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TEXT-BOOK
PRACTICAL MEDICINE
DESIGNED rOK THE TJSE OF
STUDENTS AND PRACTITIONERS OF MEDICINE
ALFRED L. LOOMIS, M.D., LL.D.,
Pbopbssob of Pathology and Practicax Medicine in the Medical Depaetilent of the UNrrEB»
siTT OF THE City of New Yobk ; Visiting Phtsician to Bellbvtts Hospital, Etc.
THIRD EDITION.
WITH TWO HUNDRED AND ELEVEN ILLUSTRATIONS
NEW YOEK
WILLIAM WOOD AND COMPANY
1885
CoPTKIfiHT, 1884,
By WILLIAM WOOD & COMPANY.
PREFACE TO FIRST EDITION.
In the preparation of a Text-book of Practical Medicine, my experience
as a medical teacher has led me to employ, quite extensively, plates illus-
trating the morbid changes and objective symptoms of disease.
The present work, both in text and illustration, is practically a revision
and an elaboration of lectures given during the past eighteen years in the
Medical Department of the University of the City of New York.
I have avoided, as far as possible, the discussion of unsettled questions,
and in order to economize space have made reference to many of these only
in brief foot-notes.
The Classification adopted is that which it has been my custom to fol-
low in teaching, and is based on our present knowledge of the etiology of
disease.
It is well known that many diseases present very different types in differ-
ent countries, and I have selected for description those types commonly
observed by the American physician;
I have considered only those diseases which come strictly within the
province of Practical Medicine, and have endeavored to indicate the
treatment usually followed in this country.
The illustrations, with but few exceptions, have been made by my assist-
ant, Dr. Maurice N. Miller (Instructor in the Laboratory of Normal and
Pathological Histology, University Medical College). The microscopical
drawings were, in most instances, made from sections prepared in the Lab-
oratory by Dr. Miller, especially for this work, and they will, I believe,
aid in the appreciation of the actual morbid processes and conditions.
In the consultation of Authorities, particularly the German and French,
in the reading of the proof, and in the preparation of the Index, I have
been assisted by Dr. Leigh Hunt, Assistant Instructor in the Pathological
Laboratory of the University.
If I have failed to give credit — either in the text or in foot-notes — to
those from whom many of the facts stated have been drawn, it has been
an unintentional omission.
19 West 34th Street, New York City,
July, 1884.
PEEFACE TO THE THIRD EDITION.
Five months after the publication of this treatise the Author has been
notified by the Publishers that they are about to issue a Third Edition.
The brief period allowed for revision has given opportunity only to
correct typographical errors, and to make important verbal changes in the
text.
The Author returns his sincere acknowledgments to the profession for
the expressions of appreciation which his labors have received.
19 West 34th Street,
April 1st, 1885.
CONTENTS.
INTRODUCTION.
INFLAMMATION.
1. — Inflammation of Serous Surfaces.
2. — Inflammation of Mucous Surfaces.
(a) Croupous Inflammation of Mucous Surfaces.
(&) Diphtheritic Inflammation of Mucous Surfaces,
(c) Ulceration of Mucous Surfaces.
3. — Parenchymatous Inflammation.
4. — Interstitial Inflammation.
5. — Fate of Pus Page 1-8
SECTION I.
DISEASES OF THE RESPIEATOEY ORGANS.
DISEASES OP THE NASAL PASSAGES.
Acute Coryza. — Chronic Coryza. — Hypertrophic Nasal Cataerh. — Atrophic
Nasal Catarrh. — Oz^na 9-17
DISEASES OP THE LARYNX.
Acute Catarrhal Laryngitis. — Chronic Catarrhal Laryngitis. — Chronic
Laryngitis of Phthisis. — Chronic Laryngitis of Syphilis. — CEdema Glotti-
Dis. — Croupous Laryngitis. — Laryngeal Ulcers. — Neuroses of the Larynx.
— Tumors of the Larynx 17-41
BRONCHITIS.
Acute Catarrhal Bronchitis. — Acute Capillary Bronchitis. — Chronic Catar-
rhal Bronchitis. — Croupous or Plastic Bronchitis. — Bronchiectasis. . . 41-69
DISEASES OP THE LUNGS AND PLEURA.
Acute Lobar Pneumonia. — Lobular Pneumonia. — Interstitial Pneumonia. —
Pulmonary Hyperemia. — Pulmonary (Edema. — Pulmonary Infarction. —
Pulmonary Apoplexy,— Pulmonary Gangrene. — Pulmonary Collapse. —
VI CONTENTS.
Pulmonary Emphysema. — Parasitic Diseases. — Morbid Growths in the
Lung AND Pleura. — Pleurisy, {a) Acute. — {h) Sub-acute. — (c) Suppurative. —
(d) Adhesive. — (e) Cancer of the Pleura. — (/) Hydropneumothorax. — {g) Hydro-
thorax. — Qi) Ecemothorax.) — Pulmonary Phthisis, (a) Acute Phthisis. — (&)
Chronic Phthisis. — (c) Chronic Fibrous Phthisis. — (d) Chronic Tubercular
Phthisis Page 70-207
SECTION II.
DISEASES OF THE DIGESTIVE SYSTEM, INCLUDING DIS-
EASES OF THE LIVER, SPLEEN, AND PANCREAS.
DISEASES OP THE MOUTH.
Stomatitis, (a) Catarrhal. — (5) Follicular. — (c) Gangrenous. — {d) Ulcerative. —
Thrush. — Diseases of the Tongue, (a) Glossitis. — (J) Camcer. — Paro-
titis 208-219
DISEASES OP THE PHARYNX.
Tonsilitis. — Inflammations. — Retropharyngeal Abscess 219-224
DISEASES OP THE CESOPHAGUS.
Inflammations. — Cancer 324-227
DISEASES OF THE STOMACH.
Inflammations, (a) Acute. — (b) Sub-acute. — (c) Chronic. — {d) Phlegmonous. — Dys-
pepsia. — Cancer and Ulcer. — Neuroses. — H^matemesis. — Dilatation. 228-256
DISEASES OF THE INTESTINES.
Enteritis. — Diarrhcea. — Cholera Morbus. — Cholera Infantum. — Dysentery.
— Typhlitis and Perityphlitis. — Intestinal Ulcers. — Intestinal Hemor-
rhage. — Intestinal Obstkuction. — Waxy Degeneration. — Cancer. — Rec-
titis. — Intestinal Parasites. — Intestinal Colic. — Constipation. — Perito-
nitis. — Ascites 257-336
DISEASES OP THE LIVER.
HYPER.SMIA. {a) Active. — (5) Passive. — Inflammations, {a) Interstitial Hepatitis
or Cirrhosis. — (J) Circumscribed Hepatitis or Abscess. — (c) Diffused Hepatitis or
Acute Yellow Atrophy. — Perihepatitis. — Pylephlebitis. — Degenerations.
(a) Amyloid. — (b) Fatty. — (c) Pigmentary. — {d) Atrophic. — New Growths (a)
Cancer. — (b) Gummata. — (c) Hydatids. — (d) Tubercle. — Diseases of the Gall-
ducts and Gall-bladder. — Jaundice. — Functional Derangements 337-409
DISEASES OP THE PANCREAS.
Acute Diseases. — Degenerations. («) Fatty. — (6) Waxy. — Morbid Growths
(Cancer, Tubercle, etc.). — Cysts.— Calculi 410-413
CONTENTS. Vii
DISEASES OF THE SPLEEN.
HYPERiEMiA. — Inflammation, including Embolism and Infarction. — Htpeeteo-
PHY. — Degenerations. — Morbid Growths. — Parasites Page 413-419
SECTION III.
DISEASES OF THE HEAET, BLOOD-VESSELS, AND KID-
NEYS.
DISEASES OP THE HEART.
Pericarditis. — Endocarditis. — Valvular Lesions. — Hypertrophy. — Dilata-
tion. — Myocarditis. — Degenerations. — Atrophy. — Thrombosis. — Aneurism.
— Morbid Growths and Parasites. — Tuberculosis op the Pericardium. —
Neuroses. — Hydropericardium. — Pneumohydropekicardium. — Syphilitic
Disease of the Heart 420-510
DISEASES OF THE BLOOD-VESSELS.
DISEASES OF THE ARTERIES.
Acute Endarteritis . — Chronic Endarteritis. — Periarteritis. — Degenera-
tions, (a) Fatty. — (b) Waxy. — (c) Calcareous. — Syphilis. — Hypertrophy,
Atrophy, and Narrowing 511-535
DISEASES OF THE VEINS.
Acute Phlebitis. — Chronic Phlebitis. — Dilatation 535-539
DISEASES OF THE KIDNEYS.
THE URINE.
NoemaIj Constituents. — Urinary Sediments. — Acute Uremia 539-543
THE KIDNEYS.
BbnaXi HYPERiEMiA. — Renal HEMORRHAGE. — Bright's DISEASES, (a) Parenchy-
matous Nephritis. — (b) Interstitial Nex>hritis. — (c) Amyloid Degeneration. —
Pyelitis. — Acute Suppurative Nephritis. — Hydronephrosis. — Cystic Kid-
ney. — Renal Calculi — New Growths {Cancer, etc.). — Parasites. — Perine-
PHRiTic Abscess. — Hematuria.— Chyluria. — Cystitis .543-607
SECTION IV.
ACUTE GENEEAL DISEASES.
MIASMATIC CONTAGIOUS DISEASES.
Ttphoid Fever. — Yellow Fever. — Cholera. — Diphtheria. — Cerebro-spinai.
Meningitis. — Septic^mla.. — Pyaemia.— Erysipelas. — Acute Miliary Tuber-
culosis 609--710
Vni CONTENTS.
ACUTE CONTAGIOUS DISEASES.
Typhus Fever. — Relapsing Fever. — Small-pox. — ^Varicella. — Scarlet Fever. —
Measles. — German Measles. — Miliary Fever. — Influenza. — Whooping-
cough.— Hydrophobia Page 710-805
MALARIAL DISEASES.
Intermittent Fever. — Remittent Fever. — Continued Malarial Fever. —
Pernicious Fever. — Dengue Fever.— Chronic Malarial Infection. . . .806-856
SECTION V.
CHEONIO GENERAL DISEASES.
Rheumatism. — Gout. — Diabetes. — Anemia . — Chlorosis. — Progressive Perni-
cious Anemia. — Leucocyth^mia. — Pseudo-Leukemia. — Addison's Disease. —
Ammonemia. — Hemophilia. — Scurvy. — Purpura. — Myxcedema. — Scrofula.
— Rickets. — ^Alcoholism. — Trichinosis. — Syphilis 856-923
SECTION VL
DISEASES OF THE NERVOUS SYSTEM, INCLUDING DIS-
EASES OF THE BRAIN, SPINAL CORD AND FUNG
TIONAL NERVOUS DISEASES.
GENERAL SYMPTOMATOLOGY
Op Nervous Diseases 925-830
DISEASES OP THE BRAIN.
Cerebral Hyperemia {Active or Passive). — Cerebral Anemia. — Meningitis. —
Cerebral Thrombosis and Embolism. — Cerebral Softening. — Cerebral
Apoplexy. — Abscesses of the Brain. — Cerebral Tumors. — Sclerosis of the
Brain. — Hypertrophy of the Brain 930-990
DISEASES OP THE SPINAL CORD AND ITS MENINGES.
Spinal Hyperemia. — Spinal Meningitis. — Acute Myelitis. — Chronic Myelitis. —
Non-inflammatory Softening. — Acute Bulbar Paralysis. — Progressive
Bulbar Paralysis. — Infantile Spinal Paralysis. — Acute Spinal Paralysis
OF Adults. — Chronic Anterior Myelitis. — Progressive Muscular Atrophy.
— Cerebro-spinal Sclerosis. — Locomotor Ataxia. — Spasmodic Tabes Dor-
SALis. — Amyotrophic Lateral Sclerosis. — Pseudo-Hypertrophic Paraly-
sis.— Spinal Apoplexy 990-1034
CONTENTS. IX
FUNCTIONAL DISEASES OF THE NERVOUS SYSTEM.
Epilepsy. — Htstebia. — Hystebo-Epilepsy. — Catalepsy. — Neurasthenia. —
Chorea.— Sunstroke. — Spinal Irritation. — Tetanus. — Facial Paralysis. —
Paralysis Agitans. — Localized Spasm and Paralysis. — Chronic Lead
Poisoning. — Chronic Mercublalism. — Vertigo. — Neuralgia. — Megrim. —
Eclampsia. — Sea-sickness Page 1034-1079
LIST OF ILLUSTEATIONS.
Fie. Paob
1. Inflammation of omentum i. 3
2. Epithelium and pus cells from serous inflammation 3
3. Inflammation of a serous membrane 5
4. Inflammation of a mucous membrane 6
5. Diphtheritic inflammation of a mucous surface 7
6. Membrane and exudation in croupous laryngitis 28
7. Position of vocal cords in the dift'erent forms of laryngeal paralysis 36
8. Multiple papilloma of the right vocal cord 39
9. The trachea laid open showing same tumor as seen in Pig. 8 39
10. Morbid anatomy of acute catarrhal bronchitis 42
11. Physical signs of bronchitis 44
12. Bronchial wall in chronic catarrhal bronchitis 50
13. Various forms of bronchiectasis 56
14. Mould of bronchi in sputum of plastic bronchitis 58
15. Morbid anatomy of first stage of acute lobar pneumonia 70
16. Morbid anatomy of second stage of acute lobar pneumonia 71
17. Morbid anatomy of second stage of pleuro-pneumonia 72
18. Morbid anatomy of third stage of acute lobar pneumonia 73
19. Morbid anatomy of purulent infiltration 75
20. Temperature record in acute lobar pneumonia in an adult 82
21. Temperature record in acute lobar pneumonia, observations every sis hours. . 83
22. Temperature record in acute lobar pneumonia ending in purulent infiltration. 84
23. Physical signs of the three stages of acute lobar pneumonia 91
24. Morbid anatomy of lobular pneumonia 102
25. Temperature record in lobular pneumonia in a child 104
26. Morbid anatomy of interstitial pneumonia 109
27. Morbid anatomy of brown induration of the lung 115
28. Hemorrhagic infarctions 121
29. Morbid anatomy of emphysema of the lung 132
30. Cancer of lung ~ 140
31. Hydatids of lung 145
32. Temperature record in acute pleurisy 147
33. Physical signs in acute pleurisy with a small amount of effusion 148
34. Physical signs in pleurisy with effusion 154
35. Physical signs of hydropneumothorax 167
36. Acute phthisis ; alveolus filled with fibrin and cells 173
37. Acute phthisis ; alveolus filled with cells 173
38. Coagulation -necrosis in acute phthisis 174
39. Tubercle bacilli from phthisical sputum 175
40. Temperature record in a case of acute phthisis 176
41. Morbid anatomy of chronic catarrhal phthisis 179
42. Lung cavity 180
43 . Chronic fibrous phthisis 181
44. Morbid anatomy of anthracosis 182
xii LIST OF ILLUSTRATIONS.
Fl3. PABE
45. Chronic tubercular phthisis, with miliary tubercles 183
46. Chronic tubercular phthisis showing tubercular nodule 184
47. Physical signs of iirst stage of chronic phthisis. 194
48. Physical signs of cavities in third stage of chronic phthisis 195
49. Oidium albicans 213
50. Stricture of the oesophagus 225
51. Stomach wall in sub-acute gastritis 230
52. Mucous membrane and stomach-tubules in chronic gastritis 233
53. Sarcinge ventriculi from vomit of chronic gastritis 234
54. Cancer of pyloric end of stomach 242
55. Perforating ulcer of stomach 247
56. Dilatation of stomach 255
57. Acute enteritis, small intestine near ileum 257
58. Acute follicular enteritis ; transverse colon showing ulceration 258
59. First stage of acute dysentery 272
60. Second stage of acute dysentery 273
61. Temperature record in acute dysentery 275
62. Tubercular ulcers; ileum 286
63. Intussusception (intestinal obstruction) 290
64. Head of taenia solium (tape-worm) 307
65. Mature segment of taenia solium 307
66. Head of taenia saginata 308
67. Oxyuris vermicularis with ovum; and ascaris lumbrieoides 3l9
68. Passive hepatic hyperaemia 340
69. Interstitial hepatitis 343
70. Interstitial hepatitis, same as Fig. 69: more highly magnified 344
71. Circumscribed suppurative hepatitis (pyaemic abscesses) 350
72. Cells from a lobule in acute yellow atrophy of the liver 356
73. Amyloid degeneration of the liver 367
74. Three intralobular zones ; waxy, fatty and pigment degenerations of the liver. 368
75. Chronic atrophy of the liver 371
76. Fatty infiltration of the liver 373
77. Fatty degeneration of the liver 373
78. Pigmentary degeneration of the liver 375
79. Same as Fig. 78: more highly magnified 376
80. Cancer of the liver 379
81. Diagrammatic enlargements of liver 381
82. Hydatids of liver : budding vesicles 385
83. Hydatids of liver : head of echinocoecus 387
84. Gall-bladder filled with calculi 401
85. Section of a large gall-stone showing layers 403
86. Crystals of cholesterin 403
87. Areas of splenic enlargement as shown by percussion 416
88. Morbid anatomy and physical signs of sero-plastie pericarditis 431
89. Physical signs of pericarditis with eifusion 435
90. Changes in mitral valve in diphtheritic endocarditis 431
91. Changes in aortic valves in diphtheritic endocarditis 433
93. Section of aortic valve in acute endocarditis 438
93. Diagram showing mode of production of cardiac murmurs 443
94. Diagram showing area of cardiac murmurs 444
95. Vegetations on aortic valves in aortic obstruction 445
96. Sphygmographic tracing of pulse in aortic obstruction 446
97. Morbid anatomy of aortic insufficiency 448
98. Sphygmographic ti-acing of pulse in aortic regurgitation 450
99. Morbid anatomy of mitral stenosis 453
LIST OF ILLUSTRATI0K8. Xlll
Fig. Page
100. Mitral orifice showing button-hole slit in stenosis 454
101. Sphygmographic tracing of pulse in mitral stenosis 455
102. View of left heart in mitral regurgitation 458
103. Sphygmographic tracing of pulse in mitral regurgitation 460
104. Physical signs in left ventricular hypertrophy 477
105. Physical signs in right ventricular hypertrophy . 477
106. Section of heart wall in acute myocarditis 487
107. Teased fibres of heart-muscle in fatty degeneration of the heart 491
108. Muscle-fibres showing fatty infiltration of the heart. ... 492
109. Chronic endarteritis : " atheroma " 513
110. Diagrammatic representation of formation of thrombi and emboli _ 516
111. Re-establishment of circulation by anastomosis after embolism 518
112. Morbid anatomy of spontaneous arterial aneurism 520
113. Hippuric acid 530
114. Fat globules from chylous urine 531
115. Leucin and tyrosin 531
116. Uric acid crystals 532
117. Urate of soda 532
118. Urate of ammonia crystals 532
119. Oxalate of calcium crystals 533
120. Ammonio-magnesian, or triple phosphate 533
121. Phosphate of calcium 533
122. Cystine 534
123. Epithelium from urinary deposits 534
124. Blood in the urine 535
125. Pus in the urine 535
126. Epithelial casts in the urine 536
127. Hyaline casts in the urine 536
128. Granular casts in the urine 536
129. Fatty casts in the urine 536
130. Blood casts in the urine 536
131. Spermatozoa in the urine 537
132. Torula cerevisise ; penicilium glaucum ; and sarcinae ventriculi 537
133. Section from Malpighian pyramid in passive renal hypersemia 544
134. Hemorrhage from vascular tuft of a glomerulus in renal hemorrhage 548
135. Renal hemorrhage and renal infarction 549
136. Cortex of kidney showing cloudy swelling in acute Bright's disease 553
137. Cortex of kidney showing advanced degenerative changes in acute Bright's
disease 554
138. Cortex of kidney in chronic parenchymatous nephritis 563
139. Cortex of kidney in early cirrhotic Bright's 569
140. Cortex of kidney in advanced cirrhotic Bright's 570
141. Cortex of kidney showing commencing waxy changes 575
142. Medullary portion of kidney showing advanced amyloid change 576
143. Arterio-capillary fibrosis : two glomeruli from the cortex of a contracted kidney. 585
144. Longitudinal section of cystic kidney 592
145. A cyst of the kidney: epithelial lining shown 592
146. Renal calculi : an embedded mulberry calculus 593
147. Mucous surface of ileum in first week of typhoid fever 615
148. Mucous surface of ileum in second week of typhoid fever 616
149. Mucous surface of ileum in third week of typhoid fever 616
150. Enlarged mesenteric lymphatics in typhoid fever 617
151. Temperature record in typical (mild) typhoid fever 627
152. Temperature record in non-typical typhoid fever 628
153. Temperature record in yellow fever 655
XIV LIST OF ILLUSTRATIONS.
Fig. Page
154. Temperature record in septiesemia 695
155. Metastatic pysemic abscesses of the lung 697
156. Temperature record in pyaemia 699
157. Temperature record in a case of facial erysipelas 703
158. Temperature record in a case of acute miliary tuberculosis 708
159. Temperature record in severe typhus fever 721
160. Temperature record in a case of relapsing fever 742
161. Temperature record in a case of discrete small-pox 749
162. Temperature record in a case of confluent small-pox 753
168. Temperature record in a case of varioloid 763
164. Temperature record in a case of scarlatina 771
165. Temperature record in a case or measles 786
166. Temperature record in a ease of German measles 793
167. Temperature record in a case of influenza 798
168. Fever curve in quotidian intermittent 811
169. Fever curve in tertian intermittent 812
170. Fever curve in quartan intermittent 812
171. Section of liver from a case of remittent fever 818
172. Temperature record in remittent fever 821
178. Temperature record in a case of continued malarial fever 880
174. Temperature record in continued malarial fever. (Septic variety) 833
175. Temperature record in pernicious fever. (Comatose variety) 841
176. Temperature record in pernicious fever. (Algid variety 843
177. Temperature record in a severe case of dengue fever 850
178. Temperature record in a mild case of acute rheumatism 859
179. Temperature record in a fatal case of acute rheumatism 859
180. Deformity from articular rheumatism. (Hand) 866
181. Section of a gouty cartilage 871
182. Vertical section of a Malpighian pyramid in gouty nephritis 872
183. Deformity from gout. (Hand) 874
184. Blood from a case of leucocythsemia 891
185. Section of a leucocytheemic spleen 893
186. Encapsulated trichinte in voluntary muscle 916
187. Trichinae with calcareous deposits and degeneration of the capsule 916
188. Temperature record in the fourth week of trichinosis 917
189. Acute meningitis, showing also intact meninges 936
190. Temperature record in a case of acute meningitis 937
191. Tubercular meningitis : — tubercular deposits along blood-vessels 944
192. Temperature record in a ease of tubercular meningitis 945
193. Pachymeningitis interna. — Vertical section of skull and cerebral meninges. . . 958
194. Cerebral softening 960
195. Small blood-vessel from a focus of yellow softening. (Cerebral thrombosis and
embolism) 961
196. Cerebral apoplexy; newly formed clot in the left optic tract 964
197. Vertical section of the cerebrum 969
198. Fibroma of the cerebellum 978
199. Diagi-am showing connective-tissues of medullated nerve structure 985
200. Sclerosis of the brain 986
201. Acute myelitis .- 996
203. Chronic bulbar paralysis 1003
203. Muscle of the tongue in chronic bulbar paralysis contrasted with normal
muscle 1003
204. Section of spinal cord in early stage of infantile spinal paralysis 1006
205. Same as 204 after establishment of sclerotic process 1006
206. Teased fibres from abductor poliicis in progressive muscular atrophy 1013
LIST OF ILLUSTRATIONS. XV
Fig. Pagk
207. Sketch of a hand in progressive muscular atrophy 1013
208. Cerebro-spinal sclerosis 1015
209. Regions of degenerative changes in spinal cord. — Diagrammatic. 1018
210. Locomotor ataxia. — Section of cord in cervical region 1019
211. Spinal apoplexy : — clot in the left anterior comu 1029
A TEXT-BOOK
07
PRACTICAL MEDICINE.
INFLAMMATION.
According to the older writers the cardinal symptoms of inflammation
are pain, heat, redness and swelling, features which are more striking in
those forms of inflammation which come under the care of the surgeon than
in those which the physician is called upon to treat. As the knowledge of
tissues and processes became more detailed and complete, and as the hidden
changes underlying these grosser ones were brought to light, pathologists
sought to discover the essence of the inflammatory process, to find its cause,
and to determine in which tissues or organs th'e primary causative change
occurred. The history of the theories and definitions of inflammation is a
record of the varying importance that has been attached to one or another
of the changes observed. Into these theories, and the arguments by which
they have been in turn supported and assailed, it is not desirable here to
enter. It will be sufficient to describe the changes observed in the tissues
and to define the associated terms of which use will hereafter be made.
Hyperaemia. — Except in the non-vascular tissues, as the cornea and
cartilage, the earliest change observed is in the circulation, and this
change is manifested by a change in the color of the affected part, which
becomes red and congested. This redness is due to an increase of the
quantity of blood in the part ; at first the hyperaemia is active, that is,
blood is brought to the part and passed through the capillaries in
1
INFLAMMATIOIT.
larger quantities than before ; but it may become passive, a condition in
•which, while the quantity of blood present in the part is greater than
usual, the current is much slower, the amount which actually passes
through the capillaries in a given time being less than normal ; finally,
this retardation of the flow may end in actual arrest : stasis. That hyper-
aemia is only an accompaniment,
and not the essence, of inflammation
is shown by the fact that the hyper-
semia which is caused by section of
the sympathetic nerves is not accom-
panied by the other symptoms and
changes observed in inflammation.
Exudation. — The swelling which
has been mentioned as one of the
four cardinal symptoms is due main-
ly to the presence of a liquid infil-
trated through the tissues. This
liquid comes from the blood by
exudation through the walls of the
capillaries ; but it is not simply the
plasma or serum of the blood ; its
chemical composition is different, it
is the plasma of the blood, with the
addition of materials furnished, pre-
sumably, by the elements of the
tissues which it bathes. It is this
addition which distinguishes the
F, G. Red and^ white corpuscles from Jmrsting of liquid from the normal iuices of the
CCtDZllClTZSS
H. Exfoliated epithelium, x 300. part, or from that of oedema, and
which makes it an inflammatory exudation.
Cellular Elements. — In order to furnish these peculiar constituents to
the exudation, the cellular elements of the tissues undergo change in form
and nutrition. The chemical interchanges whicb constitute normal nu-
trition, and which are carried on between the cells of the tissues and the
liquid furnished to the cells by the blood, are modified in character or
extent, and the cells themselves are correspondingly modified in form. On
the one hand, the cells may show a tendency to return to their earlier
embryonal form, to become swollen, globular, pale and succulent, perhaps
to divide, to form new cells by proliferation ; on the other hand, the exag-
gerated activity of the cell may prove too great a strain upon it, and it dies
or becomes disabled by passage into the condition known as fatty degenera-
tion. The former of these two results is the one seen most commonly in
the connective-tissue framework and envelopes of the various parts and
organs, and the latter in the specific cells that constitute their parenchyma.
Suppuration. — Examination of fresh normal tissues shows, scattered
through them, free cells which closely resemble the colorless coi'puscles of
the blood and lymph. Like them, they possess the power of amoeboid
Fig. 1.
Inflammation of tbe Omentum.
A. Arteriole.
B. Venule.
C. Inflammatory stasis with escape of blood glob-
ules.
D. Extravasated blood corpuscles.
E. Infiltration of connective-tissue with pus coi'pus-
cles.
INFLAMMATION".
movement, of rapidly changing their shape by throwing out processes, of
moving from place to place by means of this change of form, and of multi-
plying by division. They are called " wandering cells," or leucocytes,
because of their supposed identity with the colorless corpuscles of the blood.
Under normal conditions the leucocytes contained within the blood-vessels
may occasionally be seen to pass through the unbroken wall of a capillary
by means of this power of amoeboid movement which they possess ; when
the tissue adjoining the capillary is inflamed, the number of cells -'' migrat-
ing " through its wall is notably increased. Furthermore, when a part is
inflamed the fixed corpuscles of the omnipresent connective-tissue swell,
as has been described, and give rise
by proliferation to other cells, which
cannot be distinguished morphologi-
cally from the normal wandering cells
or leucocytes. When these cells ac-
cumulate in great numbers (whether
by transformation of connective-tissue
cells or by migration from the vessels)
they constitute pus, and suppuration
is said to have occurred. The process
is accompanied by more or less de-
struction of tissue, either by the trans-
formation of the cells into pus-cells,
or by necrosis, death of the tissue
In consequence of pressure or of modi-
fication of its nutritive conditions. When the process takes place upon a
free surface it is called ulceration; when within the substance of an organ,
the collection is called an abscess.
Resolution ; Cicatrization. — The inflammatory process, as thus described,
maybe arrested at any point. If the irritation is slight or of short duration,
if the change has not progressed to the point of tissue destruction and for-
mation of pus, the withdrawal of the prim.ary cause is followed by a dimi-
nution of the swelling and congestion, and by return to the normal state ; —
this is called resolution. When, on the other hand, necrotic changes have
taken place the simple arrest of the inflammation is not sufficient, the losses
must be made good, the destruction repaired. Thi^ is cicatrization, and it
is accomplished largely by cells of the connective-tissue. As the conditions
become more favorable, the cells newly formed by proliferation no longer
remain stationary, lose their vitality, and become pus, but they progress in
the direction of a normal development and form new tissue. The irregular
pink granulations seen within a wound or upon an ulcerated surface are
formed of masses of young cells crowded with capillary loops of new forma-
tion. The cells, at first large, soft, finely granular and Juicy, become
smaller and firmer, and the intercellular substance increases and becomes
fibrous. If the inflammatory process has taken place in the interior of an
organ, involving only a small portion of tissue, and has stopped short of
the formation of a distinct collection of pus, the result of the reparative
Fig. 2.
Desquamated epithelia audpus cells from an in-
flamed serous surface, x 500.
4 I^sTFLAMMATIOIS".
process is a mass of fibrous connective-tissue, a cicatrix ; and if a collection
of pus has actually formed, but is only of small size, the pus may disappear
by liquefaction of its cellular elements and absorption. If, on the other
hand, a larger abscess has formed and has been opened, its cavity becoming
filled by the granulatiens, the same change into fibrous tissue follows, and
a cicati'ix is again the result. The same is true of ulceration of a free sur-
face, with the addition that the surface of the cicatrix is covered by a layer
of epithelium resembling more or less closely the original layer which has
been destroyed by the ulceration. When the irritation has been less active
but more prolonged, and has perhaps involved an entire organ, its effect
again appears in an increase of the connective-tissue of the part involved ;
but the consequences of this increase are most serious. The original " fixed
cells" of the connective-tissue multiply as in the other case mentioned, and
develop into fully formed tissue, and the amount of this tissae becomes in
consequence much greater than normal. In its natural evolution it retracts,
and by its quantity and its retraction it presses upon, and interferes with
the nutrition of the specific cellular elements of the organ, so that they be-
come less fit to perform their functions. This change is called induration
or cirrJiosisj common examples are cirrhosis of the liver, and '^contracted
kidney " or interstitial nephritis.
INFLAMMATIOTSr OF FREE SURFACES.
First : Serous Surfaces. — The most common form of inflammation of serous
membranes is that which results in the production of serum, fibrin, or pus,
in variable proportions ; these products may infiltrate the substance of the
inflamed membrane, be poured out upon its free or attached surface, or
collect in cavities lined by it. The first change in this inflammatory pro-
cess is in the blood-vessels, which contain more than their normal quantity
of blood, and it is from the blood circulating in the vessels that most of the
characteristic inflammatory products are derived. After the initial hyper-
gemia, the fibrinogen of the exudation comes in contact with the fibrinoplas-
tic material of the tissues (there being a ferment present), coagulation takes
place, and layers of fibrin containing few or many cells are formed on the
free surface. These layers are called pseudo-membranes, or coagulable
lymph. If the inflammation occurs in a membrane whose normal conforma-
tion makes a free effusion possible (as the pleura and peritoneum) some
serum is always present. It may be only infiltrated through the meshes of
the tissues, or it may accumulate at some point as a sero-fibrinous
collection. When leucocytes are present in great numbers the exu-
dation is fibrino-purulent. The greater the intensity of the inflammation,
and the more enfeebled the patient, the greater is the liability to pus forma-
tion. In certain serous inflammations the exudation may be hemorrhagic ;
the blood may come from a ruptured capillary vessel, or the coloring matter
of the blood corpuscle may be set free and color the exudation without
vascular lesion. Such inflammation of serous membranes may end in
necrosis or in resolution. If the inflammation is intense, and stasis occurs
INFLAMMATIOX.
throughout a wide area of tissue, it will result in necrosis. Stasis is the
expression of a higher degree of injury than that which exists in simple in-
flammation/ The intensity of the inflammation determines whether the
result shall be a return to the normal condition or a destruction of tissue.
An uncomplicated serous inflammation is neither reproductive nor infective.
It has no tendency except to stop as soon as its primary cause ceases to act.
"When resolution occurs, the emigration of leucocytes ceases, the serous
fluid disappears, and the fibrin and the cell elements, after they have
undergone molecular change, are absorbed.
A second variety of inflammation of serous membrane is characterized by
the production of new connective-tissue cells either with or without a sero-
purulent exudation. It
may be an acute or chronic
process. The inflamed
membrane becomes
thickened, and there is
abundant cell develop-
ment in its substance and
on its surface. These cells
are not pus-cells, but are
embryonic cells from the
fixed cells of the tissue.
If the inflammatory proc-
ess is prolonged, or if the
membrane becomes very
much thickened, eleva-
tions are formed on the
surface of the membrane,
and thus adhesion takes
place between opposing
serous surfaces, or the
membrane becomes thick-
ened and indurated. If
bands of adhesion form,
they have the appearance of delicate membranes. This new tissue at first
is exceedingly rich in capillary vessels, which are distinguished from the
normal capillaries of the membrane by their large calibre and thin walls.
As the new tissue contracts, it may shut oS its own blood supply, and then
undergo fatty change and be absorbed, leaving no trace of its existence.
Second ; Mucous Surfaces. — Inflammation affecting mucous membranes
may be either catarrhal or croupous. Catarrhal mucous inflammations are
either acute, sub-acute, or chronic. In the acute variety the affected
Fig. 3.
Inflammation of Serous Membrane.
Viriical section of irijlanud diajjhragmatic ■pleura.
A. Free S'irface coTered wilh jihnnoiis exudation.
B. EndotJuTial layer with cdh chanqerl an'! displaced; at (a) t?ie
cells are seen- detached, icithin the exudation.
C. Sub-endothelial tissue loith nvmerous and enlarged blood-
vessels, d d d.
e ee. Lyiiiph spaces, x 250. After Thi&rf elder.
1 If inflammation is an arrest of function, and ?)(7/ diversion of agents of nutrition into new channels of
activity, restoration of a part to the natural state must he as simple as its departure from it, and resolution
of inflammation means, either that tlie temporarily arrested process goes on again, or if the process has
proceeded to its ultimate issue (deatli of the affected part), that the destroyed part has to be repaired, not
by a continuation of the morbid process, but simply by the restitution of the normal condition.
INFLAMMATION".
mucous membrane, at the very beginning of the process, is congested and
drier than normal, the functional activity of the mucous glands being di-
minished. After a time an abnormal quantity of mucus is poured out on
its surface, the result of an increase in the functional activity of the glands.
This mucus may be thicker or thinner than normal, and may have an acrid
or irritating quality. Mucous exudations do not coagulate, but adhere
somewhat closely to the surface of the inflamed membrane ; these changes
are accompanied by desquamation of the superficial epithelial cells. If the
catarrh assumes a purulent character in addition to the above changes, the
mucous surface assumes a darker and livid hue, and pus-cells are developed
both in the mucous membrane and in the deeper substance. The amount
of pus will indicate the intensity and character of the inflammation. In
some cases there are very few pus-cells, in others the quantity of pus is very
large, and the tissues are extensive-
ly infiltrated , with them. In
chronic catarrh the blood-vessels
of the inflamed membrane are
either increased in size and num-
ber, or they are less numerous and
more swollen than normal, giving
to the membrane a grayish appear-
ance. The production of mucus
will be increased or diminished,
according as the functional activity
of the mucous glands is increased
or diminished. When it is dimin-
ished, the membrane assumes a
"^ dry and shining appearance. The
■^ stroma of the affected membrane
may be hypertrophied or atro-
phied. The mucous glands may
also undergo hypertrophy or at-
rophy. If their ducts become ob-
structed they may suffer cystic
change : superficial erosions some-
Veriical section of nasal se2)timu ,. „ ^ , ■/] "^-i
a. Pi/swrpvsdes and degenerating epithelium on the timeS OCCUr irom a rapid, epitne-
/; ee svrface-
b. Superficial layers of epithelium.
c- Svb-epHliehal tissue.
In the submucous tissue beneath the last ivill be seen —
//. !7 0- Longitudinal and transversely divided arteries,
increased in number and size.
li h. Veins.
i i. Portions of enlarged mucous glands,
jj. Gland ducts.
A portion of the cartilage of nasal sej)tum is seen at (d),
with its ijerichrondrium (e). ' x 800. After Thierf elder.
FiCx. 4.
Inflammation of Mucous Membrane.
lial desquamation.
Croupous Inflammation of Mucous
Membranes. — In croupous inflam-
mation, the hypersemia is more
intense than in catarrhal, so that
the mucous surface usually assumes
a dark livid color and becomes
swollen ; soon its free surface is covered with a fibrinous exudation, which
takes the place of the epithelium, and lies upon the subepithelial structures
in the form of a network or in irregular masses. Enclosed in its meshes
are epithelial and pus-cells ; it varies in thickness from an exceedingly
IISTFLAMMATION".
thin semi-transparent membrane to one that may be an eighth of an inch
in thickness. This membranous exudation may be limited to small
patches, or extend over a large surface. At first it is firm in consistency
and adheres closely to the tissues which it covers ; afterward it becomes
soft, and is easily separated from the subjacent membrane ; when fully
formed it may be cast off in patches or shreds. Its separation is accom-
plished by the returning secretion of the follicles, which have been ob-
structed, as well as by the serous effusion from the inflamed surface. It
may sometimes undergo fatty, and more rarely a mucous degeneration, and
so become a fluid resembling mucus. Generally in simple croupous in-
flammation the submucous tissue is but slightly involved, and its meshes
are rarely infiltrated.
Diphtheritic Inflammation of Mucous Surfaces. — By some this is regarded as
identical in character with croupous. It differs from it in a more intense
hypersemia, and a more extensive infiltration of the affected tissue. The
fibrinous exudation is more abundant and granular, and there is a greater
metamorphosis of the epithelial and tissue cells. The membranous exuda-
tion seems to be a part of the mucous and sub-mucous tissues, and cannot
be removed without the loss of their substance. In the surface exudation,
and in the infiltrated tissues underlying it, are found multitudes of bacteria,
especially the micrococci. When the mucous and sub-mucous tissues are
so infiltrated as to cause undue pressure, and to cut off their nutritive sup-
ply> the affected tissue dies and sloughs away. Between simple croupous
and diphtheritic exudation
there is every possible
gradation. Some claim
that the fibrinous degen-
eration of the epithelium
cells is the source of the
diphtheritic exudation ;
nearly all agree that the
primary changes are epi-
thelial. This form of
inflammation mnst be re-
garded as the local expres-
sion of a constitutional
affection.
■Ulceration of Mucous Sur-
faces. — Necrotic processes
may be the result of intense
purulent catarrhs or diph-
theritic inflammations of
mucous surfaces. Super-
ficial loss of substance from
rapid epithelial degeneration, and ulcers formed by the bursting of small ab-
scesses are the chief varieties of necrosis, except in those catarrhal inflamma-
tions where the blood supply is so suddenly and completely shut off that
1 -^r?v3?!'.-;*
somewhat increased in frequency, and there is a sensation of constriction
with oppressed breathing which may be somewhat laborious, but there if
no evident dyspnoea. The cough, an essential feature of the disease, a*
first is dry and hacking, sometimes incessant, especially on lying down, and
on waking after a long sleep ; it may be paroxysmal in character. After
one or two days the cough becomes loose, and is attended with an expec-
toration of frothy mucus, of a yel-
lowish color and a saline taste ;
gradually this becomes muco-puru-
lent and even purulent. As soon as
^^ the expectoration becomes free the
'_Jj' patient is relieved. The disease
lasts from four or five days to two
or three weeks, and ends in complete
recovery or in chronic bronchitis.
Physical Signs. — In slight attacks
of acute bronchial catarrh of the
larger tubes, there may be no physi-
cal signs to indicate its existence.
The severer forms are attended by
easily recognized physical signs.
As a rule, inspection and palpation
give negative results. ^\\q percus-
sion sounds are normal, unless there is a very considerable accumulation of
mucus in the bronchial tubes ; in such cases, the normal resonance is dimin-
ished posteriorly in the infra-scapular region. On auscultation over the
Sibilant rales
Subcrepitant rales
Fib. 11.
Diagram illustrating the Physical Sign? of Bronchitis.
ACUTE CATAERHAL BRONCHITIS, 45
affected tubes, the respiratory murmur is feeble, temporarily suppressed, or
sonorous in character. In the dry stage, sibilant and sonorous rales may
be heard on both sides over the whole chest, more distinctly posteriorly. In
the stage of secretion with the sibilant and sonorous rdles, moist rales, large
and small in size, are heard on both sides of the chest. These rales are in-
constant, coming and going, and changing their situation ; after a violent
fit of coughing, they may entirely disappear for a time. When they are
abundant and very loud, they often altogether mask the respiratory mur-
mur. When the secretion is watery, they have a " rattling " sound. In
some cases, secretion takes place so rapidly that moist rales are heard from
the first. Vocal resonance in bronchitis is normal.
DifiFerential Diagnosis. — It is hardly possible to confound bronchitis of the
large tubes with any other pulmonary affection. The absence of lancina-
ting pains in either side, the bronchial character of the cough and expec-
toration, the coryza and hoarseness which precede the attack, are usually
suflBcient to distinguish it from pneumonia and pleurisy ; besides, its
physical signs, if properly appreciated, render the diagnosis easy and
positive in all cases. The early stage of whooping-cough may be con-
founded with it, until the characteristic cough is heard.
Prognosis. — This form of bronchitis, unless it occurs in the very young,
or very old and feeble," never directly destroys life. It usually terminates
by resolution in from three to four days to two or three weeks ; some-
times it becomes chronic : in such cases the inflammation is likely to
extend into some of the smaller tubes, giving rise to circumscribed capillary
bronchitis.
Treatment. — In the majority of cases, this form of bronchitis is easily
managed. In mild attacks the patient is not sufficiently ill to consult a
physician ; it is simply regarded as a severe cold. At the onset, while the
coryza is present, it may generally be arrested by a Dover's or Tully's pow-
der and a warm bath at night, followed in the morning by a brisk saline
purge — in the case of children by a full dose of castor oil. The patient
should remain in a warm, moist, equable temperature for a day or two.
gr. XX. of quinine or of salicylic acid acts oftentimes as an abortive in
adults. If this plan has not been resorted to, or has not proved successful,
then moderate but continued action of the skin and kidneys should be in-
duced by the administration of mild diaphoretics and diuretics, the patient
remaining in a warm, even temperature. In the early stage of the disease,
especially in the case of children, great benefit is often derived from steam
inhalations. Counter-irritation, by means of cups and mustard sinapisms,
to the upper part of the chest, is of great service in its late as well as in its
early stages. If the disease shows a tendency to pass into the chronic
stage, or to extend into the smaller tubes, from eight to ten grains of
the sulphate of quinine should be daily administered ; in children, cod-
liver oil with lime-water should be given. A succession of small blisters
applied to the posterior portion of the chest will be of service after the
acute stage is past. When simple bronchitis occurs in those of a gouty
or rheumatic diathesis, colchicum must be given in connection with alkalies.
46 DISEASES OF THE KESPIEATOKT OKGANS.
ACUTE CAPILLAET BRONCHITIS.
When acute catarrhal inflammation invades the small-sized bronchia!
tubes, it is termed capillary bronchitis. It is also known as " catarrhus
senilis," bastard pleurisy, and suffocative catarrh. In most instances, this
form is an extension of simple bronchitis, whose characteristic symptoms
have preceded ; but sometimes the smaller as well as the larger bronchial
tubes are affected, or the smaller bronchi may be the primary seat of the
inflam^matory process. General capillary bronchitis is much more fre-
quently met with in infancy and old age than during any other periods of
life. If the inflammation is limited, and only a few of the smaller tubes
are involved, it is called localized capillary bronchitis ; but when the bron-
chial inflammation is intense, and diffused over the lining membrane of
all the bronchial tubes, it is termed general capillary bronchitis. In the
symptoms which attend its development, and in its tendency to destroy
life, it differs very much from bronchitis of the larger tubes. The morbid
anatomy of this form of bronchitis has been already sufficiently described;
but its symptomatology, prognosis, and treatment require separate consid-
eration. The causes which give rise to capillary bronchitis are similar to
those which have been named in connection with the etiology of simple
bronchitis, except in those instances where it occurs as a secondary affection.
The danger from acute catarrhal inflammation of the smaller tubes in pa-
tients with Bright's disease, typhus fever, measles, and the chronic bron-
chitis of old age, should never be lost sight of. Some of the worst cases
are met with in connection with emphysema of the lungs.
Symptoms. — The milder types of this form of bronchitis are usually pre-
ceded by inflammation of the larger tubes, and the symptoms of invasion
are not marked. In fact, the capillary element of the disease might not be
recognized, were it not for its physical signs, and difficult or labored respi-
ration. On the other hand, the severe forms may be ushered in by distinct
chills, high febrile excitement, and great dyspnoea. The patient is unable
to lie down on account of the difficulty of breathing, and the countenance
is anxious and flushed. Paroxysmal orthopncea is not uncommon. The
respirations are accelerated, reaching 60 and 70 in a minute, attended by
great muscular effort. The pulse is feeble, beating from 100 to 130 in a
minute. The axillary temperature is raised to 103° F., but as the disease
advances it may fall to 100° F., although the pulse and respiration remain
frequent. The patient, at the commencement of the attack, has an inces-
sant hacking cough, which is often so violent as to compel him to sit up,
bend forward, and hold his sides. At first, there is little if any expectora-
tion ; if expectoration is present, it is a thick, tenacious mucus ; later, it
becomes more abundant and less tenacious. So viscid and tough is the ex-
pectorated material, that cast-like masses of the bronchioles may be formed.
When some of the sputa is put in water, the froth floats and is connected
by filaments with the heavier masses underneath the surface. The cough
may be accompanied by a rattling sound in the trachea. There is great
ACUTE CAPILLARY BEONCHITIS. 47
exhaustion. If the disease progresses, all the phenomena of deficient oxy-
genation are developed. The face betokens great distress and has a livid
aspect, the lips become blue, and there is blueness of the finger-ends, with
fulness of the jugular veins. The respiratory acts become more and more
labored and imperfect, the expectoration becomes more and more abun-
dant, and the matter expectorated thin, frothy, and less tenacious. There
is great restlessness, with signs of impending suffocation, and the surface
of the body is covered with a cold, clammy sweat. As death approaches,
the pulse becomes small and thready, the respiratory efforts are less violent
and. less frequent, muttering delirium comes on, or the patient lies in a
state of partial coma, both cough and expectoration cease, and he dies
asphyxiated. These symptoms vary somewhat with the age and peculiari-
ties of the individual affected, and with the diseases which it may com-
plicate. In aged persons, or in those who are constitutionally weak from
any cause, the fever is very apt to take on an adynamic type. When it
occurs in connection with acute blood diseases, it is likely to come on very
insidiously, without any of its usual symptoms being prominent. ■
Physical Signs. — In addition to the signs belonging to simple bronchitis,
the percussion sound in the early part of the disease may be somewhat
exaggerated in the infraclavicular regions, the percussion resonance may
be diminished on account of the attendant pulmonary oedema, and the
accumulation of morbid products in the small bronchi. While resonance
is diminished in the lower portions, the superior portions of the lung may
give an emphysematoas percussion note.
Auscultation. — If the bronchitis is extensive, the vesicular murmur over
both lungs is feeble or suppressed, and the inspiration may be masked by
high-pitched, hissing, sibilant rales ; as the disease advances the subcrepi-
tant distinctive rale of capillary bronchitis is heard all over the chest, but es-
pecially in the infra-scapular region. {See Fig. 11. ) If the subcrepitant rales
are abundant and are heard over the whole chest, they indicate very positively
the existence of a general capillary bronchitis. These rales may be present
over circumscribed spaces posteriorly, as the result of the gravitation of the
fluid secretion from the larger into the smaller tubes. If they are confined
to the apex or base of one lung, with resonance on jDercussion, they indicate
the existence of a localized capillary bronchitis.
Differential Diagnosis. — Capillary bronchitis may be confounded with 'pneu-
monia, pulmonary oedema, and phthisis. It differs from simple bronchi-
tis in the higher temperature, greater frequency of the respiration, the ex-
treme dyspnoea, the interference with the general capillary circulation, and the
presence of the hissing, sibilant, and subcrepitant rales. It is distinguished
from 'pneumonia by the absence of pain in the side, prolonged initial chill,
and the characteristic pneumonic sputa, by the greater frequency and labor
of respiration, and the more intense dyspnoea, by its lower temperature, by
the normal or exaggerated resonance on percussion, by the presence of the
subcrepitant rales on loth sides of the chest, and by the absence of bronchial
breathing and of increase in the vocal fremitus. The points of differential
diagnosis between capillary bronchitis and phthisis will be considered
48 DISEASES OF THE EESPIRATORY ORGANS.
under the latter head. The existence of the physical signs of capillary
bronchitis at the apex of one lung, accompanied by evidence of pulmon-
ary consolidation at that point, always leads to the suspicion of incipient
phthisis. The physical signs, pyrexia, and history of the patient will suf-
fice to distinguish it from asthma.
Prognosis. — General capillary bronchitis is a disease attended with great
danger, especially when it occurs in infancy or old age, or when it super-
venes upon some grave organic disease, as phthisis, Bright's, heart disease,
and acute blood diseases. When it occurs in persons suffering from pul-
monary emphysema, although for a time the symptoms are urgent, it rarely
proves fatal. It usually lasts from three to five days ; but when very exten-
sive may prove fatal in twelve hours. Among the unfavorable symptoms
may be named great difficulty of expectoration, shallow breathing, cessa-
tion of cough, urgent dyspnoea with evidences of incipient asphyxia, and
the presence of adynamic symptoms. In this disease, death results from
asphyxia caused by imperfect oxygenation of the blood.
Treatment. — All the so-called antiphlogistic remedies lessen, if they do
not destroy, the chances of recovery. From the commencement of the
attack, the treatment must be supporting. In general capillary bronchitis,
the patient must be kept in bed, the surface of the body covered with flan-
nel, the temperature of the apartment must range from 75° to 80° F. and the
air must be moistened with steam. Children should be placed in the steam
tent, as advised in the treatment of membranous croup. Dry cups should
be applied over the whole surface of the chest, after which it should be
covered with an oil-silk jacket. The inhalation of steam usually increases
the bronchial secretion, facilitates expectoration, and for a time, at least,
relieves the difficult breathing. If symptoms of imperfect oxygenation
are developed, the inhalation of oxygen gas in connection with the steam
will often afford the most marked relief. The internal administration of
muriate of ammonia, or chlorate of potash in five or ten grain doses every
two hours to the adult (two grains may be given to a child two years of
age), often seems to have a controlling influence over the inflammatory
processes. Iodide of potassium is of benefit in children threatened with
atelectasis and lobular pneumonia. The so-called expectorants are of little
service. Sometimes, when suffocation is imminent and the power of ex-
pectoration is entirely lost, stimulating emetics will be found of service,
especially in very young children ; the action of the emetic seems to sup-
ply the want of voluntary power to expectorate, and it dislodges the accu-
mulated secretion in the bronchial tubes ; care must be taken not to repeat
emesis so often as to produce exhaustion.
In the advanced stage of the disease, when the pulse becomes small and
thready, quinine and stimulants must be freely administered. The chief
object of treatment in this disease is to sustain the life of the patient until
the inflammatory process has passed through its different stages. As re-
gards the use of stimulants, there is no disease (especially of childhood) in
which their judicious use is so markedly beneficial. They should be
commenced early, and given in sufficiently large quantities to overcome the
CHRONIC CATARRHAL BRONCHITIS. 49
Bigns of exhaustion, which are present very early. To allay spasm of the
bronchial tubes, which is occasionally present in this form of bronchitis,
and gives rise to the most distressing paroxysms of dyspnoea, full doses of
hydrocyanic acid may be given, and this is often followed by most marked
relief. Opium should never be given, for by its action the power of expec-
toration is often diminished, and it favors the dangerous accumulation of
inflammatory products in the bronchial tubes. Each case should be stud-
ied by itself, with attention to the constitutional conditions under which
it occurs, and the treatment should be so modified as to meet the indica-
tions. The general management of capillary bronchitis associated with
Bright's disease is very different from that of capillary bronchitis occur-
ring in a person previously healthy. During the whole course of the dis-
ease when this complication is present the patient should receive the largest
possible amount of concentrated nutrition — the yolk of eggs and milk are
generally well borne by this class of patients. Precaution must be taken
against the slightest exposure to changes in temperature during convales-
cence.
There are certain peculiarities which attend the capillary bronchitis of
young children. It differs from the bronchitis of adults in the greater
liability to extension of the bronchial inflammation to the alveoli, with
consequent lobular pneumonia; also, in the liability to the occurrence of
atelectasis or collapse of the lobules, the result of the plugging up of the
small bronchi by accumulation of secretion in them, with intense swelling
of the mucous membrane. The occurrence of lobular atelectasis cannot
be determined with certainty either by the rational or physical signs. It
may be suspected in young children whenever physical signs indicative of
extensive capillary bronchitis are associated with extreme dysj^noea and evi-
dence of defective oxygenation of the blood, the physical signs and other
symptoms of broncho-pneumonia being absent. The development of lobu-
lar pneumonia is certain to follow lobular atelectasis, if the life of the pa-
tient is sufficiently prolonged after the occurrence of the latter. In the
treatment of bronchitis of young children, the liability to these complica-
tions should always be borne in mind.
CHRONIC CATAEEHAL BEONCHITIS.
This is a very common disease, and results from any cause which excites
and keeps up a low grade of inflammation of the bronchial mucous mem-
brane. It is usually a disease of adult life. One of its chief characteristics
is its tendency to recurrence ; the attacks increase in severity and duration
at each return, until the individual is rarelyfree from it. Chronic bronchitis
may hQ primary ov secondary. Primary, when it is the result of exposure
to wet or cold, or when it is excited by the daily inhalation of dust, vapors,
or other irritating substances. Secondary, when due to some constitutional
vice, as gout, rheumatism, syphilis, etc.; or some local affection, as cardiac
or renal disease. It may occur as a complication of other pulmonary affec-
tions, as phthisis, pulmonary emphysema, etc.
4
50
DISEASES OF THE KESPIRATOET ORGANS.
Morbid Anatomy. — As in acute broncliitis, any portion of the bronchial
and tracheal membrane may be the seat of the inflammatory action. Thus
it may be limited to the large bronchi, or it may extend into the capillary
tubes. Usually, the inflamed membrane has a slaty, reddish blue, or even
a violet color. In the more chronic cases, its tissue is frequently hyper-
trophied, its glands are enlarged and prominent, and their ducts so in-
creased in size that their mouths are readily visible. The mucus secreted
may be in transparent gelatinous masses and small in quantity, it may be
muco-purulent, or a serous fluid may be exuded in great abundance. As a
rather infrequent occurrence, the
surface of the membrane |)resents an
uneven appearance, due to the pres-
ence of little villosities covered by
normal epithelium ; occasionally fol-
licular ulcerations are met with.
These papillary excrescences and
ulcerations are usually arranged lon-
gitudinally. In the early stage, the
other coats of the bronchial tubes
may be weak or yielding ; later, an
increase in connective-tissue takes
place, leading to thickening and in-
duration. The cartilages are some-
times normal, at other times hyper-
trophied, and at times calcified. In
the posterior wall of the trachea and
e-.'
Fig. 13.
Transverse Section of Bronchial Wall in Chronic
Catarrhal Bronchitis.
A. Epithelium covered with mucus and pus.
B. Internal elastic coat.
C. Muscular layer- On the right an erilarged duct is
seen piercing the last two coats.
D.-Sufymucous tissue containing hypertrophied carti- ,, , , -, . ,. » , ,
lage, increased connective-tissue, enlarged glands the larger bronchl, Separation 01 the
and vessels, x 250. i j^i i i j.- «
muscular nbres, and relaxation oi
the bronchial wall occur, with a protrusion of the mucous membrane
through fissures in its middle coat. These diverticuli may involve a large
or small extent of the posterior bronchial wall. The submucous coat shows
increase in connective-tissue. In very old subjects the ultimate bronchi
may be changed into calcified cylinders, each with a minute canal running
ihrough it.
In very chronic cases, where there has been a puriform secretion for a
long time, the bronchial mucous membrane not infrequently presents
slight, or no apparent alteration. The results of chronic bronchitis are
dilatation and stenosis of the bronchial tubes, an accumulation of secre-
tion in a state of cheesy degeneration more or less obstructing their
calibre, pulmonary emphysema, and induration of lung tissue adjacent
to the inflamed bronchi. Ulcerations of the bronchial membrane rarely
occur ; if present they are slight and superficial, and for the most part
are found in the bronchitis which accompanies phthisis. In old age
deep ulcers may be formed, and fistulous communications may be estab-
lished with the oesophagus, aorta, pleural cavity, large blood-vessels, pul-
monary parenchyma, or, very rarely, externally. In tertiary syphilis,
(chronic bronchitis may be accompanied by gummy tumors of the mucous
CHEONIC CATARKHAL BROJTCHITIS. 51
membrane of the trachea and primary bronchi, or by a fibrous induration
which leads to stenosis.
Fetid Bronchitis. — An excessively fetid order of the breath and of the
matter expectorated in the course of a chronic bronchitis, may find no ex-
planation after death, except decomposition of the accumulated bronchial
secretion. This decomposition usually takes place in bronchial dilatations ;
it may arise independently of any bronchial dilatation. It is claimed that
germs, usually atmospheric, enter, and, lodging in a cavity, cause putres-
cence. This decomposition of the secretion may exert no special injurious
influence, or it may give rise to gangrene of the bronchial mucous mem-
brane, and may thus involve the adjacent lung tissue, causing more or less
extensive gangrene of the lungs. About the tubes the characteristic
changes of peribronchitis are nearly always found ; these changes are best
marked at the periphery of the lung. The changes that take place in the
small bronchi, in that form of bronchial catarrh which accompanies
phthisis, will be considered under the head of phthisis.
Etiology. — The most interesting part of the history of chronic catarrhal
bronchitis is its etiology. When primart/, it arises almost always from ex-
ternal causes ; such as exposure to cold and wet, the inhalation of dust or
unwholesome air. It is unquestionably the exception for chronic bronchi-
tis to be developed from exposure to what are termed the ordinary causes
of ''taking cold," without some special predisposition, such as long-contin-
ued mechanical irritation of the bronchial membrane, constitutional vice,
or some previously existing organic disease. Acute bronchitis may fre-
quently be the result of some temporary exposure, but if it becomes chronic,
there will almost invariably be found to exist a predisposing cause. Bron-
chial irritation may exist, perhaps for years, as the result of some mechan-
ical irritation (as in the case of stone-cutters, grain-heavers, etc.), and not
particularly inconvenience the individual, until an acute catarrh is devel-
oped from exposure ; this invariably becomes chronic, and sooner or later
leads to the develojament of broncho-pneumonia, and a condition called
knife-grinders' or stone-cutters' phthisis follows.
Secondary/ chronic bronchitis, or that which arises from some previously
existing acquired or congenital dyscrasia, is of more frequent occurrence.
An hereditary tendency to gout frequently manifests itself in a form of
chronic bronchitis. Sometimes in the same individual attacks of bronchitis
and gout alternate. In some instances the gouty diathesis only produces a
strong predisposition to bronchitis, which requires for its development some
external exciting cause much slighter than would produce the disease in
health ; in other instances, there is for a long time a slight bronchial ca-
tarrh, which, as life advances, slowly merges into chronic. 'Not infre-
quently chronic bronchitis occurs in connection with psoriasis and eczema,
and these affections alternate one with the other ; as one disappears the other
manifests itself ; under such circumstances it seems evident that these dif-
ferent affections are manifestations of the same constitutional vice. Pul-
monary emphysema is produced in many instances by chronic bronchitis ;
sometimes, however, it occurs independently of it, and then it is a strong
53 DISEASES OF THE EESPIEATORT ORGANS.
predisposing cause to the development of the latter. Disease of the left
side of the heart predisposes to bronchitis, which is sub-acute in character
and chronic in duration. Chronic bronchitis is very often associated with
asthma. Chronic alcoholismus is one of its frequent causes.
Symptoms. — The symptoms of this form of bronchitis vary with the con-
stitutional and local causes under the influence of which it is developed.
There are, however, certain prominent characteristics common to all varie-
ties, the most constant of which are cough and expectoration. The pecu-
liarity of the cough, and the quantity and quality of the matter expectorated,
determine to a great extent the character and severity of the bronchitis.
In some cases the cough is slight, the expectoration moderate in quantity,
and muco-purulent in character; this occurs in the mildest variety — a
variety which comes on in the winter and disappears, or is mitigated, in
summer. After a time it becomes permanent, and is liable to exacerbations
in cold, damp weather. It is the simplest form of chronic bronchial
catarrh. In another class of cases the cough is violent and more constant,
severest in the morning — the expectoration is either tenacious and scanty,
or thin, semi-transparent and abundant ; it is sometimes streaked with
blood, and frequently is difScult to expectorate. So severe is the cough that
vomiting is very commonly induced, the contents of the stomach and
bronchi being simultaneously expelled. The matter expectorated varies in
color from an ashy-yellow to a deep green ; it is slightly aerated, and not
infrequently sinks in water. Its odor varies : sometimes it is sweet and
nauseous ; at other times it has a fetor similar to that of gangrene of the
lungs. The microscope shows it to be composed of granular matter, broken
down epithelial and pus-cells, and sometimes blood-globules and small fila-
ments of bronchial tissue. Some cases of this form of bronchitis are at-
tended by loss of flesh, fever, and night sweats. It occurs most frequently
in strumous, broken-down subjects, especially those given to alcoholic
excess. More or less extensive bronchial dilatations are usually present in
this variety of bronchitis.
Again, there is a class of cases in which the cough is exceedingly
troublesome and paroxysmal in character--the expectoration is scanty,
consisting of small, rounded, semi-transparent masses of tough mucus.
This variety is met with almost exclusively in connection with pul-
monary emphysema, gout, spasmodic asthma and irritant inhalations,
and has received the name of "dry catarrh." There is also a variety
of chronic bronchitis, not infrequently met with in old people, especially
in connection with heart disease, in which the cough is paroxysmal, and
often violent, and the paroxysms are attended by a peculiar flux from the
bronchi. The expectoration often amounts to four or five pints in twenty-
four hours, and is either watery and transparent, or gelatinous and ropy,
resembling an emulsion of white-of-egg and water. The patient often finds
great relief after a paroxysm of coughing and expectoration. In some cases
this variety of bronchitis is accompanied by loss of strength and flesh ; it
has received the name bronchorrhoea. In some cases of simple chronic
bronchitis the sputa are moulded in the form of the smaller tubes. Blood
CHROKIC CATARRHAL BROKCHITIS. 53
in the sputa indicates superficial ulceration. A brownish fluid expectora-
tion is sometimes present ; and in this are fatty granules and crystals of
cholesterin and margarin. In all these varieties there is dyspncea and
labored respiration — the respiration is much more accelerated in other
chronic pulmonary affections than in bronchitis, but it is never so labored.
The pulse in a purely chronic bronchitis does not exceed the normal fre-
quency, and on this account it may readily be distinguished from pneu-
monia and phthisis ; besides, in chronic bronchitis the temperature is rarely
much above the normal, excepting in those cases which are accompanied by
a fetid expectoration. A little uneasiness or soreness is often felt behind
the sternum, which is increased by violent coughing ; but pain in the side
is rarely present. Individuals with any form of chronic bronchitis are un-
able to sustain prolonged physical exertion without great exhaustion, and
they are markedly affected by atmospheric changes.
Physical Signs. — These are very nearly the same as in acute bronchitis.
Inspection shows labored respiration with diminished expansion on inspi-
ration. The chest may appear more convex than normal.
Palpation. — Vocal fremitus varies : if the bronchial walls of the larger
tubes are thickened, it is exaggerated ; if the tubes are obstructed, or much
dilated, it is diminished or absent. In the simple forms of chronic bron-
chitis the vocal fremitus is normal.
The percussion sound rarely differs from that in health : if the accumu-
lation of a thick secretion gives rise to obstruction in some of the bronchi,
then localized temporary dulness on percussion is the result.
On auscultation, the vesicular murmur is more or less deficient over the
whole chest, and the respiratory sound is coarse, loud, and harsh, with
prolonged expiration. After free expectoration, it will often be audible at
points where it had been inaudible a moment before ; it is accompanied,
and sometimes entirely masked, by rdles of every variety, but chiefly sono-
rous and sibilant. Large and small mucous rales are present in those cases
in which there is abundant liquid secretion. These rales are constantly
varying in size and character — at times they may be altogether absent;
they are altered in character and position by coughing and by full inspira-
tion. Vocal resonance may be normal, diminished, or slightly exaggerated.
Large and persistent gurgles in the lower portion of the lung suggest the
existence of bronchiectasis.
Differential Diagnosis. — The diagnosis of chronic bronchitis is rarely at-
tended with difficulty, except in connection with pulmonary phthisis. It
may be distinguished from pleuritic effusions, not only by the cough and
expectoration which attend it, but by the continuance of vocal fremitus,
and the existence of resonance on percussion. From pneumonic consolida-
tion, by the absence of bronchial breathing, of rusty expectoration,
accelerated breathing, and high pulse-rate and temperature. In those
cases of chronic bronchitis in which the general health suffers, ema-
ciation takes place and bronchial dilatation occurs. The bronchitis
sometimes so closely simulates phthisis in its rational and physical signs,
that the differential diagnosis is exceedingly difficult ; the points of
54 DISEASES OF THE EESPIRATOEY ORGAN'S.
difference will be more fully considered under the head of pulmonary
phthisis.
Prognosis. — This disease rarely, if ever, directly destroys life ; but when
it occurs in the old and feeble, it is always attended with danger, on ac-
count of the frequent occurrence of acute attacks involving the small bron-
chi. Any pulmonary affection associated with chronic bronchitis renders
the condition of the patient more serious, on account of the liability to
bronchial obstruction from the accumulation of the secretion in the bron-
chial tubes. It is very apt to lead to the development of pulmonary em-
physema, pulmonary collapse, dilated bronchi, and fibrous phthisis. It is
rarely recovered from when it occurs in those past middle life. Hepatic
congestion, abdominal dropsy, and general anasarca are frequent attend-
ants of chronic bronchitis. Seventy-five per cent, of such cases are compli-
cated by the presence of small, granular kidney.
Treatment. — The one important fact to be borne in mind in the treat-
ment of this affection is, that it rarely occurs as a primary disease, but is
due to some constitutional disorder. The patient must be removed from
every possible source of bronchial irritation, and be protected from expos-
ure to sudden changes of temperature ; flannels should be worn next the
skin, and if a suitable climate cannot be obtained, the patient must keep
in-doors during bad weather, in well -ventilated apartments, the tempera-
ture of which should range from 65° to 70° F. Night air and cold
winds must be avoided. The region best adapted to patients affected with
any of the forms of bronchitis, is one with a moderately warm, dry atmos-
phere, protected from cold winds, and of moderately high altitude. In cases
that are attended by emaciation, a long sea-voy age is often of the greatest
benefit. The diet at all times should be most nutritious. As regards the
use of stimulants, no definite statement can be made, but, as a rule, mod-
erate stimulation is of service.
In no disease is a careful study of each individual case more important.
The immediate and remote cause of the affection must, if possible, be
determined. If the bronchitis is the result of an irritant inhalation,
removal from exposure to this is of the greatest importance. If cardiac
disease exist, which keeps up the bronchial affection by inducing hyper-
semia of the mucous membrane, the treatment should be directed to
the cardiac affection, and, if possible, the heart's action regulated. If
a gouty or rheumatic diathesis exist, the use of colchicum and alkalies
is indicated. Steam inhalations of hyoscyamus, conium, or stramonium
are often of great service in gouty bronchitis. When pulmonary emphy-
sema is associated with, or is the apparent cause of the bronchitis, the
internal administration of iodide of potassium will be followed by most
marked relief. Dilute nitric acid, and the ethereal extract of the acetate
of iron are beneficial. In general anasmia accompanying bronchitis, prepa-
rations of iron are indicated ; in fact, in the majority of cases of chronic
bronchitis, a general tonic plan of treatment is attended by the most
marked benefit. Quinine, mineral acids, bitter vegetable infusions com-
bined with iron, often prove of great service. Bronchial catarrh, alternat-
BRONCHIECTASIS. 55
Ing with chronic skin affections, yields most readily to preparations of
arsenic and sulphate of zinc.
The treatment of the immediate symptoms must depend upon the quan-
tity of the expectoration, the degree of difficulty which attends its dis-
charge, and the presence or absence of any sj)asmodic action of tlie
bronchial tubes. When the bronchial secretions are excessive in quantity,
steam inhalations of tar, creosote, copaiba, and naphtha are often of
great service in limiting their formation ; the vapor of iodine, muriate
of ammonia, and the different balsams are also of service in accomplish-
ing the same purpose. These remedies may be given internally at the
same time. When the power of expectoration is deficient, owing to the
adhesive character of the expectoration, stimulating expectorants are
indicated, such as senega, serpentaria, camphor, tincture of benzoin,
combined with such alkalies as carbonate of j)otash and soda. In those
cases where the bronchial membrane is extremely irritable, the secretions
scanty, and the cough attended by violent paroxysms, narcotics and seda-
tives should be administered in full doses ; opium, hydrocyanic acid, hy-
oscyamus, belladonna, and conium are the most trustworthy agents of this
class. Where there is much spasm of the bronchi, shown by the breath-
ing and cough, a few drops of ether or chloroform may be inhaled ; when
the tendency to the spasm is great, the narcotics and sedatives already re-
ferred to should be administered. Tincture of cannabis indica acts well
in some of those cases. In all varieties of chronic bronchitis, localized
counter- irritation over the seat of the most extensive bronchial changes
may sometimes be employed with benefit, such as may be produced by dry
cups, sinapisms, blisters, croton-oil, and turpentine. It is never necessary
or desirable to abstract blood, either locally or generally. Occasionally,
emetics may be employed with benefit, when the bronchial secretion accu-
mulates in the larger tubes and cannot be expectorated. The close con-
nection of chronic bronchitis with dilatation of the bronchi renders
it necessary to consider briefly some of the prominent features of the
latter.
BRONCHIECTASIS.
Bronchiectasis, or dilatation of the bronchial tubes, is closely connected
with chronic troncliitis. '
Morbid Anatomy. — It may be general or partial. When partial, it is
called saccular or ampullar. The dilatation may be cylindrical, fusiform,
or sacculated. When dilatations are connected together by tubes of norfual
calibre, the condition is distinguished as the " monil if orm" di\sita.tion, of
Cruveilhier. In bronchiectatic cavities, the result of chronic bronchitis,
the walls are hypertrophied, the mucous membrane is thickened, and may
be covered over with small papillary outgrowths. The submucous tissue
is hypertrophied and loses to a great extent its elastic fibres, and the mu-
' First described by Laennec.
DISEASES OF THE RESPIRATORY ORGANS.
Fig. 13.
Diagram illustrating forms of dilatation
of the Bronchi.
A. " Moniliform" dilatation— the tube ii i , ■,^
between the enlargements being of may result; Dut neither gangrene nor
vwmal size. ..i i i • i ti j i-
B. •■' saccifwrn" diiaiation-severai of occurs With bronchial dilatation as
c! FmmaampZc^^^y'^l^^^^ as colkpse and fibroid tliickening.
IM conneciiug tube.
cons glands are atrophied. The muscular fibres are often dissociated.'
Bronchiectasis is rarely met with independent of some stenosis ; we often
find alternate stenosis and dilatation. On the tracheal side these bronchial
dilatations usually communicate with a slightly enlarged bronchial tube;
but, on the peripheral side, the continuity
of the tube is almost or entirely lost by
narrowing or actual obliteration. Cystic
cavities may be found ; these are isolated
bronchial dilatations, whose supplying bron-
chus has become permanently obstructed.
Pus, muco-pus, crystals of margarin, fibres
of lung-tissue, and even chalky debris
have been found in these cavities. The
lung tissue close to the bronchiectases is
altered in various ways ; there may be fibroid
induration, emphysema, lobular pneumonia,
and atrophy. The contents of a bronchiec-
tatic cavity may decompose and, ulceration
occurring, gangrene or abscess of the lung
abscess
often
and fibroid thickening. The
small bronchi, and the bronchi in the lower
lobes, are the parts most often involved in bronchiectasis.
Etiology. — Chronic bronchitis is the most frequent cause. Atelectasis,
lobular collapse, fibroid induration, and old pleuritic thickenings also
cause it. Phthisical processes are nearly always accompanied by more or
less bronchial dilatation.
Symptoms. — Many of the symptoms are referred to under the head of
^^ fetid bro7ic1iitis.'" An abundant, fetid, purulent, and often nummular
expectoration, frequent and paroxysmal cough, a very fetid breath, some
emaciation, occasional profuse haemoptysis, and not infrequently night
sweats, associated with the symptoms of chronic bronchitis, are the character-
istics of bronchiectasis. The pulse is accelerated, and there is hectic fever
during its advanced stage.
Physical Signs. — Insijection shows retraction, prolonged expiratory motion,
with diminished expansion on the afl'ected side, or of the whole of the chest
if both sides are involved.
Palpation, — There is increased vocal fremitus. ,
Percussion elicits dulness if the dilatation is filled, or if it is sur-
rounded by consolidated lung. There will be extra resonance if the dilata-
tion is empty and superficial, and there may be a cracked-pot resonance if
the dilatation is very large, surrounded by fibrous tissue, and near the surface.
Auscultation. — The respiratory sounds maybe harsh, blowing, bronchial,
cavernous, or amphoric, according to the seat, size, and condition of the
dilatation. Large and small gurgles are often heard.
' In children these bronchiectases not infrequently disappear when the bronchitis which caused them
disappears.
CROUPOUS BROKCHITIS. 57
Its differential diagnosis will be considered in connection with phthisis.
This condition cannot be cured. It may exist for many years without ma-
terially impairing the general health. Death may be caused by gangrene,
abscess, exhaustion, or some complication.
Treatment. — Its treatment is that of chronic catarrhal bronchitis {q. v).
It is benefited by the daily use of antiseptic sprays of creosote, carbolic
acid, etc.; by a residence in a moderately high, warm and dry locality; by
a carefully regulated, nourishing diet, and a proper hygiene ; and in most
instances by tonics in addition to cod-liver oil.
CROUPOUS BRONCHITIS.
Under this head will be considered croupous, pseudo-membranous, or
plastic inflammation of the bronchial mucous membrane, as it occurs inde-
pendently of laryngeal croup on the one hand, and of croupous pneumonia
on the other, or of that form of catarrhal bronchitis during the course of
which a few membranous flakes are expectorated. This disease may pursue
either an acute or chronic course. Both forms are rare ; the acute is the
more infrequent.
Morbid Anatomy. — It differs from catarrhal bronchitis in the character of
the exudation, as plastic material is poured out into the tubes in the form
of casts, which are either solid or hollow, according as the small or large
tubes are affected. In the chronic form, the membranous exudation occurs
over a circumscribed portion of the bronchial membrane ; in the acute, it
is distributed over a greater portion of the bronchi. The membrane may
be firmly adherent or loosely attached to the mucous surface. These casts
are of a whitish color, sometimes dotted over with blood-spots. Microscop-
ically, they consist of fibrillated fibrin, abundant granular matter, oil-
globules, exudation corpuscles, and fusiform ovoid cells. They always
consist of concentric laminse. Acetic acid causes them to swell. In some
cases no membrane exists ; the bronchial membrane is pale and congested.
Etiology. — There is no known special exciting or predisposing cause to this
disease — it is supposed to be due to some diathetic state. It is most fre-
quently met with in young adults, and occurs more frequently in females than
in males, and in those of feeble, delicate constitutions, rather than in those
who are strong and healthy. It has been seen associated with asthma and
emphysema. The strumous and phthisical are markedly predisposed to it.
Symptoms. — The acute form is usually preceded by catarrhal symptoms
of short duration. It is attended by fever, by dyspnoea (often severe), by
a dry, hoarse, ringing cough (not as stridulous as in croup), and by a sense
of constriction and oppression across the chest. After severe paroxysms of
coughing, either fragments of membrane, or membranous casts or cylin-
ders are expectorated, usually in small masses. The membranous expecto-
ration, in rare instances, is wanting, and occasionally not even cough is
present. There are no symptoms of laryngeal obstruction. When the dis-
ease progresses toward a fatal termination, the dyspnoea rapidly increases
in severity, and is finally superseded by those phenomena which precede
death by asjihyxia.
58
DISEASES OF THE EESPIKATORT ORGAlSrS.
TJie cJirofiic form is generally preceded by catarrhal bronchitis, which
sometimes has lasted for a long time; severe haemoptysis may have preceded
its development. Not infrequently, in pulmonary phthisis, where haemop-
tysis has occurred, casts of bronchial tubes are expectorated, which are
nothing more than decolorized blood-clots. The history of the chronic
form of plastic bronchitis is rarely a continuous one, but is made up of in-
tervals of health and paroxysms of disease ; during the latter, expectora-
tion of membrane in fragments or casts occurs. Their removal is often pre-
ceded by fits of severe coughing, and by paroxysms
of dyspnoea of variable intensity, lasting usually a
few hours, sometimes a day or more ; at other
times, simple sneezing effects their removal. Gen-
erally, along with the membrane, there is catarrhal
expectoration, in which small portions of mem-
brane may be hidden. In about one-third of the
cases, haemoptysis (generally slight) has either pre-
ceded or accompanied the membranous expectora-
tion. The membranous exudation, if it comes from
the large bronchi, is in the form of casts ; if from
the small, it is in the form of cylinders. Occasion-
ally, there is mucus or blood in the interior of the
casts, while streaks of blood are often present on
the exterior. The casts are of variable thickness
and length — usually two or three inches long,
laminated, and of a whitish or grayish color.
Microscopically, they are composed of a structureless mass, more or
less fibrous in character, in which cells are imbedded, more particularly
pus cells. During the interval between the paroxysms, in uncompli-
cated plastic bronchitis, the general health is good and fever is not present.
Physical Signs. — These depend upon the obstruction produced by the
membrane, sometimes upon the vibration of a portion of it, and on coinci-
dent catarrh. When the bronchial tubes are obstructed, there is feebleness
or absence of the respiratory murmur, — in the chronic form, over a limited
portion of the chest, in the acute, over a large extent. At the same time,
the percussion note may be normal, extra resonant or dull ; the latter ex-
isting when collapse of the lung has taken place, disappearing, it may be,
immediately after membranous expectoration, while the respiratory mur-
mur regains its normal character, thus masking the exact seat of the dis-
ease. Flapping and rubbing sounds have been described as a result of vi-
bration of the membrane. Dry and moist rales are also usually present, due
either to the narrowing of the tubes, or to coincident bronchial catarrh.
Diiferential Diagnosis. — This form of bronchitis may be mistaken for acute-
catarrhal bronchitis, pjieumonia, or pleurisy. The history of the case, the
character of the paroxysm, the membranous expectoration, and the accom-
panying physical signs, will generally enable one to make the diagnosis of
plastic bronchitis ; without the membranous expectoration, howe\"er, the dif-
erential diagnosis between acute croupous and acute catarrhal bronchitis
Fig. 14.
Mould of bronchial twigs
expectorated in a case of
Plastic Bronchitis. One-
half the original size.
BRONCHIAL ASTHMA. 59
cannot be made. The absence of the symptoms which usually attend pneu-
monia and pleurisy serves to exclude them from the question of diagnosis.
Prognosis. — With the acute form, more than one-half die ; with the
chronic form, if death occurs, it is due to some complication ; so that, in
uncomplicated cases of chronic plastic bronchitis the prognosis as re-
gards life is good ; but the disease, having once occurred, it is very apt to
return. The duration of the disease varies. In the fatal cases, when the
disease is acute, it lasts from three to ten days ; in those cases that recover,
it lasts from ten to fourteen days. In the chronic form, the paroxysms
usually last ten or twelve days, and recur, at longer or shorter intervals, for
months or years. Complete recovery is rare. Croupous bronchitis is very
likely to lead to pneumonia and pulmonary phthisis.
Treatment. — The acute form is to be treated the same as croupous laryn-
gitis. In the chronic form, during the paroxysm, alkaline steam inhala-
tions should be resorted to, with the hope of removing the membrane as
quickly as possible. The patient should be kept in a warm, equable
temperature. Durmg the interval, the general system should be invigorat-
ed in every possible way, and all exposure to the causes of bronchial irri-
tation should be avoided. The internal administration of iodide of potas-
sium has been highly recommended ; quinine, iron, and cod-liver oil are
often called for. If the paroxysms continue to recur, a change to a warm
climate, or a long sea voyage must be tried. There is no known remedy o^
plan of treatment which promises a cure in this disease.
BEONCHIAL ASTHMA.
This is a spasmodic affection of the bronchial tubes, which gives rise to
dyspnoea of a paroxysmal character. The spasmodic contractions may be
regarded as due to a neurosis loliicli depends upon the existence of a peculiar
diathesis. Some muscular spasm or contraction of the circular muscular
fibres of the bronchial tubes is the essential element of the asthmatic parox-
ysm ; and the consequent narrowing of the tubes is a necessary mechanical
result. Bronchial catarrh, when present, may precede the paroxysm, or it
may not come on until its close. Although bronchitis plays an important
part in the development of asthma, it only acts as an exciting cause, as there
must exist a special neurotic condition, without which the paroxysm would
not occur.
Etiology. — Unquestionably, the primary cause of asthma is some consti-
tutional idiosyncrasy, which is frequently hereditary. Heredity is traced
in about forty per cent. It is a diathetic disease, and, like all such dis-
eases, may be readily transmitted from parent to offspring. It is believed
by some to be connected with a gouty or rheumatic diathesis. No period
of life is exempt from it ; I have seen a well-marked paroxysm of asthma
in an infant six weeks old, born of an asthmatic mother.
The exciting causes of the asthmatic paroxysms may be grouped into
three classes :
First. — Those cases in which the bronchial spasm is produced by some
60 DISEASES OF THE RESPIRATORY ORGAI^TS.
material respired which acts directly on the bronchial mucous membrane.
In this class are included all those cases of asthma in which the paroxysms
are excited by irritating inhalations, such as ipecacuanha powder, many
chemical vapors, smoke, dust, fog, emanations from newly mown hay,
stables, roses, sulphur matches, burning sealing-wax, certain atmos-
pheric conditions, and the emanations from certain animals, cats, horses,
etc., etc. A pure mountain air excites it in some, and relieves it in others.
Asthmatics present remarkable peculiarities as to the conditions of atmos-
phere which suit them best. Second. — Those cases which are of more dis-
tinct reflex origin. In this class are included those in which the asthmatic
paroxysms follow errors in diet, an overloaded rectum, uterine irritation,
the sudden application of cold to the surface, the irritation of an enlarged
prostate gland, or of hemorrhoidal tumors. Third. — Those cases which
occur as complications, or in connection with bronchitis, heart disease, or
emphysema, and are most likely to occur after fatigue and physical exer-
tion. Bronchial catarrh is one of its most frequent causes.
Each individual subject to asthma is susceptible only to his own peculiar
exciting cause. The retrocession of gout and rheumatism, syphilis, renal
diseases, disappearance of chronic skin eruptions, the stoppage of an habit-
ual discharge, or the healing of old ulcers may be followed by asthmatic
paroxysms. Certain organic diseases of the brain induce it. Angina, neu-
ralgia, gastralgia and asthma often alternate. That form of asthma termed
hay asthma, which is produced by emanations from newly mown hay, oi
other vegetable emanations, is always preceded or accompanied by coryza
and bronchitis ; persons may have the coryza and bronchitis for years with-
out having the asthmatic paroxysm, yet the paroxysms are certain to come
sooner or later, and differ in no respect from other asthmatic paroxysms.
Symptoms. — An attack of asthma may or may not be preceded by precur-
sory symptoms ; the majority of those suffering from asthma know when
the attack is coming on, by some peculiar symptom which they alone rec-
ognize. There may be languor, drowsiness, depression of spirits, or tha
opposite condition, abnormal buoyancy of spirits. Often a large amount
of ''hysterical " urine is passed before the attack, or there may be wakeful-
ness, headache, itching of the chin, etc. Ordinarily, the individual goes
"to bed as well as usual, and quietly falls asleep ; after an hour or two, while
he is still asleep, the characteristic wheezing commences, and soon he is
awakened by a most distressing attack of dyspnoea. He feels as if his chest
were compressed, and he were about to be suffocated ; sits up in bed and rests
his elbows on his knees, and with fixed head, elevated shoulders and mouth
open, labors for breath. There may be immoderate sneezing, attended by
running at the nose. There may be flatulent distention of the abdomen.
His face becomes red, turgid or livid, his eyes prominent, his surface cov-
ered with perspiration ; he springs out of bed, and hastens to an open win-
dow in search of air ; respiration is noisy and wheezing, the inspirations
are short and jerking, while the expirations are prolonged, and terminate
with a sudden effort at expulsion. The number of respirations varies from
sixteen to thirty a minute. All the auxiliary muscles of respiration are
BEONCHIAL ASTHMA. Ql
brought into play ; yet the chest remains almost motionless. The laboi
may be so great that the patient is in a dripping perspiration. The mouth
is wide open, the nostrils are dilated, the cervical and facial veins are tur-
gid. If the bronchial spasm is prolonged, the surface temperature falls be-
low the normal, the extremities become cold, blue and shrunken, and the
patient seems to be dying. The pulse during the paroxysm is small, rapid,
thready, and feeble in proportion to the intensity of the dysj^noea. The
duration of the paroxysm varies ; at one time it lasts only a few minutes,
at another an hour or two, in rare instances it may continue two or three
days without intermission.
As the paroxysm passes off, the patient begins to cough and expecto-
rate ; in some patients the expectoration consists of a few small, rounded
masses like pearls of mucus, and contains neither pus nor watery con-
stituents ; in others it is profuse and watery. The expectoration occurs
after the bronchial spasm has ceased ; it does not cause its cessation ;
and even when the attack begins "dry," there is some expectoration at
the end of the paroxysm. Occasionally in severe attacks, there are
blood-streaks ]n the sputa, and sometimes quite profuse hemorrhage occurs.
The paroxysm /ecurs after intervals of varying length ; some experience
an attack only annually, others monthly, and others only when sub-
jected to their own peculiar exciting cause. Less violent attacks may
last five to six days. During the interval, if the asthma is not due to any
organic disease, the condition of the asthmatic subject varies ; some are
perfectly well ; others constantly have a sense of thoracic constriction,
which renders the breathing somewhat labored, especially during active
exercise. Some suffer severely from a bronchial or nasal catarrh. When
the catarrhal element predominates, the asthmatic paroxysms are excited
by slight exposure. The longer the attack, the less abrupt its cessation
and more profuse the sputa. Immediately after a paroxysm, there is usu-
ally a feeling of exhaustion, aching and ''soreness," which passes off in a
few hours, and the individual experiences a sense of relief, and has for a
time an almost certain immunity from a repetition of the attack. Some
claim that the urine exhibits a remarkable diminution in chloride of so-
dium and urea just after an attack, while later both return to the normal.^
Analysis of expired air shows oxygen to be almost wholly replaced by car-
bonic acid, which may be eleven per cent, above the normal quantity.
Physical Signs. — During the paroxysm inspection shows labored respira-
tion, while the upper part of the chest is almost motionless, and the
muscles of the neck rigid; the inferior costal and abdominal respiration is
labored, the act of inspiration is slower than in health, and expiration is
more active and violent, and also longer than normal. Vocal fremitus and
vocal resonance are normal. The percussion sound is slightly exaggerated.
On auscultation the respiratory murmur is jerking and irregular ; some-
times it is exaggerated, at other times it is suppressed. Sibilant and sono-
rous rales of a high-pitched, hissing and wheezing character are diffused
' Sidney Ringer.
62 DISEASES OP THE KESPIRATORT ORGANS.
over the whole chest, often loud enough to be heard at a distance from the
patient. These are best marked over and between the scapulge. The
respiratory murmur is very faint or absent, especially in the old and where
expiration is prolonged and low pitched. All sounds are loudest during
expiration. The rale sounds are often musical. These rales are constantly
changing their character and site, disappearing at one point and making
their appearance at another. At the close of the paroxysm some moist
rdles may be heard ; or if bronchial catarrh exists then the sounds will be
moist throughout.
Differential Diagnosis. — Spasmodic asthma will rarely be confounded with
any other disease, if its rational and physical signs are properly appreciated.
The phenomena of a paroxysm are quite distinctive, while the physical
signs are unmistakable. The afEections with which there is a possibility of
its being confounded are spasmodic affections of the larynx, acute capillary
tronchitis, angina pectoris, liydrotliorax, pulmonary oedema and congestion
and emphysema. It is easily distinguished from laryngeal affections by the
absence of the change in the voice which is so characteristic of laryngeal
spasm, and by the presence of auscultatory signs never heard in spasm of the
glottis. It is distinguished from ironchitis by the slowness of respiration,
by the absence of subcrepitant rales and pyrexia, and by the suddenness of
its advent. In angina pectoris there are no sibilant and sonorous rales.
Angina pectoris is accompanied by lancinating pain — absent in asthma
— and there are no attendant physical lung symptoms. In hydrothorax
there is no resonance on percussion over the entire thorax, no succussion,
and no change in the line of dulness. In pulmonary mdema there is
dulness ; in asthma extra resonance. Liquid, bubbling, stationary rdles
are heard in oedema ; in asthma the rdles are dry and constantly change
position and character. There is profuse watery expectoration in oedema,
absent in asthma. Asthmatic dyspnoea and cardiac dyspnoea are some-
times confounded ; in some respects they resemble each other — both are
paroxysmal, both are intense, and both generally occur at night. There
is little wheezing in cardiac dyspnoea. In both, the respiration maybe per-
fectly normal between the attacks, but a careful physical examination will
enable one to determine whether the dyspnoea is asthmatic or cardiac.
Emphysema has a vesiculo-tympanitic percussion note, not present in
asthma. Prolonged low-pitched expirations exist in emphysema; in asthma
the expirations are never loio pitched. The barrel-shaped chest and change
in the position of the heart are absent in asthma, and are notable signs of
emphysema. The two conditions are often found together. In croup the
dyspnoea is inspiratory ; in asthma it is expiratory. The condition most
likely to be mistaken for asthma, in old age, is latent pericarditis with
effusion. Spasmodic dyspnoea often accompanies it ; but it is marked by
a feeble, often an irregular pulse, diminished cardiac impulse, obscure
heart sounds and increase in precordial dalness, and there are no rdles
present.
Prognosis, — Death rarely, if ever, occurs from uncomplicated asthma.
Asthmatic patients are frequently long-lived, which may be accounted for by
BEONCHIAL ASTHMA. 63
the fact that they are compelled to observe the most rigid hygiene in order
to avoid their asthmatic attacks. The fact that a person has had one
asthmatic attack, is presumptive evidence that he will have another. The
prognosis, as to recovery, is hopeful in proportion to the youth of the
patient. If the attacks only come on at long intervals and are not severe
and prolonged ; if during the intervals the patient is well and there is no
organic disease; if the paroxysms can be traced to some obvious cause which
may be avoided, the prognosis as to the complete recovery is good. At first,
the attacks are violent and exhausting ; then they lose their periodical
character and run together, as it were, so that the patient is never wholly
free from asthmatic dyspnoea. The periodicity varies from one year to one
month. Emphysema, chronic passive pulmonary hypersemia, right car-
diac hypertrophy and dilatation, and chronic bronchitis are among its
complications.
Treatment. — There are two things to be considered in the treatment of
this affection, viz., the relief of the paroxysms and the prevention of their
recurrence. The first thing is to ascertain the exciting cause of the
paroxysm, and, if it is still in operation, to remove it if possible. If the
paroxysm is dependent on an overloaded stomach, an emetic should be ad-
ministered; if upon a loaded rectum, an enema should be given; if smoke,
dust, or any animal or vegetable emanation is the cause of the attack, it
must be removed. " Eose fever" and '' hay fever " are only relieved by
removal from places where there are roses or hay. If, in a certain locality,
the attacks of asthma are of frequent occurrence, the patient should re-
move to one where he is free from asthmatic paroxysms. Not infrequently
the removal of the exciting cause will be all that is necessary for the relief
of the patient. If the exciting cause cannot be removed, or if its removal
is not followed by relief of the paroxysm, free ventilation should be secured,
and the patient should be placed in a position in which respiration may be
carried on with as little mechanical impediment as possible. Curtains and
obstructions to the free entrance of the air should be removed from the
room. Usually the best position during an attack is the sitting posture —
in a chair which will give support to the arms and so elevate the shoulders.
Some old people are relieved by sitting before a hot open fire in a close
room.
Having placed the patient under the most favorable circumstances for the
relief of the paroxysm, the next thing is to select those remedial agents
best adapted to the case. This selection will be very much influenced by
the patient's own experience and idiosyncrasy. The great majority of
asthmatics know the remedies that will give them relief. The remedies
that give relief to asthmatics maybe divided into three classes: 6?ej5ress«w/s,
sedatives, and stimulants. Among the leading depressants are antimony,
ipecacuanha, tobacco, and lobelia. Ipecacuanha is to be given in quanti-
ties /ws^ sufficient to produce nausea, and tobacco till it begins to sicken.
If a patient has been previously relieved by the use of depressants, it is well
to inquire which one of this class he made use of. The relief obtained by
this class of remedies is by bringing the asthmatic into a condition of com-
64 DISEASES OF THE KESPIRATORY ORGANS.
plete relaxation. Sometimes this may be accomplished by the administra-
tion of one full dose of ipecacuanha.
Sedatives seem to act in two ways : some act locally on the nervous
supply of the lungs, but the majority give relief by their action on the
general nervous system. Those which experience has shown to be most
efficacious in arresting the asthmatic spasm are stramonium, chloroform,
belladonna, conium, assafoetida, the bromides, ether, opium, cannabis
indica, hyoscyamus, and the fumes of burning nitre paper. Smoking
stramonium often relieves when the internal use of the extract is inert.
The datura tatula is by many regarded as more efficacious than the datura
stramonium. Smoking tobacco often relieves a paroxysm. Some will be
promptly relieved by the inhalation of the fumes of stramonium leaves ;
others by the inhalation of chloroform. Perhaps there is no agent in this
class that will so speedily and completely relieve the spasm as chloro-
form ; but the relief is only temporary ; so soon as the stupefying effects
have passed away the paroxysm generally returns with increased violence.
Ether is pleasanter to inhale than chloroform, and has no such after
effects. A combination of the two is often efficacious. Trousseau advo-
cates inhalation of vapor of ammonia. Quebracho has proved efficacious
in a few instances. Kecently grindelia robusta has been strongly advo-
cated. In this class of remedial agents that which I have used most suc-
cessfully is opium given in full doses — small doses are unavailing. One-
half a grain of the sulphate of morphia should be administered at once. I
prefer its hypodermic use. Atropine may be combined with the morphia ;
there are cases which are quickly relieved by this combination, which are
not relieved by the use of either of these drugs alone. Conium, hyoscya-
mus and belladonna act much less certainly. They should be tried, how-
ever. Nitrite of amyl is not so successful as its physiological action Avould
indicate. Iodide of ethyl is advocated by some.^ Fumes of nitre paper is one
of the oldest and best remedies. The paper is prepared by dipping filter
or blotting paper in a solution of saltpetre. How it acts is not well under-
stood ; certainly not by relieving the bronchial irritation, for, as a rule,
the patient is not relieved if bronchitis is associated with the asthma. When
this remedy is employed it is necessary that the apartment occupied by the
patient should be filled with its fumes. If it acts favorably it will do so
quickly, and its administration must not be prolonged if relief is not
promptly obtained.
Among stimulants, the two principal remedies are coffee and alcohol.
Coffee is the more efficacious. It should be taken strong without
milk or sugar, and as hot as it can be swallowed ; it should always be
taken on an empty stomach. Not infrequently a paroxysm of asthma
can be warded off by taking two or three cups of strong coffee imme-
diately upon the accession of the first asthmatic symptom. Alcohol
is another stimulant which experience has led me to regard very highly.
It is of little importance what alcoholic stimulant is employed, but it
must be taken hot and strong, that is as a "hot toddy," and in suffi-
1 Gazette Medical de Paris. 1878, p. 69.
BROKCHIAL HEMORRHAGE. 65
ciently large doses for the patient to feel its intoxicating effects. As a
rule asthmatic patients will bear large quantities of alcoholic stimulants
without becoming intoxicated. By whichever class of remedial agents the
patient is relieved, after a time the remedy will fail or cease to have the
desired effect. The three most reliable remedies are ipecacuanha as a de-
pressant, opium as a sedative, and coffee as a stimulant. Compressed air I
have never found to give the relief promised by its advocates ; nor does
inhalation of oxygen allay the paroxysms as a rule. Certain mineral springs
are beneficial for asthmatics ; the most noted are Cmiterets, Mont-Bore,
and Baux Bonnes. Faulkner paints the track of the pneumogastric in
the neck with iodine and claims remarkable results. Nitro-glycerine and
pilocarpin have both been used.^ In the intervals the treatment is hygi-
enic ; no known remedies can prevent the return of the paroxysms, whereas
the observance of certain hygienic rules may often prevent or delay their
return. When skin diseases alternate with attacks of asthma, arsenical
preparations are beneficial. "Where the cause is undiscoverable, many state
that iodide of potassium not only prevents, or delays, an impending attack,
but even effects a permanent cure. Asthmatic patients are usually dysjoep-
tic ; and it is a noticeable fact that, in such cases, as long as they exercise
proper care as to diet they are free from asthmatic attacks. This is not to
be overlooked in the management of asthmatics betioeen the paroxysms. A
change of residence is all important in cases dependent for their develop-
ment upon certain atmospheric causes. There is no definite rule for this
change ; each one must decide for himself, finding by experience the place
in which he is free from his attacks. If the patient is anaemic and poorly
nourished, cod-liver oil and iron must be administered during the interval.
1 have quite a number of asthmatics under observation who, by taking
daily from gr. xv. to gr. xx. of the sulphate of quinine can prevent parox-
ysms of asthma. As soon as the daily use of the quinine is discontinued
the asthmatic symptoms begin to manifest themselves, and soon culminate
in a paroxysm. Helmholtz found relief by injecting into the nostrils a
solution of quinia when he suffered from "hay fever." The diet, espe-
cially in old age, should be strictly regulated. 'No fats, no water within one
hour before dinner or supper, or till three hours after — these should be
laws never to be broken. Flannel must be worn next the skin. Exercise
should be constant but moderate. Should the frame, however, be defect-
ively developed, active gymnastic exercise is then to be advised.
BRONCHIAL HEMORRHAGE.
In the majority of instances, when blood is expectorated in considerable
quantities, the source of the hemorrhage is the bronchial mucous membrane.
Spitting of blood occurs in pulmonary congestion, pulmonary apoplexy,
and. in the inflammatory processes affecting the lungs and bronchi ; but
hemorrhage from the bronchial tubes is by far the most frequent cause of
" British Medical Journal, Yol. I. 1880, p. 960.
66 DISEASES OF THE EESPIEATOEY ORGANS.
blood-spitting or hmnoptysis ; * and when blood comes from the bronchial
tubes the hemorrhage is properly called hronchorrliagia.
Morbid Anatomy. — If the bronchial mucous membrane is examined soon
after or during a bronchial hemorrhage, at the seat of the hemorrhage it
will be found swollen, relaxed, bleeding on slight pressure, and of a uni-
formly dark-red color, with here and there spots of ecchymosis. The lungs
are pale but are marked by bright pink spots, corresponding to the air-cells
into which blood has been inhaled. If the examination is made some time
after the bleeding, the bronchial membrane will either present a pale and
bloodless appearance, or no traces of the seat of the hemorrhage can be
found. If the examination is made during or soon after the hemorrhage,
the bronchi may be found more or less completely filled at points with
blood-clots ; these clots are usually exsanguinated. The healthy portions
of the lungs are inflated. In haemoptysis occurring in advanced phthisis
there will either be aneurism of a pulmonary vessel in a cavity, or ulcera-
tion of an exposed vessel. In the early stage of phthisis the walls of the
small blood-vessels suffer nuclear proliferation and stasis. If the blood has
been forced from the bronchi into the air-cells, small, red, dense nodules
wiJl be found scattered through the lung-substance, very closely resembling,
in their gross appearance, pulmonary infarction.
Etiology. — Ulceration of the bronchial mucous membrane is rarely a
source of bronchial hemorrhage ; and seldom does an aneurism open into a
bronchus. The two prominent causes of bronchial hemorrhage are : first,
over-distention of the capillaries of the bronchial mucous membrane ;
secondly, weakness of the capillary walls of the bronchial membrane. Such
weakness of the walls of the capillaries may be an hereditary or an acquired
condition. In both cases there is probably rupture, which may escape
detection at the autopsy. The tendency to bronchial hemorrhage from
weakened capillaries is much stronger between the ages of fourteen and
thirty, especially in young, delicate persons born of phthisical parents, than
at any other time. There is also a strong disposition to this form of hem-
orrhage in those who are already suffering from developed phthisis, or
who have an acquired phthisical diathesis.^ Usually in these cases the
direct cause of the hemorrhage is a sudden distention of the weakened
bronchial capillaries from violent physical exertion, or from certain peculiar
■atmospheric influences. In rare instances it occurs without any appreciable
cause. That form of bronchial catarrh which precedes or attends the devel-
opment of phthisis is very frequently preceded or attended by bronchial
hemorrhage. Here, probably, the exciting cause of the hemorrhage is act-
ive hyperasmia of the bronchial membrane. Bronchial hemorrhage may
be induced by the inhalation of irritating gases or vapors and by the rare-
fied air of high elevations ; in both of these instances the hemorrhage fol-
lows over-distention of the capillary vessels of the bronchial membrane.
1 Haemoptysis means spitting of pure blood only : i. e., the rusty blood-stained sputa of acute pneu-
monia do not constitute an haemoptysis.
2 Rindfleisch thinks that when phthisis follows hcemoptysis the hemorrhage is due to " vascular tuber
£ular infiltration."
BRONCHIAL HEMOREHAGE. 67
Any form of obstructive heart disease that leads to passive hyperaemia of the
lungs will predispose to bronchial hemorrhage. Intense active hyper-
semia will also cause it. The violent coughing of bronchitis, pertussis and
pneumonia oftentimes induces it. It may follow suppression of any habit-
ual discharge, and is then called ** vicarious bronchorrhagia."
Symptoms. — The symptoms which attend a bronchial hemorrhage vary
with the profuseness of the hemorrhage. If the quantity of blood expec-
torated is very small no symptoms will be developed except the spitting of
the blood, which is of a bright red color. It is not often, however, that
the symptoms that attend a bronchial hemorrhage are so trivial, for these
hemorrhages are usually profuse. All bronchial hemorrhages are attended
by the spitting of bright red, frothy, arterial blood. A very profuse bron-
chial hemorrhage may come on suddenly without any warning, but usually
the patient has had some previous indication of its occurrence, such as a
sense of constriction at the upper portion of the chest, or a sense of uneasi-
ness during inspiration, which he cannot account for. Those who have had
haemoptysis may suffer prodromata, such as headache, dizziness, palpitation,
increased pulse-tension and a general constriction about the chest. Cough
may or may not precede the hemorrhage. Usually the patient feels as if
some fluid had suddenly commenced trickling under the sternum, and he
notices an unusual sweetish taste in the mouth. He spits and finds that
the fluid is blood, although there may have been no cough previous to the
hemorrhage. Now he feels more or less bronchial irritation, which is fol-
lowed by a cough. Loud moist rales are heard, more or less blood is expec-
torated, short intervals occur between the fits of coughing, and in this way
blood may continue to be expectorated for several days, or the expectoration
may continue only for a few hours.
The amount of blood expectorated varies ; sometimes, when the hem-
orrhage is profuse, the whole quantity may reach a pound or more ; at
other times not more than an ounce or two is expectorated. During the
occurrence of the hemorrhage the countenance of the patient assumes an
anxious expression ; he becomes tremulous and often faints. This, how-
ever, is not owing wholly to the loss of blood, but is probably due to
the shock to the nervous system from the sight of blood and knowledge
of the fact that a hemorrhage from the lungs has taken place. The pulse
becomes rapid and tense, and, unless the bleeding is profuse, the face
is red. The temperature during the bleeding is usually depressed, but
soon returns to the normal. All these symptoms may be present when
the individual has not lost more than half a pound of blood. Hemorrhage
from the lungs weakens a patient more than an equal amount of hemor-
rhage from any other organ of the body. After the profuse expectoration
of blood has ceased, the patient goes on coughing for a few days,
expectorating small, dark, coagulated masses of blood or blood-streaked
sputa. Sometimes bronchial hemorrhage is so profuse that the blood
spouts out of the mouth and nose. This is followed by nausea and
vomiting of blood, but it is worthy of notice that the nausea and bloody
vomiting follow and do not precede the hemorrhage. Death may occur
(58 DISEASES OF THE KESPIKATORY ORGAKS.
from suffocation in these cases. Eapid and profuse (but wow-phthisical)
haemoptysis should lead to the suspicion of the rupture of an aneurism.
Attacks of bronchial hemorrhage are rarely single ; usually for a week or
two they recur at intervals. At length the patient becomes pale and
feeble, then recovery gradually takes place, so that in a few weeks he may
feel better than before the hemorrhage. This is the most favorable termi-
nation that can be hoped for, except in those cases in which the hemor-
rhage is comparatively insignificant. It is important to remember that
attacks of bronchial hemorrhage, however profuse, are generally recovered
from in spite of extreme prostration and tendency to syncope which some-
times attend their occurrence. When the recovery from a bronchial
hemorrhage is not speedy it is quite likely to be followed by more or less
febrile excitement, the temperature rising, perhaps, to 101° ¥., the pulse
becoming accelerated and feeble. The patient becomes paler and weaker,
has almost complete loss of appetite, and is troubled with a hacking cough,
almost constant, which is accompanied by a tenacious, scanty, muco-pur-
ulent expectoration. The respiration is hurried, and there is dyspnoea
on slight exertion. Under these circumstances the bronchial hemorrhage
is followed by broncho-pneumonia, Avhich, in the majority of cases, within
a few weeks goes on to more or less complete resolution, and the patient,
by means of change of air and proper hygiene, may finally recover. There
is another class of cases in which the hemorrhage is followed by still more
active febrile symptoms, the temperature rises higher, the pulse is more
rapid and feeble, emaciation follows, usually accompanied by profuse night
sweats, and the patient dies of acute phthisis within a few months after the
fiirst hemorrhage. Previous to the hemorrhage he has good health, and
there were no physical evidences of disease of the lungs or bronchi. (This
subject is more fully considered under the head of Acute Phthisis.)
A physical examination of the chest during a bronchial hemorrhage usu-
ally gives negative results. On auscultation nothing abnormal is found,
with the exception of a few large and small moist bronchial rales. It is not
well to disturb the patient by frequent examinations of the chest.
Differential Diagnosis. — There are four conditions which may be con-
founded with bronchial hemorrhage, namely, epistaxis, pulmonary apO'
plexy, hcematemesis, and aneurisms rupturing into the air-passages.
Epistaxis is very easily distinguished from bronchial hemorrhage, for
the nose-bleed occurs before the apparent bronchial hemorrhage, and the
blood is always coagulated and dark colored. It is not attended or fol-
lowed by a cough, and blood can always be detected in the nostrils, posterior
nares, or pharynx. The characteristics of the hsemoptysis which occurs in
connection with pulmonary apoplexy will be considered under that head.
The diagnosis between these two forms of hsemopytsis rests upon the char-
acter and quantity of the blood expectorated, and the existence or non-
existence of cardiac disease or pyaemia ; and here a physical examination
is of great importance.
Hmmatemesis is to be distinguished from bronchial hemorrhage by the
fact that the blood in haematemesis is always coagulated and grumous, of
BKONCHIAL HEMORKHAGE. 69
a dark red color, and vomiting precedes or accompanies the hemorrhage.
In bronchial hemorrliage if nausea and vomiting are i)resent they follow the
spitting of arterial blood ; and hamatemesis is not accompanied or followed
by a cough. ' The gurgling in the bronchi, loose cough, and bright frothy
appearance of the blood are never met with in hsematemesis. Blood is
alkaline when from the lungs, and acid from the stomach. "Spurious
hcemoptysis " (bleeding from gums, pharynx, etc., as from bad teeth) may
be confounded with bronchorrhagia, but an examination of the mouth soon
reveals the true state of affairs. When an aneurism ruptures into a bron-
chial tube, the hemorrhage is generally profuse, and it is soon followed by
death. The long history of aneurism which precedes the rupture, as well
as the physical signs, which at* least will have led to the suspicion of
aneurism, are in most instances sufficient to enable one to determine the
nature of the hemorrhage.
Prognosis. — Bronchial hemorrhage rarely proves immediately fatal, or
directly endangers life. The prognosis as to final result is always unfavor-
able ; it is in a large proportion of cases either the precursor of phthisis,
or a sign that phthisis already exists. It certainly always demands serious
consideration. The prognosis is much more favorable when the hemor-
rhage is due to the excessive action of the heart, or bronchial hypersemia
induced by the inhalation of irritating substances or gases than when it
occurs without any apparent exciting cause. Should haemoptysis be suffi-
cient to induce angemia, the latter condition is very obstinate and persist-
ent, more so than when it follows other hemorrhages.
Treatment. — Absolute rest in a cool room is of the greatest importance.
The patient should be placed in bed and not allowed to sit up, turn over,
or even speak above a whisper. If the cough continues and is constant, or
induces the hemorrhage, it must be quieted by full doses of opium. Ergot,
tannin, gallic acid, acetate of lead, spirits of turpentine, persulphate of
iron, or common salt may be administered ; the balsams, copaiba or sweet
spirits of nitre, maybe given, if their administration wiJl quiet the anxiety
of the patient or friends. It has never seemed to me that styptics or astrin-
gents have any control over bronchial hemorrhages. The application of ice
bags to the surface of the chest may be resorted to in extreme cases, but it
must be carefully done, for the reason that patients to whom ice bags are ap-
plied are exceedingly liable to have broncho-pneumonia follow their attacks
of bronchial hemorrhage. Dry cupping over the surface of the chest is of
service whenever the hemorrhage is preceded or attended by marked pul-
monary hyperaemia. Patients with hasmoptysis should be urged to eat ice
and drink freely of cold drinks. In all cases it is important to keep the
patient under observation until all bronchial irritation produced by the
presence of blood in the bronchial tubes has subsided. If there is tendency
to a return of the hemorrhage, everything likely to bring on an attack
must be carefully avoided, and the nutrition of the patient must be im-
proved by the administration of iron combined with a most nutritious but
non-stimulating diet. Moderate exercise should be taken daily in the open
air, and all mental and physical exertion should be avoided.
70
DISEASES OF THE RESPIRATORY ORGANS.
DISEASES OF THE LUNGS AND PLEURA.
I shall consider the diseases of the lungs and pleura under the following
heads :
Pulmonary Anmmia.
Pulmonary Collapse.
Pulmonary Emphysema.
Morbid growths in the Lung
and Pleura.
Parasitic Diseases. {Hydatids.)
Pleurisy.
Pulmonary Phthisis.
I.
Acute Lobar Pneumonia.
IX.
II.
Lobular Pneumonia.
X.
III.
Interstitial Pneumonia.
XL
IV.
Pulmonary Hypercemia.
XII.
V.
Pulmonary (Edema.
VI.
Pulmonary Infarction.
XIII.
VII.
Pulmonary Apoplexy.
XIV.
VIII.
Pulmonary Gangrene.
XV.
ACUTE LOBAE PlSTEUMOlSriA.
Acute Lobar or croupous pneumonia or pneumonitis is an acute general
disease characterized by an inflammation of the vesicular structure of the
lungs, with an exudation into the alveoli which renders them impermeable
to air : a condition called
" hepatization." A single
lobe, the whole of a lung or
both lungs may be simulta-
neously involved.
Morbid Anatomy. — Ana-
tomically as well as clinical-
ly, lobar pneumonia may be
divided into three stages.
First : Sb stage of congestion
or engorgement. Second: a
stage of consolidation or red
hepatization, lliird : a stage
of gray hepatization. Arte-
rial injection preceding en-
gorgement cannot be demon-
strated. Some have called
this injection the "dry stage''
of pneumonia.
Stage of Congestion or
Engorgement. — In this stage
the portion of lung involved
in the pneumonic process
does not collapse when the
thoracic cavity is opened ; it has a firmer feel than normal, and is more
or less distended ; its resiliency is lost ; it crepitates less than normal ;
Fig. 15.
Section of Lung showing a single Alveolus in the first Stage of
Lobar Pneumonia.
A, A. Wall of alveolus.
B, B. Distended, varicose and tm-tuous capillaries.
C, C. Alveolar epilhelial cells.
2>, 2). Blood globides in cavity of the alveolus, x 300.
ACUTE LOBAK PNEUMONIA.
71
Fig. 16.
Section of Lung in the second Stage of Lobar Pnenmonia.
The pulmonary alveoli are seen, filled ivith Pus corpuscles {A, A), changed Epithelial cells (B, S),
fibrillated Fibrin (C, C), and red Blood globules (Z>, V). x 250.
and often pits on pressure. It is not wholly airless, for air can be pressed
from one part to another. It is somewhat friable ; its color is a dark
brownish red, often purple; and its weight and specific gravity are
increased.
Pig. 17
Vertical Section of tlie Lung and Pleura in tlie second Stage of PI euro-Pneumonia.
a. Plastic emidation on the thickened pleura.
b. Infiltration pus.
c. Loose epithelial cells.
d. Enlarged blood-vessels.
The alveoli contain red blood-corimscles ie), pus cells (/), changed epithelial cells (g), and fibrillated
fibrin (i). The blood-vessels (h) in the alveolar ivalls are seen filled with red corpuscles, x 200.
73 DISEASES OF THE RESPIRATORY ORGANS.
On section a thin, frothy, blood-stained serum exudes. Sometimes
it flows freely on pressure ; it may be tenacious. When alcohol is
added to the fluid it coagulates into a granular and amorphous mass.
Dark blood flows from the distended capillaries. Occasionally, just under
the pleura and between the air sacs, there are small spots of extrav-
asation. ,
On microscopical examination of a thin section of the affected lung tis-
sue the lumen of the alveoli will be found diminished by the distended,
varicose and tortuous capillaries. Early in the disease some of the air-
sacs may be collapsed from pressure. The alveolar epithelium is swollen
and granular. In the air-cells are exfoliated epithelial cells, a few pus cells,
red globules and serum.' At the autopsy it is sometimes difficult to distin-
guish the stage of pneumonic congestion from pulmonary oedema and con-
gestion. In the latter the fluid in the alveoli is serum and contains no
cell elements. When a stream of water flows over the cut surface of a
pneumonic lung the color remains ; in oedema and congestion it dis-
appears.
Stage of Red Hepatization. — This stage receives its name from the color
of the lung and its resemblance, when cut, to liver-tissue. The aflected
portion has a dark liver or mahogany color, and is mottled, the mottling
becoming more marked as the stage advances. The volume of the affected
lung is increased; so much so that it often bears the impress of the ribs.
It is solid, firmer, and heavier than normal. Pressure does not indent, but
tears it ; it is friable, easily torn, and its torn surfaces have a granular
appearance. Its specific gravity is increased. It is airless, and there is
entire absence of crepitation. Artificial inflation is impossible.
On section the cut surface has a granular appearance ; the granules
correspond to plugs of inflammatory exudation, which fill the air-cells
and the small bronchi. Torn surfaces show the granulations better than
cut surfaces. The granules can be lifted out by means of a fine needle.
When cut a dirty red viscid fluid slowly oozes from the surface, or it may
only appear after twelve or twenty-four hours' exposure to the air. This
may be scraped from the cut surface. A piece of the inflamed lung quick-
ly sinks in water. Small spots of extravasation are sometimes seen. When
a stream of water is poured over the cut surface the color changes from a
maroon to a gray or a yellow-gray.
On microscopical examination the alveoli are found filled with a solid
exudation composed of a net-work of fibrillated fibrin, in whose meshes are
pus-cells, red globules, and changed epithelial cells. The latter are in
various forms — round, oval, quadrangular, triangular or irregular — and
have received dift'ereht names, according to the views entertained by differ-
1 It is still a disputed question whether the bronchial or pulmonary vessels are the chief source of the
pneumonic exudation. The lung-tissue is nourished by tlie bronchial arteries, while the pulmonary ves-
sels are the medium for the interchange of gases. Hence it is claimed that only the bronchial vessels are
implicated. Virchow has shown that pneumonic processes can be established when large branches of the
pulmonary artery are plugged; yet he admits that the pulmonary capillaries have, secondarily, much to do
with the exudation. Again, it is claimed that early in the disease the parts supplied ny the bronchial
vessels are not injected as they would be were they alone at fault. Probably both sets of vessels are
involved.
ACUTE LOBAR PNEUMONTA.
73
ent observers in regard to their origin. At first these cells contain fibrinous
material, but later they become granular, and then fat globules accumulate
in them. They may become discolored from imbibition of haematin. The
whole contents of an alveolus now present a more or less round form. The
interstitial connective-tissue between the lobules may be infiltrated with
pus and fibrin ; the pulmonary pleura is always coated with fibrin if the
surface of the lung is involved; and if the pleurisy precedes the pneu-
monia, or if it is extensive and an abundant plastic exudation covers the
Section of Lung in third Stage of Lobar Pneumonia, showing the Alveoli filled with Granular Matter and
Crlls.
A. Granular fibrin.
B. Ptis cells.
C. Mono-micleated cells.
The blood-vessels (D) of the alveolar walls are much less distended than in the preceding stages, x 850.
pleura over the inflamed portion of the lung, it receives the name oi pleuro-
pneumonia. The anatomical changes within the lung are, however,
unmodified by the more extensive pleurisy, although it undoubtedly delays
the processes of pneumonic resolution in the third stage. The red blood
globules give the color to the lung. This stage may last from twenty-four
hours to several days.
Gray Hepatization. — In the early part of this stage the lung remains of
the same consistency as in the second stage. There is no sharp transition
from red to gray hepatization. The mottling gradually becomes more
74 DISEASES OF THE RESPIEATORT ORGANS.
marked, so that the affected portion becomes " marbled," or has a " gran-
ite" look. The surface is gray. The consistency becomes less and less
until the tissue is a mere pulp, readily breaking down on pressure. The
change in color is due to pressure on the blood-vessels, to the decoloration
of the red blood globules, and to the fatty and granular change in the
inflammatory products. The weight, friability, and density of the lung
are increased.
On section the surface presents a uniformly dirty gray appearance. A red-
dish gray or dirty white puriform fluid flows either spontaneously or on slight
pressure from the cut surface. The " granular " look of the second stage has
disappeared or is indistinct. The amount of the accompanying oedema va-
ries ; when it is excessive a large quantity of serum exudes, and the tissue
does not break down so readily as in other forms of gray hepatization.
On microscopical examination the alveoli are found filled with numerous
round, mono-nucleated cells ; and the intercellular fibres that bound the
elements together have become granular. The alveoli are filled with a fluid
or semi-fluid mass, in which numbers of discrete oil globules and protein
granules are freely mingled. The contents of the alveoli are shrunken, and
between them and the alveolar wall is a layer of fluid, so that, in a thin
section, the contents of an air sac are readily lifted out by a camel's-hair
brush. The pleura over the affected portion is covered with a thin plastic
exudation.
Lobar pneumonia may terminate : (1), in resolution (recovery) ; (2),
suppuration (purulent infiltration) ; (3), abscess; (4), gangrene; or (5),
cJironic pneumonia.
During resolution the lung is moist, lighter than during hepatization,
has a yellow or a yellow-green color, and shows a marked loss of elasticity.
On section it is now granular, of a yellow-gray hue, and a tenacious puriform
fluid readily escapes when the section is pressed. Some oedema may still
remain. Microscopically the vessels are seen to have returned to their normal
calibre ; the alveolar epithelium is restored, the cells in the alveoli are
degenerated and broken down into a detritus. The coloring matter of the
blood gives origin to the pigment so plentifully scattered throughout the
liquefied mass. The contents are either expectorated or absorbed ; and the
lung returns to its normal condition.
When purulent infiltration or suppuration occurs, the surface of the lung
becomes yellow, its substance is soft, friable, moist, and it feels " miry," as
if an abscess were being pressed. On section a diffluent purulent fluid ex-
udes from the cut surface. The yellow color is due to the cells that are
undergoing fatty change and to the anaemia resulting from over-distention
of aveoli with pus. Microscopically the pus cells are seen to crowd the
alveoli and to infiltrate the inter-alveolar tissue. This infiltration may,
by its presence, interfere with the nutrition of the lung tissue, and the
alveolar walls may become thin, indistinct and rupture.
Abscess may follow purulent infiltration, a small anfractuous cavity be-
ing formed by the rupture of several alveolar septa. These abscesses vary
in size from that of a pea to one which may occupy an entire lobe. They
ACUTE LOBAE PNEUMON'IA.
75
may have a thick well-defined wall. Their interior is crossed by shreds
of broken-down tissue. They increase either by peripheral growth or by
fusion of several small abscesses. Their most common seat is in the
lower lobes. These abscesses may be obliterated by a process of granula-
tion and cicatrization. In such cases the abscesses are small, and com-
municate with a bronchus which allows a free discharge of their contents ;
or they may be encapsulated in firm cicatricial tissue, their contents sub-
sequently undergoing cheesy and then calcareous changes. They may open
into the pleural cavity (causing pyo-pneumothorax), or into the pericar-
dium. External fistulous openings have occurred.
Gangrene occurs in about two per cent, of all cases. It is liable to occur
when there is great constitutional weakness, and in chronic alcoholismus or
in septicaemia. It may be circumscribed or diffused. The gangrenous
portion consists of a dirty pulpy debris,
sometimes without the " gangrenous
fetor." When the part becomes dif-
fluent a cavity is formed and shreds
of gangrenous lung tissue are found
in a fetid fluid. About this there is
a zone of gray hepatized friable tissue,
which in turn is bounded by normal
lung tissue. In diffused gangrene,
the cavities are large and shreds of
tissue and vascular bands cross from
side to side, and the cavity swarms
with bacteria. Sloughing of the
pleura may follow such a process.
Chronic pneumonia may be a result
of lobar pneumonia, when resolution
Fig. 19.
Purulent Infiltration.
Section of Lung showing a single alveolus.
^ ^ ^ . • • 1 • n ^' ^^'^^olar ioall, largely inflUrated.
IS delayed and an interstitial mflam- -B. Transverse section of a small artery with infil-
. . , 1 T 1 T T . traf.ionofits walls.
matory process is established during C. Epithelial cells of alveolar wall.
j_-i„„i j; r .•!• rm D. Capillaries Of Wall of the air-vesicle.
the stage ot gray hepatization. The e. Pas corpuscles.
nponlinrlv >iQvr1 anri mrlorviaf/Mics n^n The alveolar cavify IS filled With pvscorpuscles^
peculiarly nara ana oeaematOUS con- gramdar fibrin, ana a few large nucleated cells.
dition that sometimes marks gray "* ^^'
hepatization is, by some, regarded as an intermediate stage between croupous
and interstitial pneumonia. Finally, the alveolar contents in the third stage
may undergo subsequent cheesy changes. Whether this occurs independent
of tubercle is doubtful. This is sometimes called cheesy infiltration as
opposed to tubercular infiltration.
In childhood, except before the second year, croupous pneumonia is rare.
Double pneumonia is, however, more frequent than m adult life. The
morbid appearances are the same as in adults. In old age the changes are
somewhat different ; the process usually begins in the upper lobes. In the
stage of engorgement crepitation is absent; and in the second stage the lung
is blue or nearly black. A section shows granules that are much larger
than in adult life. "Granulations" are very often absent in senile pneu-
monia. Gangrene is far more frequently a termination of lobar pneumonia
76 DISEASES OF THE EESPIRATOKY ORGANS.
in old age than at any other period. The highly rarefied state of the lungs
at this time of life seems to favor the development of the small abscesses so
common in the aged.
The most frequent seat of lobar pneumonia is the lower lobe of the right
lung ; the next most frequent seat is the lower lobe of the left lung ; then
the upper lobe of the right, the middle lobe of this lung being least fre-
quently involved.
Double pneumonia has been variously estimated as occurring in from 5
to 15 per cent, of cases. Even in ei)idemics it rarely ranges above 12 to 15
per cent. Double pneumonia is more frequent in the senile than in the
adult period of life.
The stage of congestion lasts from one to three days ; red hepatiza-
tion from three to seven days ; and gray hepatization from two to thirteen
days. In old age the stages merge rapidly into each other ; abscess
of the lung may occur within 36 or 48 hours after the onset. Ked hepa-
tization is not infrequently reached within the first six or eight hours
in the aged. The changes in the pulmonary pleura over a pneumonic
lung are quite characteristic. An uneven, thin, downy-looking layer of
plastic exudation covers its surface. This plastic layer may conceal the
liver-brown color of the pneumonic lung. As the third stage is reached
the opposing surfaces of the pleura may become agglutinated. The pleurit-
ic changes follow very closely those which occur within the lung. The
cells in the pleuritic exudation are mainly pus. The pleuritic membrane
is opaque, congested and ecchymotic. It may become so thick as to give a
dull note on percussion after resolution is reached. The right heart is
dilated ; and immediately after death both ventricles may contain clots.
The pulmonary vessels going to the involved part may contain thrombi.
Pericarditis is so frequent that it must be regarded as more than a coin-
cidence or complication. The liver and spleen are congested. The splenic
changes resemble those which occur in fevers. The lymphatics of the
lung are choked with fibrin and blood corpuscles. The deeper lymphatics
contain products identical with those in the pulmonary alveoli. In the
lymphatic vessels and in the bronchial glands there is always some evidence
of inflammation.
Gastro-intestinal catarrh is sometimes present ; and may be attended
by hemorrhage. The vessels of the brain are more or less engorged. Men-
ingitis is a not infrequent complication of pneumonia.
Etiology. — The specific cause of pneumonia is as yet undetermined.
The very existence of such a cause is, as yet, conjectural. Among the pre-
disposing causes age ranks first. There are three periods in life in which
the liability to pneumonia is greatest : early childhood ; 20 to 40 ; and after
60. Though catarrhal pneumonia is very frequent in children,' the state-
ment that lobar pneumonia is rare at that period is not correct. From reli-
able data it appears that lobar pneumonia is five times more frequent in the
first two years of life than in the whole succeeding eighteen. Nine-tenths
of all deaths after the sixty-fiftli year are caused by lobar pneumonia.
1 Yogel. Kinderkr. s. 222.
ACUTE LOBAE PNEUMOKIA, 77
Sex. In early life (before the third year) both sexes are equally at-
tacked. Between twenty and forty, when the condition of the sexes is
most diverse, the proportion of males to females attacked is 3 or 2 to 1.
After sixty, when the condition of the sexes again is similar, there is little
disproportion ; but always in favor of males. Whenever women work, or are
exposed, as men, the disease makes no discrimination as to sex. The inier-
peral state does not seem to increase the predisposition to pneumonia; but
it is more apt to occur at the time of the catamenia.
The general hodily condition oi and before the pneumonic seizure has but
little predisposing influence. It is a question whether the strong or the weak
are oftenest attacked. Convalescents from acute and severe illness, habitual
alcohol drinkers and those who are " malarious " are far more liable to pneu-
monia than those who are free from such conditions. Enervating habits,
poverty, dyscrasia (cancer and chronic nervous diseases especially) and anti-
hygienic surroundings are predisposing causes. Diphtheria, measles, erysipe-
las, small-pox and the other acute infectious diseases must be regarded as pre-
disposing causes. Chronic and acute uraemia and all diseases which arise
from the retention of excrementitious products are powerful predisposing
causes. Chronic blood diseases act in like manner. Long-continued passive
pulmonary hyperaemia — e. g., from heart disease or from hypostasis — leads to
pneumonia. The pneumonia that frequently occurs during acute articular
rheumatism has been regarded by some as " metastatic from the joints." A
more rational view is that it is due to the blood changes which are part of the
rheumatic fever. One attack of pneumonia predisposes to others ; twenty-
eight attacks have been noted in one individual. When pneumonia follows
a severe blow or injury to the chest or shock from any traumatic cause, the
injury or shock must be looked on as a predisposing cause. In the aged
lobar pneumonia has developed as soon as four hours after fracture in the
hip joint. Cold does not affect the pneumonia rate except in the old.
March and April statistics usually exhibit the highest pneumonia rate. A
continuously low or high temperature has much less influence than a
changeable temperature. Its etiology shows that it is a disease predisposed
to by all things that depress the vital powers. Children and the aged are
greatly depressed by the intense cold of winter and the chilling winds of
March and April. In Europe it is often called the " May epidemic."
Pneumonia is unknown in the Polar regions ; it -is common along the
coast of the Mediterranean Sea. Elevation above the sea seems to predis-
pose to it both in hot and cold climates. North and east winds favor its
development. Eainy seasons do not influence the pneumonia rate to any
appreciable degree; nor do damp or marshy districts. But both have a
marked influence over bronchitis and other local pulmonary diseases. It is
a well-established fact that pneumonia occurs oftener among the poor than
among the rich, the private soldiers than their officers, the sailor on shore
oftener than on ship, the soldier oftener than the civilian at the same mili-
tary post. All this is explained by the better hygienic surroundings of the
one class as compared with the other. The less the resistance capable of
being opposed to some (unknown) pneumonic influence, the more strongly
78 DISEASES OF THE EESPIRATOEY ORGAN'S.
predisposed is the individaal. Every increase in population in a district
increases the pneumonia rate. ^ In New York City from 1840 to 1858 the
mortality rate of pneumonia was 5.85 per cent. From 1859 to 1877 it was
6.2 per cent.
The question now meets us : is pneumonia a specific constitutional dis-
ease, an acute infectious disease, or a local inflammation ?
The following tend to prove that it is not a local malady. All kinds of
solid and gaseous inhalations and traumatism have failed to produce lobar
pneumonia.^ They always induced lobular and not lobar pneumonia. Sec-
tion of the vagi produces hepatization, but not croupous pneumonic con-
solidation. Cold does not influence the prevalence of pneumonia as it
would were it a local disease {e.g., bronchitis). Wet and cold increase a
bronchitis but not a pneumonia rate. Lobar pneumonia is more prevalent
in our Southern than in our Northern States. Epidemics in the West
Indies were more devastating than those in Iceland. On our continent
the prevalence of pneumonia increases from pole to equator. All acute
general diseases increase with the population ; pneumonia does this. Sta-
tistics show pneumonia to be more frequent in New York City now than
twenty years ago.^ While cold has something to do with its development,
the exciting effect of cold cannot be accepted. Again, there is no relation
between the amount of lung involved and the intensity of the symptoms.*
In local inflammations the reverse of this is true. No second chill occurs
when another lobe, part, or the other lung is attacked.^ Prodromata some-
times occur in pneumonia. But the absence of regular and constant pro-
dromata, the absence of a (known) period of incubation, of a typical tem-
perature range, and of characteristic surface phenomena, the fact that the
disease is not contagious — these are the reasons advanced by those who re-
gard it as a local, not a general disease. The resemblances of pneumonia
to acute general diseases are : distinct initiatory chill, an orderly pyrexia,
a rather typical course, i. e., a day of abrupt crisis, a definite duration, and
the symptoms following in regular sequence. There is a peculiar facies ;
an occasional herpetic eruption ; nephritis is not rare ; the cerebral symp-
toms resemble those of the exanthems ; there are sweats and sudamina ;
and its mode of commencement — coma in the old and convulsions in the
young — indicate that it is an acute general disease. Etiologically it is often
developed under conditions similar to those which attend the development
of diphtheria and cerebro-spinal meningitis ; atmospheric conditions
are acknowledged factors in its causation. English writers describe a
*' sewer-gas pneumonia." There have been epidemics of pneumonia in
garrisons and aboard ship where there was overcrowding, bad hygiene,
1 Hirscti says: " The amount of mean fluctuation in the mortality from pneumonia is in inverse ratio to
the density of the population."
^Virchoiu's A7-chiv,Bd. LXXX. Reidenhain, Sityl. K. K. Akad zaWien,867. Beitz, GendHn, Hist. Anat.
des Inflam
^ N. T. Med. Record : Article on Causes of Death in Acute Pneumonia. — Loomis.
■*"The local inflammation * * * offers no sort of parallelism to the accompanying fever. "^
Slurges.
^ " Small consolidations with high fever and severe constitutional symptoms, and extensive infiltrations
with a comparatively slight fever— this is the rule, not the exception."— Ziemssen's Cycl. Vol. 5, p. 146.
ACUTE LOBAR PNEUMOKIA. 79
etc., etc.^ There is a ^'pythogenic" pneumonia arising under miasmatic
influences which is contagious." The epidemic form of pneumonia at cer-
tain times bears the distinct characteristics of a specific infectious disease.*
Miasmatic and zymotic pneumonia are names indicative of a supposed
origin. We have abortive cases of pneumonia, just as we have abortive
typhoid and cerebro-spinal meningitis. Again, the names sthenic, asthenic,
malignant, icteric, etc., etc., indicate varieties similar to those found in
fevers and acute general diseases. Pneumonia is allied to acute general
diseases by the fact that certain complications occur with more or less
regularity — lesions in the peri- and endocardium and albuminuria — and
that abortion is usually induced when it attacks pregnant women. It has
visceral and blood changes very like those of fevers. Pneumonia is some-
times a disease of intra-uterine life. No local disease occurs in the foetus,
but fevers frequently do.
The success of modern methods of treatment based on this belief bears
evidence to its being a general (self-limiting) acute febrile disease. The
nature and action of the poison that may be supposed to cause pneumonia
are indicated by the following facts : — hyperinosis does not seem capable
of causing pneumonia : fibrin increases as hepatization advances and does
not ante-date it or the pyrexia.^ Its resemblance to the acute general diseases
is mainly in its nervous phenomena, and the complications which render
pneumonia dangerous are those which diminish the nerve supply or weaken
the muscle-power of the heart.
Symptoms. — Subjective or rational symptoms. The invasion in about
one-fourth of the cases is preceded by prodromata.^ In old age they are
more frequent than in adult life (60 per cent.). They rarely occur in chil-
dren. For a day or longer there may be malaise, anorexia, headache, dull
pains in the limbs, back and lumbar region, vertigo, epistaxis, and slight
diarrhoea, or there may be slight jaundice, flashes of heat and rigors. Fly-
ing pains in the limbs and chest are common in old age. Eise in tempera-
ture is sometimes a prodrome. In Bellevue Hospital in 1877 a patient, for
two or three days preceding the initial chill, had a temperature of 102°
-103° F. In epidemics febrile symptoms and diarrhoea are common.'' In
most cases the invasion is sudden and the disease is ushered in by a distinct
chill.'
Generally the patient is seized with a chill in the night. This chill is
1 In the U. S. Sanitary Conimission Meynoirs Dr. Russel reports : " The surgeons on duty with the reg-
iments in the barracks (Benton, Mo.) report that men occupying the same bunks with those afEected were
Tery much more liable to be attacked than those more remote. Some of the most intelligent surgeons
believed that it was actually contagious."
2 Dublin Med. .lournfxl, Vol. I. 1874.
3 Berliner Klinische Wochenschrift, 1879, No. 'S^%.—Kuhn.
■* Pneumonia resembles quinsy and acute articular rheumatism. Trousseau finds a resemblance between
erysipelas and pneumonia. Sturges places it in a "middle class " between specific diseases and local in-
flammations. Cohnheim calls it a miasmatic contagious disease. The idea of its being a specific general
disease dates from the eighteenth century.— A'tw. Theo. More/. 1786, StracMns.
^ Grisolle found them in about 25 per cent, of his cases. Fox found them in 28 per cent.
* London Lancet^ 1878, Vol. II.
' 77-80-92 per cent, are the figures given by Pox, Louis, Hubs, Grisolle and Lebert as representing the
frequency of the initiatory chill.
80 DISEASES OF THE RESPIRATORY ORGAN'S. "
intense and prolonged, more so than in any other disease except pyaemia
and malarial fever. It lasts from one half an hour to three hours. Its
abruptness and violence are characteristic. In children, headache, nausea,
vomiting, delirium and convulsions may usher in the disease, its onset
resembling that of an exanthem ; when these do not occur in all their in-
tensity, the child is restless or stupid, and there are thirst and anorexia,
increasing towards night. Again, a child may awake in the middle of the
night with a burning skin, bounding pulse, flushed face and hacking cough.
When, in children, the pneumonia is ushered in by convulsions followed
by a loss of consciousness, the consolidation is usually at the apex,
A distinct chill is less frequent in the pneumonia of old age ; yet when an
old person has a marked chill pneumonia may always be suspected ; although
less frequent it is more diagnostic than in adults. A protracted fit of shiv-
ering and pain in the side are the two initial symptoms in about 50 per
cent, of the cases of acute sthenic senile' pneumonia. In the other half of
the cases the onset is attended by slight increase in the frequency, and
irregularity of the respirations, slight pyrexia, short hacking cough, and a
feeling of great exhaustion. Intense weakness may be the only symptom.
Nausea, vomiting, diarrhoea and collapse, or a semi -comatose condition, not
infrequently usher in a senile lobar pneumonia. In a very few cases, stu-
por, coma, and disturbance of intellect may be the only early noticeable
symptoms, and they may persist during the whole course of the disease.
The initial cliill (whenever occurring) is rarely repeated.
With the initial symptoms there is a rapid rise in temperature accom-
panied by pain in the side, which is aggravated by coughing and by deep
inspiration. The breathing is accelerated, there is dyspnoea, cough, expecto-
ration, the countenance is flushed and anxious, there is headache, loss of
appetite, and intense thirst. The urine is scanty and dark. The bowels are
constipated. The tongue is heavily coated. The symptoms increase until
the day of crisis, when they either suddenly remit and the patient breaks
out in a profuse sweat, or they subside by lysis. The defervescence is usually
reached between the fifth and ninth day.
The following is an analysis of the prominent objective symptoms of
pneumonia :
The respiration is more constantly increased in frequency in pneu-
monia than in any other acute disease, and varies from 30 to 80 per min-
ute. Usually, in acute diseases, the respirations increase with the pulse
rate ; in lobar pneumonia the ratio between pulse and respiration is early
perverted. The respiration may be 80 per minute and the pulse rate not
more than 100. The acceleration is not in proportion to the amount of
lung involved, and it does not depend on the pain in the chest or the py-
rexia. It \^ panting, not "catching," in character. It may or may not be
accompanied by dyspnoea. In children accelerated breathing is more
marked than in adults. The discrepancy between the pulse and respiration
is not as marked as in adults ; in the former the pulse may range between
150 and 160, and in the latter between 80 and 90. Expansion of the nos-
trils is an early symptom in the pneumonia of children. In old age expi-
ACUTE LOBAR PN"EUMONIA. 81
ration is sudden, the whole act is '' panting." The average number of respi-
rations per minute is 22, and the duration of inspiration is to that of expi-
ration as 6 to 9. It is rarely accompanied by dyspnoea. An exaggeration
of (normal) senile " catching breathing" is one of the most frequent forms
of abnormal respiration in senile pneumonia.
Dyspnma, although frequent, is by no means constant. It does not de-
pend upon the amount of lung involved, since double pneumonia may
be accompanied by less dyspnoea than when only a single lobe is involved.
It is often so great that the patient is unable to lie down. The greatest
dyspnoea occurs where there is marked nervous prostration. In " second-
ary" and complicated pneumonia the dyspnoea is greater than in primary
uncomplicated pneumonia ; it is panting, not labored. In cMUlren, dysp-
noea is most marked when the apex of the lung is involved. In old age
dyspnoea is so infrequent that even with respiration at 70 they do not
complain of difficult breathing. When a patient over seventy years who is
asthmatic, or who has chronic bronchitis, develops a pneumonia, the dysp-
noea that may have accompanied the previous condition diminislies. He
simply feels exhausted, and usually dies suddenly.
Pain follows the chill ; it is situated underneath the nipple of the af-
fected side. It is sharp and stabbing, often located over the pneumonic
spot, and is intensified by coughing, sneezing and deep inspirations. In
central pneumonia there is no pain ; it is the pleurisy that causes it. Pneu-
monia itself is a painless disease. Pain in the affected side rarely continues
beyond the third or fourth day. If it continues beyond the eighth day it
is evidence of pleuro-pneumonia. It is present in 85 per cent, of all cases.
In old age pain is never severe. It is rather a dull, uneasy feeling referred
to the whole chest or to the abdomen.
Cough is present in over 90 per cent, of the cases. It comes on within
twenty-four hours after the advent of the disease. At first it is short,
'Slacking "in character. It may entirely cease just before a fatal issue.
It is more constant in children than in adults; it is sometimes parox-
ysmal. Old people with pneumonia often have no cough. When present
it may be so slight as to escape the notice of both patient and physician.
Should bronchitis or asthma have preceded the pneumonia, the cough
diminishes, and may wholly disappear on the advent of the latter. The
expectoration is characteristic. In the first forty-eight hours of the dis-
ease it is simply frothy mucus. Then it becomes semi-transparent, viscid,
gelatinous and tenacious, but never opaque. So tenacious is it that the
cup containing it may be inverted without spilling the mass. It can be
drawn out between the thumb and finger into thin strings. This tenacity
in great part causes the difficulty of expectoration. Its color varies. About
the second day the "brick-dust" or "rusty" sputa may be observed.
This color is due to the presence of blood. The sputa may be creamy and
yellow, or of a very dark or prune-juice color ; the latter is indicative of a
depraved blood state, and occurs especially in alcoholic subjects. As death
approaches the sputa become scanty, less tenacious, more diffluent and
often of a greenish hue. Greenish sputa may occur in the middle of the
6
82
DISEASES OF THE RESPIRATORY ORGAKS.
pneumonia and during resolution, and in "bilious pneumonia." When res-
olution occurs the sputum becomes abundant, and of a yellow, creamy color.
There may be no sputum throughout ; or it may not appear until the
sixth or even the twelfth day. The sputum may remain brick-dust till
the ninth or tenth day. In pneumonia of the apex and in that compli-
cating acute articular rheumatism the sputa are often entirely wanting.
In children sputa are usually absent ; but brick-dust masses may be de-
tected in the matters vomited. In senile pneumonia expectoration is never
an early symptom, and is liable to cease suddenly during any period of
the disease. Rusty sputa are present in about 33 per cent, only of such
cases ; frothy or "catarrhal" sputa are the rule. A chocolate-looking
serous sputum, appearing soon after the onset of a pneumonia, shows a
depraved condition and indicates "typhoid pneumonia." Examined under
the microscope the sputum is found to contain swollen spheroidal red and
white blood discs, minute fat spherules and the other elements described
under morbid anatomy.^ In about 75 per cent, of cases there will be found
in the sputa (when floated in water) casts of the alveoli and bronchioles.
The chemical constituents of the sputa are albumen and mucin. Tyrosin
and sugar are sometimes found in it. There are two explanations of the
acid reaction of the sputa : Verdeil
thought it due to excess of pneumic
acid ; Bamberger claims that it is due
to deficiency in alkaline phosphates.*
Early in pneumonia there is an increase
in the chloride of sodium in the serum,
and it has been thought that, from the
rapid and excessive cell-transformation
in the lung, chloride of sodium is at-
tracted to that organ. ^ The expired air
in pneumonia is colder than normal,
and there is a diminution in the amount
of carbonic acid excreted.
The temperature-range of a typical
case of lobar pneumonia indicates that
it belongs to a remittent or sub-remit-
tent type, rather than to the class of feb-
rile disorders marked by a continuously
high temperature. Earely, it is inter-
mittent. The temperature rises sud-
denly during the initial chill, and in
two to three hours after it may range from 102° to 105° F. After the first
iwenty-four hours the temperature is subject to morning and evening exacer-
FiG. 20.
Temperature Record in a case of Acute Lobar
Pneumonia, ending in Recovery.
' Dr. Walshe affirms that pus cells are not found in the brick-dust sputum.
^ Catarrhal sputa contain 10 to 14 per cent, of alkaline phosphates : pneumonic sputa none. In catarrh,
soda is to potash as 31 to 20 : in pneumonia, 15 to 41. There is .5 per cent, more sulphuric acid in pneu-
monic sputa than in catarrhal.
3 In one case where there was no chloride of sodium in the urine, 10 per cent, of the solid material of
the sputa consisted of that sail.
ACUTE LOBAR PNEUMOJSriA.
83
DAY:
2.
3,
4
5.
G,
7
a
9.
10.
,
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= z
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i
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Fig. 21.
Temperature Record in a case of Acute Lobar Pneu-
monia, with observations every six liours. Re-
covery.
bations and remissions ; but the morning temperature is rarely 2° F. lower
than the evening — the difference in the .SMZ>-remittent type may amount to
only -^-° or 1° F. At midnight a second exacerbation may occur, but not so
marked as that occurring early in
the evening. Rarely, remissions
occur in the evening and exacerba-
tions in the morning. The tem-
j)erature is usually highest on the
evening of the third day. In some
cases the maximum is not reached
till a few hours before the crisis.
Just before death the tempera-
ture may rise very high, even to
1091° F. If, after the fourth day,
a marked remission is followed by
a high temperature, it indicates
either an extension of the pneu-
monia, or the occurrence of some
active complication. If, in a mild
pneumonia, the temperature sud-
denly rises, it indicates a grave
complication. The sudden fall of
temperature on the fifth or sixth
day indicates a crisis, and the beginning of convalescence : it may occur in
the morning or after the evening exacerbation. In a typical case it is usual
to find the temperature on the morning of the fifth, sixth, or seventh day
two or more degrees lower than on the preceding night. Then it falls
gradually until a normal, often a subnormal temperature is reached. The
crisis may show itself by successively increasing remissions, while the tem-
perature during the exacerbations rises to the same height as before. It is
usual for the remission to be exaggerated just before the crisis ; again,
the fever may reach its highest point Just before the final fall. When
the temperature declines gradually {"lysis"), a, normal point is visu-
ally reached by the ninth day, sometimes not until the twelfth or
fourteenth. A protracted, slow fall is met with oftenest in the weak,
debilitated, and in those who have been bled or depressed by treatment.
A continuously high temperature after the tenth day indicates purulent
infiltration. (See Fig. 19.) Pneumonia at the apex has the highest
temperature range. The fifth and seventh are the days of crisis in the
majority of uncomplicated cases. Of 867 cases, 677 ended before the
eighth day. Neither the height of the fever nor the amount of lung in-
volved influences the day of crisis. In hilious pneumonia occurring in mi-
asmatic regions, the temperature is paroxysmal. In children the tempera-
ture rises very rapidly, sometimes reaching 106° in the first twelve hours.
The highest recorded temperatures are in the pneumonias of children. The
critical fall is remarkable, the temperature quite often reaching 2° to 2^**
5e?ow normal. This low temperature may continue two or three days. In
84
DISEASES OF THE KESPIRATOKT OEGAN"S.
old age it is mainly by the temperature that the exact time of invasion ia
determined. The rectal temperature may be 103° to 104'' on the first days,
and then continue at the initial point for three or four days^ with morning
and evening oscillations of a degree or l|-°. The temperature does not be-
gin to rise until several hours after the chill, if the chill occur. (See Fig.
21.
^he pulse varies with the severity, extent and stage of the pneumonia.
In mild cases it ranges from 90 to 120 ; if it continues above 120 the case is
severe. The pulse is soft
full
l^a.y
xof
J03.
^r
/
5
n
^
z^
^
m
Z=?5
^23^
/O
//
/-2
^ Later it
and
Fig. 22.
at the onset.
becomes small
and feeble. In severe
cases, and when the ner-
vous system is markedly
implicated, it is rapid,
small and feeble, and may
be 130 to 140 or 160 at
the onset. High temper-
ature is usually accom-
panied by a rapid pulse,
and vice versa. When the
critical fall of tem|)era-
ture occurs, the pulse
falls correspondingly.
After the third or fourth
day the pulse exhibits
Temperature Record in a case of Acute Lobar Pneumonia passing dlCroHsm IXi many CaSCS I
into purulent infiltration and ending in Death on the 12th day. • , , . ■,
it may be jerky, very
compressible and intermittent. Just before death, it becomes markedly
slow in many instances. It is not the most extensive pneumonia that
is accompanied by the greatest flagging of the heart. Heart-failure may
exist before,^ or just as hepatization is commencing. The pneumonia
with the highest temperature is not the one where heart failure is
most marked or occurs earliest. When the heart is failing, the pulse
shows that the artery is unequally filled by each beat. First, the force
varies ; then waves occur, and finally true intermission. I have been able
to detect heart-insufficiency by these variations in the pulse within twenty-
four hours after the onset of the pneumonia, and occasionally during the
initial chill. In children the pulse-rate is greatly increased : it may be 200
per minute. It is small, unequal and irregular, but never intermittent. In
senile pneumonia the pulse is not a reliable indication. Its average rate is
73 to 78 ; rarely does it reach 120. In old age, both in health and disease,
the pulse has a fictitious hardness, on account of arterial rigidity. It may
not be irregular or intermittent when the heart is, and vice versd. Inter-
mittence of the pulse in senile pneumonia is common, independent of any
cardiac disturbance. In all cases of senile pneumonia, the pulse should he
counted at the heart.
ACUTE LOBAR PNEUMONIA. 85
The shin is often hot and dry until the crisis ; but it may be bathed in
perspiration from the onset. A moist surface is regarded as a favorable
sign, but when, at the acme of the disease, the parched skin becomes moist
and the patient is not relieved, it is an unfavorable symjDtom. In most
cases, the expression of the countenance is characteristic. The face is anx-
ious, and over the malar bones is a mahogany flush, not diffused as in ty-
phus fever, but well defined and circumscribed ; it is called the ^^pneu-
monic sjjot." The rest of the face is pale.' Usually, one cheek is more
flushed than the other ; this is due to disturbance of the vaso-motor sys-
tem. When there is a great disturbance of the circulation, or when vaso-
motor disturbance is excessive, the lips become cyanosed. At the time of
the crisis the lips become pale. In about 50 per cent, of cases, pneumonia
is attended by an herpetic eruption upon the cheeks, nose, li2)s or eyelids.
It is rare before the second or third day, and it may not occur until the
crisis is reached. Herpes occurs with varying frequency in different years,
and is more commonly met with in pneumonia than in any other febrile
disease. One winter, nearly every case of pneumonia in Bellevue Hospital
was accompanied by "herpes labialis." Sudamina may accompany profuse
sweatings. In children, while the surface of the body is hot and dry, the
extremities are cool, and the pneumonic flush is bluish or violet-colored.
Cyanosis of the extremities is more frequent than in adults, and herpes la-
bialis is more constant. All the cutaneous symptoms are exaggerated in
children. In old age the pneumonic flush is often the first objective sign
of pneumonia. The eyelids alone are cyanotic. If the face is at first
dusky, it later assumes a sallow hue, and the surface heat is succeeded
by a cold, clammy perspiration.
The cerebral symptoms are not very significant in the early stages of
pneumonia. Headache is the first to occur, and may continue throughout
the entire course of the disease. It usually diminishes after the third day.
When severe in the evening there will be slight delirium at night, so slight
as often to escape notice. Delirium and convulsions rarely occur except
in the debilitated and in those of dissipated habits. It is most frequently
met with in drunkards, and then assumes the character of delirium tre-
mens. Sometimes in non-alcoholic pneumonia the delirium assumes an
active, violent character. Whenever delirium is present it is important
to make diligent search into the former habits of the patient. Pneumonia
of the apex is oftenest accompanied by severe cerebral symptoms. The
delirium may pass into coma. When delirium and headache are marked
symptoms, muscular tremors ("subsultustendinum") are very apt to occur
with insomnia and frightful hallucinations. These cerebral symptoms
occur so early and are so marked in alcohol drinkers that they mask the
pneumonia ; a physical exploration alone reveals the disease. When de-
lirium is present in the weak and feeble it is of the low, muttering,
" typhoid " type, and soon passes into a state of stupor. Photophobia,
' Bouillard regards the flush as best mai-ked in pneumonia of the apex. Some regard the flush as best
marlied, or existing solely, on the cheek corresponding to the affected side ; others us on the opposite
side. —Juccoud.
86 DISEASES OF THE KESPIRATORY ORGANS.
disturbances of vision, and deafness are rare. In cliildren the cerebral
symptoms are more prominent than in adults. Stupor and restlessness on
the one hand, or headache, delirium and convulsions on the other, may
usher in pneumonia in children, and they may rapidly pass into a semi-
comatose condition. Convulsions are as common in children as they are
rare in adults. They may be general, resembling those of epilepsy
("Eclamptic Pneumonia"), or they may attack single muscles or groups.
Tetanus and opisthotonos are uncommon. Delirium and coma occurring
late are usually followed by fatal coma. The cerebral disturbances often
strikingly resemble those of acute meningitis. In senile pneumonia head-
ache may persist throughout the disease. It is usually accompanied by
mild delirium, especially when the pneumonia is at the apex. It is a busy,
active delirium, and the patient has a constant desire to get out of bed.
The symptoms referable to the digestive tract are not important.
Nausea and vomiting are among the initial symptoms, and occur in
about 75 per cent, of cases. At first the tongue is covered with a white
fur ; later it becomes dry. Anorexia is marked, and thirst is intense.
The lips and tongue may become brown, dry and cracked, and sordes
collect on the teeth. Diarrhoea may be an initial symptom ; it usually
accompanies nausea and vomiting. The bowels are usually constipated.
In children nausea and vomiting are not only common, but in 25 per
cent, usher in the pneumonia. They usually cease by the second day.
Persistent diarrhcea often precedes death. In senile pneumonia the tongue
early becomes dry, brown and shrivelled, and is protruded with difficulty.
Although these patients may not complain of thirst, they drink with
avidity when fluid is placed to their lips. Dysphagia is frequent. At the
crisis critical diarrhoea is more frequent than critical sweats. Loss of
strength occurs early, and is more marked in pneumonia tlian in any other
acute disease except typhus fever. Eecovery is rapid when convalescence
begins.
The wrme in pneumonia is scanty, high colored and of high specific grav-
ity. The amount of urea and uric acid excreted is two or three times
more than normal ; it increases until the crisis, and then suddenly dimin-
ishes, falling below normal. Inorganic salts, chloride of sodium especially,
are constantly diminished and may be wholly absent. Eeappearance of the
chlorides marks the approach of convalescence. At the crisis they are
present in excess. Urea and uric acid are also sometimes retained in the
system ; and at the crisis there will then be a critical diarrhoea followed
by prolonged convalescence. Bile pigment and sometimes the bile acids
appear in the urine. Slight albuminuria is present in 35 per cent, of the
cases. The severer the pneumonia the more marked the albuminuria.
Epistaxis may occur at any time, but is most frequent at the onset and
at the crisis. Swelling of the veins of the hands in children is an unfavor-
able symptom . When pneumonia is to terminate fatally dyspnoea greatly
increases, the patient suddenly " sinks," the pulse becomes small, rapid,
intermittent and dicrotic ; moist rales are heard in the larger bronchi or
trachea, and there are physical evidences of pulmonary oedema. The sputa
ACUTE LOBAE PNEUMONIA. 87
become frothy, liquid, and blood-stained ; they may be entirely suppressed.
The respirations are more and more hurried, and the radial pulse becomes
imperceptible. The face is sunken and livid ; the extremities become
cold, and the capillary circulation more and more imperfect. Tlie body is
bathed in a profuse cold sweat. Death is usually preceded by a semi-coma-
tose state. The temperature may steadily rise up to the time of death, or
there may be " defervescence." Death may occur at any period of the dis-
ease. In alcoholic pneumonia death is preceded by active brain symptoms.
In children death is often preceded by convulsions or coma ; sometimes
exhaustion or collapse is most marked. Cyanosis and extreme rapidity of
pulse are common in children before death.
Senile jpneumonia may end fatally within a few hours after the onset
in a most unexpected and quiet manner. In other cases sallowness of the
skin, cold, clammy sweat, working of the auxiliary muscles of respiration,
a feeble, rapid, irregular and intermittent pulse, and a sudden rise or fall of
the temperature may precede the fatal issue.
Abscess. — Acute pneumonia terminates in abscess in \\ to 3 per cent, of all
cases. It is met with oftenest in debilitated weak subjects. The sputa are
copious and fetid, yellowish in color, consisting almost wholly of pus. The
fever is of the hectic type, and is accompanied by rigors and sweats. The
patient grows weak and emaciated, death resulting from exhaustion, from
asphyxia, or from discharge of the abscess into some neighboring cavity or
organ. ^ The physical signs of the cavity are the most reliable evidences
of an abscess. Abscess is rare in children. In old age there are no well-
marked signs.
Gangrene as a termination of pneumonia has been found in about 14
per cent, of cases. This, however, is an exceptionally high percentage.
Its occurrence is marked by signs of sudden collapse. The pulse is raj^id,
feeble and intermittent ; the face is pale and "death-like ; " there is pro-
fuse expectoration of blackish-green masses containing shreds of decom-
posed lung substance having a gangrenous odor. The breath is offen-
sive and the body has a cadaverous smell. The sickening odor of pul-
monary gangrene is most perceptible after coughing. Gangrene has its seat
in the lower lobes of the lung, and it is here we must search for its ill-defined
physical signs. In old age when pneumonia is to terminate in gangrene
typhoid symptoms are present early and death occurs in collapse, usually
within five days from the onset.
Purulent infiltration has symptoms that differ but slightly from those
of the third stage of pneumonia. When resolution does not take place at
the period of crisis and the temperature remains high, accompanied by
symptoms of prostration and profuse purulent expectoration, purulent
infiltration may be suspected. Somnolence and mild delirium 'are quite
frequent during " purulent infiltration." The sputum contains a large
number of cells in various stages of fatty degeneration. The fever has
regular evening exacerbations, and it may range higher than at any other
1 Fox and Green state that abscess is located preferably at the apex ; Da Costa says at the base.— Guy's
Hospital Reports. Ser. VII. 1848.
88 DISEASES OF THE RESPIRATORY ORGANS.
period in the disease. The tongue becomes brown and dry, and sorde*
collect on the teeth and mouth. Eecovery is slow and convalescence
tedious. Death results from exhaustion.
Typlioid pneumonia is a term that has been applied to a pneumonia
attended by tyj)hoid symptoms. It has also been called ''asthenic,"
*' low," or "nervous " pneumonia. It is marked by extreme prostration that
may exist from the onset. In the majority of cases, well-marked pneumonic
symptoms, after having been present for a short time, soon give place to
intense nervous prostration and adynamic symptoms. There is no sputa,
no dyspnoea, no pain, no cough. Sordes collect on the teeth and gums.
The tongue is thickly coated, and later, covered with black crusts. There
is incontinence or retention of urine. The pulse is small and rapid. There
is stupor, somnolence, and continual low, muttering delirium. This form
is common in the aged. In some cases there is marked disturbance of the
special senses — the speech being most affected. Tremor and subsultus
tendinum are frequent. Typhoid pneumonia may be accompanied by
glandular swellings, sharp and darting muscular pains, arthritic symptoms
or vomiting. It is not infrequent in epidemics, and it may follow
Bright's disease, erysipelas, alcoholismus, or phlebitis. Eecovery is always
possible, but is slow and tedious, and may not begin until the twelfth or
fourteenth day. A modification of typhoid pneumonia sometimes accom-
panies dysentery, intestinal catarrh or phlegmonous gastritis. There is
great sweating, profuse colliquative diarrhoea and high fever.
Bilious, or gastric pneumonia, is lobar pneumonia occurring in mala-
rial districts, and accompanied by gastro-enteritis with hepatic symptoms.
It is sometimes called "malarial pneumonia." It has the characteristics
of a severe pneumonia, but the fever is paroxysmal. The tongue is heavily
coated ; nausea and vomiting are common and may be persistent. The
epigastrium is distended and tender, the skin more or less jaundiced ; the
liver is enlarged, and there is constipation or exhausting diarrhoea ; the
latter is accompanied by greenish-black, viscid and inodorous discharges.
" Bilious" pneumonia may be sthenic or asthenic ; but prostration is apt
to be nearly as marked as in the typhoid variety. The symptoms of bilious
pneumonia have frequently led to the diagnosis of ^^ typlioid gastric
fever.''"' It runs a much more protracted course and has a much longer
period of convalescence than the typhoid variety ; vomiting is "bilious,"
and somnolence and stupor may indicate a fatal issue.
Latent pneumonia seldom occurs in adults unless it complicates some
disease whose symptoms are so severe that the pneumonia is obscured.
Inter-current senile pneumonia is always latent; and Grisolle states that
a physical exploration gives negative results in the majority of instances.
Senile pneumonia may run its course without expectoration, dyspnoea,
flushed face or physical signs. Its diagnosis is then difficult. It is to be
remembered that of all phlegmasia of advanced life, pneumonia is the
most frequent ; and of all the acute diseases of advanced life it causes the
highest temperature range and the greatest prostration. When an old
person has a slight rigor, followed by a febnle movement attended by great
ACUTE LOBAR PNEUMONIA. 89
prostration for which there is no explanation, pneumonia may be suspected
even though all its usual signs are absent.
Intermittent 'pneumonia, which is by some described as a distinct type,
is a form of acute pneumonia in which a malarial element is so pronounced
that all the subjective and even the physical signs undergo distinct inter-
missions, returning each day with increased severity. It may assume the
quotidian or the tertian type. During the intermission the temperature
may fall to the normal. Recurring chills and sweats are often present ;
and the pneumonia is not infrequently double. By some it is regarded as
peculiar to old age ; it is very rare at any other period. Those malarial
influences that give rise to this type of pneumonia are more frequently met
with in our Southern and Western States than in any other part of the
world.
Physical Signs. — First Stage, or Stage of Congestion.— The physical signs
indicative of the first stage of lobar pneumonia are usually present within
twenty-four hours after its invasion. If the pneumonia commences in the
central portion of the lung their appearance may be delayed till the third
day. By studying these signs in connection with tlie anatomical stages of
the disease their importance in diagnosis and prognosis can best be appre-
ciated.
Inspection. — The movements of the affected side are more or less re-
stricted. The unaffected side moves as in health. In double pneumonia
the respiratory movements will assume the costal type, attended by increase
in the abdominal breathing.
Palpation. — There is more or less marked increase m the vocal fremitus
over the affected lung; the degree of increase corresponding to the extent
of the congestion.
Percussion. — There is slight dulness over that portion of the chest
which corresponds to the affected portion of the lung. It is not well marked
until the end of this stage, although the pulmonary capillaries are engorged
with blood from the very first. Even at the end of this stage there some-
times remains a slight tympanitic note. Very extensive central pneumonia
may fail to give any signs until the second stage is reached. Absolute
dulness in this stage is very rare.
Auscultation. — During the ^^dry" stage — which, according to some,
precedes the exudation — there will be noticed a feebleness and unnatural
dryness of the respiratory murmur. This murmur is sometimes harsh,
sometimes weaker than normal, losing the '^ breezy," rustling quality of
normal breathing. Elsewhere it is exaggerated. As soon as the conges-
tion is well marked, fine crackling sounds are neard at the end of inspira-
tion — '' crepitant rdles " — which have been regarded as characteristic of
this first stage, but which are usually pleuritic crepitation. These sounds
resemble those produced by throwing salt on hot coals or rubbing the hair
between the fingers. They are as numerous as they are minute, are un-
affected by coughing, and remain audible for from twelve to twenty-four
hours. This rale is of an unvarying character, and continues, i. e., is not
inter- or remittent. If the pneumonic stages succeed each other in rapid
90 DISEASES OF THE EESPIRATORT ORGANS.
succession, the crepitant rale may not be heard. They are rare in pneumonia
developed with acute articular rheumatism. The respiratory murmur is
feeble or assumes a broncho-vesicular character. Bronchial breathing may
be heard in this stage {Traube). The voice sounds are slightly increased
in intensity over the engorged spot. In children the " pneumonic crepita-
tion ■' is usually absent ; and though it may be heard at the end of a full
inspiration after crying, it is never as fine or as distinct as in adults. There
will be no marked increase in vocal fremitus. In old age the physical
signs are modified by a more complete bony union of the chest walls, by
curvature of the spine, rigidity of the bronchial tubes, by the rounded
form of the chest, and by senile rarefaction of the lungs.
Second, or Stage of Red Hepatization. — The physical signs of this stage are
more diagnostic than those of either of the other stages.
Inspection shows the expansive movements of the affected side more
markedly diminished than in the first stage ; while those of the other side
are increased. There may be absolute loss of motion over the affected lung.
Palpation. — There is usually marked increase in the vocal fremitus over
the consolidation. In some instances this is so slight that no difference can
be detected. Very rarely it is less than on the normal sid«. The heart
may be slightly displaced. Earely can pulsation be felt over th^^i inflamed
lung. The majority of authorities regard this pulsation as due to increased
pulsation in the arteries of the inflamed spot, but there is ne reason to
doubt that the cardiac impulse itself can be transmitted through t)io solid-
ified lung as well as the arterial impulse or the vibrations from the ^Jiordm
vocales. In central pneumonia, vocal fremitus may be normal. Pleuritic
effusions mask the signs.
Percussion. — There is marked dulness over that portion of the lung-
which is the seat of the pneumonia. Over the unaffected lung there is ex-
aggerated resonance. The nearer the hepatization to the surface the more
marked the dulness. There is a sense of resistance accompanying the per-
cussion. A pneumonic lung is more resistant than any other form of con-
solidated lung. When an entire lobe is consolidated its exact outlines can
be defined. The percussion may have a tympanitic quality anteriorly,
but there will always be dulness posteriorly. There may be slight tympa-
nitis Just around the pneumonic spot. When an entire upper lobe is con-
solidated a tympanitic percussion sound may be caused by vibration of the
air in a large bronchus. The " cracked-pot sound " is occasionally met
with in pneumonia over the relaxed and permeable parts of the lung in the
immediate vicinity of the consolidation. When heard over the condensed
portion it is caused by the sudden expulsion of air from the large bron-
chus. This occurs most frequently in the young with thin chest walls. In
basic pneumonia the percussion note under the clavicle of the affected side
may be amphoric.
Auscultation. — As soon as the air-cells are completely filled with the
pneumonic exudation the crepitant rdles cease, and bronchial respiration
is heard over the affected lung. It often has a metallic character ; or it may
sound like tearing a piece of linen. Bronchial respiration is more intense
ACUTE LOBAR PNEUMONIA
91
in pneumonia than in any other disease.^ At the commencement of the
second stage tubular breathing attends expiration only. Later, it accom-
panies both acts. Pleuritic exudation may mask the auscultatory signs.
Plugging of a large bronchus will prevent tubular breathing ; a violent fit
of coughing may allow it to occur when the mucus is dislodged. The
voice sounds are increased in intensity, and bronchophony is heard over
the whole of the consolidated lung. Bronchophony has the same diagnos-
tic significance as bronchial respiration because it is produced by the same
physical condition of the lung. When the pleural cavity is partly filled
with fluid, bronchophony is indistinct or absent below the level of the fluid;
while at the level the voice sounds may be asgophonic. Pectoriloquy may
First stage.
Diminished respiratory movements
Slight diilness on percussion
Broncho-vesicular breathing
Crepitant rales
. Slight increase of vocal resonance ..
Second stage. -
I^st movement
Increased vocal fremitus
Complete dulness on percussion.
Bronchial respiration
. Bronchophony
f Returning respiratory movemen'-.
Diminishing dulness
Third stage.
Bronchial, giving place to
Broncho-vesicuiar breathing
EaZeredux
Pig. 23.
Diagram Illustrating the Physical Signs in the Three Stages of Lobar Pneumonia,
be heard independent of fluid in the pleural cavity. The heart sounds are
abnormally intense. In children dulness is especially marked in the infra-
clavicular region. Some speak of a feeling of greater solidity below than
above the scapula which can be perceived before the ear can detect dulness
on percussion. Vocal fremitus may be increased, but this is not always
to be expected. In old age, inspection and palpation give negative results.
What is dull on percussion in old age might be regarded as resonant in
1 Laennec taught that bronchial respiration was due to the superior conducting power of condensed
lung. Skoda combats this view, and s.iys that bronchial respiration is generated or magnified in caverns
and in the bronchi of condensed lung substance by the air in the«e cavities and bronchi vibrating in con-
sonance with that of the trachea ; the condition necessary for this consonMnce is provided in the circunk-
stance that the air is pent up in confined spaces whose solid walls reflect the sonorous undulations.
92 DISEASES OF THE EESPIRATOEY ORGANS.
adults. Hence dulness on percussion is a relative term in senile pneumo-
nia. When the pneumonia is superficial there is actual dulness. Tubu-
lar or bronchial breathing marks the second stage, and is even more intense
than in adult life. Small gurgles or mucous rales are heard in this stage.
Bronchophony is not very common, and never distinct, ^gophony is fre-
quent. By causing the aged patient to cough and expire violently tubular
breathing may be heard.
Third, or Stage of Oray Hepatization. — There is no abrupt transition
from the second to the third stage ; the physical signs of early gray hepati-
zation are the same as in the second stage.
Inspection. — As resolution progresses, expansive motion on the affected
side becomes more and more apparent.
Palpation. — Vocal fremitus gradually diminishes.
Percussion. — Dulness becomes less and less marked. Of all the signs
this is the last to disappear. As the percussion sound becomes more and
more resonant the tympanitic note is again heard in spots. It is a long
while before normal pulmonary resonance is re-established. The dulness
may disappear in patches. As the dulness diminishes the pitch of the
percussion note rises.
Auscultation. — The bronchial respiration that was present in the second
stage gives place to broncho-vesicular breathing, which soon becomes
*^ blowing," then indeterminate, dindi finally normal. Bronchophony gives
way to exaggerated vocal resonance. In connection with these changes in
the respiratory and vocal sounds the crepitant rale returns, but is soon
obscured by larger and moister crepitating sounds — the ''resolving sub-
crepitant rale " of pneumonia — the "rale redux.''^ Large and small mucous,
sibilant, and sonorous rales accompany the sub-crepitant sounds, to disap-
pear only when resolution is complete. Not infrequently the bronchial
rdles that are developed during the stage of resolution are " consonant " or
ringing.^
The physical signs of this stage are all retrogressive, and they disappear in
the opposite order to that in which they appeared. In rare cases resolution
is so rapid that the sub-crepitant rale is not developed. In this class of
cases bronchial breathing and dulness on percussion continue for some
time after the crisis.
If the consolidated lung becomes the seat of purulent infiltration, the
temperature remains high and symptoms of great prostration are developed.
Bronchial breathing continues, and becomes more intense, dulness persists,
and when rales occur they are high-pitched, sharp, and resemble fine
gurgles. The occurrence of aiscess and gangrene is indicated by the
physical signs which attend the formation of a cavity in consolidated lung
substance, No one of the physical signs present during a pneumonia is
sufficient for a diagnosis ; but the manner and order of their occurrence
and their relation to the subjective symptoms enable one to reach a positive
diagnosis in all typical cases. The only diagnostic symptom is the sputum.
In children bronchial breathing rarely disappears before the seventh day ;
J Skoda and Traube.
ACUTE LOBAR PNEUMONIA. 93
it IS often accompanied by the sub-crepitant rale. When resolution takes
place, bronchial breathing and the sub-crepitant rdle will disappear simul-
taneously. If purulent infiltration occurs, large gurgling crepitation will
be heard. "Vesicular breathing is rarely heard before the eighth or ninth
day.
In old age, inspection, palpation and percussion give similar results to
those in adult life. Auscultation shows the crepitating sounds to be louder,
and gurgles large and loud are often heard at a distance from the chest.
The rdle redux is not distinctive of, or j)eculiar to the third stage of senile
pneumonia. The sound heard afc this stage is a muco-crepitating sound,
i. e., a sound produced in bronchi of medium size. The physical signs of
pulmonary abscess in the aged are very generally wanting. Distinctly local-
ized gurgling and cavernous respiration may, with the rational signs of
abscess, suffice for a diagnosis. The sputa will also aid, but the diagnosis
is only approximate. In old age the physical signs are subject to greater
variations than in adult life.
Differential Diagnosis. — Lobar pneumonia may be confounded with pul-
monary congestion and oedema, capillary bronchitis, j)leurisy, hypostatic con-
gestion, catarrhal pneumonia (in children), pulmonary infarction, incipi-
ent phthisis (especially in children), meningitis and typhoid fever.
Pneumonia begins with a chill, followed by a rapid rise in temperature
and pain in the side ; in pulmonary congestion and oedema, there is no chill
or rise in temperature, and no pain. The sputum of pneumonia is viscid,
rusty and (microscopically) diagnostic ; in pulmonary congestion and oedema
there is profuse watery, blood-stained expectoration. Pneumonia is com-
monly unilateral, and may occur in any portion of the lung ; pulmonary
oedema is bilateral, and usually occurs in the most dependent portions of
the lungs. In pneumonia there is complete dulness on percussion, crep-
itant rales and bronchial respiration ; in pulmonary oedema the dulness is
not complete, there is no bronchial breathing, and there occur numerous
large, liquid, sub-crepitant rales.
The resolving stage of pneumonia may be mistaken for acute capillary
'bronchitis ; but in the latter the sub-crepitant rale is heard all over the
c?iest ; while in pneumonia it is usually limited to a small area. The ex-
pectoration is muco-purulent in bronchitis, and the temperature range is
lower than in pneumonia. There is no dulness on percussion, no bronchial
breathing in capillary bronchitis ; the vesicular murmur is feeble, and
cyanosis is more marked. The breathing is labored in bronchitis, and pant-
ing in pneumonia.
Pneumonia is ushered in by a distinct chill folloAved by fever ; acute pleu-
risy begins with chilliness or several rigors, and the temperature rarely
rises above 100° F. The dry, hacking cough of pleurisy is accompanied by
slight mucous expectoration, and the characteristic j)neumonic sputum is
absent. In pleurisy the face is pale and anxious, and the pulse is firm,
small, tense and wiry ; in pneumonia the face has a mahogany flush, and
the pulse is full and compressible. The breathing in pleurisy is "catch-
ing ;" in pneumonia it is "panting." There are no critical days in pleu-
94 DISEASES OF THE RESPIRATOEY ORGANS,
risy. Vocal fremitus is diminished or absent in pleurisy with effusion,
there is flatness on percussion, and the sound of the percussion changes
with a change in position of the patient. In pneumonia vocal fremitus is in-
creased, and there is dulness — not flatness — on percussion. In pleurisy the
respiratory sounds are feeble, and a grazing, rubbing or sticky friction-
sound is heard ; in pneumonia there are crepitant rales and bronchial
breathing. Bronchophony and bronchial breathing may exist in pleurisy,
but they are always diffuse — never sharp and tubular as in j^neumonia.
Hypostatic congestion is accompanied by copious, loatery, blood-stained
expectoration ; it occurs in the most dependent portions of the lungs, dis-
appears when the patient sits up, and is accompanied by no rational symp-
toms except dyspnoea and expectoration.
Lobular pneumonia in children is always secondary ; it is not ushered in
by a chill, usually follows n bronchitis, and is developed in both lungs.
There are no days of crisis, and the physical signs of pneumonia are lim-
ited to circumscribed spots. The range of temperature in the two forms
of pneumonia differ ; the two curves represented by Figs. 20 and 25 show
the differences.
Pulmonary infarction is rarely met with independent of cardiac disease
or pyemia. It is a non-febrile disease, and intense dyspnoea, coming on
abruptly, is its prominent symptom. In pneumonia dyspnoea comes on
slowly. The expectoration in infarction consists of small black coagula ; in
pneumonia it is viscid and contains few blood-globules. The dulness of
an infarction is circumscribed, and around it moist rales are heard ; in
pneumonia the area of dulness is extensive, and there are no moist rales.
There is a peculiar garlic-like odor to the breath, in pulmonary infarction,
never present in pneumonia..
When lobar pneumonia has its seat at the apex, it may be confounded
with the first stage of phthisis. But the history of a well-marked chill,
followed by the characteristic pneumonic symptoms, will enable one to
exclude phthisis. Moreover, the fever in phthisis is subject to irregular
exacerbations and remissions. If the signs of consolidation persist with lit-
tle or no change, if the temperature at no time falls to normal, if there are
night sweats, if emaciation is progressive — then the case is to be regarded
as one of phthisis, even though pneumonia may have complicated it.
In children pneumonia is so often accompanied by cerebral symptoms that
it may be mistaken for meningitis. Meningitis comes on insidiously, the
temperature rarely rises above 103° F., the pulse is often lower than nor-
mal, there are no thoracic symptoms, no dyspnoea, the face is pale and anx-
ious, and the physical signs of pneumonia are absent.
Sometimes latent pneumonia may be mistaken for typhus fever, especially
when typhus is prevailing. While in charge of the typhus fever patients
on Blackwell's Island, I frequently saw cases where such a mistake had been
made during a typhus epidemic. In these cases there will be dry tongue,
delirium, and high temperature. The countenance resembles that of pneu-
monia, but the presence of the typhus eruption and the absence of the
physical signs of pneumonia will establish the diagnosis.
ACUTE LOBAR PNEUMONIA. 95
Pneumonia with typhoid symptoms is sometimes mistaken for typhoid
fever. The differential diagnosis is not difficult, if one remembers that the
pneumonia which complicates typhoid fever does not come on until late in
the fever, and the regular history of typhoid fever precedes its development.
On the other hand, when the typhoid symptoms are present from the be-
ginning, or come on at the end of the second stage of pneumonia, the phys-
ical signs of pneumonia will precede the typhoid symptoms. If a patient
over sixty years of age, with this type of pneumonia, is not seen until the
second or third week of his sickness, although evidences of lung consolida-
tion maybe found, it will be very difficult to decide whether the pneumonia
is or is not complicating a typhoid fever, and under these circumstances
the diagnosis will be difficult if not impossible.
Prognosis. — The phenomena of the crisis of pneumonia are a sudden fall
of temperature followed by profuse sweats and a diminution in frequency
of respirations and pulse. The cough becomes loose, the dyspnoea abates,
the flush disappears from the face, the sputum is more copious, loses its
rusty hue, diminishes in viscidity and becomes ''creamy," thin and watery.
Thirst decreases, the appetite returns, pain ceases and the patient
falls into a quiet sleep, waking extremely exhausted. Epistaxis, hge-
maturia and hemorrhage from the bowels may occur at the cri-
sis. After the crisis the amount of urea in the urine, which was aug-
mented before, becomes normal and the chloride of sodium reappears. The
crisis in children is marked by a greater fall in temperature and by a more
profuse sweat. When children have been restless or delirious the crisis is
marked by a state of stupor. In old age the crisis is marked by a critical
diarrhoea rather than by a sweat.
The fatality of pneumonia is shown by the following statistics : of
12,431 cases treated in the hospitals at Stockholm, 11 per cent. died. In
the Vienna hospitals 24 per cent. died. The Basle Hospital Reports for
thirty-two years give 23 per cent, of deaths. Grisolle reports 59 per cent, of
deaths in those over sixty. In the " U. S. Medical Reports," May 1st,
1861, to July, 1866, of 61,202 cases which occurred among the white troops,
14,738 died— more than 24 per cent. ; and of 16,133 among colored troops,
nearly 33 per cent. died. The deaths from all other inflammatory diseases
of the respiratory system for the same time were only one-seventh as many
as from pneumonia.' Of 255 cases treated in Bellevue Hospital during a
period of four years the rate of mortality was 34 per cent. The statistics of
private practice are very different : of Lebert's 205 cases, only TyVper cent.
died. Ziemssen lost only 3^^ per cent, of his cases. Rennet lost none of
his 105 cases. (He says, however, that no complications existed.) Brundes,
of Copenhagen, lost over 21 per cent, of his 142 cases. Fox gives to pneu-
monia the fifth, and Walshe the third place among fatal diseases. The
average mortality-rate from all the published reports to which I have had
access gives 20^o P^^ cent, of deaths. But the rate varies in different
years.
1 The Confederate Hospitals' Reports give over 30 per cent, of deaths from pneumonia for the same
period.
96 DISEASES OP THE KESPIKATORY ORGANS.
The prognosis depends more on the age than on any other single ele-
ment. In infancy the mortality is greater than in early childhood. Be-
tween the ages of forty and sixty the death-rate is from 10 to 25 per
cent., while from ten to thirty years almost all of the uncomplicated cases
recover. After sixty the prognosis is always unfavorable. Pneumonia is
the most fatal of all acute diseases at this period of life ; most " sud-
den deaths" in the old. are from acute lobar pneumonia. Some of the most
reliable modern authorities state that nine-tenths of deaths after the seventy-
fifth year are from acute pneumonia. It is more fatal in females than in
males. In some years the proportion of deaths is far greater in summer
than either in the spring or winter ; and certain — as yet unknown — atmos-
pheric influences are of the utmost imj)ortance in determining the death-
rate. The extent of lung involved influences the prognosis ; double pneu-
monia is rarely recovered from. When an entire lung is involved, the
prognosis is not as good as when only a single lobe is involved. Apical
pneumonia — esjoecially in the old and very young — is more often fatal than
basic. The feebler the patient the more unfavorable the prognosis.
Complications render the prognosis unfavorable : of 225 of my own cases,
87 Avere fatal and 168 recovered. Of these, 124 were complicated and 131
uncomplicated. Of the complicated cases, 75 died; of the uncom]3licated,
12 died.^ The most dangerous complications are those which exert a
direct influence on the heart, diminishing its power and obstructing the
flow of blood from the right ventricle. Acute infectious diseases are
dangerous complications because they hasten heart failure.
Pneumonia may be regarded as mild when the temperature is below 104°.
When the fever ranges above 106° for two days, the case is unfavorable.
A gradual rise in temperature after the fourth day is always an unfavor-
able sign. A low temperature is dangerous only when the respirations
are greatly accelerated. When the pulse is 120 to 130 for two or three
days, the prognosis is bad. If the pulse reach 150 per minute, or if it
becomes irregular, intermitting, or dicrotic, the patient rarely recovers. In
children a rapid pulse is of less significance, and in old age the pulse is
never a reliable guide. Prune-juice expectoration is an unfavorable sign,
indicating extensive blood changes. When expectoration is absent in
the second or third stage, or if it become scanty and difficult, the prog-
nosis is unfavorable. Sudden suppression of the sputa, with coincident
tracheal rales, indicates impending death. Delirium coming on after the
sixth day, convulsions in children, with jactitation and subsultus, or, in
the aged, a tendency to coma, are unfavorable signs. Exhaustion and
prostration, accompanied by a sunken pallid face and cold, clammy sweat,
are always dangerous. In children, bronchial breathing, after the
seventh day, numerous subcrepitant rdles, copious and persistent diar-
- Lebert states that he lost only 5>^ per cent, of hisimcomplicated,andaZ^of his complicated cases. Huss
lost 6 per cent, of uncomplicated and 20 per cent, of complicated cases. Fox states that pneumonia com-
plicated by endocarditis is fatal in 75 percent, of cases ; by pericnrditis,in 54 per cent.; by Bright's disease,
in 50 per cent.; and by alcoholismus, in 25 per cent. Brundes (of Copenhagen), in 120 uncomplicated cases,
lost 6% per cent.; of 22 complicated, he lost all. The danger of complications is markedly shown by
these statistics.
ACUTE LOBAR PNEUMONIA. 97
rhoea, and swelling of the veins of the hands are bad symptoms. In
old age a sudden rise or fall in temperature, apathy, somnolence, and a
sallow, anxious countenance are dangerous symptoms. Pulmonary con-
gestion and oedema in the unaffected part of the lung often precede a fatal
issue. The occurrence of purulent infiltration, abscess, or gangrene ren-
ders the prognosis unfavorable.
In pneumonia the fibrin-factors of the blood are increased (often 400
per cent, more than normal), the heart-power is diminished, so that
the ventricles cannot empty themselves, the columns and cords whip
Tip the residual blood (already prepared for clotting), and ''heart
clots" always form when the death struggle is prolonged and cardiac
contractions feeble. The " heart failure " is the beginning of death.
Post-mortem results can never give all, or the true causes of death,
but only the modes of death. If, on account of heart failure, pulmonary
oedema and congestion occur and heart clots form, these clots cannot be
called causes of death. Jiirgensen states that in fatal cases of pneumonia
oedema of the lungs is probably always present, and heart clots are fre-
quent. Death may occur, then, from heart-insuflficiency, from complica-
tions (cardiac especially), or from asphyxia. Fatal collapse may follow an
apparently regular and well-marked crisis.
Treatment. — If we regard pneumonia as a general disease with a charac-
teristic local lesion, the treatment must be modified by the constitutional
condition of each patient and by the type of the pneumonia. If it is un-
complicated and occurs at certain periods of life, it will terminate spon-
taneously in recovery by crisis ; but when certain complications exist, when
certain conditions are present, and at certain ages, it is almost necessarily
fatal.
Any plan of treatment in such a disease, if resorted to indiscriminately,
will prove unsatisfactory. Although a large proportion of cases will re-
cover without treatment, yet well-directed therapeusis will save lives and
render convalescence less tedious. The pneumonic lung no more requires-
treatment than the intestinal ulcers of typhoid fever. It is i\ie ge7ieral con-
dition of the patient, not the local changes, which is to govern us in the
management of each case. Agents for the arrest of local inflammation
have no place here ; hence venesection, once generally practised, has been
almost entirely abandoned. A careful study of the pathology of pneumo-
nia not only leads to the conclusion that bleeding does harm, but it
strongly contra-indicates the use of all those agents which have been em-
ployed for the arrest of simple pulmonary inflammation. Hence veratrum
viride, aconite, antimony, calomel, the tartrate of potash and antimony,
iodide of potassium, and all so-called "cardiac sedatives" have been dis-
carded, for it is evident that they add a new load to an already overburdened
heart. They may, for a time, lower temperature and pulse-rate, but this
wiU be accomplished at the expense of heart-power. Cardiac insufficiency
will therefore appear earlier and be more profound.
Counter -irritafAon by blisters, or other irritants, to the chest (in the
early stages) is apt to do harm ; but blisters may be applied during the third
7
98 DISEASES OF THE EESPIRATOET OEGAKS.
stage, to hasten resolution. The application of leeches, followed by a lin-
seed-meal poultice or other soothing fomentation, will relieve the pain in
the side, which is often so urgent at the onset, and, if the condition of the
patient will allow, may be of service. If extensive pulmonary oedema oc-
curs, dry cups applied to the chest will relieve the dyspnoea, and for a
time dispel the oedema. It has come to be a rule to incase the chest in
a cotton-batting or flannel jacket, covered with oiled silk. This has no
influence over the course of the pneumonia, but it promotes diaphoresis,
protects the surface from sudden clianges of temperature, and it is always
grateful to the patient. The " Jacket " is especially beneficial in children.
Absolute rest is important ; the patient should be moved as little as
possible, and should not be kept in a constrained posture. If signs of
heart failure occur, he should not be allowed to sit up or talk. The sick
room should be large, cheerful and well ventilated, and its temperature
should range between 65° and 70° Fahr. A most important adjuvant is
a carefully-regulated diet. The food should be fluid or semi-fluid, and
highly nutritious, e. g., milk, eggs, beef -tea, and concentrated broths.
Milk is preferable to all other nourishment.
The nervoiis slioclc which attends the onset of acute lobar pneumonia is
greater than in any other acute disease, except, perhaps, acute peritonitis,
and the important question presents itself: what measures shall be em-
ployed to counteract, or mitigate, the impression made on the nerve centres
by the morbific agent which is operating to produce the jDneumonia ? The
exiDcrience of the last five years leads me to the conclusion that during the
developing period of the disease, when the pneumonic blow is first struck,
and until the infiltration is complete (usually for the first four days), the
patient is to be brought under the full influence of opium and held in a
state of comparative comfort, by hypodermic injections of morphia, re-
peated at regular intervals ; and that by this course a pneumonic patient
is placed in the best condition, not only for sustaining the primary shock,
but for resisting the pneumonia. Thus given, opium does not interfere
with the employment of any stimulating or anti-pyretic measures which
may be demanded. And not only does it diminish the chances of the
occurrence of heart failure, but the great relief and comfort which it gives
to the sufferer in the first four days of his struggles are sufficient to com-
mend its use. After the pneumonic infiltration is completed, opium should
be discontinued, for paralysis of, and a consequent accumulation of secretion
in the bronchi may greatly increase the already deficient respirations.
In all severe types of pneumonia there are two prominent sources of
danger — heart-insufficiency and high temperature. The two prominent
indications for treatment are, therefore, to sustain the heart and to reduce
the temperature. A large proportion of deaths in pneumonia directly result
from heart failure ; alcohol, judiciously used, is the most efficient means
for preventing or overcoming it, but its indiscriminate use is more dangerous
than indiscriminate bleeding. Only a few ounces of brandy may be re.
'quired to carry a pneumonic patient through a critical period ; or its free
administration may be demanded to save life. In the old and feeble, apd
ACUTE LOBAR PNEUMONIA. 99
in those who have been accustomed to the use of alcohol, stimulation may
be necessary from the very onset. The indications in each case demand
careful study ; in no disease is so much discretion required in the admin-
istration of stimulants. The pulse is the indicator of the heart's con-
dition. A frequent, feeble, irregular or intermitting pulse calls for
stimulants. The quantity required in any case is to be determined by its
effects on the pulse. It is best to begin with small quantities, and care-
fully note the effect of the first few doses. If it acts beneficially, a favor-
able effect will be seen in a few hours ; and then the quantity administered
must be varied to suit each case. It is seldom necessary to use more than
six or eight ounces of brandy in twenty-four hours ; but, when demanded,
it is to be unsparingly given. A dicrotic pulse is always an indication for
its use. The period immediately following the crisis is the time when
stimulants are usually most required. Delirium, muscular tremor and sub-
sultus are indications for their use. Critical collapse in the aged must be
combated by a very free use of stimulants. Carbonate of ammonia is
extensively employed as a stimulant in pneumonia ; — it is claimed that
its use diminishes the danger of heart clot, but there is no evidence in
support of this statement; — and if given in sufficiently large doses to act
as a stimulant it irritates the stomach. It is unquestionably inferior to
alcohol as a cardiac stimulant. Camphor and musk are also inferior to
alcohol, and digitalis is only of service when there are evidences of extensive
renal congestion.
There are two plans of treatment advocated for reducing temperature
in pneumonia : (1) the application of cold in various ways to the surface
of the body ; and (2) the internal administration of the sulphate of quinine.
It is claimed that the temperature can be reduced by applying cold com-
presses to the chest : a cloth of some thickness is to be wrung from cold
water and applied every ten or fifteen minutes to the affected side. This
not only relieves the local symptoms, but it lowers the body temperature
and hastens the day of crisis. Some prefer the " Esmarch ice-bag " to
the cold compress. There is no doubt but that the pain in the side and
fever will be relieved by this means, but the relief is only temporary ; and
my own experience leads to the belief that pneumonia treated in this way
is more likely to extend, and that there is great danger of chilling the
patient. The other methods of applying cold to the surface for the reduc-
tion of temperature in pneumonia are the cold bath,' the cold pack and
cold sponging.
' The rules for administering the bath are as follows : as soon as the axillary temperature rises above
104° F., place the patient in a water-bath having a temperature of 70° F. or 80° F., and gradually lower the
temperature by the addition of cold water or ice until the temperature of the patient begins to fall. When
the patient's temperature begins to fall the thermometrical observations must be taken every two or three
minutes in the rectum. If it falls rapidly, the patient must be removed from the bath as soon as the tem-
perature has reached 102° F. ; (if it falls slowly, as soon as it reaches 101° F.,) and immediately placed in
bed. While in the bath cold must be applied to the head by means of sponges or ice-bags. The cold pack
consists in wrapping the patient in a sheet wrung out of tepid water, and applying over this sheet one
wrung out of cold water. The latter is to be removed as often as it becomes warm. Its application and
removal must be continued until the desired fall in temperature is obtained. To keep the temperature at
the desired point, the baths or packs must be repeated and continued night and day whenever the tem-
perature rises above 104°, until the crisis is reached.
100 DISEASES OF THE RESPIRATOEY OEGAITS.
The experience of American practitioners is against the cold bath and
the cold pack. The shock of cold causes depression, which the feeble or
old cannot rally from. And though fever is lessened, heart-failure more
rapidly follows, and is more difficult to overcome. My own experience is
decidedly against the use of cold on the surface for the reduction of tem-
perature in pneumonia. Cold "sponging" may be practised when it is
grateful to the patient.
It is claimed that sulphate of quinine is an arterial sedative ; that it has
a peculiar tonic effect on the capillary circulation ; that it arrests cell-devel--
opment, and checks the amoeboid movement of the white blood corpuscles.
Theoretically, therefore, its use is indicated in lobar pneumonia ; and, clin-
ically, it is found to reduce temperature more permanently and with greater
certainty-than any other agent. To act antipyreticaily it must be given in
doses of from gr. x. to gr. xx. within a period of not more than two hours. ^
The very large antipyretic doses of quinine which have been recommended
seem to me to be attended with danger, for in such large doses it appears
to act as a cardiac depressant, and I believe that with gr. x.-xv. given in
one dose we obtain as certain an antipyretic result as with much larger doses.
If there is great restlessness or wakefulness during the third stage, small
hypodermatics of morphia, or, better, hydrate of chloral, can be given. If
there is even slight evidence of cyanosis, these remedies should be used
with great care. When the pupils are small, belladonna or hyoscyamus may be
given. For the relief of the distressing cough which is sometimes present,
five grains of hydrate of chloral combined with one-twentieth of a grain of
morphia, or twenty-five drops of chlorodyne every two hours, may be given.
If expectoration is difficult from loss of muscular power, stimulating
*' expectorants," such as senega and turpentine, are useful. But if this
diJBBculty arises from great viscidity of the sputum, alkalies will be found
of service, and, as alkalies and neutral salines also have a diuretic and
diaphoretic action, they are especially indicated just before the crisis. For
the relief of the delirium of chronic alcoholism, tartar emetic and digitalis
are highly recommended by English authorities.
In the first stage of senile pneumonia an emetic, when not specially con-
tra-indicated, is given in the " Salpetriere Hospital." Ipecacuanha is re-
garded as especially indicated. The nitrate of potash and the hydro-
chlorate of ammonia are also highly recommended in senile pneumonia.
In children the chest should be thoroughly protected, the diet carefully
regulated. Leeching and blistering are both harmful, and should never
be employed. Stimulating expectorants are often indicated, and the mod-
erate use of stimulants in feeble children is always required. During con-
• Liebermeister gives quinbie until the temperature has been reduced by it to within \° of the normal.
Few American practitioners carry the antipyretic effects of quinine so far. In Ringer and Gill's experi-
ments upon " The Influence of Quinine on Temperature^'' m health, it took at least gr. xx. to produce a fall
of 1°. From fifty to eighty minutes elapsed before the fall occurred, and the effects lasted from forty -five
minutes to three hours. Ringer states that in pneumonia (and some other diseases) quinine does not
readilj' pass out with the urine, but is delayed in the system for considerable time, and its antipyretic
effects are continued longer than in other diseases. Prof. Flint states that he has seen pneumonia rendered
abortive in a certain proportion of cases by xs. to xl. grains of qninine daily, and even when this result has
not followed, the disease has often been favorably modified in a greater degree than by smaller doses.
LOBULAR PN"EUMONIA. 101
yalescence, iron, quinine, mineral acids, cod-liver oil, and blood-making
wines, should be given.
Very recently there has been advocated an antiseptic treatment of pneu-
monia, the origin of which is to be found in the notion, which somewhat
extensively prevails, that pneumonia is a zymotic disease. Klebs even
advocates injection of carbolic acid to kill or render inert the " monas pul-
monale," which he claims to be the contagious element found in the sputum.
It cannot be denied that a septic element exists in some if not in all cases ;
hence the sulphites and hyposulphites (30 grain doses every three hours)
are rceommended. Carbolic acid, from 1 to 5 grains, sulpho-carbolate of
soda (5 to 20 grains every two hours), have both been used quite extensively
as antiseptics in the treatment of pneumonia. Thymol and salicylic acid
have risen into favor because they are powerfully antiseptic and are almost
physiologically inert. Quinine has also been advocated for its antiseptic
power. The antiseptic treatment of pneumonia has not yet assumed a
definite aspect or been sufficiently tried for any definite statements to be
made concerning it.
LOBULAR PNEUMONIA.
Lobular, catarrhal, or hroncho-pneumonia, is always secondary, being
preceded by, or associated with, inflammation and obstruction of the smaller
bronchi, which lead to the consolidated lobules. It may run an acute, sub-
acute or chronic course, and differs very decidedly both in its clinical and
pathological history from acute lobar pneumonia.
Morbid Anatomy. — The anatomical changes in lobular pneumonia are
confined to scattered groups of air-vesicles, hence the gross appearance of
the portion of lung involved will vary with the duration and extent of the
pneumonic process. In well-marked cases there will be found scattered
throughout one or both lungs, small, circumscribed nodules of a light,
deep-red, or bluish color, which do not inflate when the lung is inflated.
If they are situated near the surface of the lung, they cause small, rounded
elevations. When they are of minute size they resemble, and may be con-
founded with, tubercles. When they are of considerable size, a reddish
fluid oozes from their cut surfaces on section, and a small quantity of dark
blood can be pressed from them. They are less tough than healthy lung
substance and break down easily on pressure. These nodules shade off into
the surrounding zones of lung-tissue, which may be the seat of oedema,
congestion, or emphysema. The nodules vary in size from that of a pea to
that of a hazelnut, and are very rarely granular.' When the lung is in-
flated these spots of consolidation are rendered more prominent, so that
they stand out sharply defined from the adjacent lung-tissue. In some in-
stances these isolated spots of consolidation become confluent and involve
a large portion of lung — perhaps a whole lobe — and become pale, firm and
dry, resembling in color the gray hepatization of lobar pneumonia. The
smaller bronchi are congested ; their walls are often thickened, and they
may contain a thick, tenacious, puriform secretion which, later, may be-
* Jtlrgensen says : " Granulation is never obseired."
102
DISEASES OE THE EESPIRATORY ORGANS.
come dry and inspissated. When a section of the lung is made they often
stand out prominently or even rise a little above the level of the cut sur-
face. A peri-lroncJiitis i&'^Qvy often associated with these changes. Cy-
lindrical and fusiform dilatations of the tubes are not infrequent. Often,
when a small patch of consolidation is cut across there will be found at its
centre a dilated bronchiole filled with pus. Discoloration begins at this
point and extends towards the periphery. The connective-tissue of the
portion of lung involved is increased, and this, in long-standing cases, is
often pigmented. Bronchiectasis may occur at various points.
A microscopical examination of an affected lobule may distinguish three
stages in the inflammatory process. First, the air vesicles may be more or
less completely filled with pus and serum, containing swollen and granular
epithelium. The capillaries in
the walls of the air vesicles are
usually elongated, and red globules
may escape into the air-sacs. In
the unaffected portions of lung-
tissue the epithelial cells appear
large and more distinct than in
healthy lungs. In the second stage
the affected lobules become solid
and airless. Their color changes
to a pinkish gray. The other
changes are similar to those that
take place in the stage of red
hepatization in lobar pneumonia,
except that no fibrillated fibrin is
found in the exudation, the pus
and epithelial cells are more abun-
dant and there are fewer red blood
globules. The anatomical differ-
ences between the second stages
of acute lobar and acute lobular pneumonia are as follows : acute lobar
pneumonia involves a whole lobe ; acute lobular only portions of a
lobe. Lobar pneumonia advances steadily and uninterruptedly from one
point, usually from the base upwards, until the whole lobe is involved ; while
lobular begins simultaneously in several lobules remote from one another.
Moreover, these lobules are in different stages of the inflammatory process,
e. g., one is dark, red and moist ; another is grayish and quite firm. In lob-
ular pneumonia the small bronchi are more or less filled with catarrhal pro-
ducts ; while in lobar pneumonia the exudation is fibrinous and does not
extend beyond the infundibula and minute bronchioles.
The third stage is the stage in which occurs either resolution, cheesy
degeneration, or purulent infiltration. Abscess and gangrene may both
occur, but they are very rare. When resolution occurs the contents of the
alveoli become fatty and granular and are absorbed, and the pulmonary
epithelium is restored. Large confluent spots of catarrhal pneumonia may
FiQ. S>4.
Alveolus from a Lung in Lobular Pneumonia.
The capillaries are distended with blood, and within the
alveolus are seen swollen epithelia (a, a) and pus cells
b. X 250.
LOBULAR PKEUMONIA. 103
undergo clieesy degeneration. And even solitary lobules may remain pale
and yellow, looking like so-called cheesy tubercles ; when cut into, a fluid
escapes from their centres. Some lobules that look like cheesy masses are
soft, never granular, and a purifonn fluid flows from their cut surfaces.
While the contents of the alveoli are undergoing cheesy changes, hyper-
plasia of the interstitial connective-tissue is taking place, which leads to
more or less fibroid induration or " sclerosis'^ of the lung. On the pleura
covering the superficial nodules an exudation of plastic lymph occurs ;
the bronchial glands are swollen and hyperaemic' Catarrhal pneumonia
in adults occurs independently of lobular collapse or atelectasis.
Etiology. — Lobular pneumonia is always secondary to obstruction in the
air passages, especially those of capillary size. It may be excited either by
the gradual extension of inflammatory processes from the tubes to the air-
cells, or by the entrance of inflammatory products from the tubes into the
air-cells. It is most frequently met with between the ages of one and three.
The senile period also seems to predispose to it. The more imperfectly
nourished the child, the more anti-hygienic the air, surroundings and food,
the more liable is it to develop lobular pneumonia. Debility and a long-
continued recumbent posture predispose to it. Indirectly, any cause of
bronchial irritation is a predisposing cause. The bronchitis of measles,
whooping-cough, influenza, and that which accomjDanies the acute infec-
tious diseases, often leads to lobular pneumonia. It occurs in lung-tissue
adjacent to spots of hemorrhage, or pyaemic infarctions; traumatism may
induce it. It is intimately associated with all varieties of acute and chronic
phthisis. '
Symptoms. — The phenomena which attend this form of pneumonia are
always more or less obscured by those of the disease by which it has been
preceded. It has no early distinctive symptoms. From an anatomical
standpoint it is evident that its symptoms should resemble those of capillary
bronchitis. It rarely runs a regular course, — terminating after a definite
period in either death or resolution, — but may be protracted for weeks or
months. A large number of cases occur in the course of whooping-cough
and measles or other diseases complicated by bronchitis. The acute form
is met with almost exclusively in children. In adults the disease usually
runs a sub-acute or chronic course.
After a diffuse capillary bronchitis has existed for a variable period,
attended by its ordinary symptoms, such as a cough with muco-purulent
expectoration, slight rise in temperature and labored breathing, if lobular
pneumonia is developed the labored breathing becomes panting and ac-
celerated ; the respiration may be 100 per minute. Dyspnoea is greatly
increased. It is rarely ushered in by a rigor or a distinct chill. The tem-
perature will gradually rise to 104°-105°, unlike the sudden rise of lobar
pneumonia. It runs no typical course ; though exacerbations and remis-
sions are marked, they have no regularity ; sometimes the morning, some-
• Many patholoj^ists claim that the pulmonary alveolar epithelium takes no active part in the processes
that result, in the above described consolidation. Rindfleisch assorts an active proliferation.
^ " EUrat.or pneum.onia " is a name given to catarrhal pneumonia caused by inhalation of the dust of
grain elevators in our Western cities.
104
DISEASES OP THE EESPIRATORY ORGANS.
Dav
/
^
►. 3)
mnco-purulent expectoration, pain in the chest, a J^^/ -^ f 0/1
sense of suffocation, haemoptysis, night sweats, pallor \/ */^ps^V ^^,*3^
and emaciation. When blood is expectorated goose- l||»®<. ^j^p^'^o^^J;?
berry-like skins (the sacs of echinococci) or hook- -gJ^B.^. 1 a ^ 99^
lets may be found in the expectorated matter. Unless
the daughter-cysts, or booklets, are expectorated the
diagnosis can never be positive. When an hydatid ^_
attains any considerable size it may cause bulging Pi^ 3L
of the chest wall and displace the mediastinum and Hydatids of the Lung.
diaphragm. The circumscribed dulneSS on perCUS- Microscopical appearance of
. ^ 1-1 n , ji -11 1 p, J. 1 elements fofund in the spiitum.
sion, which may extend to the right or left of the ^ EooicsfromneaaofTcBrAa
median line, with absence of respiratory sound and EcMnococcus.
vocal fremitus over the area of dulness, is a strong ^\EedZmTdis%. x 250.
evidence of pulmonary hydatids.
Differential Diagnosis. — The rupture of the cyst and the escape of its con-
tents into a bronchial tube are its only diagnostic features and will prevent
it from being confounded with any other condition. If an hydatid is super-
ficial a portion of the fluid may be withdrawn by aspiration, and a micro-
scopical examination will establish the diagnosis. It is impossible to dis-
tinguish between hydatid tumors at the base of the right lung and those in
the right lobe of the liver.
Prognosis. — These tumors sometimes disappear by spontaneous retrogres-
sion, or by discharge into a bronchial tube ; or suppuration may be estab-
lished in the cysts which afterward undergo calcification. Recovery occurs.
in fifty per cent, of cases. Earely do patients die from emaciation or ma-
rasmus. They may die from suffocation, when the cysts rupture into the
10
Oo^V
146 DISEASES OF THE EESPIRATORY ORGANS.
bronchi, from long-continued suppuration, or from an empyema established
by the rupture of a cyst into the pleural cavity. Inilammation of any of
the three adjacent serous membranes may cause death, or this may result
from extensive hemorrhage and from gangrene.
Treatment. — They should be treated as hydatids of the liver. It is a
question if they should be injected with iodine.
PLEUKISY.
Pleurisy is either a partial or general inflammation of one or both pleuraB.
It may run an acute, sub-acute, or chronic course, and have for its pro-
ducts fibrin, serum and fibrin, serum, fibrin and pus, or new connective-
tissue. I shall describe four varieties of pleurisy : — (1) Acute or Dry
Pleurisy ; (2) Sul-acute Pleurisy, or Pleurisy luitli Effusion ; (3) Sup-
'pur alive Pleurisy or Empyema; and, (4) Adhesive Pleurisy.
ACUTE PLEURISY.
In this variety the symptoms are well defined, the course rapid, and the
exudation principally fibrinous.
Morbid Anatomy. — The first stage of the inflammatory process is marked
by a reddening of some part of the pleural membrane from hypermaeia of
the capillaries of the serous and sub-serous tissue with degeneration of the
endothelial cells. The pleura loses its natural glistening appearance on
account of a slight fibrinous exudation and the swelling and increase in
number of its fixed connective-tissue cells. These changes take place dur-
ing the first forty-eight hours. Following this, the fibrinous exudation
increases and \\\q free surface of the pleura assumes a rough, shaggy ap-
pearance. If any serum exudes it gravitates to the most dependent por-
tions of the pleural sac. In the substance of the pleura and in the fibrinous
exudation new cells are now found which are young connective-tissue or
pus cells. These cells are at first more numerous on the inner surface of
the pleura. As the inflammation progresses they increase in number
and collect on the free surface of the pleura under the fibrinous exudation.
By the fifth day of the pleurisy new blood-vessels are formed in the fibri-
nous exudation and become connected with the original vessels of the pleura.
The nature of the subsequent changes will depend upon the intensity of
-the inflammatory process ; in the milder types the fibrin gradually dimin-
ishes and disappears, some of the cells become fatty and are absorbed, and
the remainder enter into the formation of a basement substance which grad-
ually increases and finally a permanent new connective-tissue forms upon
the inner surface of the pleura. If the inflammatory process subsides with-
lout much serous effusion, the opposing surfaces of the pulmonary and costal
-j)leur8e come into contact and adhesions are formed between them composed
of permanent connective-tissue containing long, slender vessels. These
adhesions follow the general law that governs all new connective-tissue :
they may be permanent, or — ^their blood supply becoming insufficient —
ACUTE PLEURISY.
147
they may undergo fatty degeneration and be absorbed, the thickened pleura
alone remaining to tell of the past inflammation. When an individual has
once had this form of pleurisy he will always have a permanent lesion.
This pathological process may be completed in two weeks, or the sero-fibri-
nous effusion may not be absorbed for months, and then the pleuritic thick-
ening becomes very extensive.
Etiology. — The etiology of acute pleurisy is sometimes very obscure. Ex-
posure to wet and cold has been regarded as one of its most frequent causes,
but it is very doubtful if it ever occurs as the result of simple exposure to wet
and cold. In all cases that have come under my observation where it has fol-
lowed such exposure, I have been able to find some previously existing predis-
posing cause. It may be the result of a penetrating wound, or blows upon
the chest walls. Fracture of the ribs, if the broken ends of the ribs pene-
trate the pleura, may cause it. It is often a complication of other diseases,
such as pyaemia, the exanthematous fevers, acute and chronic alcoholismus,
acute rheumatism, Bright's disease, pneumonia, etc. Sometimes it is the
result of extension of inflammation from adjacent organs and tissues. There
is a strong predisposition to it in some individuals, and one attack predis-
poses to another. It may occur at any age. Although it has been claimed
that it never occurs in young children, my experience leads me to believe
that it is of quite frequent occurrence in children of two or three years of
age, and pus is usually formed in the pleurisies of children which occur
as complications or sequelae of the exanthematous fevers. Whenever acute
pleurisy occurs on the right side it is important to determine if it is, or is
not, the result of an extension of inflammation from the liver.
Symptoms, — Acute pleurisy may be mild or severe ; in either case it is
ushered in by well-marked symptoms. The most prominent and constant
at its onset is a sharp stitch-like pain in some portion of the chest ; it usu-
ally is referred to the nipple of
the affected side. Each inspira-
tion increases its severity. The
patient, to prevent motion of
the affected side, assumes a pe-
culiar position, leaning forward
and toward that side. At first
the countenance is pale and
anxious ; after a few hours it
becomes flushed. The pulse is
accelerated, beating from 90 to
120 per minute ; it is firm,
small and tense in character —
in this respect differing from
the pulse of all other pulmonary
diseases. The respiration is
hurried and difficult ; each in-
spiration is jerking in character; as soon as the general symptoms of
pyrexia are present, the pain, in most cases, diminishes — in a small pro-
Da-K
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Fig. 32.
Temperature in a case of Acute Pleurisy. Patient set. 24.
Recovery.
148
DISEASES OF THE KESPIEATORY ORGAN'S.
portion of cases it maintains its intensity throughout the attack. The
temperature follows no regular course and has no fixed relation to the pulse
or respiration ; in ordinary cases it rarely rises above 100° F. ; in very severe
cases it may reach 104° F. There is a short, dry, tearing cough, which
is very distressing ; the patient restrains it as much as possible on account
of the intense pain which it produces. In very severe cases of acute pleurisy,
where the fibrinous exudation is very abundant and takes place rapidly,
causing compression of the lung, the primary symptoms are very violent,
resembling those of pneumonia. A distinct chill is followed by high
fever, the temperature often reaching 105° F. The countenance assumes
an anxious expression, the pulse beats 120 per minute and is feeble, but the
pain in the side is not so severe as in the milder cases. Under these circum-
stances, at the onset of tiie attack it is difficult to distinguish it from croup-
ous pneumonia. Such severe cases are rare ; when they do occur they are apt
to prove fatal. There are occasionally very mild cases of acute pleurisy which
are attended by few of the subjective symptoms of pleurisy : the febrile move-
ment is slight, the pain in the side is not severe, and cough and dyspnoea may
be entirely absent. These patients continue their ordinary occupations, com-
plaining only of an uneasy sensation in the side, and the disease would
pass unrecognized but for the physical signs. Although the rational symp-
toms of acute pleurisy may vary in different cases and in some be very
obscure, the physical signs at once dispel all doubts.
Physical Signs. — During the first twenty-four hours of acute pleurisy,
inspection will show the movements of the chest wall on the affected side
to be more or less restricted. Palpation, percussion, and mensuration will
give negative results. On auscultation the respiratory murmur will be
found feeble over the affected side, and jerking in character both on in-
spiration and expiration, and a grazing friction sound will be heard ; this
friction sound will be most intense
at the end of inspiration.
As the plastic exudation takes place
inspection will show a greater loss of
expansive motion on the affected
side ; and on palpation there will be a
diminution of the vocal fremitus over
its seat. On percussion there will
be slight dulness over the seat of the
pleurisy. The amount and extent of
the dulness will correspond to the
amount of the plastic exudation.
Upon auscultation the respiratory
murmur will be distant and feeble
or entirely absent, and a crepitating
Fig. 33. frictiou souud will be heard both with
Diagram illustrating Physical Signs in Acute Pleu- :„„„,-„„4-,-p.^ ^f.A pxr>irfltion * it is
risy with a small amount of EfEusion. Alter Da ^^^P^^^*^^"" '''"" t;.spUciLiuu , iu lo
tJosta. usually most intense with inspiration ;
this sound sometimes very closely resembles the so-called crepitant rale and
Normal respiratory soundi
Crepitating friction
sounds
Eespiratory mnr-
7iiur feeble or
absent
Flatness on percus-
sion
Absent vocal fre-
mitus
Absent voice
ACUTE PLEURISY. 149
may be mistalien for it. At times this sound loses its crepitant character
and becomes rubbing and sticky ; it is always due to the rubbing together
of the two roughened pleural surfaces. Often it will not be heard unless
the patient cough or take a deep inspiration. If the pleurisy is confined
to the diaphragmatic or mediastinal pleura the friction sound will not
be heard.
If a considerable fluid effusion accompany the plastic exudation, the
expansive movements on the affected side will be more restricted, and
the vocal fremitus at the bottom of the pleural cavity will be markedly
diminished. Upon 'percussion there will be flatness over the region occu-
pied by the fluid. It is difficult, however, to recognize the presence of
a small amount of fluid effusion, for the level of the fluid is not appre-
ciably changed by changing the position of the patient. On auscultation
the respiratory sounds will be absent below the level of the fluid, and
feeble above it ; and both respiratory acts will be accompanied by the
friction sound.
During the period of absorption of the fluid and plastic exudation there
will be a gradual return of the pulmonary resonance and of the normal,
vocal, and respiratory sounds, and as the roughened pleural surfaces play
upon each other, the friction sound will assume more of a rubbing char-
acter. In some instances the friction sounds remain audible for a long
time after the disappearance of all the other signs of pleurisy. Retraction
of the affected side does not follow acute pleurisy except in rare instances,
when the inflammation has been very severe and a large plastic effusion
has taken place. In those having extensive plastic exudations in acute
pleurisy which compress the lung, the respiratory sound may assume a
bronchial character and be mistaken for that of a pneumonic condition.
Differential Diagnosis. — In the majority of cases the diagnosis of acute
pleurisy is easily made. Acute ^pneumonia is the only disease with which
it is liable to be confounded. In both affections there are dyspnoea, fever,
and cough ; but in pleurisy the temperature rarely rises above 100° F.,
while in pneumonia it usually reaches 103° F. within the first twenty-four
hours. The cough of pleurisy is short and hacking, and is attended by
little or no expectoration, whereas in nearly every case of pneumonia expec-
toration is present, and the substance expectorated is characteristic of the
pneumonia. The countenance at the onset of pleurisy is pale and anxious ;
in pneumonia it is flushed and the cheeks have a purple hue. There is also
a very marked difference in the physical signs of the two diseases. In pleu-
risy the vocal fremitus over the affected portion of the pleura is somewhat
diminished ; in pneumonia it is more or less increased. In pleurisy the
respiration is feeble ; in pneumonia it is rude or bronchial. In pleurisy a
grazing, rubbing, or crepitating friction sound is heard with both respira-
tory acts. In pneumonia the crepitant rale is heard at the end of inspira-
tion. Sometimes it is difficult to distinguish a crepitating friction sound
from a sub-crepitant rale, but, as the sub-crepitant rale is not present until
the last stage of pneumonia, the question will not arise if the patient is seen
before that period has arrived.
150 DISEASES OF THE RESPIEATOEY ORGANS.
Occasionally it is difficult to make a differential diagnosis between inter-
costal neuralgia or pleurodynia, and acute pleurisy. Intercostal neuralgia
or pleurodynia may be attended by many of the ushering-in symptoms of
acute pleurisy. They may come on after exposure, be attended by violent
pain in the side, jerking respirations, anxious countenance, and often by
considerable fever. On physical examination the respiration may be as
feeble as in the first stage of pleurisy. The presence or absence of a pleuritic
friction sound, and the painful points on pressure, are the principal points
of difference.
Prognosis. — The prognosis in acute pleurisy is generally good. Its natu-
ral termination is in recovery within two or three weeks after its commence-
ment. But it is to be remembered that patients even with the milder form
of the disease are liable to have frequent pleuritic thickenings and adhesions
between the pulmonary and costal pleurae. These thickenings predispose
to other attacks of pleurisy, and each new attack interferes more and more
with the expansion of the lungs and leads to the development of intersti-
tial pneumonia or bronchitis, and finally to fibrous phthisis. If this form
of pleurisy complicates any grave form of disease, as septicaemia, pyaemia,
Bright's disease, etc., there is a liability to acute empyema. In some very
acute cases, where there is a large plastic exudation, death may result in a
few days.
Treatment. — The only remedial agent which has seemed to me to have a
controlling power over acute pleurisy is opium. The best method of admin-
istering it is by the hypodermic injection of morphine. It has been claimed
that free blood-letting at the commencement of an acute pleurisy will arrest
its progress. But the facts deduced from recorded cases are strongly against
this statement. A free general bleeding will undoubtedly relieve the pleu-
ritic pain with great promptitude, but no more so than a hypodermic of
morphine, and the morphine does not increase the liability to a large seroua
effusion, as does general bleeding. For the successful management of
ordinary acute pleurisy all that I have found necessary is to place the
patient in bed. This is important, however mild the attack may be. The
sick room should be well ventilated and kept at an even temperature of about
65° F. The patient should be allowed to assume that position in bed which
he finds most comfortable. He should be forbidden to talk, and should be
prevented from making any unnecessary movements, and a nutritious diet
without stimulants should be given him. If he is robust, three or four
leeches may be applied over the seat of pain, and followed by an anodyne
poultice. Hypodermics of morphine must be given in sufficient quantities
to relieve all pain. After the first week the morphine can usually be dis-
continued and the patient will be able to sit up, and, at the end of three
weeks, to resume his ordinary occupation unless it requires great physical
exertion. If there is an abundant plastic or serous exudation the convales-
cence will be reached more slowly and the recovery will be less complete.
In such cases there will be some crippling of the lung, and pain and uneasi-
ness in the affected side will continue for months. After recovery it is well
to inform the patient that he may expect pain after active physical exer-
cise. If the patient presents the signs of anasmia, the syrup of the iodide
SUB-ACUTE PLEURISY. 151
of iron should be given in teaspoonful doses three or four times each day.
Stimulants should rarely be allowed before the third week. Counter-irri-
tants by means of cups and blisters, are rarely of service in the treatment of
this form of pleurisy. I have found in some cases, when the pain in the
side continued after the friction sound had disappeared, that the use of the
constant current over the affected side for twenty minutes at a time, gives
almost instantaneous relief.
SUB-ACUTE PLEURISY.
{Pleurisy with Effusion.)
This is the most common form of pleurisy, and the inflammatory proc-
ess usually invades the whole of the pleura on the side affected. It may
commence at any point on the pleural surface, but it most frequently com-
mences on the costal portion.
Morbid Anatomy. — The anatomical changes in this form are similar
to those which take place in acute pleurisy, except that the new tissue
formations are more extensive, the pleural membrane more uniformly
thickened, and there is more abundant serous effusion containing flocculi of
lymph. The pleural cavity may be partly or completely filled with fluid.
The entire pleura becomes coated with a layer of fibrin varying in thick-
ness, usually most abundant on its costal portion. New connective-tissue
cells and basement substance are mingled with the exudation. Sometimes
the serous effusion contains blood globules from the rupture of the thin-
walled vessels in the new connective-tissue. It is the large amount of
serous effusion, containing more or less cellular elements, that distinguishes
sub-acute from acute pleurisy. This indicates a difference in the grade
rather than in the nature of the inflammatory process. When the cell ele-
ments are abundant it is characterized as a sero-purulent effusion. If the
pleural cavity is not filled with fluid, the effusion will occupy the most
dependent portion of the pleural cavity. It may be confined to circum-
scribed portions of the pleural cavity by adhesions. If it occupy the most
depending portion of the cavity the adjacent lung-tissue will be compressed
and pushed upward. When the pleural cavity is filled with fluid the in-
tercostal spaces will be more or less bulging, the diaphragm will be pushed
downward, and the abdominal viscera upon either side may be displaced
downward ; the heart will be displaced either to the right or left, accord-
ing as the fluid occupies the left or right pleural cavity. The lung on the
affected side is compressed either toward the vertebral column or upward
and inward against the mediastinum. Occasionally the lung occupies
the anterior portion of the pleural cavity and the fluid the posterior
portion ; the direction of the compression is influenced by the location
and extent of previous pleuritic adhesions. If no adhesions exist the
lung may be compressed to one-eighth of its normal size, and assume a
pale-red or greenish color, have a tough, leathery feel, and be entirely
void of air. With the compression of the lung there may be compression
of the bronchi, but the larger bronchial tubes usually remain pervious.
If recovery takes place the fluid disappears by absorption, the fibrin
152 DISEASES OF THE RESPIRATORY ORGANS.
undergoes fatty metamorphosis, liquefies, and slowly disappears. As the
fluid disappears the thickened pleural surfaces come in contact, and more
or less extensive adhesions form between the two surfaces. On account of
the changes which take place in the pulmonary pleura the lung-tissue does
not expand to its normal dimensions, but more or less retraction of the
chest walls on the affected side takes place. The longer the fluid remams
in the pleural cavity the more extensive will be the retraction. As the
fluid disappears, the orgafls which have been displaced by its pressure re-
turn to their normal positions. If the retraction is considerable they will
be displaced upward, and the heart may be drawn from its normal position
to the right or left.
Etiology. — The causes of this form of pleurisy may be the same as those
of acute pleurisy. In a large proportion of cases it is secondary to some
form of organic disease, as chronic Bright's disease of the kidneys, pulmo-
nary phthisis, etc. Occasionally it seems to occur idiopathically, or at least
from causes not well understood. It is a clinical fact familiar to every
careful observer that sub-acute pleurisy is not infrequently the first step
to the development of phthisis. The pathological relations between these
two diseases are exceedingly interesting, but not at all times ajiparent. The
weak and enfeebled, rather than the strong and robust, are liable to attacks
of sub-acute pleurisy.
Symptoms. — This form of pleurisy may come on suddenly with active
symptoms, or insidiously with very mild symptoms. In the majority of
cases the symptoms are mild. There is no chill of invasion ; it comes on
insidiously after exposure to wet, cold, and fatigue, in the enfeebled or in
those who are suffering from some chronic disease. It is rarely attended
by any noticeable pain in the side, or at least not by the severe pain which
attends acute pleurisy. On close questioning the patient will state that
some time before exposure an uneasy sensation in the affected side, attended
occasionally by a sharp pain of short duration, was experienced. This
form of pleurisy is often so insidious in its approach that the patient will
be unable to tell when he commenced to be sick ; for a period of several
weeks he will have gradually lost flesh and strength, yet will have been
able to attend to his ordinary avocations if they required but little physi-
cal exertion. There will be slight dyspnoea on exertion, with slight febrile
excitement at night. Sometimes there is an almost continual cough with
a scanty muco-purulent expectoration ; at other times the cough will be
entirely absent. Usually when this class of patients consult a physician
the only subjective symptoms will be a frequent, small, feeble pulse, and
slight heat and dryness of the skin, the temperature rarely rising above
101° F. The countenance will be pale and anxious, and the breathing short
and catching in character. On speaking, especially after exercise, the sen-
tences are uttered in a broken, interrupted manner. The patient will be un-
able to lie comfortably except on his back, or on the affected side with his
head slightly elevated. The pulse, usually small and feeble, will vary from
110 to 120 beats in the minute ; in fact, there will be no subjective symptom
which will enable one to reach a positive diagnosis.
In those cases which are ushered in by active symptoms the invasion wiU
SUB-ACUTE PLEURISY. 153
resemble that of acute pleurisy. There will be rigors followed by a tem-
perature of 102° or 103° F. ; the joulse will be full and frequent, the pain
on the affected side well marked and the breathing rapid and shallow.
Patients will sometimes ascribe the pain to the lumbar I'egion, as in ne-
phritic colic, for which it is sometimes mistaken. After a few days the fe-
brile symptoms abate, but do not entirely subside, and the serous effusion,
which is much larger than that in acute pleurisy, for a time steadily in-
creases, then remains stationary for a number of days or even weeks, and
then there is a sudden renewal of the febrile symptoms, the dyspnoea is
greatly increased, the cough becomes more constant and harassing, the pa-
tient is unable to lie down, and the fluid rapidly increases ; in twenty-four
hours the pleural cavity, — which previously has been only half full of
fluid, — becomes entirely filled, and the dyspnoea becomes so urgent, and
the danger from collateral congestion and oedema of the opposite lung so
imminent, that immediate relief is demanded by paracentesis. With the
rapid increase of the effusion the pain in the side subsides. However ill-
defined the rational symptoms may be in acute pleurisy, its physical signs
are more distinctive than in any other thoracic disease.
Physical Signs. — The physical signs of pleurisy with effusion will vary with
the amount of the fluid effusion. At its onset, before there is much fluid
effusion, a friction sound will be heard over the -affected side with more or
less feebleness of the respiratory sound. After the pleural cavity partly fills
with fluid, the vocal fremitus will be diminished cr absent at the bottom
of the pleural sac below the level of the fluid ; there will be flatness on per-
cussion, and an absence of vocal and respiratory sounds. A change in the
position of the patient will change the level of the fluid and the line of
flatness. Above the level of the fluid the percussion resonance will be nor-
mal or exaggerated, and in some cases tympanitic in quality. The respira-
tory murmur will be exaggerated, and at the level of the fluid it may as-
sume a bronchial character. The vocal sounds may be intensified, or a
distinct bronchial voice may be heard. All of these physical signs are
most marked posteriorly.
When the pleural cavity is completely filled with fluid, and the lung is
compressed backward against the spinal column, important modifications
in the physical signs take place.
Inspection will show an enlargement of the affected side, and a bulging
of the intercostal spaces. The respiratory movements on the affected side
will be changed from an up-and-out movement to a direct up-and-down
motion, while on the unaffected side the expansive respiratory movements
are increased. If the effusion is in the left pleural cavity the heart will be
displaced to the right, and the apex beat may be noticed under the right
nipple ; if it occupies the right pleural cavity the apex beat will be carried
to the left, beyond its normal position.
The circumference of the affected side at the end of expiration, will be
one or two inches greater than that of the healthy side ; but at the end of
inspiration the difference will be but slight. The expansive motion in in-
spiration on the healthy side may be two or three inches greater than on
the affected side.
154
DISEASES OF THE RESPIRATORY ORGANS.
On palpation there is usually complete absence of vocal fremitus over the
affected side. There are a few cases, however, in which the vocal fremitus
persists even when the cavity is filled with fluid.
Upon percussion there will be flatness over the whole of the affected side,
and the flatness will extend below the normal limits of the lung.
On auscultation there is usually entire absence of the respiratory sounds
over the affected side, and the vocal sounds will be distant and indistinct.
Not infrequently, however, at the upper and posterior portion of the
pleural cavity distant bronchial respiration and bronchophony will be heard.
The bronchial respiration and the bronchial voice are sometimes diffused
and heard over the whole of the posterior portion of the affected side.
As the fluid subsides in the pleural cavity, inspection shows that the en-
largement of the affected side is decreasing, that the intercostal spaces
are regaining their normal condition, and that the respiratory movements
are returning. Mensuration shows a gradual diminution in the size of the
affected side until it becomes smaller than the other. On percussion the
pulmonary resonance will gradually return, first at the upper portion of the
pleural cavity ; but it is not completely restored until some time aftei*
the fluid has disappeared, especially over the lower portions of the pleural
cavity.
On auscultation, as the fluid disappears, the vocal and respiratory sounds
will gradually return. At first, the respiratory sounds are feeble and dis-
tant ; gradually they become more and more distinct. As the two rough-
ened pleural surfaces come in contact and move on each other, a creaking.
Absent respiratory motion
Diminished or absent vocal fremitus
Flatness on percussion.
Absence of respiratory murmur in
front, bronchial breathing behind.
Vocal sounds distant or absent
Fig. 34.
Diagram showing Physical Signs in Pleurisy with EfEusion ; pleural cavity filled with fluid.
rubbing, friction sound is heard. These rubbing friction sounds are often
audible for months after the fluid has disappeared. If, as sometimes hap-
pens, the lower portion of the affected lung remains permanently imper-
vious to air, the upper portion of the lung becomes emphysematous. Un-
der such circumstances the emphysema is compensatory, and the percussion
SUB-ACUTE PLEURISY. 155
note in the infra-clavicular space on that side will have a tympanitic
quality, and the expiration in this space will become prolonged, harsh, and
blowing in character.
Differential Diagnosis. — The diagnosis in uncomplicated cases of sub-
acute pleurisy is usually very readily made. The diseases with which it is
most likely to be confounded are pneumonic or phtldsical consolidation of
the lung, enlargement of the liver or spleen, cancer of the lung and i^leura,
and intra-thoracic tumors. It is hardly possible for a thoracic aneurism
to be developed in such a manner as to be mistaken for sub-acute pleurisv.
Pleurisy with effusion may be distinguished from phthisical and pneu-
monic consolidation by the history of the case, by the absence of the charac-
teristic expectoration, and by the lower range of temperature. Upon phys-
ical examination it may be distinguished by the enlargement or retraction
of the affected side, by the diminution or absence of vocal fremitus, and by
the flat note of the percussion sound. If the cavity is partly filled, by
the change in the line of flatness on change in the position of the patient,
and by the feeble or absent respiratory sounds over the fluid. The bron-
chial respiration which is sometimes heard over a pleural cavity filled with
fluid differs from the bronchial respiration of pneumonic or phthisical con-
solidation, in that it is more diffused and less tubular in quality. In
phthisical consolidation the progress of the physical signs is usually from
above downward ; in pleuritic effusion they advance from below upward.
Phthisis of an entire lung rarely exists without the other lung being in-
volved, while any amount of pleuritic effusion may exist in one cavity, and
the other remain unaffected. If doubt exists after considering all these
points of difference, it may be removed by the use of an exploring
trochar.
Serous effusion into the right pleural cavity is distinguished from an
enlargement of the liver upward, by the fact that when percussion is made,
the patient being in a sitting posture, the line of flatness in liver enlarge-
ments is higher in front than behind. The liver does not enlarge in such
a manner as to fill the pleural cavity posteriorly and anteriorly to the same
level.
Sub-acute pleurisy of the left side will rarely be mistaken for enlarge-
ment of the spleen, for when the spleen is sufficiently enlarged to encroach
upon the left pleural cavity the enlargement will be downward as well as
upward, the splenic tumor will be readily felt in the abdominal cavity, and
the flatness on percussion at the lower portion of the pleural cavity will
be continuous with the tumor in the abdomen.
The diagnosis between pleurisy with effusion and cancer of the lung or
pleura is often very difficult, and in some instances, if one relies only upon
the rational symptoms and physical signs, it will be impossible. All such
doubtful cases can only be decided by the use of the exploring trochar.
The needle of the exploring trochar can be introduced into the thoracic
cavity without the least danger, whether the needle enter a pleuritic effusion,
a hepatized lung, a cancer of the pleura or lung, or an aneurism.
Prognosis. — The prognosis in sub-acute pleurisy varies greatly in different
cases. While the majority will terminate in recovery, sudden death occurs
156 DISEASES OE THE KESPIRATORY ORGANS.
in a limited number without lesions to account for it. A large serous effu-
sion may take place suddenly, and cause death by its interference with res-
piration and circulation. Cases may be protracted over a period of months,
and finally a sero-fibrinous effusion may change into a sero-purulent one,
and a sub-acute pleurisy may thus become an empyema ; in giving a prog-
nosis it is to be remembered that in most cases that recover, more or less
extensive adhesions result, which cause permanent crippling of the lung,
and lead to the development of more or less extensive compensatory emphy-
sema, chronic bronchitis, and fibroid induration of lung-tissue. When
the new tissue formations are extensive, and the general health much im-
paired, in those who have a strong hereditary or acquired tendency to pul-
monary phthisis, there is always danger that the new tissue may become the
seat of tubercular developments. One of the greatest dangers after recovery
from sub-acute pleui'isy is a relapse.
Treatment. — The main thing to be accomplished in the treatment of sub-
acute pleurisy is to remove the fluid effusion as rapidly as possible, at the
same time taking care to sustain the patient. The principal means which
have been employed for the accomplishment of this object are hydragogue
cathartics, diuretics, diaphoretics, and blisters applied in succession over
different parts of the affected side. On account of the anemic condition
of the majority of these patients, general or local bleeding, as well
as the use of mercury, is now very rarely employed ; for a like reason I
very much question the beneficial effects claimed for cathartics, diuretics
and blisters ; it is very questionable if the condition which favors the ab-
sorption of the fluid in the pleural cavity can be reached by the employ-
ment of any of the so-called depurative remedial agents. It is claimed that
the use of hydragogue cathartics and diuretics quickly removes large quan-
tities of fluid from the body, and consequently the fluid portion of the
blood is greatly diminished, and that whenever a cavity contains fluid, the
absorbents and blood-vessels of the part take it up to replace that lost by
the blood, and thus fluid in the pleural cavity is absorbed. There is little
doubt but that hydragogue cathartics and diuretics will hasten the absorp-
tion of non-inflammatory serous effusion in simple hydrothorax, but there is
no evidence that they have power to promote the absorption of inflammatory
products from the pleural cavity in sub-acute pleurisy. It is certain that
by the action of these depurative means the vital powers of the patient are
greatly enfeebled and the processes of digestion and nutrition seriously in-
terfered with. It is also well established that when the nutritive processes
are going on most rapidly absorption takes place most rapidly. Conse-
quently anything that interferes with these processes is contra-indicated in
the treatment of this form of pleurisy. There are also other conditions
which greatly impede the absorption of the fluid effusion in pleurisy.
When the pleural cavity is distended with fluid, its absorption is impeded
or prevented by the obstruction offered to the flow of blood throngh the
pleural and sub-pleural vessels by the pressure. Under such circumstances it
is useless to resort to diuretics and hydragogue cathartics. The mechanical
withdrawal of a sufficient amount of liquid to relieve the tension of the cavity
and remove the pressure from the lung and the sub-pleural veins is an abso-
SUB-ACUTE PLEUEISY. 157-
lute necessity before the processes of absorption can commence. If the surface
of the pleura is covered by a thick layer of exudative material, this layer is
interposed between the sub-pleural vessels and the fluid effusion, and must
greatly interfere with the absorption of the liquid ; as it becomes thicker
and thicker by successive deposits of fibrin, it is obvious that the longer the
liquid remains in the pleural cavity the thicker the fibrinous deposit be-
comes, and the less is the probability that the liquid will be absorbed.
Against these conditions cathartics and diuretics are powerless.
For many years I have rarely employed any depurative agents in the treat-
ment of sub-acute pleurisy. The remedial agent which seems to me to have
the greatest power in promoting the absorption of an effusion is the syrup
of the iodide of iron. In connection with the administration of iron the
patient should take the largest amount of the most nutritious food, with
wine or some form of alcoholic stimulant. The principle of treatment
is to employ all those remedial and hygienic measures which improve
nutrition.
As so little can be done by medication to excite or hasten the absorption
of pleuritic effusion, the question of the employment of mechanical means
for its removal presents itself. There is some difference of opinion in the
profession upon this point. One class of observers claim that a single re-
moval of the fluid is of little service, and that the danger of admitting air
into the pleural cavity is so great that if the operation is frequently per-
formed a serous effusion is very apt to be changed into a purulent one, thus
jeopardizing life. On the other hand, the advocates of the operation main-
tain that if the fluid is permitted to remain in the pleural cavity it becomes
purulent. The causes which impede or render impossible the absorj^tion of
the fluid seem to me reasons in favor of its early mechanical removal, es-
pecially as the practice of aspiration has inaugurated a new era in the
management of these cases, and has removed all objections to such early
removal. When a perfect instrument is used and a small needle intro-
duced into the pleural cavity, the entrance of air is impossible. In any
case of pleurisy, when the accumulated fluid remains stationary for one
week, or is increasing after the cavity has become half filled, and especially
when the cavity is completely full, there should be no delay in aspirating.
With every day that the lung remains compressed, and with every addition
to the plastic deposit upon the pleural surfaces, the chances of its absorp-
tion are diminished, and the danger that the lung will be permanently
crippled is increased.
The following rules should be observed in the performance of aspira-
tion of the chest. Place the body of the patient in the erect posture, lean-
ing somewhat forward, with the arm of the affected side thrown partly
across the chest. This position of the arm is preferable to any other for
the reason that the integument is not made unnaturally tense over the inter-
costal spaces. Select a needle of small size for the first tapping, and in-
troduce it to the depth of at least one inch into the fifth or sixth inter-
costal space, at the junction of the axillary and infra-scapular regions.
After the needle has been introduced the fluid may be permitted to flow
through the instrument until the patient complains of a sense of con-
158 DISEASES OF THE EESPIEATOKY OEGANS.
striction about the chest, when the withdrawal of the fluid must b8
stopped. The amount of fluid that can be withdrawn at the first aspiration,
if the cavity is distended, will depend upon the length of time which the
fluid has remained in the pleural cavity. If it has accumulated rapidly,
the cavity may frequently be emptied without giving rise to any un-
pleasant symptoms ; if, however, it has been slow in its accumulation
and the pleural cavity has contained a large quantity of fluid for a consid-
erable time, only a small amount can be withdrawn without producing a
severe attack of dyspnoea. When this is the case the patient may be per-
mitted to remain quiet for a few days, and then the operation should be
repeated as often as it can be without producing unpleasant symptoms.
The sense of constriction about the chest always indicates that no more
fluid should be withdrawn at that time. It is claimed by some that aspira-
tion of the chest in pleurisy may cause death suddenly or within twenty-four
hours after the aspiration, and that the cause of death under such circum-
stances cannot be accounted for, as there are no lesions found after death
which are sufficient to produce it. I cannot understand how this is pos-
sible if the aspiration is performed with sufficient care ; it certainly has
never happened in any of my cases. I can conceive how the sudden with-
drawal of a large quantity of fluid from the left chest might cause a severe
attack of syncope from which a crippled heart might not rally. I have no
hesitation in recommending this operation in all cases, provided it be done
according to the rules just given, and I am not disposed to delay aspiration
long after the pleural cavity has once become filled with fluid, for I am
convinced that its early removal tends to promote a more rapid recovery,
and prevents those changes in the pleura which lead not only to a tedious
convalescence, but also to an incomplete ultimate recovery.
EMPYEMA.
{Plev/risy with a Sero-fibrinous and Purulent Effusion.)
This is a suppurative inflammation of the whole pleura, usually confined
to one side of the chest. It may be primary or secondary. When it is
primary it usually commences as an acute affection ; when secondary, it is
sub-acute or chronic from its commencement.
Morbid Anatomy. — The pathological changes in this form of pleurisy are
most extensive and best marked on the costal, diaphragmatic, and medias-
tinal portions of the pleural membrane. In primary suppurative pleurisy
there is poured out a large amount of plastic material which undergoes
histological transformation into pus, and thus a large amount of thick pus
is rapidly formed in the pleural cavity. In the secondary variety of sup-
purative pleurisy a sero-purulent effusion will slowly accumulate in the
pleural cavity, varying in consistency in different cases, sometimes being
quite thin and mainly composed of serum, at others extremely thick and
containing comparatively little serum. This purulent fluid usually occu-
pies the most dependent portion of the pleural cavity ; it may, however, be
confined either to the posterior or anterior half of the chest by old adhesions.
The manner in which large purulent accumulations are formed in the
EMPYEMA. 159
pleural cavity is as folloy>^s : — in acute suppurative pleurisy with sero-fibri-
nous exudation, a large number of pus cells form in the connective-tissue of
the pleura and also on its surface, from which they are waslied into the
cavity, along with the fibrinous exudation, by the serous effusion. Some-
times the accumulation is very large and takes place very rapidly. This is
characteristic of the pleurisies which occur in connection with pyaemia. A
sero-fibrinous exudation may become purulent when a fresh cause of in-
flammatory irritation gives rise to an active cell-exudation ; the new irrita-
tion may come from the admission of a>r into the pleural cavity, or from
some change in the fluid which has previously occupied the cavity, or, per-
haps, from suddenly developed sepsis. Under these circumstances a variety
of cell-formative processes are established. Some are produced in the plas-
tic exudation, and some in the pleura itself. The clear serum becomes tur-
bid, shreds of false membrane are loosened from their connection with the
underlying tissue and undergo liquefaction, and the whole, or a large por-
tion of the pleural membrane becomes a suppurating surface, and thus a
large amount of pus is formed in the pleural cavity. If the pleural cavity
is aspirated at the commencement of the purulent process in such cases, the
first fluid removed will be found to contain a moderate number of cells ; at
a second operation, a week or two later, a large number of cells may be
found, and it is usual under such circumstances to attribute the increased
number of cells to the effects of the first aspiration. This is not, however,
a legitimate inference, for the increase in the cell develoj)ment is the
natural result of the morbid process which was in operation at the first
aspiration.
Purulent accumulations in the pleural cavity may become so large that
death may ensue in consequence of the depression caused by their pro-
duction. The tendency of sujopurative pleurisy is never toward convales-
cence, unless by spontaneous openings. The inflammatory process is not
limited to the pleura ; it may extend from the costal pleura to the connec-
tive-tissue underneath, to the periosteum of the ribs, causing necrosis,
or it may perforate the walls of the chest and be discharged externally. In
some instances the lung may be perforated and the discharge take place
through a bronchial tube, or the diaphragm may be perforated and the pus
find its way into the abdominal cavity. If the patient survives the empty-
ing of the pleural cavity, repair is accomplished by the rapid and abundant
formation of cicatricial tissue ; the pleural cavity is contracted in every di-
rection like a huge cicatrix, the chest walls on the affected side retract to
their fullest extent, and the thoracic and abdominal viscera are dragged out
of their normal positions to help fill the space formerly occupied by lung-
tissue. In some cases of circumscribed empyema the fluid portion of the
pus is absorbed and the solid constituents undergo cheesy transformation,
the salts of lime are deposited and the thickened pleura becomes calcified.
The bony or calcareous plates which are occasionally found in the pleural
cavity at post mortem examinations usually have their origin in an
empyema.
Etiology. — The cause of suppurative pleurisy is not always readily de-
termined. It may be of traumatic origin. When it occurs spontaneously
160 DISEASES OP THE KESPIEATORY ORGAKS.
it is always associated with some vice of constitution, such as results from
some exhausting disease, or the debility which attends chronic alcoholismus.
It often complicates acute and chronic infectious diseases. In the en-
feebled it is frequently developed from a sero-fibrinous pleurisy which has
continued for a long time, but in most instances, under such circumstances^,
the occurrence of the suppurative process is due to some new infection,
or to some new local excitement of pleuritic inflammation. Pleurisies
that are developed in advanced phthisis are very apt to be suppurative in
character. It may be secondary to abscess of the liver, or to the opening
into the pleural cavity of a vomica in the lung in chronic phthisis. An
abscess in the abdominal cavity or in the chest walls may open into the
pleura, and establish a suppurative pleurisy.
Symptoms. — The rational symptoms of empyema will vary with its char-
acter. Those cases in which the inflammatory processes are acute at the
onset, accompanied by the rapid production of fibrin and pus, will be
ushered in by chills, followed by a rapid rise in temperature, and a rapid,
full pulse. There will be severe pain in the affected side, with the signs of
great prostration. The prostration is greater than in acute fibrinous pleu-
risy, and the countenance early assumes an anxious expression ; if the in-
flammatory products become gangrenous the prostration is extreme, and the
patient presents the appearance of one suffering from peritonitis ; typhoid
symptoms manifest themselves very early ; and these cases usually termi-
nate fatally within two or three weeks. In other cases the active symptoms
subside after a week or ten days, and symptoms of the more chronic form
of empyema are developed. The symptoms of chronic empyema are often
very obscure ; the presence of pus in the pleural cavity in these cases can-
not be determined either by the rational symptoms or by physical signs.
The patient rarely suffers from local pain — there is simply a sense of un-
easiness, or weight in the affected side ; there is a gradual loss of flesh and
strength ; the countenance assumes a pale, anxious expression ; and there
is an irregular diurnal chill followed by profuse sweats. Ordinarily the
patient has a cough with a scanty muco-purulent expectoration, the voice
becomes weak and there is more or less dyspnoea, and the patient gradually
assumes the appearance of one in the last stages of pulmonary phthisis. If
empyema occurs as a complication of septicaemia or pyaemia, its commence-
ment is also, at times, very insidious. In these conditions patients some-
times pass into a semi-comatose state. Not infrequently pysemic patients
make no complaints which would direct attention to the pleura, and the
pleural cavity may be found two-thirds full of pus, without having given
a single symptom of its presence.
If an empyema is about to open externally, it will usually make itself
manifest by a protrusion between the ribs, which gives a sense of fluct-
uation, and after a time grows red, and finally a valvular opening is
formed and pus is discharged. If the opening takes place through the
lung into a bronchial tube, the discharge of pus is ordinarily preceded
by symptoms of pneumonia ; the patient will have a chill, followed by
a cough and a more or less profuse expectoration containing blood, which
will be followed by a profuse purulent expectoration, which will afford
EMPYEMA. 161
marked relief. The profuse purulent expectoration will occur two or
three times a day ; the chest walls gradually retract, and finally the ex-
pectoration will cease altogether and the pleural cavity become obliterated.
If the opening takes place into the peritoneal cavity, its occurrence is
usually followed by a rapidly fatal peritonitis. If the communication
is established with the intestinal canal, pus will appear in the discharges
from the bowels. If the patient survives the establishment of either
an external or internal oi^ening, spontaneous or artificial, a connec-
tive-tissue development takes place in the pleural cavity, and as the con-
tents of the cavity are being discharged retraction of the chest and dis-
placement of the abdominal and thoracic viscera take place ; this process is
necessarily slow, and years may elapse before it is completed.
Physical Signs. — The physical signs of empyema are essentially the same
as those of pleurisy with elfusion, except that the level of the fluid is not so
readily changed by a change in the position of the patient ; if, however,
the physical signs indicate the existence of fluid in the pleural cavity in
one who is very much debilitated, who has a constant cough with muco-
purulent expectoration, hectic fever with profuse sweats, and whose history
indicates tliat the fluid has existed for a long time, one may be almost cer-
tain that the fluid is purulent.
Diiferential Diagnosis. — Unless a fistulous opening exist, a positive diag-
nosis of empyema is impossible, except by an explorative puncture.
When such a puncture has been made, and some of the contents of the
pleural cavity have been drawn ofl and subjected to microscopical ex-
amination, it is not possible to confound an empyema with any other
thoracic disease.
Prognosis. — The prognosis in empyema is unfavorable. In acute sup-
purative pleurisy death may occur at the end of one or two weeks. In the
more chronic cases it may take place from gangrene produced by decompo-
sition of the inflammatory products in the pleural cavity. Statistics show
that in empyema of slow development, where spontaneous openings occur,
about one in five recover, while in those in whom artificial openings are
established the rate of mortality is greater. This class of patients die
from the exhaustion produced by the accumulation of large quantities of
pus, and from the exhaustion which attends a prolonged and abundant
purulent discharge. A large number of these patients live for a year or
more. The judicious use of the aspirator will tend to render the prog-
nosis more favorable in the acute cases. I am confident that the early in-
troduction of a drainage tube into the pleural cavity in chronic cases will
save many lives. In estimating the prognosis in this disease, the treatment
to which the patient is to be subjected must always be considered.
'Che majority of empyemic children recover, while in adults, although
for a time recovery seems almost certain, phthisis is sooner or later
developed.
Treatment. — In the treatment of this afi'ection it is useless to attempt to
produce absorption of the purulent accumulation by remedial agents. Its
removal can only be accomplished by mechanical means — either by aspira-
tion or by making a permanent opening in the chest walls. If aspiration is
11
162 DISEASES OF THE EESPIEATORT ORGAN'S.
resorted to a large-sized needle should be used, and no attempt should be
made to empty the cavity at the first operation. Eemove only a small por-
tion of the accumulation, being governed by the same rules which have been
given for the removal of serous effusions, and allow from three to six days
to elapse between successive aspirations. At each aspiration something in
excess of the amount which was taken at the previous seance should be
removed. Never continue the removal of pus in empyema after the patient
complains of constriction in breathing, even though only three or four
ounces have been removed. If the aspiration is to be successful the fluid
will become thinner at each aspiration, and retraction of the chest wall will
be noticed. If the fluid becomes thicker and emits an unpleasant odor, a
permanent opening should immediately be made. In empj^ema occurring
with septicaemia and pysemia the accumulation will exceed in quantity that
removed, unless the aspirator is used daily. Under such circumstances a
free opening should be made. If a permanent opening is to be made, let it be
made in the axillary line in the seventh or eighth intercostal space. After
a free opening has been made into the chest cavity, a quarter-inch rubber
drainage tube should be introduced, and so fastened that it will remain.
Oft-^en when there is little space between the ribs a portion of bone should
be removed, that the tube may not be compressed during respiration. A
double drainage, by making two openings in the chest cavity, is rarely
advisable. As regards the washing out of the pleural cavity after the intro-
duction of the drainage tube, although it is strongly advocated by some, my
recent experience is very positively against it, even when the purulent dis-
charge has an offensive odor. Thrice have I had reason to believe that my
patients have died from the direct effects of washing out the pleural cavity
with a weak solution of carbolic acid. From the commencement empyemic
patients must receive a most nutritious diet with moderate stimulation.
Tonics, such as quinine and iron, are always indicated ; cod-liver oil will be
of service if it does not interfere with stomach digestion. The patient
must be kept in the open air as much as possible, and a change of climate is
often attended by very marked improvement. The majority of cases of em-
pyemic children will recover if aspiration is performed early and repeated
at short intervals. In most adults it will be necessary to make a permanent
opening in the chest wall.
ADHESIVE PLEURISY.
Adhesive pleurisy may commence as a primary disease, or be the sequela
of an acute, plastic, or a sub-acute effusive pleurisy. In any case there is
more or less extensive new connective-tissue formations over a greater or
Jess extent of the pleural surface.
Morbid Anatomy. — The essential lesion in this form of pleurisy is the for-
Tuation of new connective-tissue over the pleural surfaces. This hyperpla-
sia may or may not have its origin in a pleurisy which gives fibrin, serum,
or pus as its product. As a result the pleura becomes thickened sometimes
to the extent of half an inch ; but the most important and constant lesion is
adhesion between the costal and pulmonary pleurae. These adhesions.
ADHESIVE PLEURISY. 163
however they originate, are progressive, and, after a time, become very
extensive. In some cases the two surfaces may become closely agglutinated
to each other throughout their Avhole extent, and then the entire space be-
tween them may be obliterated. As a result of these adhesions the expan-
sive motion of the lungs is interfered with, and sometimes to such an extent
as to cause constant dyspnoea. The heart may be displaced to the right and
backward. In one case where the adhesions were extensive over both lungs,
the heart cavities were much dilated, and, a loud ventricular murmur always
being heard, valvular disease of the heart was diagnosticated by good ob-
servers who saw the case during life. This form of pleurisy often leads to
the development of fibrous phthisis.
Etiology. — It occurs most frequently in rheumatic and gouty subjects. It
is often associated with general fibroid degeneration. When it occurs as
a sequela of sero-plastic pleurisy it begins with the disappearance of the
sero-plastic effusion.
Symptoms.— Its development is always slow and often intermittent. Its
most constant early symptom is a dull pain over the affected part, accom-
panied by a sense of constriction. An early symptom is dyspnoea on exer-
tion, which steadily increases with the advance of the disease, and becomes
so severe that even slight exertion, such as going up stairs, will give rise
to such severe paroxysms that signs of collapse sometimes follow. There
is usually a dry, hacking cough, frequently attended by free bronchial
hemorrhages. I have frequently found these pleuritic adhesions the only
apparent cause of quite profuse bronchial hemorrhage. As the adhesion
becomes extensive, the patient loses flesh and strength, and in some cases
the ordinary symptoms of chronic phthisis are present. If there is much
displacement of the heart the patient will be troubled with cardiac palpita-
tion on slight excitement or physical exertion, so that his dyspnoea and
cough are often supposed to be due to some obscure cardiac lesion.
Often after this class of patients have suffered much and seem to be stead-
ily getting worse, periods of remission occur, during which for months and
perhaps years they will seem to be recovering. The appetite returns, they
gain flesh and strength, the dyspnoea becomes less, and then, while they are
apparently recovering, they suddenly get worse, all their aggravating symp-
toms return greatly exacerbated, and they rapidly pass into a decline.
Physical Signs. — Inspection shows diminished expansive motion of the
affected side, or of the entire chest if both pleurae are affected.
Palpation shows diminished vocal fremitus over the seat of the adhesions.
Careful mensuration of the chest will often establish the diagnosis when
doubt exists as to the exact character of the changes.
On percussion there will be slight dulness, which will be most marked
at the part where the adhesions are most extensive.
On auscultation the respiratory sound will be feeble, sometimes scarcely
audible even during a full inspiration ; friction sounds will be heard. These
friction sounds are creaking or crepitating in character, very loud, and
often resemble mucous r41es and gurgles, for which they are sometimes mis-
taken, but the loss of chest expansion and the feebleness of the respiratory
sounds will readily correct the mistake.
164 DISEASES OF THE KESPIEATORY ORGANS.
Prognosis. — The prognosis in this form of pleurisy varies with its dura-
tion and extent. If the adhesions are not extensive and are of recent date,
the process may be arrested and complete recovery is possible ; but if they
are extensive and the inflammatory process has continued for a long time, it
is generally progressive and recovery is impossible. If it is attended by
great emaciation and progressively failing health it may cause death with-
out complications. The majority, however, die from the complication of
chronic bronchitis, emphysema, and chronic interstitial pneumonia (''fibrous
phthisis"). In some cases the disturbance of the general circulation from
dilatation of the right ventricular cavity leads to general dropsy and all
the conditions which result from heart insufficiency.
Treatment. — The first and most important thing to be accomplished in
the treatment of this affection is to improve the nutrition of the patient.
In accomplishing this the diathesis of the patient must be carefully consid-
ered. The diet must be regulated according to the indications ; the diet of
gouty subjects must he very different from that of the enfeebled, broken-
down alcoholic subject. While iron and the mineral acids will be indicated
in one class, cod-liver oil and the hypophosphites will be indicated in the
other. In all cases, the bichloride of mercury in minute doses will be found
of service. Climatic conditions are very important in its successful man-
agement ; as a rule high altitude with a warm, dry atmosphere, such as is
obtained in New Mexico, will be found most favorable. The external ap-
plication to the chest which has seemed to me to have a desired effect in
arresting its progress and removing its results, is the oleate of mercury —
its use must be continued for a long time, care being taken not to bring
the patient under the constitutional effects of the mercury.
CAlSrCER OF THE PLEURA.
Cancer of the pleura and sub-pleural tissue is never primary, and is only
met with in advanced cancerous infection. It appears either as circum-
scribed grayish thickenings of the pleura or in the form of distinct papular
elevations on the pleural surface. As the papules enlarge, they form pe-
dunculated outgrowths, which vary in size from a pea to a small orange. Ac-
companying these developments there is interstitial pleurisy, which causes
extensive thickening, adhesion, and induration of the pleura, attended by
the effusion of fluid into the pleural cavity.
Etiology. — It most frequently complicates cancer of the mamma, medi-
astinum, aud lungs.
Symptoms. — The signs of pleural cancer are always obscure. The history
of the case is always important. If the tumors are large, or the fluid effu-
sion abundant, so as to cause compression of the lung, there will be dysp-
noea, cyanosis, and vertigo, with the physical signs of fluid accumulation
and the slow development of solid tumors in the pleura. Should the evi-
dence of a tumor with slow accumulation of fluid in the pleural cavity oc-
cur in a case of long standing cancer of the breast, accompanied by gradual
emaciation and dyspnoea on slight exertion, cancer of the pleura may be
suspected. If a cancerous tumor is developed in the pleura posteriorly, with
PYOPNEUMOTHORAX. 165
the aorta in front, there may be a pulsation and bruit which will cause it
to be mistaken for thoracic aneurism. The prognosis is always unfavora-
ble, and the treatment is only palliative.
PYOPNEUMOTHOKAX.
This a condition characterized by the presence of both air and fluid in
the pleural cavity. The entrance of air into the pleural cavity is usually
promptly followed by the effusion of liquid, for it excites suppurative in-
flammation of the pleural membrane.
Morbid Anatomy. — The morbid changes which may occur in the pleural
membrane and in the pleural cavity in pyopneumothorax very nearly cor-
respond to those described as occurring in empyema ; they are increase of
tissue, granular appearance of the surface of the pleura, and the development
of pus. By the entrance of air into the pleural cavity, the lung is allowed to
collapse, to contract toward its base near the spinal column, in the same
manner as when the cavity is filled with fluid, although the opening (as from
rupture in an emphysema) may be no larger than a jDin-hole.' The heart
may be considerably displaced. The quantity of fluid varies in different
cases ; at one time the cavity will be nearly filled with fluid and contain
little air; — again it will be distended with air and contain little fluid.
"When extensive and firm adhesions of the pleural surfaces exist prior to the
entrance of air into the pleural cavity, collapse of the entire lung does not
take i^lace, but the escaped air is contained in a small space enclosed by ad-
hesions on all sides. This condition is usually present when pyopneumo-
thorax is developed from the perforation of an empyema, or suppurative
pleuritis. The air in the cavity is always deoxidized and rich in carbon
dioxide ; it may also contain sulphuretted hydrogen.
Etiology. — Eegarding the source of the air in the pleural cavity different
views have been entertained. Some have claimed that gas escapes into the
pleural cavity from the tissues or blood, in the same manner as it is claimed
to escape into the intestines from the mucous membrane ; this may be pos-
sible, but it is by no means probable. Others, again, have claimed that
it is the product of decomposition of fluid in the pleural cavity ; this ib
rarely, if ever, the case, for fluid effused into closed cavities resists de-
composition in a surprising manner, although when taken from such cavi-
ties or exposed to the contact with air within them, it rapidly decomposes.
Pus or serum will resist decomposition in a pleural cavity so long as it is not
exposed to air.
There can be little question but that in pneumothorax and pyopneu-
mothorax there is always an opening between the air-passages of the lung
and the pleural cavity, an opening which is the result of an ulcerative proc-
ess which may begin within the lung and work outward, or in its pleura]
surface and work inward. In rare instances air enters the pleural cavity
through an external opening in the chest wall. Hydatids sometimes rupt-
ure into the pleural cavity. In most cases of traumatic pneumothorax
i But them need he. no pleurisy : although a secondary pleuritia may light up around the opening and close
it, thus efifecting a cure.
166 DISEASES OF THE RESPIRATORY ORGAISTS
air does not enter the pleural cavity tliroagli the opening in the chest wall,
but comes from the lung through an opening in the pulmonary pleura, the
lung being torn at the same time that the opening is made through the
walls of the chest. The commonest example is in connection with fracture
of the ribs, in which the lung is sometimes torn by the broken end of the
bone, and air escapes through the rent into the pleural cavity. Entrance of
air into the pleural cavity usually occurs either in connection with pulmo-
nary phthisis, gangrene of the lung, empyema, or pulmonary emphysema.
It is most frequently met with in connection with pulmonary phthisis. Ab-
scess of the bronchial glands, and ulceration of the oesophagus or stomach,
may lead to it. When an empyema has existed for a long time an opening
may be established by ulceration through the lung into a bronchial tube,
thus permitting the fluid to be expectorated, and air to enter the pleural
cavity. In pulmonary emphysema, a sac containing air which has been
formed upon the surface of the lung may rupture, and air enter the pleural
cavity and develop pneumothorax ; the consequent pleurisy will rapidly
develop a pyopneumothorax. At the post-mortem examination of one who
has died of pyopneumothorax, it is often difficult, and sometimes impos-
sible, to find the opening in the pulmonary pleura, for the reason that in
some instances it becomes covered with a fibrinous deposit, and in others the
opening has been closed some time before death by an inflammatory process
in the lung substance about the opening.
Symptoms. — The symptoms which attend perforation of a lung, and the
escape of air into a pleural cavity, are usually well marked, but they are
somewhat variable. First, there is a class of cases in which the symptoms
are severe in character, the patient is suddenly seized with a sense of faint-
ness followed by hurried respiration and great dyspnoea. Pain may or may
not be a symptom ; its existence indicates inflammation. The dyspnoea is
in part mechanical, in part reflex. It is extreme, comes on suddenly, is
soon followed by well-developed cyanosis, the patient passes rapidly into a
state of collapse, and, in some instances, death occurs in a few hours.
Usually, however, the patient survives the shock of the perforation, and,
after a time, becomes comparatively comfortable, suffering, however, from
more or less dyspnoea. He is unable to lie down, able only to recline upon
the affected side. Some say they experienced a sense of "tearing," and
felt as if a fluid "were being poured inside the chest."
As the pleural cavity becomes filled with the fluid effusion (which may re-
sult from the attending pleuritic inflammation), the dyspnoea and cyanosis
increase, and general dropsy gradually develops. Aseptic air alone will not
cause inflammation or rise in temperature. It is a purulent accumulation
in the pleural cavity which proves fatal, and not the pneumothorax, for with
its development the temperature rises and the patient becomes more mani-
festly hectic, if hectic has previously existed. When the purulent accumu-
lation becomes very abundant the patient dies from the exhaustion produced
by the intensity of the fever or from collateral hypergemia and oedema of the
opposite lung. In some cases the symptoms which attend the entrance of
air into the pleural cavity come on more insidiously. The difficulty of
breathing may be gradually developed, and the existence of air in the pleu-
PYOPNEUMOTHORAX.
167
ral cavity may not be recognized until after considerable fluid has collected
in the pleural cavity. When pneumothorax occurs in connection with pul-
monary phthisis, its occurrence is marked by very active symptoms, pain
being prominent, followed by all the evidences of collapse. When oc-
curring in connection with pulmonary emphysema its development is very
insidious.
Physical Signs. — The physical signs of pyopneumothorax are very charac-
teristic, and, if properly appreciated, will always enable one to recognize its
existence. By ins;pection there will be noticed a bulging of the intercostal
Tympanitic resonance....
Amphoric respiration.... .
Metallic tinkling
Succussion sound
Absent vocal fremitys .
Flatness ^ -jj,
Absent voice •
Absent respiration
Fia. 35.
Diagram illustrating the Physical Signs of Pyopneumothorax.
space and an increase in the size of the affected side, which becomes more
prominent than in sub-acute pleurisy and has a ''rounded" look. There
will be the displacement of viscera seen in sub-acute pleurisy when the pleu-
ral cavity is distended with fluid, and there will be absence of motion on the
affected side, while upon the unaffected side the respiratory movement will
be also decreased in force and frequency, but to no such great extent, the
breathing being almost wholly abdominal.
Upon palpation there will be entire absence of vocal fremitus upon the
affected side, unless there are old adhesions. The heart, at the same time,
is felt pushed from its normal site. Thus far there is no difference between
the physical evidences of pyopneumothorax and sub-acute pleurisy.
On percussion, when the patient is sitting or standing there will be tym-
panitic resonance from the summit of the affected side to the level of the
fluid. Below the level of the fluid there will be complete flatness.^ A
change in the position of the patient will change the level of the fluid, and
also, of course, the character and site of the percussion note.
Upon auscultation there will be found an entire absence of all respiratory
and vocal sounds below the level of the fluid ; but, as soon as its level is
reached, if the opening from the bronchial tube which admits the air into
the pleural cavity still remains pervious, amphoric respiration or "echo "
will be heard, and it will be metallic in character. Metallic tinkling is al-
most uniformly associated with amphoric respiration, and is produced in a
' Except in pyopneumothorax it is rare to find an exactly horizontal line of demarcation with pleural
effusions.
168 DISEASES OF THE RESPIRATORY ORGANS.
variety of ways. It may be produced by agitation of tbe liquid from tbe
vibration of the voice, or by coughing and full inspiration, or by dropping
of liquid from the walls of the cavity upon the surface of the fluid. It is
more frequently produced by agitation of the fluid from speaking and
coughing. The characteristic physical sign of this disease is the succussion
sound, which is a metallic, splashing sound, produced by abruptly shaking
the chest while the ear is resting upon the surface. Over the affected side
no vesicular breathing can be heard, while over the healthy side the vesicu-
lar breathing is exaggerated.
Differential Diagnosis. — When pyopneumothorax is fully developed, it is
scarcely possible to confound it with any other disease, but it is possible to
confound pneumothorax with some other conditions. The only physical
evidences of a perforation which permits the entrance of air into the pleural
cavity, are tympanitic percussion, absence of all respiratory sounds on the
affected side, and intense dyspnoea ; the same development of signs might
occur in connection with complete obstruction of a large 'bronchus. Again,
it is said that pneumothorax maybe confounded with extreme pulmonary
emphysema. Patients suffering from these diseases present a somewhat
similar appearance ; in both classes there is tympanitic percussion, but in
the emphysematous patient the tympanitic percussion is present over both
lungs, while in a patient suffering from pneumothorax it is present only
upon the side on which the perforation has occurred. Besides, there is a
vesicular element to the tympanitic note in emphysema never found in
pneumothorax. In emphysema there will also be heard some respiratory
sounds. The expiration is prolonged and low pitched in emphysema ; not
so in pneumothorax. The breathing is broncho-vesicular in emphysema ;
not so in pneumothorax, where respiratory sounds are absent. Succussion
is present in pyopneumothorax ; not in emphysema. If errors in the dif-
ferential diagnosis of these two conditions are possible, they will be made
at the commencement of the attack.
A large cavity in the lung substance may be mistaken for pyopneumo-
thorax. I have never met with a pulmonary cavity of sufficient size and
with the conditions to produce the succussion sound. Amphoric res-
piration and metallic tinkling may be developed in a large cavity, but the
succussion sound will be absent ; on the other hand, when amphoric re&
piration and metallic tinkling are present in hydropneumothorax the suo.
cussion sound will also be present. In a cavity rales would be loud and
numerous ; vocal fremitus is very often exaggerated; the chest wall above it
would probably be slightly depressed, and fiinally, the heart, etc., would not
be displaced.
With a knowledge of the history of the patient and a proper appreciation
of the physical signs, it is hardly possible to confound pyopneumothorax
with any other form of disease. In no other disease are the physical signs
so characteristic and unequivocal, and in a large proportion of cases the
rational symptoms are equally diagnostic.
Prognosis. — The prognosis in pyopneumothorax is always unfavorable.
Al l authorities agree that when it occurs in connection with advanced pul-
HTDROTHOEAX. 169
monary phthisis or gangrene it generally proves fatal within five or six days ;
but in pneumothorax without pleurisy the prognosis is favorable. Every
day the patient lives betters the outlook ; the majority of fatal cases
die within two days, the period of survival in the remainder rarely extend-
ing beyond the sixth day. When recovery has taken place in cases of
pyopneumothorax, either they have been of traumatic origin, the result
of great muscular strain in connection with extensive pulmonary emphy-
sema, or an empyema has discharged itself through a bronchus. There is
record of a few recoveries where the rupture occurred in the early stage
of phthisis. When recovery does take place it is reached in the following
manner : — plastic material is poured out in the tissue surrounding the open-
ing in sufficient quantities to completely close it ; the air and fluid are thus
imprisoned in the pleural cavity ; the air is rapidly absorbed by the pleural
membrane, and if the closure is sufficiently firm to persist after the air has
been removed, the case will be thus changed from one of pyopneumo-
thorax to one of empyema. Cases have been related in which perforation
of the lung and pneumothorax were present without any fluid collecting in
the pleural cavity. Such cases are of such rare occurrence that they can
hardly be taken into consideration as regards prognosis.
Treatment. — The treatment of this affection is almost necessarily pal-
liative. At the very onset of the attack, when the patient is suffering from
the shock of the perforation, a full hypodermic injection of morphine
will be found of service, and it may be repeated once or twice a day for
the first few days. If the patient survives for a few days, stimulants
may be advantageously administered, and he must be sustained by a
most nutritious diet. Among drugs, musk and chloroform are recom-
mended by so good an authority as Dr. Walshe. Hot poultices and sooth-
ing fomentations give relief when applied over the chest. The que-
bracho bark is now given for relief of the dyspnoea. When the dyspnoea
is extreme and the distress of the patient is very great, and a considerable
quantity of fluid has accumulated in the pleural cavity, the question will
arise whether a free opening shall be made through the chest walls. As a
rule, this must be regarded as a palliative measure, and should be resorted
to only in extreme cases. If it be resorted to, a fine trochar sliould be in-
serted into the chest, and the air permitted to escape through a connecting
tube under water, until an equilibrium has been established. It may give
relief for a time, and it is justifiable to resort to it when the fluid collec-
tion is abundant and the febrile excitement is intense. It may delay the
fatal termination. Walshe recommends general bleeding or dry cupping.'
HYDEOTHOEAX.
Uydrotliorax is anon-inflammatory fluid effusion into one or both pleural
cavities ; it often accompanies general dropsy. The fluid is generally clear,
of a yellowish-green color, and may be sufficient in quantity to compress to
a considerable extent one or both lungs. It may occur in any chronio
1 JJis. of Heart, etc.
170 DISEASES OF THE EESPIEATORY ORGAKS.
exhausting disease which causes general hydraemia. It rarely occurs as the
sole morbid process in the human body. In a large number of autopsies
a small amount of clear or bloody serum will be found in the pleural cavi-
ties, which is merely the result of post-mortem changes ; such conditions
should not be regarded as evidence of hydrothorax.
Etiology. — Any disease or condition {e. g., mitral disease especially) that
impedes, and raises the pressure in, the venous circulation will cause it.
Thus it may be caused by the pressure of enlarged glands ; tumors and
venous thrombi may induce it ; also diseases of the heart and kidneys, the
cancerous and other cachexise. Hydrothorax generally occurs in connec-
tion with general anasarca, such as is developed in Bright's disease.
Symptoms. — It generally comes on insidiously, and its development is
attended by no febrile symptoms. Its occurrence is marked by steadily in-
creasing dyspnoea, until the patient reaches a condition of extreme distress,
and orthopnoea ; the lips become livid, the finger-ends blue, and the res-
piration gasping. He is unable to lie down and can speak only in mono-
syllables. On physical examination there will be found the signs of fluid
in both pleural cavities. There may be a short, dry cough. If the effusion
is large, the action of the heart will be embarrassed, as shown by a small,
feeble pulse. All the phenomena which attend this condition are due
to mechanical pressure caused by the presence of fluid in the pleural cavi-
ties, and patients die cyanosed as the result of diminished breathing
capacity.
Differential Diagnosis. — Ordinarily the diagnosis of hydrothorax is readily
made. It may be confounded with suh-acute pleurisy, but generally the
history of the case will determine the character of the effusion. Then, its
simultaneous occurrence on both sides in connection with general dropsy,
without any irritant or attendant fever, will be sufficient to enable one to^
make the diagnosis of hydrothorax. It may be mistaken for pulmonary
oedema ; the two conditions are very likely to occur together, but in pul-
monary oedema a crackling sound will be heard over the oedematous lung,
which sound is not present in hydrothorax, and there will be copious,
watery (perhaps blood-stained) expectoration, which is absent in hydro-
thorax. In emphysema the increased resonance, and in bronchitis the
sputum and rales, will suffice to differentiate the three conditions. An
enlarged (painless) liver will not be mistaken for dropsy of the chest. The
physical sign of hydrothorax is fluid in both pleural cavities which is freely
movable by a change in the position of the patient, and is not attended by
friction sounds or vocal fremitus. The introduction of a trochar and with-
drawal of the fluid will decide the case.
Prognosis. — The danger attending hydrothorax will depend to a great
extent on the general condition of the patient at the time of its occurrence.
When it occurs in connection with general anasarca in Bright's disease, oT
in extensive heart disease, it may prove the direct cause of death. The
majority of cases yield readily to treatment, and life may be prolonged
months, even years, by judicious management.
Treatment. — The general treatment of hydrothorax corresponds to that
H^MOTHOEAX. — PULMOZsTARY PHTHISIS. 171
for the removal of dropsical accumulations in other parts of the body. It
is a simple dropsical elfusion, and can be removed by the administration of
remedies which diminisli the quantity of water in the blood. Such reme-
dies are the hydragogue cathartics, diuretics and that general class of
agents employed for the removal of fluid from the areolar tissue. Elaterium
is the best. Digitalis should be given (P. Anstie), and as soon as its effects
show, the muriated tincture of iron (gtt. xx every six or seven hours) should
be given. In many cases it will be impossible to wait for the effects of diu-
retics and hydragogue cathartics, as the patient will die unless immediate
relief from the pressure of the fluid is afforded. Under such circumstances
the aspirator may be used with advantage. Those remedies may be em-
ployed which are of service in the treatment of general anasarca.
HEMOTHORAX.
Hmmothorax is the escape of blood into the pleural cavity ; it is never a
primary affection. The escape of any considerable quantity of blood into
the pleural cavity may occur in connection with cancer of the lung or
pleura, from the bursting of an aneurism, the rupture of the pleura follow-
ing an extensive pulmonary apoplexy and accompanied by escape of blood
from the lung, and the rupture of a vessel. It may be due to traumatic
causes, a vessel being injured, as in fracture of the ribs. Sometimes blood
is mixed with pleuritic effusion, the product of pleuritic inflammation in
those of a scorbutic or purpuric diathesis. Fluid blood in the pleural sac
soon excites inflammation, whose products are usually serum with a varia-
ble admixture of pus.
The symptoms of haemothorax are those of liquid accumulation in the
pleural cavity with the accompanying evidences of internal hemorrhage,
pallor, syncope, etc., etc. In haemothorax, dyspnoea is sometimes greatest
at the onset, diminishing gradually.
In those cases where there is no appreciable traumatic cause for the bleed-
ing, all that can be done is to keep the patient at rest. Opiates are not
contra-indicated. Stimulants may be necessary. In some instances relief
may be obtained by the performance of paracentesis.
PFLMOlSrAEY PHTHISIS.
At the present day there is no subject in the domain of practical medi-
cine concerning which competent observers differ so widely as in the inter-
pretation of the anatomical changes which are met Avitli in pulmonary
phthisis. For one class of observers phthisis is an inflam7natory process
which may or may not be secondarily complicated by tubercle ; another
class maintain that tubercle is the primary and essential lesion of all phthi-
sis. Still more recently certain investigators maintain that there is a
specific material in phthisical processes, which may or may not be accom-
panied by the histological elements of miliary tubercle, but which always
172 DISEASES OF THE EESPIRATORT OEGAISTS.
has a specific form of bacteria — the tulerch hacillus — as the sole exciting
cause of its development.
Clinically and pathologically two varieties of phthisis can be recognized
— the acute and clironic. The pathological changes of the former are
quite well settled ; but the great difference of opinion which exists in
regard to the morbid changes of chronic phthisis is, to say the least,
confusing. This diversity compels to the opinion that tubercle is either
absent or plays but a secondary part in a large proportion of cases.
Acute phtJiisis. — The morbid changes of acute phthisis are a complex of
inflammation and the rapid development of tubercular tissue in the lung
substance.
Clironic phthisis. — The essential pathological change of chronic phthisis
is consolidation and induration of lung substance. Tubercles may or may
not be its primary lesion, and when present they may constitute but a small
part of the morbid processes. It is difficult and perhaps impossible to
draw a sharp line of demarcation between the different varieties of chronic
phthisis. Yet by the prominence of certain lesions it is possible to dis-
tinguish : flrst, a variety in which bronchitis, pneumonia, and pleurisy are
intimately associated with the development of tubercular tissue ; this has
been recently called "tuberculous lobular pneumonia ;^' the old term " ca-
tarrhal phthisis " indicates equally well the nature of the primary changes.
Secondly, a variety where the chief lesion is the production of new tissue
in the substance of the lung, the new growth being arranged either as dense
nodules in a firm tissue, or as a diffuse infiltration ; in the latter case much
of the lung is converted into a dense fibrous-looking mass. " Tuberculou\,
interstitial pneumonia^'' is suggested as the name for this variety, but tht>
term "fibroid phthisis" better indicates its essential changes. Thirdly, a
variety which has received the name of chronic tubercular phthisis, in
which numerous disseminated nodules, larger and harder than those met
with in acute phthisis, are found scattered throughout the lung.
ACUTE PHTHISIS.
Acute phthisis usually occurs in young subjects. Its advent and br^ef
course are marked by high temperature, a rapid pulse, hurried respiration,
pain in the chest, rapid emaciation and general loss of strength, haemopty-
sis, and the physical signs indicative of rapid pulmonary consolidation.
Morbid Anatomy. — A lung in acute phthisis appears, on section, to be
consolidated throughout the whole or a part of its extent ; the consolidated
portions have a gross appearance resembling red hepatization, interspersed
with diffuse yellow and grayish spots. The external surface of the lung
may appear normal, or show spots of yellow-gray solidification. Scattered
through the lungs may also be found extensive patches of consolidated tis-
sue, the central portions of which exhibit yellow or yellowish-white masses.
The material in the alveoli is inclosed in a fibrillated mesh-work (similar to
that in lobar pneumonia) and, microscopicall}^, is found to consist of pus
and epithelial cells that have become granular, fatty, swollen or distorted in
ACUTE PHTHISIS.
173
Fig. 36.
Acute Phthisis.
Section of Lung showing a single alveolus.
A. Wall of alveolvs.—B. Pus ccymuscles.— C. Cavity of
alveolus.— D. Fibrillar mesh.—E, E. Distorted, fatty and
granular epithelial cells, x 300.
shape, associated with a shining, transhicent, homogeneous substance ; this
fibrinous exudation is less solid than that of acute lobar pneumonia.
Though its evolution is not dissimilar (as there is no tendency to cheesy
degeneration, and complete reso-
lution can take place), yet mor-
phologically it is distinct. Both
lungs may be equally involved.
This stage of so-called " red hepa-
tization " is rapidly reached. In
some cases of acute phthisis the
only change found may be an
accumulation of epithelia in the
alveoli, with more or less cellular
infiltration of the alveolar walls.
In the hepatized mass are nodules
of tubercle tissue that vary in
size. They are bloodless, hard
and white, and, agglomerating,
press upon and obstruct the vessels
in the alveolar walls. Similar
nodules surround the small bron-
chioles and air-cells. The walls
of the bronchioles are more or
less implicated and are infiltrated with cells. Their lumen is, in the major-
ity of cases, filled with changed epithelia, pus and fibrin. These are called
"tuberculous zones." They
are bloodless. A peri-bronchitis
which may be tubercular exists
in all cases and advances uninter-
ruptedly from the smaller to the
larger bronchi. Infiltration of
peri-bronchial tissue is followed
by proliferation of the lymph
follicles in the bronchial walls.
Infiltration of the bronchial walls
by tuberculous material prone to
caseous degeneration is followed
by sub-epithelial abscess' and
ulcers that gradually extend.
Dilatation follows, and the bron-
chial wall becomes disorganized,
and cavities of considerable size
are thus formed.
In the midst of the hepatized
or tubercular tissue are spots that
Tissue that has become necrotic
Fi«. 37.
Acute Phthisis.
Bection of Lung showing a single alveolus in stage of hepa-
tization.
A. Wall of alveolus, with in fllf ration of pus at B, B.
C. Cavity of alveolus nearly filled with changed epithelia
and a few pus corpuscles.
J), D. Fibrillar mesh enclosing the cell elements.
300.
have undergone "coagulation necrosis.
' Called " tubercular " by Rindfleiech.
174
DISEASES OF THE RESPIRATORY ORGANS.
in this way is very abruptly and distinctly outlined from the adjacent con-
solidated lung. It may remain thus without further change, or it may
suffer cheesy degeneration. Cheesy nodules may remain unchanged, or
they may soften and form cavities that vary in size according to the extent
of the original " coagulation necrosis." ^ The nodules may, if resolution of
the alveolar exudate occurs, pass into and be surrounded by firm inter-
alveolar fibrous tissue. Occlusion of the branches of the pulmonary artery
is one of the explanations that have been advanced to account for the
'* coagulation necrosis." Another is the rapid accumulation of tubercular-
tissue, that shuts off the adja-
cent blood supply, and thus
induces necrosis. Neither view
as yet is accepted ; but it is
evident that the areas of coagu-
lation necrosis soften and cause
a rapid destruction of lung-
tissue which resultsin theforma-
tion of cavities.^
Etiology. — The most frequent
cause of acute phthisis is defec-
tive nutrition, associated with
lymphatic and glandular en-
largements. When these con-
ditions exist all the predisposing
causes of chronic phthisis pre-
dispose to this form also. The
exact nature of its essential
cause is still obscure ; efforts
to discover the peculiar elements
which give to tubercle a specific
character have been abundant,
but the statements of various
observers who claim to have
discovered a tubercle bacillus lacked demonstrative proof until the
researches of Koch were made public, when he announced the discov-
ery of a bacillus which is found in tubercles and in them alone. Basing his
statements on a series of experiments many times repeated, in which this ba-
cillus was isolated from tubercle, cultivated in a solid menstruum under the
microscope, and, finally, shown by inoculation to produce general tubercu-
Fis.
Coagulation Necrosis.
Section of Lung through an area, near a bronchial tube, in
which the vascular supply has been cut off.
A. Area of coagulation necrosis. The alveoli are so
filled with inflammatory products that their wails
are obscwed.
B, B, B. Pulmonary tissue around the necrosed area. The
alveoli are here filled with catarrhal products.
C, C, C. Normal lung, x 30.
1 Cohnheim and Weigert.
2 The acnte phthisis described by Williams (in " Quain's Dictionary") is, according to that investiga-
tor, marked by consolidation of the lungs, adherent pleurse, indurations consisting of red hepatization and
caseous infiltration (the latter largely predominating), with but little or no miliary tubercle present. Exca-
vation quickly succeeds consolidation, and pneumothorax is often the result. Others describe an acute
tuherculo-vmiimonic phthisis, a " connecting link," as It were, between the acute and chronic varieties.
The tubercle-tissue aggregates, caseates, and rapidly forms cavities, while fresh tubercle-tissue is being
developed elsewhere in the lung.— Fox, in " Beynolds'' System;' states that in acute phthisis soft dif-
fluent miliary tubercular deposits are found with ulcerous and irregular anfractuous cavities. Engorged
" pneumonic " lung intervenes ; the bronchi are loaded with pus. The disease resembles gray hepati-
zation, and, like it, is oftenest irwst developed in the lower lobe.
ACUTE PHTHISIS. 175
losis, he concludes that the active etiological element in tubercle is a dis-
tinct lacillus, and that tubercle is not found where this organism is not
present. It is not his claim, however, that all those anatomical elements
which, from a purely histological classification, have been called tubercle,
are due to the presence of this bacillus, but only that those pathological
changes which are preceded by the presence of this oi'ganism should be
called tubercle. The applicability of these conclusions to tubercle as found
in man rests solely upon the supposition of the identity of the two condi-
tions in man and the lower animals, an identity which, while it may be very
generally accepted by pathologists, has been proven only by inoculations
fro7n man and not inversely. Observations of the truth of Koch's state-
ments, in part, are abundant, and it is the universal testimony that the
bacilli described are found in tuberculous matter. The success of various
observers in finding these bacilli is not uniform. Some report bacilli pres-
ent in all cases of tubercle, while others find them absent in a varying per-
centage of cases. Beyond this point Koch's experiments have not been
repeated.
The case at present may be stated as follows : the presence of a distinct
bacillus in connection with tubercle and its absence in all other morbid
conditions are generally confirmed by the most competent observers.
The etiological relation of this bacillus to phthisis still rests solely upon
Koch's demonstration. Observers are not wanting who deny entirely not
only any etiological relation, but even that this bacillus is confined to tu-
bercular tissues ; but they fail to present satisfactory experimental proof in
support of such statements. German pathologists, on the other hand, among
whom are Cohnheim, Frankel and Schottelius, — at one time the most able
opponents of the infectious character of tubercle, — accept its specific nature
as a fact entirely proven.
This form of phthisis is oftenest met with in the young who have grown
rapidly and who have a strong inherited phthisical taint. Children who
have been nursed by phthisical mothers are especially liable to its develop-
ment.
Symptoms. — A young adult who for some time
has had a dry, hacking cough with a gradual
but steady emaciation, is suddenly seized with a
sharp pain in the side ; the pulse becomes rapid
and feeble, and the temperature rises to 104° in
the evening, while the morning temperature may
be normal. With increase in pulse-rate and
temperature the skin becomes pungently hot.
The fever alternates with night chills and profuse
sweats. The cough is soon accompanied by an ^^^
opaque, purulent expectoration, in which are . ^ ' ^^^^. . ,
„•' ^, ' ^ .-,-,, .,,. ' T, , ,. Tubercle Bacilli from Phthisical
found numerous tubercle bacilli and yellow elastic sputum, stained with Fuchsin.
fibres. There is rapid loss of flesh and strength : a. miatea bacuu.
, . , , -^ , ■, . ? < 1 B. Groupn of the same. ^
the patient becomes extremely ansemic ; and the The unstained granular deiH*
, , , . , -, J. 1 -I of nus corpuscles and mucus are
constant harassing cough causes loss oi sleep and seekjaintiy at c, d. x 50o.
176
DISEASES OF THE KESPIEATORY OEGANS.
extreme exhaustion. The expectoration is usually not abundant until after
breaking down of the lung-tissue has occurred. Patients ascribe the ema-
ciation and weakness to the profuse sweats. The respirations and the
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Temperature in a case of Acute Phthisis. Patient a3t. 25. The larger falls of temperature, on the 5th, 9th,
16th and 24th days followed the administration of sulphuric ether. Falls of a degree and a degree antf
a half were induced by large doses of the sulphate of quinine.
Death occurred after a steady rise in temperature for a week preceding.
pulse-rate increase in frequency with the fever. The pulse ranges from
120 to 135. Cardiac palpitation and sudden acceleration of the pulse-rate
follow excitement. In some cases the chill, fever and sweat occur with
such regularity that malarial fever is suspected or a malarial element is
ACUTE PHTHISIS. 177
regarded as the prominent feature. Nausea, yotniting and diarrhoea are
often prominent symptoms, and greatly add to the exhaustion which is so
marked a feature of the disease. The skin assumes a pearly pallor, the
hectic flush is present, and the eyes are bright and glistening. HaBmopty-
sis may mark the advent of the disease and recur at intervals during its
course. It is rarely absent during the entire course of the disease.
Anorexia is always a marked symptom. Not infrequently the destructive
processes are so rapid as to cause pneumothorax. Acute phthisis usually
pursues a steadily progressive course, but it may assume an intermittent
character, and have periods of arrest and apparent amendment, followed
by periods of exacerbation and rapid progress.
Physical Signs. — The physical signs will vary with the seat and extent of
pulmonary consolidation, and with the rapidity with which destructive
processes are established.
Inspection, during its early stage, shows rapid respiration and imperfect
expansion of the upper part of the chest during a deep inspiration ; as
the disease advances the loss of expansion becomes more and more ajoparent,
but there is no infra-clavicular retraction.
On palpation the loss of motion in the infra-clavicular spaces is more
apparent; and if the pleuritic changes are not extensive there will be
increased vocal fremitus.
On percussion there will be more or less dulness over the infra-clavicu-
lar spaces. If there are large superficial cavities which contain little fluid,
there will be amphoric or cracked-pot resonance.
Upon auscultation, in the early stage, expiration is notably prolonged
and high pitched, and fine mucous rdles with fine crepitation will be heard
over the affected district. The respiration is wavy and interrupted. There
may be distinct bronchial breathing and bronchophony over a circumscribed
space posteriorly in the scapular region. Excavations take place rapidly in
the consolidated portions of the lung ; they are of varying size and are sit-
uated at varying distances from the surface of the lung. Deeply seated cav-
ities, when filled, give deep-seated dulness, and, when empty, an exaggerated
percussion resonance. Over sm.all cavities with lax walls low-pitched puff-
ing, cavernous respiration will be heard. This is very frequently heard
in acute jjMliisis wliere soft yielding walls result from rapid 'pulmonary ne-
crosis. Amphoric breathing, gurgles and metallic tinklings will be heard
over large cavities which communicate freely with bronchial tubes. The
sub-clavian murmur (discussed in chronic phthisis) is not so liable to be
heard in acute as in chronic phthisis.
Differential Diagnosis. — Acute phthisis may be mistaken for croupous pneu-
monia, troncliiectasis and acute general capillary bronchitis.
In pneumonia the prolonged ushering-in chill, the continuous high
temperature, the characteristic sputum, the dulness limited to a lobe and the
pneumonic countenance, are symptoms which readily distinguish it from
acute phthisis. In some cases the differential diagnosis cannot be made
during the first week. Bronchiectasis accompanied by wasting, fetid ex-
pectoration, haemoptysis and night sweats, with the physical signs of con-
12
178 DISEASES OF THE RESPIEATOEY OEGAKS.
■solidation, may well be mistaken for the adyanced stage of acute plitlii»/k^.
In phthisis the signs of conso\ida,tion precede those of cavities ; — in bronchi-
ectasis they follow them. Fever and emaciation are always greater in
phthisis than in bronchiectasis, and the symptoms are more steadily pro-
gressive. In capillary hroncliitis there is no dulness on percussion, sub-
crepitant rales are heard on both sides of the chest, and there is no bron-
chial character to the respirations. The temperature range is lower than
in phthisis. Emaciation is rapid in phthisis, and the signs of the forma-
tion of cavities occur early.
Prognosis. — The prognosis in acute phthisis is always unfavorable. Its
average duration is from five weeks to five months. A sudden amelioration
of the symptoms may occur before the cavities are formed, but the ameliora-
tion is one of short duration and is usually followed by a more rapid prog-
ress of the disease. It may be complicated by pleurisy, pneumothorax,
hydrothorax, peritonitis, and, rarely, by pericarditis. Death may occur
from exhaustion, asthenia, or complications. Acute capillary bronchitis
and pulmonary oedema and congestion often lead to a rapidly fatal termina-
tion.
Treatment. — Most cases are hopeless ; the dietetic and climatic meth-
ods employed in chronic phthisis have no place in the management of acute
phthisis. ' Morphia in small doses — one-twentieth of a grain hypodermic-
ally every six or eight hours — has, in my hands, been more satisfactory in
staying the progress of the disease, prolonging life and keeping the patient
comfortable, than any other plan.
CHEONIC PHTHISIS.
The first variety of chronic phthisis, — which may be designated as tuber^.
cular pneumonia or catarrhal phthisis, — is preceded or accompanied by
the pathological changes of localized bronchitis, lobular consolidation and
pleurisy.
Morbid Anatomy. — The primary changes are in the bronchi and in the
cavities of the alveoli, which become more or less filled with cellular ele-
ments mingled with other inflammatory exudation products. The bronchial
exudation is usually abundant and purulent. It has been recently claimed
that the tubercular infection is contained in it. After a time amass of cells
obstructs the bronchioles and becomes cheesy. The nutrition of the walls of
the bronchial tubes at the site of the obstruction is interfered with and they
become attenuated, or a peri-bronchitis is developed. The peri-bronchitis
may be tuberculous, fibrous, or purulent. An ulcerative process may also
be established at the site of the obstruction. Ulcers thus formed in the
tubes are usually sharply defined and shallow ; sometimes they involve the
1 Dr. McCall Anderson (in London Lancet, June, 1877) takes a more hopeful view of tliese cases, and
claims that subcutaneous injections of atropia check the exhausting sweats ; and that quinine, digitalis
and opium reduce the temperature, and if they fail, ice-cloths to the abdomen will accomplish the desired
result. His reported results are exceedingly encouraging, but the failure of his treatment as tried by oth-
ers causes many to doubt his diagnosis.
CHRONIC PHTHISIS.
179
A, A
B.
adjacent lung substance as well as the bronchial walls. These cheesy masses
are found in patches. The air-vesicles become filled in one of two ways :
(1) by polypoid outgrowths from the alveolar walls, consisting of round and
polygonal cells in a basement substance;
or, (2) a mass of similar cells — with or
without giant-cells — not in connection
with the alveolar walls, partially fills
the vesicles of the affected lobules, the
intervening space being filled with
catarrhal products. These masses vary
in size. They may be limited to a
single lobule or they may attain the
size of a hazel-nut. When they pass
into the caseous state all the elements
of the exudation become granular,
and are agglutinated by a slightly trans-
parent granular substance which glis-
tens like fibrin upon the addition of
acetic acid. These foci are friable and
present a gray homogeneous appear-
ance, resembling the so-called yellow
tubercle.
The gross appearance of lung-tissue
involved in this form of phthisis varies. "^ '''^'
It may be of a gray color, hard and glistening, described by Laennec
as "gray infiltration;"^ or it may appear as a colloid jelly-like mass
{" gelatiniform infiltration" of Laennec, or the "colloid caseous pneu-
monia " of Thaon). Early in this process lymphoid cells infiltrate the alve-
olar septa, which may break down or become hardened and thickened from
new tissue developments. Similar cellular infiltrations may also occur in
the walls of the bronchioles. Pressure causes obliteration of the vessels and
subsequent caseation ; and in this way large tracts of gray pneumonia^ are
converted into yellow masses. Charcot claims that in caseous pneumonia
he finds, as in gray granulation, two zones : (1) a central region consisting
of exudation products, cheesy debris, and fibres of lung-tissue ; and, (3) a pe-
ripheral region, made up of adenoid growths and giant-cells — " zone ernbry-
onnaire." These last two he regards as the basis of tubercle — always a
peri-bronchial product — and that caseation does not take place unless they
are present. When a few lobules only are involved, they may become en-
capsulated, or, by a proisess similar to that described in lobular pneumonia,
they may undergo resolution. It is rare, however, for a lung to return to
its normal condition unless the nodules are small and few in number.
Even should the masses be removed, obliteration of the alveoli which they
occupied is apt to occur. If a cheesy nodule is encapsulated, cretaceous or
Fig. 41.
Chronic (Catarrlial) Phthisis.
Section of Lung sfwwing two alveoli.
Wall of alveoli covered with changed epithe-
livm.
" Polypoid wxtqrowth " frmn the alveolar
wail nearly filling the air-vesicle — composed
of a delicate,^ granvlar basement substance in
ivhich are imbedded round and polygonal
cells.
C, C. Epithelial cells between the last and wall of
the air-vesicle.
D. Alveolus partly filled with epithelial and
lymphoid cells in the basement substance.
' The infiltrated tubercle of Laennec is considered as desquamative pneurrwnia by Buhl and scrofulous,
inflammation by Rindflemch.
* Called "gray infiltration."
180
DISEASES OF THE RESPIRATOKY ORGAN'S.
chalky material is found in the centre of the fibroid tissue. The lung-tis.
sue between these nodules may be anaemic, hypergemic, cedematous, or em-
physematous, or the seat of atelectasis. The larger the nodule and the
more rapidly it has formed, the more liable is it to soften. Cheesy masses
may soften and by a process of ulceration be removed through the bronchi.
Absorption of caseous matter by tlie lymphatics is attended by more or less
adenoid hyperplasia, and a group of miliary granules may be deyeloped
about a caseous centre, the remainder of the lung not being involved. Some-
times softening and ulceration are so rapid that the process becomes dis-
tinctly gangrenous.
Cavities.— The walls of a phthisical cavity are always irregular. At first
they are soft and friable ; later they become tough, smooth and fibrous.
Bands of dense connective-tissue traverse them, sometimes covered by a
layer of granulation-
tissue, and vessels and
large bronchi often
extend across them.
Sharply " cut-off" stubs
of bronchi often project
half an inch from their
walls ; portions of the
wall may stand out like
the columnse carnese of
the heart; or the sur-
face may be uneven or
ragged. The connec-
tive-tissue trabeculse ex-
tending across a cavity
frequently contain
blood-vessels, whose
rupture may cause fatal
hsemoptysis. When
„ ^ ^ cavities are formed the
A. Stump of small bronchus.— B, B. Bands of flbnn.— C. Loop of j xi
blood-vessels in bed of cavity.— D. Smaller cavities ope?iing into a luUg-tlSSUe arOUnd the
larger one. ., -mi • -, , j
cavity Will be indurated
and the cavities will be separated from one another by bands of firm
fibrous tissue, and the peri-bronchial and peri vascular connective-tissue
sheaths, and the thickened pleura, will all be involved in an indurative
process. Cavities increase in size by peripheral disintegration, or several
small ones may coalesce and form one large, irregular excavation. Phthis-
ical cavities contain air and a grumous purulent fluid of a yellowish or
greenish color, with which shreds of lung-tissue may be mingled. If the
growth of a phthisical cavity becomes arrested, a "limiting membrane
forms on its inner surface." The purulent secretion from it at first is
abundant, later it diminishes, and the case becomes one of a "quiescent
cavity." A large cavity may, by contraction of the fibrous tissue around
it, have its walls approximated but not united. True cicatrization of a
Fig. 42.
A Lung Cavity.
CHROlSriC FIBEOUS PHTHISIS.
181
chronic cavity which has a distinct lining membrane rarely if ever
occurs.
Ulcerating cavities are those which having been long quiescent take on,
for some reason, an ulcerative process. A small cavity at the surface of the
lung, after having caused a localized pleurisy and a thinning of the friable
wall of consolidated lung-tissue which separates the pleura from the cavity,
may break through into the pleural cavity and cause pyopneumothorax.
Pleurisy is rarely absent in this variety of chronic phthisis ; firm adhesions
form, and the pleura may be from three-quarters of an inch to one inch
thick. These changes — pulmonary and pleuritic — are best marked at the
apices.
The broncliial glands may be softened, cheesy, chalky, pigmented and
enlarged. The right heart is frequently dilated and hyijertrophied.
CHEOlSriC FIBEOUS PHTHISIS.
Clironic fibrous pMliisis, or interstitial tubercular pneumonia, is charac-
terized by the diffuse development in the lungs of dense fibrous tissue^
which may be associated with tubercles.
Morbid Anatomy. — The affected lung is
diminished in size. The pleural surfaces are
adherent and greatly thickened. A section
of a portion of lung that is the seat of this
variety of phthisis presents a smooth or granu-
lar surface, or it has a striated appearance.
If granular, the granules are imbedded in
the fibrous mass. The fibrous tissue contains
more or less pigment material, which gives
to the cut surfaces a bluish or gray color.
If the process is old the lung will be tough ;
if recent it is less resistant and less leathery.
When the disease has existed for a long time
the apex, and sometimes the whole lung, is
converted into fibrous tissue, all traces of the
normal lung-tissue being obliterated. The
indurated tissue may be studded with nodules.
The nodules may be small masses of dense
fibrous tissue containing a few cells at their
centre, masses of tubercular tissue, granu-
lation-tissue enveloping tubercles, or cheesy
masses with tubercles and interlacing fibrous
bands. Giant-cells may or may not be present in the nodules. The con-
nective-tissue growths may begin in the walls of the bronchi, alveoli, or
blood-vessels, in the septa, or in the pleura. The alveoli are at times
dilated, at times narrowed ; they are always deformed. The alveolar epi-
thelium undergoes slight multiplication and swelling. New cells also form
Fig. 43.
Chronic (Fibrous) Phtliisis.
Part of a section of pulmonary tvberch
showing change into fibrous-tissue with
obliteration of contiguous alveoli.
A. Centre of the tubercle. — B. Periphery
of the same altered into fibrous co7inec-
tive-tissue. — C. Growth of the fibrous
tissue in the alveolar walls.— D D. Two
air-vesicles in process of solidification,
X 100.
183
DISEASES OF THE RESPIEATORY ORGAN'S.
in the walls. Cheesy masses, specks of cretaceous material and cayitied
of varying size are found in the hard lung.
The bronchi are at times thickened, at times thinned. Bronchiectatic
cavities (cylindrical, fusiform or sacculated) are found, chiefly in the apex.
The appearance of these cavities is similar to that described in chronic in-
terstitial pneumonia. Through ulcerative processes cavities, often of large
size, result from these bronchiectases. As the disease progresses, more and
more of the tubercle-tissue is changed into connective-tissue. But while the
growth of connective-tissue is extra-alveolar, the tubercle-tissue is both
extra and intra-alveolar. The early stage of connective-tissue development
consists in the accumulation of a large number of small cells looking like
granulation-tissue and lymphoid cells, while, in the later stages, we find
dense fibrillated tissue containing a few cells — and those spindle-shaped —
and an abundant supply of irregular blood-vessels. Tubercles may also be
found in the pleura.
Anthracosis — from the deposit in the lungs of inhaled particles like coal-
dust, causing the development of interstitial pneumonia — is a form of fibrous
phthisis. One or both lungs may be involved, the diseased portions being
dense and of a slaty or black color.
They are usually elevated above the
surface of the lungs.
Upon section the indurated portions
present a smooth, shining solid surface
of slate, gray, black, or ebony color.
When the lesion is pronounced the finger
is soiled by contact with it, and a thick
fluid of the same color is obtained on
scraping it with a scalpel. The bronchi
contain a dark muco-pus.
Under the microscope the inter-alveolar
septa are seen to be much thickened and
contain small black particles scattered
along the vessels, in the cells and between
the fibres of the connective-tissue. The
„ vv ., , „ , , alveoli are diminished in size, and con-
verse section.— C, C. Alveolar walls largely- . ■ i t i _e •
piqmented.—D, D. Alveolar epithelium con- tam CClls With dark granules 01 irregular
taming pigment granules, x 250. ,,. ^ ,, , r>i-.i -,i
outline. Soon the septa are nlled with
black particles, some of which, entering the lymphatic circulation, reach
tlie bronchial and even the mesenteric glands, which suffer enlargement.
Iron and steel workers have a brown discoloration of the lung (siderosis).
In stone-cutters' phthisis (chalicosis) a slaty-gray appearance is found, due
to the lodgment of inhaled dust and silica.
FiQ. 44.
Anthracosis.
Section from a Coal-tniner's Lung,
A, A, A. Alveoli.— B, B. Small arteries in trans-
CHRONIC TUBERCULAR PHTHISIS.
183
CHRONIC TUBERCULAE PHTHISIS.
Chronic tubercular phthisis is characterized by gray granules scattered
more or less abundantly throughout the affected portion of the lung, or by
masses of them agglomerated by fibrous "tubercle-tissue."
Morbid Anatomy. — The lungs are large, emphysematous and pale, unless
pneumonia, congestion or oedema is present. The surface of the lungs is
often marbled. The apex of the lung is studded with firm, hard, gray or
cheesy nodules, varying in size from a pin's head to that of a pea.
Ul3on section of a lung which shows these changes muco-pus flows from
the cut bronchi. Peri-bronchitic and inter-alveolar interstitial pneumonia
is developed to a greater or less degree around these nodules, with irregular
dilatation of the alveoli. These nodules originate chiefly in the lymph-
sheaths of the arterioles, in the peri-bronchial adenoid tissue, or in the
small masses of cytogenic tissue in the alveolar walls.' These bloodless
nodules are incapable of suppuration, resorption, or organization. As the
'Hubercle-tissue" about the vessels increases, it causes occlusion of their
lumen. The lumen of the occluded vessel is occupied by granular fibrin,
and on transverse section a row of
white blood-corpuscles and of en-
dothelial cells is often seen between
the coagulum and the vessel wall.
In recent cases the walls of the
vessels are very easily distinguish-
ed. But if the centre of the
tubercle has become caseous the
vessel wall is also altered and is
very indistinct. Thickening of
the alveolar walls may also result
from the development of ''tuber-
cle tissue " in them. Many claim
that the commencement of the
process is a small cellular projec-
tion on one side of an alveolus,
which, as it grows, pushes the
capillaries and the epithelium with
it into the alveolar cavity. The
bronchioles are thickened and diminished in calibre ; sometimes there are
complete peri-bronchial cylinders of new embryonic or tubercle-tissue.
The alveolar cavity maybe filled by the new formation, the walls remain-
ing distinct ; or the wall may be destroyed by the growth of the projecting
nodule, and thus communication opened between adjoining air vesicles."
After coalescence of masses of tubercle-tissue anaemic necrosis occurs ;
1 Rindfleisch states that the points at which the smalleat tjronchioles become contimioyf with alveolar' sacs
are the situations of the first eiv.ption. of the tubercles, and that the first lesion is a tuberculous infiltratiion of
all the angles and projections situated at these points.
= Hamilton states that this appearance, which so resembles the condition of the lobules in catarrhal
pneumonia, has caused the mistake of regarding tubercle and catarrhal pneumonia as identical.
Pig. 45.
Chronic (Tubercular) Phthisis.
Section of Lung shoirlng a small miliary tubercle, with
surrounding pulmonary alveoli.
A. Cheesy centre of tvbercle.
B, B. Trabeculce of the basement tissue of the tubercle,
containing lymphoid elements, large cells, etc.
C, C. Divided 'arteries with inflltration of their walls
with tubercular tissue.
D.D,D. Lung alveoli filled with catarrhal products. x50
184
DISEASES OF THE EESPIEATOET OKGANS.
the cellular elements become granular, atrophied and fatty, and form cheesy
yellow masses. These caseous masses are easily removed from the paren-
chyma in which they
are imbedded. Sur-
rounding these masses
are found groups of
gray miliary tubercles.
The mode of this for-
mation of cavities and
their appearance are
the same as already
described. Between the
ulcerous cavities of
chronic tubercular
phthisis the lung-tis-
sue may be emphyse-
matous, engorged, oi
pneumonic. The iron-
chi are filled with
muco-pus ; their mu-
cous membrane is the
seat of a catarrh, and
is congested and tra-
beculated. Their walls
are thickened, tuber-
cle-tissue is found in
them, and ulcers are
not infrequent.
The pleura is con-
gested and covered with fleshy, soft vegetations over the parts involved
in the chronic phthisical processes. Organized adhesions are common;
in them tubercles may be found, and also in the pleura. Tubercles
may be found in the larynx, trachea, mesenteric and lymphatic glands, and
in the mucous surfaces of the alimentary tract, peritoneum, spleen, kidney,
liver, brain, bladder and testes. Thus a chronic local disease of slow and
seemingly intermittent progress is found associated with evidence of some
sort of general infection. Fatty heart is not uncommon. The recent dictum
is that chronic tubercular growths may heal. Many, however, believe that,
once established, the process can never become ''quiescent." ' Ulceration,
dilatation of the bronchi, and the formation of large cavities are not infre-
quent attendants on this process.''
' Rindfleisch advances a new doctrine of the "healing processes in tuberculosis of the lung," viz.: it
consists in a shrinkage of the infiltration, combined with a formation of new vessels. These vessels do not
penetrate deeply into the infiltration, but surround it and supply it with constant, though scanty, nourish-
ment. It is a "fibrinous shrinkage ;" the capsule not only encloses but nourishes.
= In a variety called by O. Clark and Rindfleisch "■ Broncho-phlMsis Pulmonalls " the central feature of
the change is f ■-■ extensive vlceraiion of all the bronchi of medium size down to the intra-lobular branches.
Spaces of all sizes are seen— on section— connected with one another. Rindfleisch states that a '
mative pneumonic process " accompanies this peculiar form of tuberculosis of the lungs.
Fig. 46.
Chronic (Tubercular) Phthisis.
Section of Lung showing a small tubercular nodule with surrounding
alveoli.
A. Cheesy centre of nodtde.
B, B. Fibrillar basement substance containing cells and nuclei.
C, C. Giant-cells.
1). Vacuoles.
E, Ey E. Alveoli, surrounding the tubercle, containing pneumonic products.
F. Part of wall of an artery infiltrated with tubercle-tissue, x 250.
CHEONIC PULMONARY PHTHISIS. 185
Etiology. — The causes of chronic phthisis are general and local.
The most effective general causes are hereditary or g-cquired feebleness of
constitution, anti-hygienic influences, climate, and soil.
The local causes are pneumonia, pleurisy, bronchitis, mechanical irri-
tants, and noxious vapors.
Inherited tendency. — The influence of heredity is so decided that many
observers claim that phthisis can never be developed by those who have no
such tendency. Every-day expei'ience disproves such sweeping statements.
My own statistics show a direct transmission in more than 18 per cent. ; it
is stronger in women than in men in the proportion of 57 to 43. Mothers
transmit phthisical tendencies more certainly than fathers. But when one
parent alone is affected the mother is more apt to transmit to the daughters
than to the sons, and vice versa. The stronger the hereditary predispo-
sition the earlier will be the development of the disease and the more acute
its course. A phthisical vice of constitution may be inherited by the
children of the aged, of drunkards, of those enervated by excesses, and of
, those who, at the time of the birth of their children were suffering from
some form of constitutional disease such as cancer, syphilis, or gout. It is
therefore necessary, in order to fully determine the influence of an heredi-
tary tendency in any given case, to know the condition of the parents at the
time of the individual's birth. Children of the scrofulous are apt to be
tuberculous early in life. Children of consanguineous marriages are es-
pecially liable to pulmonary phthisis.
Anti-hygienic surroundings. — Second only to hereditary influence are
anti-hygienic surroundings. Impure air, improper quality and insufficient
quantity of nutritious food, are among the most prolific of this class of
causes. Bad ventilation and impure air, an indoor life, especially when
large numbers are crowded into a small space, are strong predisposing
causes. The frequency of phthisis in clerks, printers, tailors, milliners,
seamstresses, factory employes— -^ho live in a hot, close, dust-laden atmo-
sphere—proves this. Of indoor workers those are most liable to phthisis
who exercise least at their vocations. Compositors suffer oftener than the
press-hands in the same room. The moister the air and the higher the tem-
perature of the apartment the more liable is phthisis to be developed. If,
in addition to these anti-hygienic conditions, are added insufficient and im-
proper clothing, want of cleanliness, alcohol drinking, prolonged lactation,
and repeated miscarriages, it is evident that the feebleness of constitution
which predisposes to phthisis can be acquired as well as inherited.
I am convinced, from a careful analysis of my records, that the phthisi-
cal developments depend as much upon the anti-hygienic influences under
which childhood has been passed as upon hereditary tendencies. These
predisposing anti-hygienic influences embrace the important problem of
infantile diet. Few mothers, especially among the wealthier classes, are in
a condition properly to nourish their own offspring. The habit which pre-
vails of feeding children until they are one, two, or even three years of age
upon barley-water and pap has a great influence upon the future physical
development of the child. In determining the influences which have pre-
186 DISEASES OF THE RESPIRATOEY ORGAN'S.
disposed to the phthisis in any case, it is important to consider not only the
condition of the parents at the time of the birth of the individual, but also
the hygienic influences under which his childhood and early life were
passed. One of the great objects of early physical training should be to
overcome hereditary physical tendencies ; this can be accomplished, in the
majority of cases, by good hygienic surroundings and systematic physical
training during infantile and early life. It is especially important that the
children of phthisical parents should be placed under such influences, dur-
ing infancy and childhood, as shall insure the greatest physical vigor. All
these predisposing influences tend to arrest physical development.
Climate has long been regarded as an important factor in the develop-
ment of phthisis. We know of no climatic condition which renders its
development a necessity, or that makes its development impossible ; yet
there is no question but that it occurs with greater frequency in one cli-
mate than in another. It is rare in the torrid and frigid zones, and fre-
quent in the temperate. It is a question, however, if climate alone can
properly be regarded as a cause of phthisis. There is something more than
climatic changes which renders certain localities especially powerful in its
development. Altitude is more important than climate, for most high ele-
vations are antagonistic to its development. The condition of the soil of a
region or locality favors, or is antagonistic to, phthisis : light, sandy, por-
ous soils are antagonistic; while heavy, hard, clayey and impermeable soils
are favorable. A damp, cold atmosphere, an impermeable soil, and sudden
changes in temperature are the most favorable conditions for developing
phthisis. Want of sunlight acts also as a strong predisposing cause.
Local causes. — One who carefully studies the clinical features of a large
number of cases of phthisis must be convinced that bronchitis of the smaller
tubes and chronic lobular [catarrhal) pneumonia are the starting points of a.
large number of cases of phthisis. Some call these "exceptional " catarrhs. '
That an apparently simple catarrh leads to the development of phthisis in-
one case and not in another may be explained by the fact that one individ-
ual is in a condition to resist the bronchitis, while in another all the predis-
posing causes of phthisis are in operation and the catarrh then results in
the phthisical developments. The relation which pneumonia bears to the
development of phthisis has been sufficiently considered under the head of
its morbid anatomy. From a clinical standpoint there seems to be no ques-
tion but that a non-resolved pneumonia is the starting point of phthisis in
quite a large proportion of cases. The question which it seems difficult ta
decide is : — are such pneumonias tubercular ?
That pulmonary phthisis not infrequently dates from a pleurisy is^
evident to every careful observer. Phthisis which is preceded by pleu-
risy is often attended by an extensive development of fibrous tubercular-
tissue. Bronchial hemorrhage is frequently the first and only sign of
phthisical developments. It is claimed that bronchihis precedes and causes
the hemorrhage. Unquestionably such bronchial hemorrhages indicate a,
' Winiams found In 1,000 cases of phthisis that bronchitis was the origin in 12 per cent. Niemeyer regards,
bronchitis ae the primary and essential developing cause in the majority of cases.
CHRONIC PULMONARY PHTHISIS. 187
vice of constitution which favors phthisical developments ; but it requires
no argument to prove that the hemorrhage is not an evidence that tuber-
cles exist in the lung at the time of tlie hemorrhage. The connection
which exists between phthisical developments and bronchial hemorrhage is
not always clear.
The mechanical irritation of the bronchi produced by the constant in-
halation of an atmosphere laden with dust leads to phthisis. The phthisis
of knife-grinders, stone-cutters, potters, silk- workers, cigar-makers and
coal-miners, are examples of this. The constant inhalation of noxious gases,
such as are generated in overcrowded, badly ventilated apartments, is a fre-
quent exciting cause of phthisis.
Pregnancy, instead of preventing phthisis, as was at one time supposed,
predisposes to it, and renders its course more rapid in those who are already
phthisical.
Empliysema and goitre have been by some supposed to afford an immunity
against phthisis, but my observations lead me to the conclusion that it is a
very frequent attendant of both these conditions. The notion that malaria
and marsh fevers are antagonistic to phthisis is disproved by every-day
experience. The relation between dialetes melUtus and pulmonary phthisis
is not well understood, but that one complicates the other very frequently
is a clinical fact. At the present day many claim that phthisis is commu-
nicable, that those who live intimately together, occupying the same apart-
ment and the same bed — husband and wife, children in nurseries, and sol-
diers in barracks — can contract the disease one from the other. It seems to
me that the question of the communicability of phthisis,— either by per-
sonal contact, inoculation, or the ingestion of tuberculous matter, — is one to
which clinical observation has as yet given no conclusive answer, and ex-
perimental observations upon man are wanting, save in a single questiona-
ble case. The proof of isolated or collated cases upon either side are but
presumptive. In animals the case is different, and the results of experi-
mental research seem to prove conclusively that tubercle is communicable
by inoculation through inhalation of tuberculous matter. The tuberculosis
thus produced is identical histologically with that caused by various irrita-
ting substances, but is entirely distinct in its power to produce general tu-
berculosis upon inoculation, a power which the tubercle of irritation has in
but small degree if at all. Cohnheim strongly believes in infection ; and
Virchowand many English physicians believe in the communicability from
person to person. Some English physicians go so far as to forbid kissing.
The frequency with which young women become phthisical after pregnancy
has given rise to the idea that they may have been infected by phthisical off-
spring."
Symptoms. — There are certain symptoms which characterize the early stages
of each variety of chronic phthisis. Catarrhal or tuhercular pneumonic'
phthisis usually commences with a bronchial catarrh. The cough is par-
> Reginald Thompson, in London Jymcfi/, January, 1881, Art. " The Tnfectirmof PhfMw," makes a spe-
cial form of " infectivf' phtliisin," not "ordinary phthisis." He calls the former " rather an ulcerative proc-
ess capable of privirig rise to pyaemia." His cases would certainly lead one to a belief in the communi-
cability of phthisis.
188 DISEASES OF THE EESPIRATORT ORGANS.
oxysmal and accompanied by tenacious muco-purulent sputa, now and then
blood-stained. There is a gradual but steady loss of flesh and strength ; the
patient grows pale and has an occasional night-sweat. These symptoms are
accompanied by the physical signs of slight consolidation at the apex of one
or both lungs, with those of localized bronchitis of the small tubes. Some-
times this variety begins with more acute symptoms, and the physical signs
of apical lobular pneamonia are present. In such cases the pneumonia does
not resolve and the fever takes on a distinctly remittent type, with a more
raj)id loss of flesh and strength, and a copious purulent expectoration, often
blood-streaked. Night sweats become profuse and exhausting, and there
are the physical signs of progressive consolidation of lung-tissue. At any
time during the early stage the physical processes may be arrested. And
during the period of arrest there may be a great improvement in the gen-
eral condition of the patient, and complete recovery is possible. But in a
large proportion of cases a return to the anti-hygienic conditions in which
its primary development occurred, or a fresh bronchitis, lights up anew the
phthisical process.
Tuberculous interstitial pneumonia— or fibroid phthisis — comes on very
insidiously ; it may be ushered in by one or more attacks of haemoptysis.
In most cases it commences with the physical signs of a localized bronchi-
tis and pleurisy at the apex of one lung. Cough and a muco-purulent ex-
pectoration, with more or less pain in the affected lung, may exist for a
long time before there is any marked impairment of the general health.
After a variable period the patient begins to lose flesh and strength, the
cough increases, and the expectoration becomes more abundant. There is
a progressive loss of appetite, but at no time is the temperature high or the
pulse rapid. Dyspnoea becomes more and more marked, especially on ex-
ertion. Eetraction of the chest walls under the clavicle commences quite
early and is steadily progressive. The limited play of the chest walls is the
most distinctive early sign. This variety of phthisis rarely occurs in young
persons, and it is often associated with a rheumatic, gouty or syphilitic
taint, or is the result of mechanical irritation.
Chronic tubercular phthisis may for a long period give no distinctive
signs, for interstitial pleurisy, chronic bronchitis and emphysema nearly
always accompany it, their prominent symptoms masking those of phthisis.
Patients with this form become emaciated ; their dyspnoea resembles that
of emphysema. The expectoration is in the earlier stages mucous, and later
it becomes muco-purulent. Hsemoptysis is common ; and hectic fever is
more pronounced than in any other variety. There are no periods of im-
provement, though there may be periods during which the disease remains
stationary. Pleurisy, laryngitis, and intestinal catarrh are more marked
than the pulmonary symptoms. As the disease advances its symptoms
resemble those of fibroid phthisis.
In analyzing the symptoms which are common in all varieties of chronic
phthisis I shall first consider the cough. It is the earliest and most constant
of all the phthisical symptoms. It is present early and continues through-
out the whole course of the disease. At first it is dry and hacking. It may
CHRONIC PULMONARY PHTHISIS. 189
exist before there are any physical signs, and then there is little or no ex-
pectoration ; it may amount only to a " clearing of the throat." The sever-
ity of the cough without expectoration is a measure of the extent to which
the pleura is involved. The younger and more excitable the patient, the
more paroxysmal is the cough. It is usually worse in the morning on rising,
or just after lying down at night. Lying on the affected side often brings
on violent paroxysms. Some cough after the slightest exertion ; others have
a varying number of paroxysms during the day and can estimate how long
an interval of rest they will have between the paroxysms. The loss of sleep
occasioned by the cough may add much to the discomfort and wasting of the
patient. In advanced phthisis, when cavities have formed, the cough be-
comes ''hollow" in character. Expectoration may accompany cough from
its commencement. At first it is tenacious, glairy, frothy and mucous;
then yellow purulent spots are found in it. It is always important to ascer-
tain whether pallor, fever, and emaciation have been preceded by cough
and expectoration, or whether emaciation preceded cough and expectora-
tion. The sputa are gelatinous and faintly pink when the infiltration is ex-
tensive. Vitreous, gelatinous rounded masses may be mingled with yellow
catarrhal expectoration, and these are evidences of a recent pneumonia.
Dots and streaks of blood in catarrhal sputa indicate a lobular pneumonia,
and when this occurs fatty, swollen, and granular bronchial and alveolar
epithelium will be found intermingled in the mass. The sputa in the ear-
lier stages — often for months — are muco-purulent. When shreds of elastic
tissue are found it indicates softening and destruction of lung-tissue. Elas-
tic fibres are generally found in compact, airless, uneven masses, which read-
ily sink in water. As cavities form, the sputa becomes more purulent, some-
times being wholly composed of fluid pus, which may be fetid and greenish,
and contain elastic fibres coming from the alveolar wall, organic matter,
fat-crystals, pigment, young cells, and small masses of cheesy matter, and
the tubercle bacillus ; the latter are present in the sputa of all varieties of
advanced phthisis. The quantity of matter expectorated varies with the
extent of the bronchial catarrh and the number and size of the cavities. It
may be expectorated readily, or only with difficulty. Usually, the more fee-
ble the patient the more difficult the expectoration. In rapidly formed
cavities the expectoration may contain fragments of bronchioles and blood-
vessels, with shreds of lung-tissue.
Hmmoptysis is a very important symptom of phthisis, and may occur
during any stage of the disease ; the blood may simply streak the sputa,
or a pound or more may be expectorated at one time. Hemorrhages that
occur in the early stage of pulmonary phthisis are, in the majority of in-
stances, bronchial ; and the blood expectorated is arterial in color. When
streaks of blood appear in the sputa, the bleeding usually comes from the
vessels of the alveolar walls. Profuse hemorrhages in the later stages of
phthisis have their origin in cavities in the lung substance. Hemorrhages
that occur in the early stages may be profuse, but they are rarely danger-
ous ; hemorrhages in advanced phthisis may be the immediate cause of
death. Haemoptysis usually comes on with coughing. There is a sen-
190 DISEASES OF THE RESPIRATORY ORGAiq'S.
sation as if a fluid were trickling underneath the sternum, and there may
be violent cardiac palpitation, oppressed breathing, and a peculiar sweetish
taste in the mouth. In profuse hemorrhage the rapid flow of blood into
the mouth may excite vomiting and be mistaken for hsematemesis. For
some time after the primary hemorrhage blood is coughed up, and the
color of the spitting becomes darker and darker. Sometimes without
warning there is a sudden filling of the mouth with hot arterial blood.
Many English writers describe a hemorrhagic phthisis. In this variety an
apparently healthy man has a sudden and profuse hemorrhage, recurring
daily for some time, and followed by cough and slight expectoration for a
few days, with no physical signs of consolidation. These cases often con-
tinue for years without any other phthisical symptoms, but sooner or later
phthisis is developed.' Haemoptysis often occurs in those who have no
physical or rational signs of phthisis at the time of its occurrence, and who
do not become phthisical after. Although haemoptysis occurs more fre-
quently in phthisis than in any other pulmonary affection, and there are few
phthisical subjects who do not have one or more hemorrhages, yet its oc-
currence is by no means a certain indication that an individual afterward
will develop phthisis.
Fever. —Rise in temperature is so constant a symptom of phthisis that it
has led to the expression, " there is no consumption without fever ; " but
in no two cases is the fever course exactly ttie same. In some cases the
temperature in the morning may be subnormal, only reaching normal in
the evening ; in others the rise commences at 2 p.m., continues until 8 p.m.,
and then falls until 5 in the morning. Between 10 and 11 A.M. the tem-
perature is nearly normal. As cavities form, the post-meridian rise occurs
later, i. e., 10 to 12 at night. Toward the end of the disease the fever
type resembles that of pyaemia. Night sweats temporarily lower the
temperature. When the alveoli are involved in pneumonic processes the
temperature rises rapidly to 103°-104° F. ; should it continue high, it
indicates that the pneumonia is tubercular in character. Hectic fever may
occur in any stage of phthisis, but is usually confined to the stage of soften-
ing and excavation. It has three stages : first, at some time during the
day there is a well-marked chill or chilly sensation, which may last from
half an hour to an hour, followed {second) by a dryness and heat of the sur-
face, the temperature rising from 102° F. to 104° F., the face assuming a pe-
culiar brilliant appearance, and the cheeks having a peculiar rosy tint called
the *^ hectic flush." After a time the fever gradually subsides, and some
time in the night (it may be toward morning) the tliird or sweating stage
comes on. The night sweats are usually profuse and exhausting, and
always indicate the existence of hectic fever. The chilly feeling may be ab-
sent, the subsequent fever may be so slight as to be overlooked, but sweats
are constant. A steady and continuous low temperature indicates that the
phthisical processes are retrogressive ; a steady and continuous high tem-
perature indicates that they are progressive. In fibroid phthisis the tem-
perature rarely rises more than a degree or two above the normal. In the
1 Fox claims that tubercular disease of the vascular walls is the primary and. chief ev»n'- in such cases.
CHROIS'IC PULMONARY PHTHISIS. 191
absence of local symptoms, the thermometer alone may detect pulmonary
phthisis in the aged.' An intermittent temperature indicates a milder proc-
ess than a remittent or continuous febrile action.
The pulse in chronic phthisis bears no uniform relation to the temper-
ature ; it is always feeble. It varies greatly in frequency and force, but
rarely in rhythm ; it is accelerated by slight exciting causes. In the early
stages its excitability is one of its most characteristic features. The ar-
terial tension is below the normal. In the early stage of fibroid phthisis
it is rarely over 100. In a few cases it is abnormally slow. An improvement
in the other symptoms is not always accompanied by an improvement in
the pulse. In the last stage of all varieties of phthisis the pulse becomes
very rapid and feeble.
The respirations are more or less accelerated, and after exertion there is
dyspnoea. When the patients are quiet, unexcited, and resting in bed,
the respirations may be normal or but slightly increased. But on exertion
the breathing becomes accelerated and labored. The accelerated breathing
is due to the fever, the diminished breathing area, to bronchial obstruction
and to pain in the chest. Anaemia and heart failure may also contribute
to it. In the absence of fever the dyspnoea and accelerated breathing dimin-
ish. The extent to which the lungs are involved influences the frequency
of the respirations. Dyspnoea is usually not marked except after exercise
and during periods of excitement. In young subjects the dyspnoea is fre-
quently periodical. During the whole course of fibroid phthisis shortness
of breath on exertion is a constant symptom.
Pain in the chest is not a prominent or constant symptom of chronic
phthisis, except in connection with pleuritic changes. Dry and intersti-
tial pleurisies are common ; yet they seldom cause severe pain, but rather a
sense of tightness and constriction on taking a full inspiration. Intercostal
neuralgia is frequent and may be confounded with the pain of a localized
pleurisy. Dragging pains in the side are most marked in fibroid phthisis.
Pain on swallowing should always cause one to carefully examine the lar-
ynx. It usually announces the co-existence of laryngeal phthisis.
Emaciation is an early and constant symptom of phthisis ; but it is not
always progressive. Fever is the chief cause of the wasting and pallor that
are so common in all varieties of phthisis. The higher the average range
of temperature, the more rapid the emaciation. The pulmonary change
may he preceded by progressive emaciation, but in all such cases the aver-
age temperature is a degree above the normal. Emaciation may be a part
of the constitutional tendency of the individual, but such emaciation forms
no part of the phthisical wasting. While emaciation, loss of strength and
progressive anaemia are recognized premonitory symptoms, they cannot be
regarded as diagnostic. Emaciation may not be continuous in all cases ;
there are periods when the patient may even regain lost weight and mus-
1 Sir William .Tenner makes three clinical types of chronic phthisis in reference to temperature— the
insiclimn, the ac/ive febrile, and the adynamic. In the first the morning temperature is normal ; in the
second, the morning temperature will be about 100° or 101", and the eveninn; temperature 10fi°-in4''. In
the third, morning and evening temperatures are both high and not very diflEerent ; but between these
times irregular fluctuations occur.
19iiJ DISEASES OF THE EESPIEATORY OEGANS.
cular strength. The anorexia, dyspepsia, diarrhoea, profuse expectora-
tion and hsemoptysis are all causes of the emaciation. Phthisical wasting
occurs not only in the fat and muscle, but in the organs and blood as
well.' Slow, gradual wasting belongs to the history of fibroid phthisis.
The symptoms indicating disturbances in the alimentary tract are im-
portant. Anorexia is often for a long time one of the most prominent
symptoms. It may be accompanied by nausea, vomiting and pain in the
stomach, due either to reflex causes or sub-acute or chronic gastric catarrh.
At the autopsy we often find a normal gastric mucous membrane in one who
during life gave the symptoms of acute gastric catarrh. The most common
cause which acts in a reflex manner to produce vomiting is a violent fit of
coughing. It is important to distinguish between the vomiting due to re-
flex causes and that due to gastric catarrh. With dyspeptic symptoms the
tongue and pharynx are frequently covered with aphthae. The most im-
portant interference with digestion which occurs during the progress of
phthisis is due to changes which take place in the small and large in-
testine. These intestinal changes are marked by more or less tympan-
itis and by diarrhoea which is often very troublesome and difficult to
relieve ; few altogether escape these symptoms. Diarrhoea may occur in
any stage, but it is more likely to occur during the later stages ; in some
cases it alternates with hectic fever. It is usually most severe at night.
The profuse watery diarrhoea which comes on late in phthisis is called
colliquative diarrhoea. Hemorrhoids and fistulce in ano are frequent
troublesome complications of phthisis, and should always be relieved by
surgical interference in the early stages of the disease. The cure of a
fistula in ano, or the healing of an old ulcer is often followed by phthisical
developments ; and scrofulous joint disease, psoas and lumbar abscesses in
children are often followed by phthisis in early adult life.
Cerebral symptoms are rarely pronounced in any stage of phthisis ; there
is no chronic disease in which the mind is so clear. The hopefulness
and buoyancy of spirits which attend its development are remarkable.
The least improvement is hailed by the patient as an indication of com-
mencing recovery. He speaks lightly of his unpleasant symptoms, and is
very reluctant to admit that his disease is of a serious nature ; rarely will
a phthisical patient admit that recovery is not possible.
Laryngeal symptoms of phthisis have been considered under the head of
Chronic Laryngitis. The pharynx is sometimes the seat of tuberculous
processes. Arrest of menstruation is a very frequent occurrence in females
who are consumptive. In young females this is sometimes the first notice-
able symptom. Its occurrence in advanced phthisis indicates extreme ex-
haustion, and it is often followed by a more rapid progress *of the disease.
The shin is pale and traversed by prominent blue veins. Sudamina and
pityriasis versicolor are often observed. The nails curve and become claw-
like. The terminal phalanges of the fingers become "clubbed," and this
1 Malassez states that the red discs are diminished in number. The haemoglobin is also diminished.
Leucocytes, fibrin, and calcic phosphate are in excess. Gr.'inular masses agglomerate into patches vary-
ing greatly in size ; and, on a warm stage, they appear to develop into, or give rise to organisms which
move about in the blood.
CHRONIC PULMONARY PHTHISIS. 193
is by some regarded as an important diagnostic symptom, but it occurs fre-
quently in other chronic thoracic affections. It has been regarded as (1) a
form of scleroderma beginning in the phalanges and extending centrally
over the body ; (2) as due to interference with peripheral return circu-
lation ; and (3) as an hypertrophy of connective-tissue/ The hair becomes
thin, dry, gray, and falls out. (Edema of the feet and legs is not an infre-
quent symptom during the last stage, and its gravity is well recognized by
the non -professional. Its occurrence indicates that a fatal issue is not far
distant. It may be due to secondary changes in the vessels, but in a large
proportion of cases it is due to thrombosis of the veins of the lower extrem-
ities, the result of an enfeebled heart.
Physical Signs. — There are thi-ee recognized stages in chronic phthisis : a
stage of consolidation, a stage of softening, and a stage of excavation.
The physical signs of the stage of consolidation vary with the extent of
the consolidation according as it involves large areas or small disseminated
patches. As a rule, phthisical developments have their seat at the upper
portion of the lungs.
Inspection reveals diminished expansion — on inspiration — in the supra-
and infra-clavicular regions of the affected side. If there are extensive
pleuritic thickenings and adhesions, or if extensive fibroid changes exist,
flattening and retraction, most marked at the end of a full inspiration,
will be found on the affected side or over the seat of ^the phthisical
development.
Palpation shows more distinctly the loss of expansion on the affected
side. Vocal fremitus is slightly increased over the affected lung, although
extensive pleuritic changes may render the vocal fremitus less distinct.
Percussion. — The percussion sound will vary with the extent of the con-
solidation and the condition of the lung-tissue surrounding the consolidated
portion. There is always more or less pulmonary resonance. If the con-
solidation is slight the percussion sound may remain normal, and local-
ized emphysema may give rise to exaggerated resonance even when consoli-
dated lung-tissue exists. When practising percussion, to recognize a slight
consolidation at the apex of the lung, it is important to percuss from the
trachea rather than toward it. In all cases percussion should be performed
at the end of a full inspiration and at the end of a full expiration. Dul-
ness usually appears first under the scapula, next over the sternal end of the
clavicle, and gradually extends down, being limited, for a long time, to the
apex of the lung. If the dulness is slight at first it gradually increases and
may reach complete flatness.
Auscultation. — The auscultatory signs vary greatly in different cases, and
at different times in the same ease. Over the affected portion the respira-
tory sounds may be feeble or exaggerated, interrupted, '' cog-wheeled " or
wavy. The breathing may be rude or IroncMal ; or, when rude in charac-
ter, it may be rude and wavy, rude and interrupted, at the same time being
exaggerated, or it may be feeble and rude. The pitch indicates the extent
of the consolidation. At the commencement there may be only a loss in
' In 1,776 cases Pollock found clubbing of the finger-ends in about 25 per cent.
194 DISEASES OF THE BESPIRATORY OEGANS.
the vesicular character of the inspirations, with a slight rise in the pitch of
the expiration.
Prolonged expiration, when MgJi pitched, is very significant. The expi-
increased vocal fremitus... ^^ ration is prolonged in cmphy-
siightduiness on percussion ..:^^K, scma, but low pitched. Wavy
E^xaggeratea vocal resonance..... ^g^R or jerking respiration is regarded
Jxuae or broncho-vesicular resjnration. jj^^^^hM^^ -■ 4; • j.- j u
Moist rales may ormay not be pres- J^^^^^^^ by SOme aS a iriction SOUnd, by
eni .^^^^^^^M others as the result of a narrow-
^1^ ing of the bronchi which inter-
feres with the entrance of air into
the lung substance. Accom-
panying or preceding changes in
the respiratory murmur, crepita-
^^^^^^^ ting sounds are heard ; they may
be crumpling or creaking in
character. Small mucous and
sub-crepitant rales, if present,
"Tig- 47. are heard loudest after cough-
Diagram illustrating Physical signs of first staee of • 1 --e j-u TJ i-
Chronic PhthisTs. =" »i»K« "^ jj^g.^ ^ud, if the Consolidation is
Partial InJUtratlon at the Apex of the Lvng. extcusive, they haVG a metallic
ring. It is claimed by some that all the rdles that are heard in this
stage of phthisis are produced upon the surface and not in the sub-
stance of the lung. This statement is too sweeping, for these sounds are
usually circumscribed. They can be changed by coughing, and are often
entirely removed by violent coughing, and can be heard before the inspira-
tion is completed. If they were pleuritic they would remain after cough-
ing, and would not be changed in size, character or position, at different
examinations. Pleuritic sounds are present in a large proportion of cases,
but they can be very readily distinguished from rdles produced in lung sub-
stance. Carefully conducted post-mortem examinations show that, in a
large proportion of cases of phthisis the pleuritic changes are secondary to
the changes in the lung substance. Besides, by inflating phthisical lungs
after they are removed from the body, sounds similar to those heard during
life are distinctly audible if a stethoscope is pressed firmly upon their sur-
face. A systolic murmur over the subclavian artery of the affected side,
heard loudest during expiration, indicates that the pleural surfaces at the
apex of the lung on that side are adherent. Vocal resonance is usually
increased in proportion to the percussion dulness ; the more marked the
dulness the more intense the vocal resonance.
In the second stage, or stage of softening, the physical signs of consolida-
tion become more marked, and new auscultatory signs are developed.
Inspection shows a greater frequency of respiration and a more marked
(depression above and below the clavicle on the affected side, as well as an
increased difficulty in local expansion. In fibroid phthisis the retraction
is more marked than in any other variety.
Percussion elicits more uniform and widely-spread dulness, which
assumes a wooden or tubular character.
CHRONIC PULMONARY PHTHISIS.
195
Palpation shows a more marked diminution in expansion of the affected
side. On forced inspiration — both hands being placed on the chest equally
far from the median line — the fingers that rest over the affected lung will
move but slightly compared with those on the opposite side. Vocal
fremitus is increased.
AuscuItatio7i. — Bronchial breathing and bronchophony become more
distinct ; numerous moist crackling rdles, unchanged by coughing, are
heard over a circumscribed space, and have a distinct, shai-p, metallic
character, unlike the crepitation and bubbling sounds which were heard
during the first stage.
In the third stage, inspection shows greater depression in the infra-
clavicular region than existed in either of the preceding stages, and there
is more complete absence of expansive movements during the respiratory
acts.
Palpation gives results similar to those of the second stage. Over large
cavities containing air and communicating with a bronchus, vocal fremitus
is intensified.
Percussion. — The percussion sound will vary according to the condition
of the cavities and their surroundings ; over large superficial cavities partly
filled with liquid there will be amphoric or " cracked-pot " resonance, if
there is a free communication with a bronchial tube. Deeply seated
cavities, when filled, will give deep-seated dulness, and, when empty, an
exaggerated percussion sound. A metallic amphoric note is obtainable only
from a cavity whose transverse diameter is at least 1^ to 1| in.^ Occasion-
ally, cracked-pot resonance will disappear and remain absent for some
time, and no evidence of a cavity can be found where one was known to
have previously existed. This happens when the bronchial tube which has
communicated with the cavity
becomes obstructed in such a
manner as to prevent the in-
gress of air and the egress of
fluid.
Auscultation. — Over small
cavities with lax walls, low-
pitched, puffing, cavernous res-
piration will be heard. When
cavities are surrounded by
firm, tense walls, and are of
large size, communicating free-
ly with a larger bronchus and
are situated near the surface,
a musical, or amphoric, respi-
ration is heard. The amphoric
echo is sometimes most marked
Cracked-pot resonance
Cavernous respiration.
Cavernous whisper. . . ,
Amphoric respiration
Gurgles
Pectoriloquy
Diagram illusirating Physical Signs of Cavities in the third
stage of Chronic Phthisis.
on inspiration ; at other times on expiration. The clearness of the amphoric
note is no way influenced by the presence of a moderate amount of fluid in
' Merbach and Leichtenstern.
196 DISEASES OF THE KESPIRATORY ORGANS.
the cavity. But, when the fluid in the cavity has its level at or above the
opening of the bronchus, the incoming air may bubble up and cause
gurgles. These have a metallic quality and vary according to the character
of the fluid — the thinner and more watery the fluid the more bubbling the
sounds ; the thicker the fluid the more crackling are the sounds. Gurgles
are always most distinct and abundant during and after cough. When very
large cavities with rigid walls contain thin liquid, metallic, tinkling sounds
may be produced by coughing and speaking. The vocal sounds over large
cavities have a metallic or musical quality. Whispering pectoriloquy is
a diagnostic sign of a cavity.
Differential Diagnosis. — The early stage of chronic phthisis may be con-
founded with 'bronchitis, ^pulmonary infarction, pleurisy, acute lohar pneu-
monia, anwmia with cough and expectoration, and cancer of the lung. The
evidence of consolidation of lung-tissue is essential to the diagnosis of
phthisis. So long as bronchitis is accompanied by a temperature of 100°
R, and the physical signs show that the bronchitis is general, phthisis ia
readily excluded ; but if the temperature rises to 103° F., and localized
crepitant rales develop at the apex of either lung, accompanied by dulness
on percussion over the seat of the rdles, with a bronchial character to the
respirations, then there is reason to believe that phthisis is being developed.
If, with these signs, there is gradual loss of flesh and strength, the cough
becoming hacking in character, and the expectoration containing fine
yellow streaks and blood stains, it is almost certain that phthisis is develop-
ing. The diagnosis between chronic bronchitis and fibrous phthisis rests
upon the evidences of consolidation and retraction in phthisis, and their
absence in bronchitis.
Infarctions are attended by haemoptysis and localized areas of dulness.
Their etiology, however, is very different from phthisis, heart disease being
their chief cause. The blood expectorated in phthisis is of a bright scarlet
color ; in infarctions it is dark and in the form of coagula. Infarctions are
most frequently situated in the lower lobes ; in phthisis the dulness is
apical. The temperature is normal in infarction, elevated in phthisis.
In pleurisy ivith effusion, flatness will exist from the base of the lungs
to the level of the fluid ; the line of flatness will change with a change in
the position of the patient ; the breathing will be exaggerated above the
line of dulness ; the range of temperature is lower and does not undergo
such marked diurnal changes as in phthisis. The cough is more hacking
and is not accompanied by expectoration, and vocal fremitus is dimin-
ished or absent. If, after the disappearance of the fluid, the lung remains
compressed and bronchial or broncho-vesicular breathing is present, with
feebleness of the patient, hacking cough and "short breath," the differen-
tial diagnosis between it and fibrous phthisis is difficult. A localized
pleurisy at the apex of the lung, not the result of a general pleurisy,
is indicative of phthisical developments.
Anmnia with cough and expectoration is attended by no febrile symp-
toms, and by none of the physical evidences of pulmonary consolida-
tion.
CHRONIC PULMONARY PHTHISIS. 197
In cancer of the lung there is usually bulging of the chest at the seat of
the cancerous development ; in phthisis there is retraction. In cancer
the temperature is often sub-normal, in phthisis it is more or less elevated.
The currant-jelly expectoration of cancer is diagnostic. Pain is constant in
cancer and intermittent in phthisis. The cancerous cachexia and swollen
lymphatic glands also aid in the diagnosis of cancer.
Whenever cavities have formed in phthisis the diagnosis is not difficult
if the physical signs are properly appreciated ; they can be confounded only
with those of bronchiectasis. The rules for the diagnosis of hroncMectatic
cavities are given under the head of chronic bronchitis.
Prognosis. — Chronic pulmonary phthisis is not necessarily a fatal disease.
Its morbid processes may be arrested in their early stage in a large propor-
tion of cases. In the advanced stage, or stage of cavities, proper treatment
will prolong life, and in some eases permanently arrest the progress of the
disease. Eecovery has occurred in one-sixth of my recorded cases during
the past ten years. Its duration depends on the variety and treatment ;
in Laennec's and Bayle's statistics, its average duration is from one to two
years. My records of chronic phthisis give an average duration of three
years and four months. The younger the subject the shorter its dura-
tion. Phthisis can in no sense be regarded as a self-limiting disease.
Some cases, after a period of activity, become stationary and then slowly re-
cover ; others slowly but steadily progress to a fatal termination ; others,
again, pursue a more rapid and fatal course. The course that any case will
take is determined more by the conditions under which it is developed than
by the natural history of the disease. If an individual has suffered from
phthisical developments from which he has apparently recovered, his chances
for recovery from a second attack are greatly diminished. The history of
phthisical manifestations in early life renders the prognosis unfavorable
when the disease develops during middle life.
The prognosis is unfavorable when there is a strong hereditary tendency,
when phthisis develops early in life, when scrofulous or glandular disease
has existed in childhood, when the patient is narrow chested or dissipated,
when the ordinary pulse-rate is high, and when there is great variation in
weight without any apparent cause. Opinions in regard to haemoptysis
vary. Many think its occurrence renders the prognosis favorable, and that
there is a larger percentage of recoveries when frequent haemoptysis occurs.
My own experience leads me to the opinion that frequent haemoptysis in an
early stage of the disease is not unfavorable. When oedema of the feet and
lower extremities comes on in advanced phthisis the prognosis is very un-
favorable, and a fatal issue is not far off. The following complications ren-
der the prognosis unfavorable : — pleurisy, pneumothorax, emphysema,
pneumonia, secondary eruptions of miliary tubercles, pericarditis, meniu'
gitis, diarrhoea, intestinal ulceration, peritonitis (with or without perforation)
sub-acute gastric catarrh, amyloid degeneration of liver, intestines, spleen,
or kidneys, chronic laryngeal catarrh and bronchitis.
But there is no general law that can be applied to all cases. The general
condition of the patient, the rapidity of the emaciation, the pulse-rate and
198 DISEASES OF THE BESPIRATORY ORGANS.
temperature, the amount of consolidation, the age of the patient, a knowL
edge of the progress of the disease in other members of the family, and the
character of the phthisical process will indicate the probable course of the
disease. In chronic phthisis of long standing the future course may be de-
termined in some degree by the past history of the case. It must be remem-
bered that phthisical patients who seem to be progressing favorably, may
suddenly develop some complication which rapidly terminates the case.
Again, a case that presents symptoms which indicate a rapid course may
suddenly be arrested and a retrogressive process be established. Advanced
cases may die suddenly from heart failure or syncope. The majority waste
to a skeleton, but the mind is perfectly clear and the patient is hopeful of
recovery, and makes plans for the future as if perfectly well.
Treatment. — I shall consider the treatment of pulmonary phthisis under
three heads, viz. :
(1) Prophylactic; (2) Medicinal — internal and local (as inhalations); and
(3) Hygienic, including the climatic treatment.
Prophylactic. — During the period when prophylaxis can be success-
fully employed it is possible to prevent the development of phthisis. In one
who is delicate and leads a sedentary life, or is engaged in an occupation
where the surroundings are unhealthy and depressing, or whose family his-
tory strongly predisposes him to phthisical developments, the occurrence of
emaciation or loss of strength should immediately lead to such a change in
habit of life, occupation and surroundings as shall arrest defective nutrition,
invigorate his constitution, and thus counteract his marked tendencies.
Children born of phthisical or decrepit parents should not be nourished in
infancy by their own mothers, but should be placed with healthy wet nurses.
During childhood they should be fed chiefly on good cow's milk, and the
greatest care should be taken in their exercise and general hygiene. Change
of climate and surroundings is often of the greatest prophylactic importance
in this class of children — ^let the child be removed from the city to the
country. There is no other agent so powerful in correcting phthisical
tendencies in childhood as systematic physical exercise in the open air. This
training should be commenced in infancy and continue to adult life. All
those agencies which tend to develop pulmonary hyperaemia and bronchial
catarrh should be avoided. Individuals with phthisical tendencies should
not breathe air laden with foul vapors or fine particles of dust. Sudden
changes in temperature must be avoided, also hot crowded apartments.
They should have the largest amount of fresh air, not only during the day
but also at night ; their sleeping apartments should be large and well ven-
tilated. Pulmonary hyperaemia may be the result of speaking a few hours
in a crowded and badly ventilated apartment, and then may be followed by
broncho- or lobular pneumonia, which maybe the exciting cause of phthisis.
Flannel should be worn next the skin the whole year. It is important that
such individuals should not engage in excessive physical exercise — as jump-
ing, running and violent gymnastics.
The diet should be simple and nutritious, and taken with regularity ; and
the digestive process should never be overtaxed by taking a large quantity
CHRONIC PULMOKAKY PHTHISIS. 199
of food into the stomach at one time. Alcohol is not to be taken, except
after severe mental or physical work, when there is a sense of exhaustion, or
after the body has been chilled. The functions of the skin must be most
carefully preserved. The soil on which the dwelling-house is built must
also be carefully chosen ; a sandy, porous earth is the best. All bronchial
catarrhs must be carefully and promptly treated until complete recovery is
reached. I know of nothing so certain to assist in the removal of bronchial
catarrhs, in this class of subjects, as a change of climate. Those living in
the mountains should go to the sea ; those at the sea to the mountains. The
" milk " and " grape-cure " so strongly advocated by some for the arrest of
early phthisis, will often be useful in those who have feeble digestive pow-
ers. The whole object of prophylaxis is to sustain and improve the nutri-
tion, and to guard against bronchial, pleuritic or pulmonary complications.
Medicinal Treatment. — The most constant and important symptom of
phthisis is fever, and its reduction is therefore one of the most important
thiligs to be accomplished in the management of a case, for the wasting,
the cough, the expectoration, and the rapidity of the phthisical processes,
are closely connected with the fever. Of all the anti-pyretics in the treat-
ment of the fever of phthisis the sulphate of quinine is the most reliable,
but it must be remembered that rest is equally important. I have often
found that when quinine had little anti-pyretic power while the patient
was " taking exercise," a reduction of temperature was effected by the same
dose if he were put to bed. Twenty grains, on alternate mornings, I have
found most efficacious. Even when cavities are forming, its administra-
tion will often be followed by a lower temperature. It seems to check
the process of consolidation and limit bronchial catarrhs. Digitalis exer-
cises no anti-pyretic power, and only temporarily increases heart-power in
phthisis. Salicylate of soda is recommended as an anti-pyretic by English
physicians, but my experience does not favor its use. Arsenic will act as
an anti-pyretic in some mild cases when all others fail. One-tenth of
a grain of morphine combined with quinine increases its anti-pyretic
power, so much so that now I rarely give quinine as an anti-pyretic to
phthisical patients without it. Aconite, veratrum, gelsemium, and anti-
mony I seldom use on account of the disturbance of digestion which they
cause. In many cases after the disease has passed the first stage the fever
cannot be controlled. When the first elevation of temperature occurs, qui-
nine rarely fails to control the fever. Its administration should be contin-
ued until cinchonism is produced, or until the temperature falls ; after the
temperature commences to fall the dose may be diminished. If the fever
can be controlled, the additional beneficial influences of a change of cli-
mate may, in very many instances, carry the phthisical patient on to recov-
ery, or, if not to complete recovery, life may be prolonged, and the patient
made comfortable. In some cases, even when cavities exist, phthisical
patients may be much improved by the judicious administration of qui-
nine. I am confident that no drug has equal power in arresting phthisical
processes during its early stage. In fibroid phthisis its use is only indicated
during those slight attacks of febrile excitement which attend its progress.
300 DISEASES OF THE RESPIRATORY ORGAl«rS.
Another medicinal agent which has been extensively employed in the
treatment of phthisis, and which, for the past twenty years, has enjoyed
the reputation of curing this disease, is cod-liver oil. It has been claimed
that if this remedy is commenced very early it has the power of arresting
the phthisical processes. I am not among those who advocate its indis-
criminate use. I doubt if it exerts any specific influence upon the disease ;
it is more than probable that all its beneficial influence is due to the fact
that it furnishes some element essential to the digestion and assimilation
of certain nutritive elements. In very many cases the exact manner in
which it acts remedially is not well understood. There are three facts
which seem to me to afford some clue to the mode of its action :— first,
unless the patient gains in weight while using the oil, it seldom or never
proves remedial ; secondly, flesh and weight may be gained during its ad-
ministration, and still the phthisical processes steadily progress; and.
thirdly, when it does act remedially the weight gained is far greater
than would result from the oil as a mere element of nutrition. A great
gain in weight will sometimes immediately follow the administration of a
small quantity of oil. It always acts remedially with more certainty in
young persons and children than in the aged ; generally, old persons are
not much benefited by its use. Those patients who improve under its
use take more food than they have been accustomed to previous to its
employment, and digest it more perfectly. In some instances diarrhoea
will be arrested by its use, and also vomiting of food after eating. In other
cases the oil itself will be rejected and its administration rendered impos-
sible. If possible, it should be given in connection with an alkali. At
first small doses should be given, not often repeated. A teaspoonful once
or twice a day is sufficient to commence with, the dose being gradually
increased to a tablespoonful three times a day. No special benefit is to be
derived from the administration of large doses. Most patients take the oil
best immediately or soon after meals. If it disagrees with the stomach,
lying down a short time after taking it will often prevent any disagreeable
sensation. Some can better take it upon going to bed at night. It should
not be administered in connection with stimulants unless the patient cannot
take it in any other way. Regularity and perseverance in its use are essen-
tial in order to obtain the full benefit it is capable of producing. If, at
times, it seems to disagree with the digestive organs, it may be tem-
porarily omitted, especially during the summer months. The best oil
in the market is '^Holler's," or what is termed ISTorwegian oil. Fish-
oils of various kinds, cream, glycerine, oils from vegetables, koumyss,
malt extracts, pancreatic and pepsin emulsions, etc., etc., have all
proved inferior to the simple cod-liver oil. Phosphorus, sulphur, the
hypophosphites of lime, soda and iron, sulphurous acid, the sulphites, are
all excellent adjuvants to the oil, but cannot take its place. When intes-
tinal digestion is imperfect, the hypojDhosphites are especially beneficial.
When phthisical subjects become anaemic, iron may be given at each meal
if the temperature is below 100° F. ; it may be combined with quinine,
arsenic and the mineral acids as tonics.
CHEONIC PULMONARY PHTHISIS. 201
There is a great diversity of opinion as regards the use of alcohol in
the treatment of phthisis. Some claim for it a curative power; others
maintain that its daily use does harm. The question, therefore, arises : —
under what circumstances has experience taught that it is of service, and
when is it hurtful ? I am convinced that benefit may be expected from
the use of alcoholic stimulants only when they increase the desire for food
and assist digestion, or when their use is followed by an increase in
strength and a disposition to take exercise. On the other hand, if their
use causes a rise in temperature and an acceleration of the pulse, followed
by a feeling of increased weakness and nervous depression, they will cer-
tainly do harm. The belief that alcohol has the power of arresting
phthisical development is one which experience does not sustain. The
daily use of alcohol for a time may mask phthisical symptoms, and the
patient and his friends may fancy that the progress of the disease is stayed;
but soon he reaches a condition in which the disease will make rapid prog-
ress, and in which a large quantity of stimulants will not give relief. It
is unfortunate for a phthisical patient to become addicted to the daily use
of stimulants. If an individual with developed phthisis reaches complete
recovery while taking alcoholic stimulants freely, I am confident that he
would have reached it more rapidly and safely without them. The
quantity and kind of stimulants to be used must be determined by the
effects: — no rule can be given; each case is a law unto itself. Malt
liquors and wines do less harm than whiskey and brandy, and are usu-
ally more serviceable. Phthisical patients tolerate alcohol to a marked
degree.
Cough-mixtures are prescribed by physicians to phthisical patients more
frequently than any other medicinal agents. Such mixtures are usually
composed of substances which are more or less nauseating ; and as the
future well-being of every phthisical patient depends upon his powers of
digestion, everything that may interfere with the healthy performance of
this function must, as far as possible, be avoided. Although a distressing
symptom may temporarily be relieved by a cough-syrup, its administration
will certainly cause digestive disturbances which will do positive harm.
The relief obtained by cough-mixtures is due, for the most part, to the
opium which they contain.
This brings us to the question : — should opium be given to phthisical
patients ? In answer to this question, I would say that opium should
neyer be given in any stage of phthisis, unless the cough is distressing and
the patient is unable to obtain the^ required amount of sleep. Under such
circumstances the milder narcotics should first be tried. Opium should be
reserved for the later stages of the disease. Its use should be commenced
with the smallest dose that will give rest. In the majority of instances I
have found that more speedy and satisfactory relief will be obtained from
the cough and restlessness during the early stages of phthisis by the inhal-
ation of a few drops of chloroform than from the use of opium; besides,
chloroform is less liable than opium to dist^^rb digestion. One must be
careful in the use of chloroform ; there is danger that phthisical patients
302 DISEASES OF THE RESPIEATOEY ORGANS.
may become addicted to its excessive use. Chloral hydrate, hydrobromie
acid, '^chlorodyne," creosote, stramonium and belladonna sometimes act
better than opium. Quite recently oxalate of cerium has been employed.
All narcotics act only as palliatives, and should be employed only when
the symptoms become suflBciently distressing to demand relief. In those
cases where a constant hacking or violent paroxysmal cough is excited
or kept up by an inflamed or irritable condition of the fauces, the topical
application of sedative or astringent remedies by means of sprays will be
found of great service. It is sometimes imperative to give a stimulating
expectorant. Ammonium carbonate in the infusion of wild cherry bark
is one of the best. It never nauseates.
Night sivents are a part of hectic. When quinine does not control
them, quinine with opium may do so. Oxide of zinc (gr. ij-iv), gallic
or suljjhuric acids, arseniate of iron (gr. ^ - ^), ext. of belladonna or sul-
phate of atropia (hypodermically), muscarine, picrotoxine, ergot, — all may
be tried at different times. Atropia is the most reliable. Cold spongings,
and sponging with acidulated or astringent waters (alum in alcohol) are-
always agreeable and sometimes efficacious. Capsicum in the sponging
water is sometimes serviceable.
Gastric and intestinal disturbances are a part of the history of nearly
every case of phthisis, and there are two conditions upon which the diar-
rhoea and distress after eating may depend : — viz., either upon a hypersemic
condition of the gastro-intestinal mucous membrane produced by indigesti-
ble food, or upon ulceration of the large or the small intestine. If it depend
upon gastro-intestinal hypersemia, the quantity and quality of the food
must be carefully attended to, and a mild saline laxative rather than an
astringent must be administered ; this should be followed by the daily use
of the lacto-phosphate of lime. If the diarrhoea is dependent upon ulcer-
ations in the small intestine, cod-liver oil and the hypophosphites of lime
and soda will often be of service. If these fail to give relief, ten grains of
bismuth, combined with the twelfth of a grain of morphine after each
movement, will almost certainly control the diarrhoea for a time. If the
diarrhoea depends upon ulceration of the large intestine, all that can be
done is to give temporary relief by opium suppositories. Vomiting after
meals is often a troublesome attendant of phthisis. Champagne with the
food, hydrocyanic acid, pepsin, and a long list of other remedies are rec-
ommended for its relief. The most certain relief is obtained by giving
the patient a glass of hot water every two hours, followed in half an hour
by a teaspoonful of raio scraped beef made into a sandwich, at the same
time keeping him absolutely quiet in a recumbent posture.
The most valuable remedies for the arrest of Ticemoptysis are rest and
opium. Lead, ergot, ice and a long list of astringents are recommended.
Ergotin hypodermically is much employed. Turpentine is more relia-
ble than any remedy except opium. Local pains in the chest may be re-
lieved by blisters and counter-irritants ; strapping the chest so as to render
the chest walls immovable often gives marked relief from the pains in the
chest caused by the circumscribed pleurisies which attend phthisical proc-
CHRONIC PULMONARY PHTHISIS. 203
esses. Dry cupping often gives marked relief from the dyspnoea which
accompanies acute phthisical processes.
The antiseptic treatment of phthisis has thus far given no satisfactory
results; carbolized inhalations have been quite extensively employed with
very favorable results, according to the statements of some recent observ-
ers, but after quite an extensive trial, my experience is decidedly against
their use. The internal or hypodermatic use of antiseptics, notwithstand-
ing the strong statements made in their favor by some of their enthusias-
tic advocates, I have found to fail not only in counteracting the sepsis of
advanced phthisis but in reducing the high temperature which so rapidly
exhausts the phthisical patients. The injection of cavities through the chest
walls has not been followed by satisfactory results.^ The injecting of cav-
ities through canulse passed into the larynx and trachea seems to me not
only dangerous but futile.
The Hygienic Treatment of Phthisis. — The quantity and quality of the air
habitually respired is a most important consideration in the hygienic treat-
ment of phthisis. Phthisical patients should sleep in large, well ventilated
and well lighted rooms with a southerly or westerly exposure. Flannels
should be worn next the skin, and the surface must never be exposed to sud-
den changes of temperature ; cold sponging or baths often act as tonics when
judiciously employed. The diet should be varied, and phthisical subjects
should become accustomed to drink from one to three quarts of milk each
day. The quantity of food taken should be determined by the power of
digestion ; a phthisical subject should never take more food at a time than
can be easily digested. Peptonized foods and preparations of pancreatin
will often aid a feeble digestion. The patient must live as much as possible
in the open air, and should avoid sedentary occupations, taking systematic
daily exercises, but never to fatigue. It is a very great mistake for a phthis-
ical subject to exercise when his temperature is ranging from 102° P. to
104° P.
The Climatic Treatment of Phthisis is a subject which has recently re-
ceived much attention, but it is to be remembered that its usefulness is con-
fined almost exclusively to the first stage of the disease and that no absolute
rules can be laid down in regard to it. It is well known that some consump-
tives thrive best in a warm, moist air, others in a cool, dry atmosphere ;
some are most vigorous in winter, others in midsummer. Each year's ex-
perience impresses on me the conviction that while climate, more than any
other agent, has a controlling influence over phthisical developments,^ each
case must be carefully analyzed before any definite directions can be given
as to the climate best suited to it. Although we know of no climatic condi-
tions which render phthisis a necessity or an impossibility, still there are
conditions which are known to be antagonistic to its development as well
as those which favor its development. Scarcely twenty years ago the great
J Dr. Pepper, American Journal Med. Science. The modus operandi of washing out hinf?-cavities and
the use of drainage tubes in such cases are fully discussed by Hosier in the October number of the Bar.
Kiln. Woch., 1878.
2 Laennec long ago wrote, " Of all the means hitherto recommended for the cure of phthisis, none have
been followed more frequently by complete cessation of the disease than change of climate. "
204 DISEASES OF THE RESPIEATOKY ORGAN'S.
desideratum was thought to be a warm, dry atmosphere, but we now know
that a cold climate not only does not hasten, but often arrests phthisical
processes. The statement has been made that " the higher the altitude the
less prevalent is phthisis," but the altitude at which such immunity exists
varies with the latitude and with the idiosyncrasy of the individual.
Mountains and elevated districts were thought to be beneficial on account
of their elevation alone. But recent investigations show that the absence
of atmospheric impurities is the chief element, and that the purity of the
air is the chief reason that elevated regions are so beneficial in phthisis.
Prof. Tyndall's experiments are of special interest in this connection. ' Or-
ganic germs are more abundant in the air in the city than in the country.
Eain and ozone free the air from them, the latter by oxidation. Rain
cleanses the atmosphere of solid particles and purifies it by washing down
ammonia and carbonic acid. The presence of ozone in the air is presump-
tive evidence of its purity. The air of high mountains and plateaux and
along the shore of the ocean is richer m ozone than that of the plains. Prof.
Tyndall's experiments show that in early summer, the mountains, and in
late summer and fall, the sea-shore, have their purest air. The benefit which
phthisical patients derive from living near pine-forests has long been known.
Turpentine exhaled from pine or hemlock forests converts oxygen into ozone,
and thus the air of pine-forests becomes pure. Direct inhalation of ozone
has little power over phthisis ; hence it is not the ozone but the purity of
air it induces that renders the air of certain localities so salubrious. It was
formerly thought that resorts where no rain fell for weeks and months were
the best suited to phthisical subjects, but experience has taught the reverse.
Long-continued rains are certainly unfavorable, but cleansing showers act
beneficially. The amount of rainfall is not a sure indication of the amount
of moisture in the air of any region, the latter depending more upon the
dampness of the soil. The atmosphere of a region with a loose, porous,
sandy soil, through which the water filters, and whose surface dries quickly,
is never damp ; but hard, compact, rocky or clayey regions that drain but
slowly and imperfectly, hold the moisture and cause a dampness which is a
strong predisposing cause of phthisis.^
Atmospheric temperature is an important element in the climatic treat-
ment of phthisis. Some patients thrive best in a warm sedative climate, oth-
ers in a cool, stimulating climate. Extended clinical observation leads one
to believe that it is neither the heat nor cold of a certain locality, but the
absence of sudden and frequent changes, which makes it so beneficial to
phthisical invalids.
Altitude is regarded by many at the present time as of more importance
1 After boiling, filtering and evaporating a vegetable infusion he hermetically sealed it in flasks, which
he transported to the Alps 7,000 feet above sea level. Some of the flasks were opened during transporta-
tion, and in these millions of organisms developed in the fluid, while the fluid in the flasks that were
opened on the mountain remained free from such organisms. By further experiments he showed that dust-
laden air was necessary to the procreation of these organisms, and that they are diffused through the atmos-
phere, although the air in different localities may be infected in different degrees.
2 Laennec states that the dampness arising from such a condit ion of soil is one of the most certain devel-
oping causes of phthisis, and he makes mention of a locality having such a soil, in which the dampness
was so constant and of such a character that two-thirds of the resident population died of phthisis.
CHRONIC PULMONAEY PHTHISIS. 205
than any other natural element. As a rule, the atmosphere at elevations
of 1,500 or 1,800 feet is purer than on the plains ; yet all high altitudes are
not thus pure ; experiment has shown the atmosphere of some elevated
regions to be impure, and that consumptives on such elevations do badly.
Something more than altitude is needed to make a given locality suitable to
plithisical subjects. Recent investigations show that the similarity in the
composition of sea and mountain air, at certain times of the year, is far
greater than was at one time supposed. Mountain air is less dense, less
humid and lower in temperature than sea air, but in both we find excess of
ozone and freedom from organic impurities. Both sea and mountain air are
cooler and less subject to frequent variations in temperature than the air of
the plains. A slight diminution in atmospheric pressure produces no palpa-
ble changes. But a great diminution (say one-quarter) produces serious dis-
turbances of nutrition, developing a condition which favors rather than
retards phthisical developments. The effects of diminished atmospheric
pressure vary so greatly in different individuals that no jjractical deduc-
tions can be made.
The question arises : — will this patient be benefited by sea or by mountain
air ? Beneke's experiments show that tissue changes take place more rap-
idly on or by the sea than in the mountains. Hence those in whom the proc-
ess of tissue-change needs no hastening, and those with exhausted nervous
systems, with an overtaxed brain from excessive mental labor or an all-
absorbing business, and who still retain considerable muscular power — those
should go to the mountains. While those past middle life, who have devel-
oped phthisis late, who are incapable of much muscular activity, and who
therefore require stimulation in order to the production of tissue change —
such patients do best in sea air. Sea air is better suited than mountain air
to those who cannot bear sudden changes of temperature, while the suscepti-
bility to such changes is greatly lessened by mountain air.
On our own continent is found every variety of climate. Permanent im-
provement only occurs after a prolonged residence in the place which experi-
ence proves best suited to each case. A change of climate should not be
made every year. The limited space which can be devoted to the consid-
eration of the localities best suited to the phthisical patients in this and
other countries will only allow of mention of the most important ones.
Every stage of fibroid phthisis, no matter how far advanced or where the
fibroid developments began, is benefited in the high altitudes found in Col-
orado and about the Rocky Mountains. But there is one grave objection to
Colorado as a winter refuge :— the enormous monthly, and also the diurnal,
range of temperature must severely try any invalid. During March, 1880,
the thermal range at Denver was eighty-three degrees, and in December,
1876, it amounted to ninety-three degrees— a change in a single month
greater than occurs at London in a whole year, and greater than occurs at
New York in a whole winter.
In my experience, catarrhal phthisis is not benefited in regions of very
high altitudes. It is during, or before, the stage of consolidation that per-
sons with this variety of phthisis are to be benefited by climatic influences,
206 DISEASES OF THE RESPIRATORY ORGANS.
and a careful analysis of each case is important before directions can be
given as to the region most likely to suit the special requirements of each
case. The patient must not wander around till he hits upon the place which
suits him ; much valuable time is thus lost. Except in those who are con-
valescing from some acute lung disease, a sojourn in a southern climate dur-
ing the winter seems after a time to hasten the degenerative processes. My
favorite resorts in the winter, for those recovering from acute pulmonary dis-
eases, are Aiken, S. C, Palatka, Enterprise and Gainsville, Fla., Thomas-
ville, G-a., and Nassau. These localities are also favorable for those in whom
there are evident phthisical tendencies, but in whom as yet, no physical evi-
dences of pulmonary consolidation exist. My best results, when the evi-
dences of consolidation were present, have been obtained in those who have
stayed from one to three years in mountain regions 1,500 to 2, 000 feet above
the sea. My most decidedly beneficial and permanent results have been
obtained in Asheville, N. C, in New Mexico, and in the Adirondack region
of New York State. The temperature, rainfall, and surroundings of the
latter region are all at variance with preconceived notions of a proper " re-
sort for consumptives," but results are strong in its favor. A camp or tent
life in the open air is best for those who can enjoy such life. Excursions
and cheerful social intercourse in the open air should always be an object.
A dreary spot, even with plenty of ozone and elevation, is not of great
material benefit.
I would advocate sanitariums for the phthisical. Not overcrowded hos-
pitals, but cottages and pavilions in sheltered spots, in appropriate climates,
and at a given elevation, where privacy and quiet are possible, and where
all shall be supervised by a capable and intelligent physician. Minnesota
has a dry, cool, exhilarating climate. Southern California, Georgia and
South Carolina have a dry, warm atmosphere. The Bermudas, Bahamas,
Florida, Turk's Island, Santa Cruz, and St. Thomas have a warm, moist
and usually healthy climate. The extraordinarily dry belt of country which
runs northward from San Antonio, Texas, has begun to endanger the su-
premacy of Florida as a winter health resort for the consumptive. That
this belt offers some climatic advantages for weak lungs over the mild but
rather humid air of Florida, cannot be doubted. Nassau, the capital of the
Bahamas, is a noted resort and one that suits most phthisical subjects past
middle life ; Matanzas, Cuba, has a dry, warm climate, suitable for a win-
ter home for the enfeebled, but not for those who have developed phthisis.
It maybe that, for various reasons, a phthisical patient prefers a residence
abroad. Dry climates near the sea are Malaga, Riviera and Algiers. Egypt
and South Africa are highly recommended by the English physicians for
phthisis. Sea voyages to Australia and New Zealand are recommended in
cases of " hemorrhagic pTitMsis.^^ J. Hughes Bennett finds the lakes of
Scotland the best resorts for consumptives in the summer. The Engadine
has been strongly advocated by many.
Recently, Davos am Platz, in the Swiss Alps, has been most extensively
visited. Williams, Albutt and other English physicians give very favorable
reports of it. It is 5,200 feet above the sea, very dry, but not windy, and not
CHRONIC PULMONAET PHTHISIS. 207
changeable.' Davos possesses, also, the unique climatic characteristic of free-
dom from high winds (the records showing that from October 1, 1880, to
March 31, 1881, there were one hundred and thirty-four days with "no
wind"), while its "sun temperature" rises even in January, as Dr. Frank-
lin notes, as high as 150° — conditions which admit of much invaluable out-
door exercise by invalids. Doubtless some high winter resort combining
these vitalizing conditions can be found in the southwestern Kocky Moun-
tain region of our own country.
' London Lancet, 1878, i. 884.
SECTION II.
DISEASES OF THE DIGESTIVE SYSTEM.
{Including Diseases of the Liver, Spleen and Pancreas.)
DISEASES OF THE MOUTH.
The following classification may be made of the diseases of the mouth
I. stomatitis.
II.
Tlie " tliru&hr
a. Catarrhal.
III.
The tongue-diseases.
l. Follicular.
a. Glossitis.
c. Gangrenous.
b. Cancer.
d. Ulcerative.
IV.
Injlammatio7i of the parotid
gland or "Mumps."
OATAEEHAL STOMATITIS.
Catarrhal stomatitis is an inflammation of the whole, or a portion of the
mucous membrane of the buccal cavity and tongae. It may be acute or
chronic.
Morbid Anatomy. — At its onset the mucous and submucous tissue of the
tongue and inside of the mouth becomes tumefied, much redder than nor-
mal, and dry. Later, the mucous and salivary secretions are very much
increased. The swelling is greatest over those parts disconnected with
bone, as the tongue and cheeks. The tongue becomes covered with a
whitish coating, and the red papillae are visible through it. A copious-
glairy secretion, slightly acid in its reaction, containing pus and epithelial
cells, covers its surface. This secretion has a sourish, but not a fetid odor.
In some cases the changes are slight and superficial, in others the tongue
is so swollen that it presses on the teeth and becomes indented by them, and
the mucous membrane of the cheek and gums fills the space outside of
them. The whole surface becomes covered with a tenacious, opaque secre-
tion.
If the process becomes chronic, the glands of the mouth become
swollen and tender, the filiform papillse become elongated and pale, and
give what is called the " hairy tongue." The tongue is less swollen than
in the acute stage ; the secretions have a fetid odor. Occasionally,
patches of exudation form over the tongue and sides of the mouth, which,
tend to collect about the teeth. Large diffuse ulcers sometimes occur in
adults.
Etiology. — The acute form occurs almost exclusively in children during
th.e period of dentition. The chronic occurs mainly in adults. Decayed
CATARRHAL STOMATITIS. 209
and ulcerated teeth, acid ingesta, and the taking frequently of too hot or
too cold fluids, often excite it. The i^rolonged administration of mercury
and preparations of iodine for their specific effect, causes a form which is
termed mercurial stomatitis. The excessive use of tobacco is a frequent
cause. Gastric catarrh may precede or follow it. It may be an ex-
tension of inflammation from wounds of the tongue and fauces. More or
less severe catarrhal inflammation of the mucous membrane of the mouth is
present in most of the specific fevers, especially in scarlatina. Improper
food, bad air, and bad hygienic surroundings will induce it in children.
Symptoms. — The acute form commences with a burning, smarting pain
in the mouth. The child refuses to take food, or allow the finger to
be put in its mouth ; it will take freely of cold drinks, is fretful and sleep-
less, and there is usually a slight rise in temperature. Vomiting and diar-
rhoea often accompany it. The salivary secretion is increased, and flows
from the corners of the mouth, excoriating the parts with which it comes
in contact. It may extend into the larynx and cause laryngeal catarrh.
When it occurs in adults, there is a slight rise in pulse and temperature, a
general feeling of malaise and much difficulty in swallowing. The patient
is constantly trying to get rid of the slimy coating on the tongue and mouth,
by hawking and spitting. The sense of taste is blunted, and there is usu-
ally an unpleasant bitter taste in the mouth. These symptoms are usually
accompanied by a dull frontal headache.
In chronic stomatitis the breath in the morning has a fetid odor, the
taste is vitiated, and there is often great depression of spirits. Earely is
the digestion interfered with.
Differential Diagnosis. — Catarrhal stomatitis may be mistaken for the
changes which take ];)lace m the tongue and mouth in some of the specific
fevers. In catarrhal stomatitis the coating of the tongue is soon followed
by a coj)ious salivary secretion; while in fevers the tongue becomes dry,
and the detachment of brown crusts leaves a glassy, smooth surface. In
catarrh, the appetite for solid food and the digestive functions are not
much changed, while in fevers there is great thirst and repugnance for
food. There are slight, if any, constitutional symptoms in catarrh, while
in incipient fever there are marked constitutional symptoms.
Prognosis. — The acute form generally terminates in recovery within a few
days. Chronic oral catarrh is very persistent and stubborn, and rarely yields
to treatment.
Treatment. — In young children the diet should be cold milk with lime-
water. The mouth should be washed with a slightly alkaline wash, and
chlorate of potash given internally. In all cases the cause should be re-
moved, and the bowels regulated with rhubarb and soda.
In chronic catarrhal stomatitis, after the removal of its exciting causes,
moderately strong alkaline washes should be frequently used, and in obsti-
nate cases a weak solution of nitrate of silver will be found most effica-
cious. Carbolic acid sprays relieve the offensive odor and other unpleasant
symptoms.
14
310 DISEASES OP THE DIGESTIVE SYSTEM.
rOLLICIJLAE STOMATITIS.
Follicular, aphthous, sometimes called croupous, stomatitis is a vari-
ety of inflammation of the mouth, in which the mucous follicles are pri-
marily and chiefly affected.
Morbid Anatomy. — On the anterior portion of the tongue, and on the
mucous surfaces of the gums and cheeks, there appear small vesicle-like
elevations, semi-transparent, and having a red zone about their base ; these
are called ''aphthae ;" some regard them as a peculiar deposit, others as a
local croupous exudation. They are often numerous ; after they have rupt-
ured they leave an irregular gray surface, resembling a small ulcer, which
heals slowly. Occasionally a number of aphthae coalesce and form irregular
ulcer-like or excoriated patches. In the majority of cases the ulcers soon dis-
appear, new crops appear and the disease may run a tedious course. Dirty
white or yellow sloughs cover the ruptured aphthae, and gradually separate,
leaving no scar. Follicular ulcers on the inner side of the lips sometimes
occur at the menstrual epoch, or during pregnancy and lactation ; ulcers
like these rarely occur in men.
Etiology. — Aphthffi may accompany any disease of the tongue or mouth.
It is, like most oral diseases, chiefly prevalent among children during den-
tition, and is rare after five years of age. It is idiopathic, or a sequela of
one of the exanthemata. Unripe fruit, candy, and indigestible food re-
maining in the child's mouth will cause it. Bad hygienic surroundings-
and a weakly, badly nourished state of the body, are its principal predis-
posing causes. It sometimes prevails epidemically.
Symptoms. — Aphthous stomatitis shows itself in very young children by
pain on taking the breast and in swallowing. Older children have pain on
talking and masticating. There is a slight febrile excitement and enlarged
and tender sub-maxillary glands. Salivation occurs, and tJie parts about
the month and chin become excoriated by the saliva, which continually
runs over them. Feculent diarrhoea is common, and there is more or less
interference with digestion.
Differential Diagnosis. — This cannot be confounded with any other dis-
ease.
Prognosis. — It is never fatal ; it generally disappears as soon as the causes
that produced it are removed.
Treatment. — Correct any intestinal disturbance that may exist with small
doses of rhubarb and magnesia, or mild salines ; restrict the diet to milk.
Wash the mouth with a weak solution of glycerine and borax, or chlorate
of potash. In severe cases the mouth should be washed every few hours
with a dilute mineral acid, or nitrate of silver. In weak children, wlien the
general health is impaired, stimulants may be given with benefit.
GANGRENOUS STOMATITIS. 211
GANGRENOUS STOMATITIS.
Grangrenous stomatitis, ''cancrura oris/' or sloughing phagedgena of the
mouth, is a formidable disease of childhood, in which the tissues of the
cheek are prominently involved.
Morbid. Anatomy. — There is first a hard swelling developed in the cheek,
the skin over it being red, shining, tense, and brawny. In the mouth, at
the side of the indenture, there is a deep, ragged, angry, unhealthy ulcer
covered with a dark, ashy, or brown colored slough. The adjacent tissue is
cedematous, and hemorrhage fi'om the livid and swollen part sometimes
occurs. The ulcer in the cheek rapidly extends and deepens, emits a
very fetid odor, and often perforates the walls of the buccal cavity. The
slough may occupy the whole of one side of the mouth, the teeth may
become loosened, and caries, or necrosis of the inferior maxilla, result. If
the ulcerative process is not extensive, separation of the slough may occur,
and the ulcer heal by granulation and cicatrization. The facial vein may
be implicated, and then pyaemia, with multiple abscesses, may result.
Etiology. — This is a very rare disease. It occurs principally in debilitated
children between two and five years of age who are convalescing from some
form of acute disease, such as scarlet fever. Whether it is contagious or
not has never been determined. It sometimes follows the prolonged use of
mercurials. Bad air, insufficient food, and anti-hygienic surroundings,
predispose to it.
Symptoms. — It commences with pain in the mouth, which is increased by
movement of the jaws. Then the local changes already described appear
on the cheek and gums, and an abnormal quantity of saliva, mixed with a
putrescent fluid, often with blood, flows from the affected side of the
mouth. The breath has a peculiarly offensive odor. The adjacent glands
become enlarged and tender. As the disease advances, the constitutional
symptoms of septicaemia are developed. In most cases the child after a
time becomes drowsy, passes into coma, and dies.
Differential Diagnosis. — Cancrum oris maybe mistaken for "malignant
fustuW Malignant pustule attacks the skin and exposed parts -first,
while gangrenous stomatitis begins in the mucous membrane of the cheek
or about the gums, involving the skin secondarily. Malignant pustule is
at once accompanied by constitutional symptoms, and soon followed by the
phenomena of a septic or typhoid fever, while cancrum oris is without
pyrexia or loss of appetite at its onset, and severe general symptoms do not
come on till late.
Prognosis. — This is an exceedingly fatal disease — nineteen out of twenty
die. In the few cases where the process has been mild, recovery has
occurred within two weeks from its commencement. The complications
are pneumonia, bronchitis, and pyaemia. Death may occur from exhaus-
tion or from one of the above named complications.
Treatment. — Prompt measures are indicated at the onset of this affection.
Nitrate of silver, and even strong nitric acid, should be thoroughly applied
212 DISEASES OF THE DIGESTIVE SYSTEM.
to the slough, and the mouth frequently washed with solutions of carbolic
acid and chlorate of potash. The best internal remedies are quinine and
hydrochloric acid. The diet should be highly nutritious ; stimulants may
be freely given, if indicated. "When the child cannot swallow, beef tea and
brandy enemata should be administered.
ULCERATIVE STOMATITIS.
Ulcerative stomatitis, or noma, is a variety of inflammation of the mouth
chiefly affecting the gums and spreading over a large extent of surface.
Morbid Anatomy. — The gums are hypera^mic and tumefied. Sometimes
they assume a purplish color, separate from the teeth, and are covered with
a pulpy gray- white material which disintegrates, becomes soft and dark,
and gradually spreads to the lips and side of the cheek. This gangrene-
like slough may gradually extend until the gums are destroyed. In some
few instances little vesicles precede the slough. If the slough is removed
as soon as it appears, the gums underneath will be found red, bleeding and
granular. The teeth become loosened and often drop out, the tongue
enlarges and has a sodden a]3pearance, and the mucous membrane of the
cheek swells so that it often receives the impression of the teeth. Some-
times the bones about the face lose their periosteum and exfoliate. When
recovery takes place deep cicatrices may remain and cause more or less
distortion of the face.
Etiology. — Noma, or ulcerative stomatitis, is met with only in children
from one to ten years of age. It occurs among those who inhabit filthy
localities, who are badly fed and compelled to breathe unwholesome air.
Dampness seems to exert a predisposing influence, and the disease is most
prevalent during the autumn months. It is probably contagious, for well-
marked epidemics of it are recognized. It is common after asthenic in-
flammation and the eruptive fevers. The prolonged use of mercurials will
cause ulcerative stomatitis.
Symptoms. — The mouth is hot and painful for some time, and then ap-
pear the changes already described. There is pain on chewing or speaking,
and there may be slight febrile excitement, although constitutional symp-
toms are not prominent. There is an increased flow of saliva which has
a very offensive odor, and is mixed with blood and shreds of the pulpy
mass. There is enlargement and tenderness of the sub-maxillary glands.
In some cases the child will pick at its mouth and throat, and very often
loosens and swallows some of the shred-like sloughs. The appetite may
not be impaired, though the bowels are disordered, and the child is restless
and sleepless. The upper lip becomes swollen, dark-red, and projects out-
ward, while the mouth is kept widely open to prevent painful contact with
the lips or tongue. The excessive salivation soon decreases, but the un-
pleasant fetor of it and of the breath persists. Late in the disease the adja-
cent glands become enlarged and tender.
Differential Diagnosis. — Ulcerative stomatitis maybe mistaken for " can-
crum oris," or gangrenous stomatitis. It is a local disease, while cancrum
THRUSH. 213
oris is attended by constitutional symiotoms ; it begins in the gums, while
gangrenous stomatitis begins in the cheek. The j)rogress of noma is slow
compared with the very rapid extension of cancrum oris. The livid red-
ness, the dark swelling, and the ashy slough of cancrum oris are absent in
ulcerative stomatitis.
Prognosis. — This is good. Its duration is about eight days, but slough-
ing about the gums may continue for weeks.
Treatment. — The treatment is the same as in aphthous stomatitis. The
chlorate of potash may be used as a wash or gargle and internally, and will
usually arrest it. In many instances, fresh air, cleanliness and a restricted
diet are all that is necessary to effect a cure. If the ulceration spreads,
the application of nitric acid, and sometimes the employment of the ac-
tual cautery, must be resorted to. For the profuse salivation which is
sometimes so troublesome, belladonna has proved efficacious.
THEUSH.
Thrush, sjjrtie or muguet is an aphthous disease of the epithelium of
the mouth and tongue, due to the growth of the germs of the thrush-fun-
gus, the oidiutn albicans. It was formerly classed as an exudative inflam-
mation.
Morbid Anatomy. — The mucous membrane of the mouth assumes a dark
red color, and upon the most superficial layer of the epithelium there ap-
pear numerous small, round whitish spots, — " aphthas," — which give to it a
flocculent or curdy appearance. These spots are often aggregated in
groups of two or three ; at first, as they enlarge, they fall off or can be
readily removed, but are soon reproduced and run
together m patches. The development in thrush
of the oidium albicans and of its frequent j)arasitic
companion, the leptothrix buccalis, in and between
the epithelial cells may continue until the mucous
tissue is invaded. The epithelium becomes swollen
and loosened, the tongue and inside of the mouth
are covered with a yellowish pultaceous, creamy
mass, underneath which the. mucous membrane is
of deep red color, and the papillfe are enlarged. In
the new-born it occurs most abundantly about the
boundary line between the hard and soft palates ;
in adults, on the mucous membrane of lips, cheek '*^' ^^'
, , „ , -ri -TIT Oidium Albicaiis. From the
and end of tongue. It may invade the pharynx, tongvein a case of ''Thrush:''
oesophagus and stomach. It has been found in the uai tiireads^^''^ m. ' ^^'
lungs and air-passages and about the breasts and
genitals of infants. A microscopic examination of a patch shows it to con-
tain mucous and epithelial cells, fat spherules, and the spores and filaments
of the oidium albicans. The spores are round or ovoid and form masses of
varying sizes, while the filaments coming out of the spores are cylindrical,
curved or branched, and consist of long cells, which are constricted where
they Join one another, each cell being filled with granules.
314 DISEASES OF THE DIGESTIVE SYSTEM.
Etiology. — In children this disease occurs from birth to the second year,
and is very rare after that time until adult life. These parasitic plants
grow best in the presence of acids, hence the acid secretion of the mouth
for the first six or seven months predisposes to it. All food or drink that
will produce irritation of the stomach or intestines, and make the intestinal
contents acid, jDredisposes to it. Want of cleanliness in the care of nursing-
bottles, spoons, etc., is one of its principal causes, consequently it is more
frequently met with in children brought up on the bottle, especially in asy-
lums. In adults thrush occurs toward the end of any long exhausting
disease, such as cancer, or consumption.
Symptoms. — In children the mouth becomes hot and painful. The child
will not allow its mouth to be touched. An examination shows the mu-
cous membrane to be drier than natural ; soon after, the peculiar thrush
aphthae appear, and there is salivation, which is always markedly acid.
The lips swell and become everted. Diarrhoea is frequent and the passages
are often green and smell of fatty aci^s ; so acid are they at times that
they cause an erythema about the anus. If this condition persists, the but-
tocks and parts around the genitals become excoriated. Besides this diar-
rhoea, vomiting and purging give additional evidence of gastro-intestinal
disturbance. In adults suffering from exhausting disease, the mouth be-
comes hot, dry and painful before the thrush appears, and there is diffi-
culty in swallowing, after which the mouth and tongue soon present the
characteristic appearance of the disease.
Differential Diagnosis. — The presence of the parasite establishes the diag-
nosis.
Prognosis.— In vigorous children the average duration of this affection
is from eight to ten days, but in feeble infants it often lasts for months.
Its only serious complication is gastro-intestinal catarrh. Death may result
from the exhaustion of the diarrhoea.
Treatment. — The most important thing to be accomplished in the
treatment of this affection is to arrest or counteract the acidity of the se-
cretions of the mouth. After each feeding the mouth must be thoroughly
cleansed with borax and glycerine, or a weak solution of carbolic acid, and
sulphate of soda. The diet should be restricted to milk with lime-water ;
when there is emaciation, cod-liver oil and the lactophosphate of lime will
be of service. The bowels must be regulated as in follicular stomatitis.
GLOSSITIS.
Glossitis is an inflammation of the parenchyma of the tongue. It may
be acute or clironic, and when chronic, is generally circumscribed.
Morbid Anatomy. — There is first intense hypersemia, causing slight swell-
ing and intense redness of the tongue. This is soon followed by so great
an enlargement of the organ that it entirely fills the mouth and protrudes
beyond the teeth. Its surface is covered by a thick secretion, and its sub-
stance assumes a pale or grayish color. The oedematous condition may
rapidly subside and leave the tongue in its normal state, or the inflammac
GLOSSITIS. 215
tion may be so intense that small abscesses form which leave deep cica-
tricial depressions, giving the tongue an uneven and lobulated appearance.
In some instances the tongue may remain enlarged and hardened for life.
There is a rare variety of glossitis which does not invade the deeper struct-
ure of the tongue, but is confined to its mucous and sub-mucous tissue,
causing thickening and sloughing of its surface, with depressions similar to
the cicatricial depressions of the parenchymatous variety.
Chronic glossitis occurs chiefly in patches along the edges of the tongue ;
the thickening, induration, and cicatricial depressions occur in circum-
scribed spots. When chronic glossitis is general, the tongue is uniformly
enlarged and its color is much redder than normal, some spots being
darker than others ; its movements are interfered with, and its surface pre-
sents the appearance of eczema of the skin.
Etiology. — Acute glossitis may develop under the influence of mercurial
poison, or as a consequence of direct injury. Croton oil and other acrid
matters taken into the mouth may cause it ; burns, blows, and the poison
of insects have caused it. Chronic glossitis occurs in the old without any
apparent cause. It may be produced by disease of the teeth, or of the maxil-
lary bones, and may, in some instances, result from the action of the mate-
rials of which false teeth are made.
Symptoms. — With the enlargement of the tongue in acute glossitis, there
is great restlessness and anxiety, accompanied by an increase of the pulse-
rate, and an elevation of the temj)erature. In some cases, there is profuse
salivation, and the swollen tongue protrudes between the lijDS. There is a
sensation of heat in the mouth, and the swelling often causes severe pain.
The glands at the angle of the jaw are enlarged and tender, and all move-
ments of the tongue in talking, chewing or swallowing become exceedingly
painful and frequently impossible. Dyspnoea and inability to lie down are
sometimes caused by the obstniction to the free entrance of the air into the
lungs. When the veins in the neck are compressed, cyanosis of the face is
marked. The patient is anxious, and very much depressed, and may show
signs of asphyxia ; indeed death has occurred from suffocation in extreme
cases. When it terminates in suppuration, the constitutional symptoms be-
come severe, and all the oral symptoms are intensified. When clefts remain
in the tongue after glossitis, the ulcers in them are painful, but otherwise
there is no inconvenience. In superficial glossitis, which is apt to be pro-
tracted, any movement of the tongue is painful, and there is constant sali-
vation. In chronic glossitis patients sometimes complain of a dull aching
in the tongue, and in some cases movements of the tongue induce pain of
a burning character.
Differential Diagnosis. — Chronic circumscribed glossitis may be mistaken
for cancer. Cancer develops rapidly, and chronic circumscribed glossitis al-
most imperceptibly. Cancer tends to speedy ulceration, and hemorrhage is
frequent, while glossitis passes on to induration and there is no hemorrhage.
Fetor of the breath is present early in cancer, while it is slight or altogether
absent in glossitis. In cancer the pain is sharp and lancinating, running
along the branches of the fifth nerve, while there is only a dull pain in
216 DISEASES OF THE DIGESTIVE SYSTEM.
glossitis. In cancer the adjacent lympliatics are early involved, in glossitia
they are uninvolved. In cancer, emaciation and cachexia are marked ;
these are absent in glossitis. A microscopical examination of a portion of
the diseased tissue will establish the diagnosis.
Prognosis. — In acute glossitis, the prognosis is uncertain, for suffocation
may occur unexpectedly; generally it subsides in from three to seven days.
Of the modes of termination, that of thickening and induration is the most
common, and is rarely entirely recovered from.
Treatment. — In acute glossitis, ice should be freely applied to the tongue
and a mild cathartic administered. If the patient is not able to swallow
castor oil, a turpentine enema may be given. If the swelling interferes with
respiration, free and deep incisions on the upper surface must be at once
made, and if abscesses form they should be promptly opened and washed
out with some disinfectant fluid. The ulcerations occurring in glossitis
should be treated in the same way as those of ulcerative stomatitis. In the
chronic form, if possible, remove the cause. In superficial glossitis, the
local application of carbolic acid will be found the best remedy. If suffo-
cation becomes imminent in either variety, tracheotomy should be per-
formed.
CAlSrCER OF THE TONGUE.
The most common variety of cancer of the tongue is epithelioma.
Morbid Anatomy. — At some point that has been subjected to constant
irritation, or in some ulcerative cleft in the tongue, there appears a small
unhealthy ulcer or a small deeply seated nodule. When appearing on an
otherwise healthy tongue, its locality is usually on its edge. In whatever
way it may begin, an ulcer quickly forms, circular in shape with ragged
everted edges, and a wide indurated base. The surface of the tumor has a
dirty white or grayish-red appearance, is papillated and friable, and com-
monly of a firm consistency. As the disease advances, it may involve the
whole tongue, which is then larger than normal, unevenly lobulated, and
covered with small ulcerations. The mucous membrane on the floor and
sides of the mouth may be secondarily invaded. As the deeper tissues are
encroached upon, hemorrhages occur. The sub-maxillary and sub-lingual
glands early take part in the cancerous development, and the oral cavity
may be filled with the cancerous mass. On scraping the surface of an epi-
thelial cancer, a grayish granular mass is found beneath, a portion of which
under the microscope will show the characteristics of an epithelioma.
Etiology. — Cancer of the tongue is met with most frequently in middle
life, between the ages of thirty-five and sixty, and occurs in men more often
than in women. Its chief exciting cause is some local irritation, as from a
projecting or carious tooth. It may develop in syphilitic fissures. Oc-
casionally it appears on a tongue whose mucous membrane has, for a long
time, been thickened and indurated. Usually there is an hereditary pre-
disposition to cancerous develojDment. It may develop without any discov*
erable cause.
Symptoms. — In most cases, from the onset there is a sharp pain at the seat
PAROTITIS. 217
of the disease. This pain is aggravated by any movement of the tongue,
and generally runs along the branches of the fifth nerve. Salivation is pro-
fuse, and swelling of the lymphatics in the neighborhood is present early.
Hemorrhages not infrequently occur, which increase the anaemia that at-
tends the cancerous cachexia. The disease runs a very rapid course, the
pain becomes agonizing, and a fatal termination may at anytime occur from
hemorrhage from the lingual artery, or suffocation may result from me-
chanical interference with respiration.
Differential Diagnosis. — This disease may be mistaken for syphilitic ulcer-
ation. A syphilitic ulcer is long and oval or irregular in shape, while can-
cer is circular. A syphilitic ulcer is developed slowly and with little or
no localized pain, but cancer spreads rapidly and is accompanied by severe
pam. The constitutional symptoms of syphilis are usually well marked,
and the ulcer improves under anti-syphilitic treatment, while the evidences
of syphilis are absent in cancer. A microscopical examination of a small
portion of the ulcerating surface removes all doubt in diagnosis.
Prognosis. — The disease advances rapidly; its average duration is about
fourteen months. I have known cases to last two years. Death results
from the cancer, marasmus, exhaustion from hemorrhage, or from starva-
tion, as the intense pain in eating causes the patient to refuse food. The
constant and long-continued pain hastens the fatal termination. If, after
removal, it does not reappear, death may result from cancerous develop-
ments in other parts of the body.
Treatment. — The relief of pain and the maintenance of the vital powers
are the principal indications. The hypodermic use of morphia is the best
means of relieving pain. Antiseptic gargles are grateful, and counteract
the offensive odor of the breath and the unpleasant taste. The checking
of hemorrhage, removal of the growth, removal of the tongue, ligation of
the lingual artery and division of the gustatory nerve, belong to the surgical
rather than to the medical treatment of the affection.
PAEOTITIS.
Parotitis, or " mumps," is a catarrhal inflammation of one or both pa-
rotid glands ; rarely are the other salivary glands involved. It is of two
varieties, specific and non-specific. The latter is also called symptomatic.
Morbid Anatomy. — The left parotid is usually first affected. The disease
commences in the gland-ducts, not, as was formerly supposed, in the
intercellular substance. Both varieties begin as a catarrh, the intense
initial hypersemia of the parotid being followed by a serous exudation and
a soft swelling of the gland. From the few cases that have been examined
at this stage, we learn that there is oedema of the acini, and that the gland
is reddened and injected, presenting a fleshy appearance. The connective-
tissue about the parotid and often the parts beyond it are involved. The
gland which is so enormously swollen may decrease to its normal size by
the absorption of the exudation; or, when the process is very severe, the
idiopathic variety may end in abscess ; this termination is much less fre-
218 DISEASES OF THE DIGESTIVE SYSTEM.
quent than in metastatic parotitis. Occasionally, the gland remains per-
manently enlarged. It may atrophy.
Metastatic parotitis begins with a catarrh of the ducts ; there is first
hypersemia, followed by an exudation into the ducts, which is semi-transpa-
rent or yellow. The acini are wholly or partly filled with pus, and there
result numerous little spots of suppuration, but if the process is severe and
rapid the interstitial tissue becomes involved, and the whole gland may be
converted into an abscess. The suppurating process may extend to the
neighboring bones, muscles, connective-tissue, or, rarely, to the cranial
bones and meninges. As in "cancrum oris," if the adjacent veins are in-
volved, pyaemia and multiple abscesses are the result. The Eustachian
tube may be involved, and sometimes pus burrows under the muscles at
the back of the neck.
Etiology. — Specific parotitis seldom occurs except as the result of conta-
gion. It is contagious, but not infectious, and seems to be favored in its
development by dampness. Consequently, it is common in autumn and
early spring, and among those who live in cold, damp cellars. It prevails
most in crowded localities, such as asylums and foundling hospitals. It
resembles the exanthemata, in that it attacks the same gland but once.
The exact cause of metastatic parotitis is obscure. The reason of its devel-
opment in small-pox, typhus, typhoid, measles, pyaemia, septicaemia, chol-
era, and rarely in pneumonia, cannot always be given. The period of
incubation in specific parotitis varies from seven to fourteen days.
Symptoms. — In specific parotitis for a short time preceding the glandular
enlargement there is chilliness followed by flashes of heat, frequently by
dull pains in the limbs, general lassitude and loss of appetite. In nervous
children headache, delirium, and often convulsions are its premonitory
symptoms. In from thirty-six to forty-eight hours after these phenomena,
there is a sensation of stiffness about the angle of the jaw, followed by pain.
and swelling in the parotid region. The pain is increased by speaking,
swallowing, and by pressure. Both glands may be simultaneously affected
but usually only one is involved at a time. The tumor is firmer over the
centre than at its circumference, the outer rim being slightly cedematous
and pitting on pressure. Moderate salivation occurs in a few instances.
The disease reaches its height in from three to five days, and the swell-
ing of the gland begins to subside on the seventh or eighth day.
In the non-specific variety, if abscess form, constitutional symptoms in-
dicative of the formation of pus are developed, and the adjoining lymphat-
ics become enlarged. These abscesses may open externally, into the mouth,
pharynx, or external ear. During or after the decline of specific parotitis,
metastasis to the testicles, mammae, or ovaries may occur. Metastasis to the
meninges of the brain (a rare occurrence) is indicated by delirium and active
cerebral symptoms, which terminate in coma and death. Non-specific paro-
titis, developing during some severe constitutional disease, produces few
symptoms of its own, excepting the physical evidences of the tumor, which
shows a tendency to suppurate from its beginning ; very soon a lobulated red
swelling exhibiting fluctuation at various points is developed, which soon
TONSILLITIS. 219
discharges laudable pus. In this variety, but one gland is usually in-
volved.
Diflferential Diagnosis. — There is little difficulty in recognizing this disease
by the situation of the swelling.
Prognosis. — In the specific variety the prognosis is favorable, the gland
usually returning to its normal si e and consistence in from ten days to two
weeks. If an abscess forms and implicates the ear or Eustachian tube, per-
manent deafness may result ; when orchitis, mammitis, meningitis and
other metastases complicate the parotitis, the prognosis is more or less un-
favorable. Death may result from meningitis with active brain symptoms.
Non-specific parotitis, occurring in the course of any acute general disease,
must be regarded as a very unfavorable symptom.
Treatment. — Specific parotitis is a self-limiting disease ; during its active
period the patient must be kept in an even temperature, and a mild saline
cathartic may be administered. The diet should be non-stimulating. If
the parts are painful, warm fomentations may be applied. If the patient
suffers severe pain or is restless, the bromide of potassium or hydrate of
chloral may be given. Inunctions of oil, when the swelling is disappear-
ing, are said to aid in reducing it. When orchitis or meningitis occurs it is
to be treated as a complication. During convalescence tonics are indicated.
The non-specific variety requires no treatment except the use of means
which hasten suppuration and support the patient.
DISEASES OF THE PHAEYNX.
I. Tonsillitis:— {a.) Acute ov Quinsy ; and {h.) Chronic— 11. Inflam-
mations:— {a.) Catarrhal which is either Acute or Chronic; and, {h.)
Memhranous, which is either Croupous or Diphtheritic. — III. Retro-
pharyngeal Abscess.
TOl^SILLITIS.
" Quinsy sore throat," sometimes called phlegmonous pharyngitis, is an
inflammation of the parenchyma of one or both tonsils, and may be acute or
chronic.
Morbid Anatomy.— It must be remembered that beneath the external cov-
ering of the tonsils fibrous trabecular enclose numerous groups of lymph-fol-
licles, and that this interstitial stroma is very vascular. In acute tonsillitis
there is first hypergemia and swelling of the gland and of the parts adjacent
to it. The angry, red, lobulated surface of the enlarged gland and the
back part of the tongue are covered with a tough, gelatinous or creamy
secretion, and the uvula and anterior pillars of the fauces become swollen
and oedematous. When suppuration is to occur a point on the surface of
the inflamed tonsil becomes prominent, soft and fluctuating. The loose
cellular tissue surrounding the tonsils may be involved in the suppurating
processes. If chronic tonsillitis follows, subsidence of the acute hypertrophy
of the stroma occurs, accompanied by enlargement of the supplying ves-
sels. Chronic enlargement of the tonsils may also be developed slowly
220 DISEASES OF THE DIGESTIVE SYSTEM.
without being preceded by the acute, and then the glands may become so
large that they touch each other and are much firmer and harder than the
normal gland. Their surface presents a pitted appearance, the mucous
membrane usually being paler than natural.
Etiology. — Quinsy is rare in those under twelve years of age, but it is more
common in youth than in adult life. Certain atmospheric influences pre-
dispose to it. There is a strong hereditary predisposition to it in certain
persons. It ^'runs in families." Certain diseases, as scrofula and syphilis,
favor its development. Exposure of the surface to cold almost always pre-
cedes an attack. After a first attack it is liable to occur at stated intervals
each year. Tonsillitis frequently occurs with scarlatina, measles, typhoid
fever, and with inflammatory conditions of the mouth or tongue. Chronic
tonsillitis, which is not a sequela of the acute, is almost always hereditary.
Symptoms. — Acute tonsillitis is usually ushered in by a distinct chill fol-
lowed by a rapid elevation of temperature ranging from 103° F. to 105° F.,
with a corresponding increase in the frequency of the pulse. In from
twelve to thirty-six hours after the initial fever there is heat, pain and
swelling in the region of the tonsils, and dryness of the tongue and throat.
The attempts which the patient makes to swallow an imaginary substance
in the fauces increase the pain. Fluids are often regurgitated through the
nostrils. The respirations become difficult on account of the obstruction to
the ingress and egress of air. The tumor produced by the swollen tonsil
can be readily felt externally. Thick mucus is expectorated, and the
tongue becomes swollen and covered with a thick pasty coating. The
breath is offensive, the jaws are often immovable, any attempts to move
them causing darting pains along the Eustachian tube to the ear. There
is a peculiar "nasal " tone to the voice, and if the throat can be examined,
the passage to the pharynx is found obstructed by the swollen glands, the
cedematous uvula, and the oedematous anterior pillars of the soft palate.
These symptoms steadily increase in severity. The patient is unable to
sleep, and suffers constantly from a sense of impending suffocation. He is
sometimes delirious. The constitutional and local symptoms increase for
several days, and then gradually subside, or something is felt to give way in
the throat, and suddenly the patient is entirely relieved by the discharge of
fetid yellow pus. Convalescence is rapid. "When a chronic enlargement is
the result of quinsy, violent paroxysms of coughing and loud snoring dur-
ing sleep are caused by the enlarged tonsils and elongated uvula, which lat-
ter, in some cases, produces an inclination to vomit. The Eustachian tube
being pressed upon, partial or permanent deafness results, and the voice
has a thick and often husky tone. Chronic catarrhal stomatitis frequently
accompanies this form of tonsillitis ; acute attacks may be engrafted upon
the chronic condition. Slight dysphagia and impediment to full and deeji
inspirations, as well as a permanent change in the voice, are caused b}
chronic tonsillitis.
DifFerential Diagnosis. — It is hardly possible to mistake quinsy for an}
other disease if a proper examination of the throat is made.
Prognosis. — The prognosis in acute tonsillitis is always good. The onl}i
CATARRHAL PHARYKGITIS. 221
thing to be feared is that chronic enlargement of the tonsils may result.
The duration of the urgent symptoms is from four to five days — the entire
duration is eight days. It may be complicated by inflammatory conditions
of the tongue and mouth, by inflammation of the Eustachian tubes, by
pharyngitis and oedema glottidis. Death in rare instances may result from
suffocation, exhaustion, or cedema glottidis.
Treatment — When seen early, astringent gargles and the carbolized spray
will afliord relief, and in some instances seem to arrest its progress. After
the chill, suppuration can rarely be prevented. Warm poultices of linseed
meal, the wet pack, or external applications of turpentine, are then found
most efficacious and agreeable. I have been able in a large number of
cases to abort a quinsy by a twenty-grain dose of quinine administered at
the time of the chill, followed by a large dose of bromide of potassium.
Mild cathartics should be administered at the commencement of the at-
tack ; a combination of belladonna, quinine and aconite has been thought
by some to have a controlling influence over this disease. Acetate of am-
monia, chlorate of potash, or some effervescing draught is generally grate-
ful to the patient ; the diet should be highly nutritious ; moderate stimula-
tion is often required. As soon as an abscess forms it should be opened.
Warm poultices may be applied over the region of the glands for some time
thereafter. If suffocation threaten at an early stage of the disease, free
scarification of the swollen and oedematous parts, or excision of the tonsils
must at once be made. In chronic tonsillitis, tannin and glycerine, or a
strong solution of alum or iodine, should be carefully and regularly ap-
plied ; at the same time iodide of potash or iron may be given. It may
be necessary to excise a part or all of the gland, and part of the uvula, af-
ter other remedies have been tried and found unavailing.
CATARRHAL PHARYNGITIS.
This is an inflammation of the mucous membrane of the tonsils, uvula,
soft palate and pharynx. It may be acute or chronic, and may affect all or
only portions of the pharynx.
Morbid Anatomy. — The morbid changes in the mucous membrane are the
same as in catarrhal laryngitis and stomatitis. The uvula is enlarged, and
the calibre of the pharynx is lessened. In chronic catarrhal pharyngitis
the mucous membrane is either generally thickened and indurated, or the
thickening occurs in irregular patches. The uvula is relaxed, and the af-
fected parts, are covered with a viscid mucus of a slightly offensive odor.
The lymphatics are enlarged, especially at the back part of the pharynx,
and small round nodules (often aggregated into masses of considerable size)
present the appearance called "follicular pharyngitis." Tlie escape of secre-
tions from the glands being prevented, the latter dilate and form cysts
whose contents undergo cheesy degeneration, or, after forming vesicles, ul-
cerate. The cheesy masses in the cysts may, after a time, become calca-
reous, or undergo purulent change. Follicular pharyngitis may extend
upward and involve the posterior nares, or downward and involve the larynx.
222 DISEASES OF THE DIGESTIVE SYSTEM.
Etiology. — The acute form occurs most frequently in children and in
young adults. There seems to be a predisposition in some persons to this
affection. One attack predisposes to others. The causes which predispose
to quinsy induce acute pharyngitis. Chronic follicular pharyngitis may be
produced by prolonged use of the voice in public speaking or singing, or
by the excessive use of tobacco or of spirituous liquors. Weak, scrofulous
persons, and those with chronic thoracic disease are frequently affected with
it. Its chief cause is repeated acute attacks.
Symptoms. — Slight fever may usher in an attack of acute pharyngitis, or
precede the development of its local symptoms. The throat first becomes
dry and redder than normal, and movement of the parts produces pain in
the direction of the Eustachian tubes, so that swallowing and speaking be-
come painful. The elongated uvula may induce violent fits of coughing.
The local symptoms are very severe ; there will be more or less regurgita-
tion of food through the nose. If particles of food do not readily pass into
the oesophagus they may enter the larynx and cause severe fits of coughing.
In these severe cases there is a nasal twang to the voice, and any movement
of the throat, tongue, or mouth is carefully avoided on account of the pain
it produces. If the inflammation invades the Eustachian tube, deafness
may result, and not infrequently the tympanum is perforated by the pus
which collects in the middle ear. The extension is more often forward, so
that the mucous membrane of the tongue and mouth presents the same
condition as that of the pharynx. These symptoms may gradually subside,
after a few days, and the viscid secretion disappear from the tongue,
mouth and pharynx. If it becomes chronic, the voice becomes hoarse,
and there is a stridulous cough accompanied by a thick, tough mucous
expectoration, often containing small firm, yellow masses. There is
constant irritation of the throat, which is variously described as dry, tick-
ling or tingling, and the secretion may be so much diminished that slight
hemorrhage may occur from the membrane when pressed upon. All these
symptoms are most marked in the morning. The symptoms in a long
standing case may lead to anxiety on account of the supposed existence of
pulmonary phthisis. These are all aggravated by '' catching cold," atmos-
pheric changes, and the prolonged use of the voice.
Differential Diagnosis. — Follicular pharyngitis may be mistaken for pul-
monary disease, and the early stage of mild chronic catarrh often excites
suspicion of syphilis. In the former case an exploration of the chest and
an examination of the throat will at once decide, while the presence or ab-
sence of the constitutional signs of syphilitic infection will establish the
diagnosis in the latter instance.
Prognosis. — Acute catarrhal pharyngitis is a very mild disease, subsiding
completely in most cases within one week from its onset, while chronic phar-
ingitis is the most persistent of all catarrhal affections.
Treatment. — In acute pharyngitis, ice-cold carbonated water affords the
greatest relief during the first twenty four hours. The throat and mouth
should be frequently sprayed with a solution of alum, tannin, or sulphate
of zinc, and at the same time the wet pack should be applied to the throat
MEMBKAjSTOUS PHARTJS'GITIS. — EETRO-PHARYNGEAL ABSCESS. 223
either hot or cold, but they should not be alternated. In chronic pharyn-
gitis, the first thing to be done is to remove the cause and live an out-
door life. Spraying the parts two or three times a day with the astringent
just named, or a mild solution of nitrate of silver, will generally afford
temporary relief. In some cases capsicum or guiacum may be advan-
tageously combined with the astringents, and in obstinate cases the local
use of iodine or a twenty per cent, solution of carbolic acid may be resorted
to. In chronic (follicular) pharyngitis a nutritious diet is especially im-
portant. German physicians recommend very highly the use of mineral
waters, but alkaline gargles are as effective as a residence at some *' spring."
MEMBRANOUS PHARTISTGITIS.
Under this head are included both croupous and diphtheritic inflamma-
tions of the pharynx. Croupous inflammation may be primary, but diph-
theritic inflammation is always secondary. This form of pharyngitis is
considered in the history of membranous laryngitis and diphtheria.
EETEO-PHAETNGEAL ABSCESS.
Suppuration behind the pharynx, in the areolar tissue between it and
the vertebrse, is known as retro-pharyngeal abscess.
Morbid Anatomy. — This is a cellulitis, and its morbid anatomy is the
same as that of cellulitis terminating in an abscess anywhere. It belongs
properly to the province of surgery.
Etiology. — Eetro-pharyngeal abscess occurs more frequently in children
than in adults. It is developed during the progress of caries of the cervical
vertebrge. It is rarely if ever due to the extension of inflammation from
the pharynx. A strumous diathesis predisposes to it. Sometimes it appears
late in pyaemia, septicaemia, typhoid, typhus, scarlet fever and measles.
Now and then it occurs without any obvious cause.
Symptoms. — The first symptom is dysphagia. With this there is stiffness
of the neck, slight difficulty in articulation, and a change in the tone of
voice, which becomes nasal in character. On examining the pharynx its
calibre will be found diminished by a bulging from behind and perhaps a
little to one side ; the pharyngeal mucous membrane is redder than normal,
and there may be a slight swelling about the angle of the jaw. The head
is thrown backward, and any attempt at flexion causes dyspnoea ; the jaws
seem to be partially locked. There is regurgitation of food through the
nose. In young children there may be snuffling, choking, coughing and
great dyspncsa, with a certain hoarse tone to the voice. The mouth is
filled with a mucous secretion.
As the abscess increases in size the tumor may be seen nearly filling
the space behind the soft palate. This swelling is soft, elastic and
fluctuating, sometimes rupturing when pressed upon, and discharging
an offensive pus. If it opens spontaneously the pus is vomited, swal-
lowed, discharged through the nose, or is inspired into the trachea and
may cause suffocation. Again, the abscess filling the pharynx may press
on the rima glottidis and epiglottis and cause oedema glottidis. In rare
224: DISEASES OF THE DIGESTIVE SYSTEM.
instances the pus makes its way around to the opposite wall of the
pharynx, and then breaks into the oesophagus or trachea, or burrows into
the pleural cavity or even the pericardium. It may burrow between the
tracheal muscles and appear at the anterior part of the neck.
Differential Diagnosis. — When fully developed, a careful examination of
the pharynx will detect at once the existence of a retro-pharyngeal abscess.
Prognosis. — The prognosis is bad whenever caries of the spine has caused
the abscess. The complications which may cause death are oedema glot-
tidis, pleurisy, pneumonia, and pericarditis. Death may result from suffo-
cation from pressure.
Treatment. — Open the abscess early, and never wait for its spontaneous
rupture. The position of the child when the bistoury is used should be
such that the escape of pus through the mouth is facilitated.
DISEASES OF THE (ESOPHAGUS.
The following diseases of the oesophagus will be considered :
I. Inflammation, either catarrhal or membranous, including Stricture
of the (Esophagus ; and, II. (Esophageal Cancer.
OESOPHAGITIS.
QEsophagitis, or inflammatory dysphagia, is a catarrhal inflammation of
the mucous membrane of the whole or a part of the oesophagus. It is an
exceedingly rare disease.
Morbid Anatomy. ^ — In the acute variety the mucous membrane is red,
swollen, softened and covered with a layer of mucus containing epithelium
and pus. In the chronic variety the mucous surface is of a dull pink or
slaty blue color. The sub-mucous tissue is thickened, and a thick viscid
mucus or pus covers its surface. It may cause dilatation of the oesopha-
gus, which may affect the whole tube uniformly or form a pouch at its lower
portion, or it may give rise to a hernial protrusion of the mucous mem-
brane through the muscular coat. In all cases of oesophageal dilatation due
to chronic catarrh, there is more or less thickening of the oesophageal walls.
In some cases the thickening may diminish the calibre of the tube. Ulcer-
ation of the mucous membrane at the seat of the catarrh sometimes occurs.
The ulcer may be superficial, or extend through the walls of the tube.
Membranous Inflammation of the oesopliagus may be either croupous or
diphtheritic. In either case the morbid changes are the same as in croup-
ous or diphtheritic inflammation of other mucous surfaces.
Etiology. — Acute oesophagitis has its most common cause in the irritation
produced by acrid fluids or solids in their passage to the stomach. Irritat-
ing drugs and corrosive poisons may excite it. Too frequent introduction
of instruments into the stomach may cause it, and it may arise from the
excessive use of alcohol. Extension of inflammation from the parts above
or below it often induces acute oesophagitis. Chronic oesophageal catarrh
may occur as part of a similar process affecting the whole alimentary tract.
It may develop as the result of a strumous or phthisical diathesis, or follow
CESOPHAGITIS. 235
an acute attack. Membranous oesophagitis is always secondary and results
from, or occurs with similar processes in the respiratory or other portions
of the digestive tract. It also may appear after some of the eruptiye fevers,
cholera, pyaemia and septicsemia.
Symptoms. — Varying with the intensity of the inflammation, an aching
or severe burning pain is felt at the back, between the shoulders, or deep
behind the sternum. Even the ingestion of fluids causes dysphagia, the
pain being greatest as the fluids pass through the upper portion of the
oesophagus. More or less febrile excitement and great depression and anxi-
ety accompany the disease, and throughout its course the thirst is torment-
ing. In severe cases there are paroxysms of coughing, and perhaps slight
dyspnoea with hoarseness. Vomiting sometimes follows attempts at swal-
lowing. All these symptoms gradually increase in severity. If extensive
ulceration is present, sudden rupture of the oesophagus may occur during the
act of deglutition. In chronic oesophagitis there is dysphagia and pain only
on swallowing solids. If ulcers exist, there may be vomiting of viscid mucus
tinged with blood, accompanied by the symptoms of oesophageal stricture.
Stricture of tlie cesophagus is accompanied by gradually increasing
dysphagia, emaciation and debility, which finally terminate in death from
inanition. The most frequent seat of stricture of the oesophagus is at its
cardiac extremity. It may be caused by structural changes in its wall, as
in oesophagitis with or without ulceration, and cancer, or by compression
from mediastinal and other tumors. As oesophageal strictures develop
slowly, for a long time the only symptom
is slight difficulty in swallowing solids, the
patient usually referring the difficulty to a point
behind the manubrium sterni. As the constric-
tion increases there is difficulty in swallowing
liquids. Food and drink collect in the oesopha-
gus, and after a longer or shorter delay are re-
gurgitated with the saliva through the mouth and
nose. With oesophageal stricture there are usually
painful eructations. Sometimes the pain is lan-
cinating in character, shooting from the region of ^'^''^^i showing stricture of the
° ' o o CEsopnaguB near cardiac extrem-
the oesophagus back to the spinal column. The ity-
introduction of a bougie will determine the seat, ± E^:^':ZZl%''o/sf^T.^-
extent, and form of the stricture. ' _ ^; ^7^^ ,^^ ^,^^.^^^^^_
Uniform dilatation cannot be recognized dur-
ing life. When dilatation is partial, or when pouches exist, there may be
vomiting of undigested offensive food some hours after eating. In all cases
of alteration in the calibre of the oesophagus, the oesophageal bougie will
determine the amount of narrowing and the locality of the pouches.
Membranous inflammations of the oesophagus cannot readily be determined
during life. A portion of membrane may be vomited, but it cannot be
determined whether it comes from the oesophagus, or has been swallowed
and regurgitated.
> The treatment of stricture of the CESophagus belongs to surgery.
15
326 DISEASES OF THE DIGESTIVE SYSTEM.
Differential Diagnosis. — This disease may be mistaken for cancer of the
oesophagus ; the diagnostic points will be considered in the history of
oesophageal cancer. At the onset it may also be mistaken for hydropholia,
but the diagnosis is soon established by the development of the character-
istic nervous phenomena of the latter disease.
Prognosis. — The immediate prognosis in acute oesophagitis caused by
chemicals or mechanical irritants depends more on the changes which have
occurred around the larynx and in the stomach, than upon, the oesophagitis.
The prognosis in croupous and dijjhtheritic inflammations of the oesophagus
is also determined by the conditions of the primary disease. In chronic
oesophageal catarrh without stricture the prognosis is good.
Treatment. — In acute oesophagitis, if the inflammation has been excited
by foreign bodies lodged in the oesophagus, they must at once be removed ;
if corrosive chemicals have been swallowed, the proper antidote must be ad-
ministered. In severe cases, all movement of the parts must be prevented.
Ice in the mouth is grateful and does no harm. Nutrient enemata may be
given, and, if the pain is severe, hypodermics of morphine must be given
in sufficient quantities to afford relief. Hot anodyne fomentations applied
locally are usually of service. In chronic oesophageal catarrh, if ulcers ex-
ist, spray the parts with astringent fluids, such as a solution of nitrate of
silver. Surgery directs that if starvation seems imminent a gastric fistula
should be made. In oesophageal stricture, bougies must be daily intro-
duced for a long time, with the hope of dilating the stricture. No treat-
ment is required in oesophageal dilatation.
CANCER OF THE (ESOPHAGUS.
The most frequent variety of oesophageal cancer is epithelioma, but
scirrhus and medullary cancer are not unknown. It occupies the upper and
middle third of the oesophagus more often than the cardiac portion ; in the
former, it is associated with pharyngeal and laryngeal cancer, and in the
latter with cancer of the cardiac extremity of the stomach.
Morbid Anatomy. — Epithelioma begins in the mucous tissue, and pursues
ihe same course as cancer of the tongue. The ulceration may be limited
io a circular patch an inch in diameter, or may involve the whole circum-
ference of the oesophagus. The growth after a time invades all the tissues
of the oesophagus, and causes stricture of its calibre. Above the stricture
there is either uniform dilatation or a pouch, sometimes as large as an
orange. If the cancerous mass involves the entire oesophageal wall, it may
press upon and destroy one or both pneumogastrics, and lead to the devel-
opment of pneumonia or pulmonary gangrene. If the oesophagus is rupt-
ured, openings may be made into the trachea, through the diaphragm into
Ihe peritoneal cavity, or into the posterior mediastinum. Cancer has some-
times ulcerated into the aorta, pulmonary artery, and even into the right
subclavian artery.
Etiology. — Two-thirds of the cases of cancer of the oesophagus occur in
males between the ages of forty and sixty. It is generally primary ; it
CANCER OF THE CESOPHAGUS. 227
may be secondary to cancer of the mouth, pharynx, mediastinum, or
stomach.
Symptoms. — The first thing noticed in cancer of the oesophagus is difficult
deglutition ; soon well-marked dysphagia occurs. Pain is present early,
and may be dull, burning, or lancinating in character ; it is located about
the centre of the sternum, in the throat, or in the interscapular space. It
varies greatly in kind and degree, but it is greatly aggravated when food
reaches that portion of the oesophagus which is the seat of the cancer. As
the stricture grows narrower, flatulence, regurgitation of food and vomiting,
with steadily increasing emaciation, become prominent symptoms, and a
well-marked cachexia is developed. Cough, dyspnoea, and hoarseness some-
times result from pressure of the cancerous tumor. As the disease advances,
the pain becomes more constant, the cachexia is better marked, and hem-
orrhages are frequent ; the bloody fluid vomited often contains shreddy
masses which contain cancer elements and show the character of the dis-
ease. The neighboring lymphatic glands may also be implicated, and, by
pressure on a main bronchus, cause feeble respiration in the lung to which
the bronchus is distributed. If rupture occurs, it is followed by a sudden
sharp pain in the chest, fainting, and coldness of the extremities, followed
almost immediately by death.
Differential Diagnosis. — (Esophageal cancer may be mistaken for stricture
of the cesophagus from chronic catarrhal inflammation. In cancer, pain is
constant and greatly aggravated by taking food, while in non-cancerous
oesophageal stricture pain is absent, or is only present on swallowing. The
glands about the neck are early involved in cancer, but are normal with
chronic catarrh. Chronic pulmonary disease is rarely absent when oeso-
phageal cancer is present, but is never induced by non-malignant stricture.
Hemorrhage is frequent in cancer, and does not often occur with stricture
from chronic catarrh. The bougie may bring up shreddy masses, with evi-
dences of cancer in the one case, but merely meets with obstruction in the
other.
Prognosis. — This is always a fatal disease. Its average duration is one
year, but death may occur in a few weeks. The prognosis as to time varies
with the presence or absence of complications. Death may result from any
of the complications, from hemorrhage or septicsemia.
Treatment. — Early in cancer let the food be finely chopped and taken in a
semi-fluid state ; later, it should be entirely fluid, and when the patient
cannot swallow, nutrient enemata must be given. The diet in all cases
must be nourishing in the highest possible degree, and stimulants can usu-
ally be given with benefit. When the pain is intense morphia per rectum
or hypodermically should be administered in doses sufficient to relieve it.
Bougies should be used with great care ; early, they should only be used to
locate and diagnosticate the disease ; later, tubes must only be used for the
purpose of introducing food into the stomach, as fatal hemorrhage or rupt-
ure has followed their use. The subject of gastrotomy comes within the
domain of surgery.
i2ii DISEASES OF THE DIGESTIVE SYSTEM.
DISEASES OF THE STOMACH.
I. Inflammations of its mucous membrane and its submucous or areolae
tissue.
a. Acute or Toxic Gastritis.
b. Sub-acute Gastritis, or Acute Gastric Catarrh.
c. Chronic Gastritis, or Chronic Gastric Catarrh.
d. Phlegmonous Gastritis.
II. Dyspepsia. IV. Neuroses or Gastralgia.
III. Cancer and Ulcer. V. Hcematemesis.
VI. Dilatation.
ACUTE GASTEITIS.
Acute or toxic gastritis is a general inflammation of the mucous and sub-
mucous tissue of the stomach. It is of rare occurrence, unless the result of
the introduction into the stomach of irritating poisons.
Morbid Anatomy. — On opening a stomach which is the seat of toxic gas-
tritis a thick layer of tough, viscid mucus will be found spread over its
mucous surface. Beneath this there will be found an intense redness of the
membrane, which is most marked along the edge of the rugse, near the car-
diac orifice. The mucous and submucous tissues will be soft and oedema-
tous. In some rare instances the whole or a portion of the mucous mem-
brane will be found to present the appearance of a detached brown or black
slough ; it may be entirely eroded. Fibro-plastic exudation may cause com-
plete occlusion of its cardiac or pyloric orifices. When the muscular tissue
is involved it becomes soft, easily torn, often gelatinous. In severe cases
perforations may exist.
Etiology. — Acute gastritis is almost always caused by the entrance into
the stomach of irritant poisons, such as sulphuric, nitric, and oxalic
acids, arsenic, the chloride of zinc, and large quantities of concentrated
alcohol. Mechanical irritation, such as results from the introduction into
the stomach of knives, pins, false teeth, etc., may produce a local acute gas-
tritis. Introduction into the stomach of boiling water, hot lead, or steam
may cause a most intense gastric inflammation, with extensive sloughing of
its mucous surface.
Symptoms. — Soon after the introduction of corrosive substances into the
stomach, there will be a dull, uneasy feeling, sometimes one of warmth,
over the epigastrium. This is rapidly followed by an intense burning pain
shooting through to the back. The epigastric region becomes extremely ten-
der. With, or preceding these symptoms, there is nausea, and vomiting of
tenacious macus ; the vomiting is very distressing ; the ejected mucus often
contains blood, and, at first, portions or traces of the substance which has
caused the gastritis. As the pain becomes more severe the vomiting is more
distressing ; there is intense thirst, and frequent spasms of the abdominal
muscles. The temperature rapidly rises, sometimes to 105° F.; the pulse
SUB-ACUTE GASTRITIS. 229
reaches 120 or 140 per minute and is feeble and irregular. If the oesophagus
is implicated, there is dysphagia. The urine becomes scanty and high
colored, and is sometimes suppressed. These violent symptoms soon give
place to a condition of general prostration, in which there is almost con-
stant hiccough. The surface becomes cold and clammy, the radial pulse
grows feeble and finally imperceptible, while the respirations are hurried,
short and irregular, the mind remaining clear to the last. There are cases
on record of poisoning by chloride of zinc and sulphuric acid, in which
there was no pain in the epigastrium during the whole course of the disease.
Differential Diagnosis.— The diagnosis is not difficult. The history of
its cause and the character of the vomiting establish it.
Prognosis. — The prognosis depends upon the cause. The more intense
the pain, the more extensive the gastric inflammation. Death may occur
in a few hours, or it may be delayed two or three weeks. Acute gastritis
may be complicated by analogous conditions of the mouth, pharynx, or
oesophagus, by enteritis, laryngitis, or oedema glottidis, and as sequelae there
may remain constrictions at the cardiac or pyloric orifices. Death may
result directly from the shock of the gastritis, from the constitutional effects
of the poison which produces it, or from resulting peritonitis.
Treatment. — The fia^st thing is to administer the proper antidote to the
poison which has caused the gastritis, and thoroughly wash out the stom-
ach, after which the gastritis should be treated as a local inflammation. Four
or five leeches may be applied over the epigastrium, followed by warm poul-
tices or fomentations. Some prefer the application of ice to the epigas-
trium. Unless contra-indicated by the chemical constitution of the poison,
the intense pain should be relieved by hypodermic injections of morphia.
During the whole period the patient should be kept absolutely at rest in
the horizontal position.
SUB- ACUTE GASTRITIS.
Suh-acute gastritis, or acute gastric catarrh, is always a secondary affec-
tion.
Morbid Anatomy. — The parts principally involved in this form of gas-
tritis are the ridges between the depressions, the vessels which lie in imme-
diate proximity to them, and the apertures of the tubules. The mucous
membrane is mottled by red spots scattered over it in irregular patches ;
sometimes there are extensive ecchymoses and blood extravasations. The
gastric Juice is much diminished in quantity, and being mixed with much
mucus loses its acidity and to a great extent its digestive power. The sur-
face of the mucous membrane is covered with an abundant, tenacious mu-
cus ; there is also a moderate production of pus cells on the surface of the
mucous membrane. The gastric tubules become filled with granular mat-
ter. Late in the disease the solitary and lenticular glands, especially
about the pylorus, increase in size and stud the surface as small white
specks. The inflammatory processes are superficial and do not involve
the deeper tissue of the mucous membrane. Superficial sloughs are some-
330
DISEASES OF THE DIGESTIVE SYSTEM.
times formed varying in size from a pea to that of a three-cent piece ; they
rarely involve the submucous tissue.
Fig. 51.
A Vertical Section of the Stomacii walls in Sub-acute
Gastritis.
A. Mvscular fibres in longitudinal section.
B. The same cut tranfwehely .
C. Submucous tissue, in which are seen at
J), D. Blood-vessels enlarged and filled with blood.
E. Mucous coat. The gastric follicles are shown Jillei
with granular detritus and covered with pus— G.
F. Small vessels betioeen the follicles, x 40.
Its most prominent lesion is the
coating of the gastric mucous
surface with tenacious mucus.
Etiology. — No period of life is
exempt from this form of gastri-
tis. It occurs most frequently
under two conditions : — first, with
acute alcoholismus ; secondly,
with those diseases in which there
is extensive blood-poisoning, as in
scarlet fever, small-pox, measles,
typhoid and typhus fevers, diph-
theria, pneumonia, pysemia and
septicgemia. It sometimes com-
plicates pulmonary phthisis, and
may follow the disappearance of
gout, rheumatism, or affections
of the Joints.
Symptoms. — Vomiting is its
first and most prominent symp-
tom. The matter vomited con-
sists of the substances which have
been taken into the stomach,
mingled with a grayish, stringy mucus, and sometimes streaks of blood.
"When the vomiting is severe and prolonged, bright green, bitter fluid
is often ejected. The fermentation which takes place in the fluid con-
tained in the stomach sometimes develops gases which cause distention
of the stomach and a prominence of the epigastrium. The patient has no
desire for food, but constantly craves ice and cooling drinks. The thirst is
intense. The smallest quantity of food taken into the stomach causes nausea
and vomiting, which may be so severe as to induce extreme exhaustion or
collapse. Accompanying the nausea and vomiting there is more or less
pain at the epigastrium. This pain is sometimes intense, and shoots back-
ward between the shoulders, but usually it is not severe unless firm pressure
is made over the stomach. The tongue is coated with a yellow or ash-col-
ored material, and becomes dry and red at the tip. The papillae are prom-
inent. The breath has an offensive odor. Late in the disease, herpetic
eruptions make their appearance about the lips and in the mouth. Often
during its course there will be flashes of heat, with a burning sensation in
the palms of the hands and the soles of the feet. The thermometer may
indicate an axillary temperature of 103°, or even 105° P. The patient be-
comes restless and irritable and often has attacks of syncope. In alcoholic
cases the anorexia is absolute, and vomiting occurs mostly in the morning.
Delirium tremens is often a complication. Its symptohas are always more
or less varied by the diseases with which it occurs. In rare instances I have
seen an icteric and sometimes a bronzed hue of the skin come on during a
CHRONIC GASTRITIS. 231
prolonged attack of acute gastric catarrh. Diarrhoea is usually present, the
stools having a very offensive odor. Obstinate constipation is rare. The
urine is scanty and high colored, and in severe cases presents slight traces
of albumen. Nitric acid gives a deep red color to it, or there is a copious
deposit of lithates.
Differential Diagnosis. — The diagnosis is easily made, and it is not likely
to be confounded with any other affection, if its etiology and symptoms are
carefully analyzed.
Prognosis. — The prognosis is decided by the disease which it complicates.
Unless associated with acute alcoholismus, it rarely becomes chronic. Its
duration is from ten days to two or three weeks. It may be complicated by
catarrhal conditions of the oral and pharyngeal mucous membranes, and in
very rare instances by implication of the intestines (gastro-enteritis). It only
causes death when it is extensive and complicates some grave acute general
disease, as septicsemia, pyaemia, typhoid or puerperal fever.
Treatment. — The most important thing in the treatment of this affection
is rest to the stomach. In mild cases, entire abstinence from food for twenty-
four hours, and then milk with lime-water in small quantities at stated in-
tervals, is all that is required. In severe cases, and in all cases occurring
in children, nourishment must be given jiger rectum as long as the gastric
symptoms are urgent. One or two leeches applied over the epigastrium,
followed by warm fomentations, usually afford marked relief. In adults,
if the pain is so severe as to prevent sleep, or if there is great restlessness,
small hypodermics of morphia may be administered. After the patient has
passed twenty-four hours without vomiting, milk and lime-water may be
given in small quantities. In those cases in which vomiting is persistent,
and there are symptoms of collapse, stimulants must be freely administered
by the rectum. None of the remedies which are so often employed for the
relief of vomiting are serviceable in the treatment of this affection. Dur-
ing convalescence, if the stomach is in an atonic condition, mineral acids
and the vegetable bitters will be found of service ; great care must be exer-
cised in the diet during the whole period of convalescence. The improve-
ment of the diet must be gradual, and those who have been spirit drinkers
should be warned of their danger, and the use of stimulants prohibited.
CHRONIC GASTRITIS.
Chronic gastritis is known under the names of simple gastritis, chronic
catarrh of the stomach, morbid sensihility of the stomach, and chronic in-
flammatory dyspepsia.
Morbid Anatomy. — The morbid appearances in chronic gastritis vary
with its character and duration, and are usually best marked around the py-
loric extremity of the stomach. Over all, or part of the mucous surface,
there is a layer of gray mucus, varying in thickness and tenacity with the
duration and character of the disease. On its removal the mucous mem.-
brane is seen studded with ecchymotic and pigmented spots, the result of
small extravasations. In some cases the mucous tissue is oedematous and
233 DISEASES OP THE DIGESTIVE SYSTEM.
presents a well-marked granular appearance. The walls of the stomach are
usually thickened and more or less indurated, especially about the pyloric
orifice, which gives rise to more or less constriction, or ^'pyloric stenosis.'^
The thickened membrane is often "leathery" to the feel, and the indura-
tion may be so great that it tears with difficulty and can be stripped
off the submucous tissue. The submucous tissue may also be thickened
and congested, the color varying from an inflammatory blush to a livid, al-
most purple red. When the submucous tissue is involved, there is an infil-
tration of cells into it ; and upon their organization into new connective-
tissue, and the subsequent contraction of this tissue, there will be more or
less interference with the peristaltic motion of the stomach. Besides this
there will be hypertrophy and distention of the gastric tubules, for their
secretion is retained by the tissue-increase in the intertubular structure,
which will cause them to stand out as small granulations in the atrophied
tissue, presenting an appearance denominated " mammilla t ion." This condi-
tion may also be the result of hypertrophy of the glandular layer, which thus
becoming too large for the basement muscular layer is corrugated and gives
rise to another form of mammillation. It is only in rare instances that
there is any mammillation about the cardia.
In long-continued chronic catarrh of the stomach the muscular coat of
the organ may become involved, and then the peristaltic movements
will be still more impaired ; finally, the peritoneum may become thickened
and adhesions take place between it and the adjacent parts.
A microscopic examination of tlie gastric tubules in chronic gastritis will
sometimes show that their epithelium has undergone granular degeneration,
and in others there is a complete loss of epithelium, the tubules being filled
with a granular detritus. Occasionally there will be found on the
mucous membrane dirty white spots in
irregular patches, which appear like de-
pressions on the mucous surface. Under
the microscope, there will be found in
those spots some tubules completely filled
with discrete fat spherules, and others
whose epithelium has undergone fatty de-
generation. If the tubules are constricted
near their openings, cysts are formed from
distention of the portion near the base by
A Vertical Section of Mucous Membrane Of , , , . i • ^ , t
the Stomach, showing changes in the Tu- the SCCrctlOn WhlCh CanUOt CSCapC. in
buiesin Chronic Gastritis. ^^^^ ^^^^^ ^j^^ ^^^. degeneration will in-
A. Mn ocularis mucogce. , , ., i-.-ii- n tj»
B. Small blood-vessels armmd the. follicles. VOlve the interstitial tlSSUe aS Well. il
C. Tiibide with qrannlar epithelimn and filled ■, ^ • l j.- • j. j-1,„
with ammdar detritm. hemorrhagic extravasation occurs into the
^•i':f^?/;;;*;;f^A%r^/»t/.f'''''^'^''''"^' gastric mucous membrane, the tubules
f: fS^'c^t&SZS^t^nun.th Will have their epithelium stained and
t^Xat'f^zC^'-^'''''^'"'''''^^''''^'' ■t^eir base blackened as a result of the
sanguineous infiltration. Sometimes there
is an increase in the intertubular lymphatic elements, with hyperplasia of
the nuclei in the sheath of the vessels.
CHEOKIC GASTETTI8. 333
In long-standing chronic gastritis there may be abrasions of the mu-
cous surface and formation of ulcers (chiefly about the lesser curvature
and the pylorus), circular in shape, varying in diameter from half an inch
to an inch. These ulcers are very superficial, rarely extending beyond the
mucous coat. They are pale in color, and their surface is covered with
mucous cells, nuclei, and epithelium ; between the ulcers the rugae are con-
gested. The intervening tissue is rarely normal. There may also be small
follicular or punctate ulcerations, originating, it is supposed, in the enlarged
solitary and lenticular glands. The base of these ulcers is infiltrated with
lymph-cells and granular detritus ; they are never present except in the ad-
vanced stage of chronic gastric catarrh. Chronic gastric catarrh may
involve a large portion of the mucous surface of the stomach, and is gen-
erally associated with a like condition of the intestinal mucous membrane.
Waxy degeneration may be associated with these morbid changes, but in
such cases other organs, as the liver and spleen, will have been primarily
affected by the amyloid infiltration. The size of the stomach varies : some-
times it is smaller than normal ; at others it is dilated.
Etiology. — Chronic gastric catarrh is essentially a secondary affection ; it
is rarely the sequela of sub-acute, much less of acute, gastritis, unless the
former has been caused by an abuse of alcoholic stimulants. In many persons
there is an hereditary tendency, after middle life, to chronic gastric catarrh.
The principal general cause of this affection is ancBinia. The most common
local cause is the daily use of alcoholic stimulants.
Mechanical obstruction to the capillary circulation of the stomach, induc-
ing continued passive hyperemia (congestion) will cause it, and hence we find
it associated with cirrhosis of the liver and other chronic hepatic affections
where the blood is dammed back in the formative branches of the vena
portEe. In the same way, valvular and other cardiac lesions, and pulmon-
ary diseases, such as emphysema, chronic bronchitis, and phthisis, which
offer an obstacle to the venous return, will induce chronic gastric catarrh.
Pressure on the walls of the stomach by tumors produces first congestion,
and then chronic catarrh. Degeneration of the capillaries — '' arterio-
capillary filrosis" — occurring in the cirrhotic form of Bright's disease,
causes it, and it often accompanies ulcer and cancer of the stomach.
Those causes which may be denominated recent are rapid ingestion of
food, improper quality of food, or food which is known *Ho disagree with
the stomach," and the sudden arrest of the digestive process after hearty
meals. The prolonged use of arsenic, mercury, cubebs, and purgatives
often causes it. Finally, scrofula, syphilis, and gout seem to predispose
to it, and I am inclined to regard the chronic gastritis which is so often
found associated with these diseases as the result of some degeneration of,
or alteration in, the hlood-vesseh of the stomach.
Symptoms. — The early symptoms of chronic gastric catarrh are chiefly
those of indigestion. There is at first a sense of weight and fulness in the
epigastrium, sometimes amounting to constriction, which comes on from
half an hour to an hour after meals. Later there is actual pain and
heat in the epigastrium (*' heart-burn "). Pressure increases the pain and
234 DISEASES OF THE DIGESTIVE SYSTEM.
causes it to shoot backward and upward toward the scapulae. Following,
or with the advent of, these symptoms there is loss of appetite, first for
solids such as meats ; later there is complete anorexia. Nausea and eruc-
tations accompany the anorexia ; the stomach, and often the intestines
become distended with gas, but vomiting is not usually present unless
pyloric stenosis exists. The most important of the dyspeptic symptoms are
the acid risings after meals, and the vomiting or regurgitation of acid
mucus in the morning, which may be regarded as characteristic, and with-
out which the diagnosis is uncertain. It is this acid material belched up intO'
the oesophagus that causes " heart-burn." If there is actual vomiting of
food, traces of butyric acid are present, with the sarcinm ventricuU, cuboid
cells averaging 1-2500 inch in diameter, each being divided into-
four equal parts containing nuclei, usually heaped into large
cubes.
As the disease progresses, the feeling of malaise and un-
easiness following meals changes to one of languor or ex-
Fig. 53. haustion, and there is a sensation of heat in the epigastrium r
mii. X 750. thirst becomes a promment symptom, one person craving
cold, another hot drinks. The thirst is greatest in the evening, but
the taking of fluids is usually followed by a sense of weight in the
epigastrium, and by acidity and flatulence. The appearance of the tongue
varies : it may be normal, paler than normal, florid and "beefy," or may
be covered with a white or brown coating. The general symptoms which
accompany the ansemic condition which attends this diwsease are headache,
vertigo, cardiac palpitation, a gradual loss of strength and emaciation.
Constipation and hemorrhoids are usually present, and the stools are often
coated with mucus. In the chronic gastric catarrh of phthisis, diarrhoea is
present. In cases of long standing, the hair becomes harsh and loses its
lustre or turns gray ; the skin is dry, sallow, and shrivelled, sometimes
covered with an eczematous eruption ; the nails are corrugated and exhibit
a tendency to split, while in some there is premature caries of the teeth.
Hypochondriasis, despondency, and irritability of temper are generally
more or less marked. Hseraatemesis often occurs in that form of gastritis
which accompanies cirrhosis of the liver, and the bleeding may for a time
relieve the unpleasant gastric symptoms. Vomiting in the morning al-
ways accompanies the gastritis of Bright's disease.
The urine in chronic gastritis is cloudy, usually alkaline in reaction,
depositing urates, phosphates and oxalates. Its specific gravity is highest
at evening. The alkalinity is due either to imperfect gastric digestion or im-
paired function of the liver and pancreas. The greater the mental depres-
siion the more of earthy phosphates will be found in the urine.
If hemorrhagic erosion exist in a stomach which is the seat of chronic
catarrh, the pain in the epigastric region is constant, frequently shoot-
ing back to the scapulae. Vomiting occurs not only in the morning, on
rising and after meals, but also in the intervals. The vomited matter con-
tains traces of blood, and bile mixed with mucus ; all of the gastric symp-
toms are augmented in hemorrhagic erosion. Punctate ov follicular vlcer-
CHKONIC GASTRITIS. 335
ation presents few, if any, symptoms differing from those of ordinary chronic
catarrh. In most instances where a post-mortem has revealed this patho-
logical state, there was vomiting of coffee-ground material during life.
Differential Diagnosis. — Chronic catarrh of the stomach is to be differ-
entiated from atonic dyspepsia, from cancer, and ulcer of the stomach.
Atonic dyspepsia is associated with anaemic conditions dependent uj)on
habits of life and an unhealthy occupation ; while chronic catarrh is
associated with the immoderate use of alcoholic stimulants, or is secondary
to chronic thoracic, renal or hepatic disease. In atonic dyspepsia there is
little or no pain or tenderness in the epigastric region, which is always
present in chronic gastritis. In atonic dyspepsia the tongue does not
present the coated appearance so constant in chronic gastritis, but is
broad, pale, and flabby. In atonic dyspepsia there is loss of appetite, but
never the complete anorexia and constant thirst which are present in
chronic gastritis. Spices and stimulating ingesta often relieve the gastric
symptoms of atonic dyspepsia, while in chronic gastritis they aggravate the
gastric symptoms. The constitutional symptoms in atonic dyspepsia are
slight, while in chronic gastritis they are marked and severe. The urine is
unaltered in atonic dyspepsia, while it is cloudy and alkaline, and deposits
urates, oxalates and phosphates in chronic gastritis. Nausea and vomiting
are more apt to occur in chronic gastritis than in dyspepsia, and eructations
are never present in simple dyspepsia.
The points in the differential diagnosis between chronic gastritis and
ulcer of the stomach are given under the latter heading.
Prognosis. — The duration of chronic gastric catarrh is variable; it may
last for months or years and may terminate in ulcer or stenosis of the
pyloric orifice. It is amenable to treatment except when associated with
advanced hepatic, renal, or pulmonary diseases, or where stricture at the
pyloric orifice exists. A not infrequent complication is disease of the supra-
renal capsules, and the connection between the two diseases has by some
been supposed to be a "sympathetic" one, but no rational explanation has
yet been offered. Sub-acute gastric catarrh sometimes complicates chronic
gastric catarrh and renders the prognosis unfavorable. G-astro-enteritis is
a very rare complication. Death may result from heematemesis or from
stricture of the pylorus. The general feebleness which results from long
standing gastritis predisposes to acute disease.
Treatment. — The most important thing to be accomplished in the treat-
ment of chronic gastritis is the removal of its cause. Each case requires a
special treatment suited to its special indications and to its complicating
causes. When alcohol is the cause, all stimulants must at once be pro-
hibited, and the patient placed on a diet in which there are few fats or
carbo-hydrates. The food should be taken slowly in small qiiantities, at
shorter intervals than in health, and thoroughly masticated. I have found
" underdone beef " and milk to be especially adapted to this class of cases.
In catarrh induced by dram-drinking the best drug to allay morbid
sensibility of the stomach and the morning sickness is opium, which also, by
inducing sleep, relieves the nervous symptoms, which are always prominent
236 DISEASES OF THE DIGESTIVE SYSTEM.
in this variety. Strychnia and zinc in combination with mineral acids have
a wide reputation in this class of cases, acting favorably on both the nervous
and digestive disturbances. The vegetable bitters as tonics are often
serviceable when the craving for alcoliol is excessive.'
When there is marked anaemia, j)reparations of iron and pepsin may be
given. When chronic catarrh is associated with cardiac disease, granules
of digitaline, 1-50 of a grain each, may be given twice a day with advan-
tage. When associated with pulmonary diseases, an out-of-door life in a
suitable climate not infrequently effects a cure. In phthisical gastritis, a
form that is very obstinate, hydrocyanic acid with the alkaline carbonates
combined with bismuth is often of service. If hepatic disease exists tho
portal congestion may be relieved by ^leeches about the anus, and an
occa^onal brisk mercurial purge ; a course of mineral waters will in a
large proportion of cases give temporary relief. The daily use of cold water
enemata will in these cases preclude the necessity of resorting to cathartics.
Scrofulous subjects should be treated with iodine and cod-liver oil. The
Vichy waters in combination with colchicum are indicated in gouty
patients. Free purgation and warm alkaline baths are also serviceable in this
class of cases. There is, perhaps, no remedy which will for a time relieve
the irritability, pain, and acidity after meals as certainly as bismuth.
When it fails in cases of long standing, zinc, alum, tannin, or nitrate of
silver may be tried. The habitual constipation which often complicates
these cases will be relieved by daily use of aloes and strychnia, or rhubarb
and soda. When there is evident deficiency of gastric juice, five or six
drops of hydrochloric acid in a wine-glass of water and ten or fifteen grains
of saccharated pepsin will greatly assist the digestive process. If there is
an excess of gastric juice, alkaline waters should be freely used during, and
after meals. When fermentation is very active and flatulence is annoying,
sulphite of soda or creosote given after meals is serviceable. If the stomach
rejects food as soon as it is taken, rest is essential, and the patient must be
nourished for a time by the rectum and then placed on a milk diet. Mi-
nute doses of arsenic and of belladonna have been recommended as curative
agents, but there is no evidence that they have any such power. Blisters,
moxae and issues over the stomach are sometimes of service in very chronic
cases.
PHLEGMOXOIJS GASTEITIS.
Phlegmonous gastritis is a suppurative inflammation of the areolar (sub-
mucous) tissue of the stomach ; it has also been called " suppurative
Unit is.'''
Morbid Anatomy. — The suppurative process may be circumscribed oi
diffused. On removal of the stomach its wall is found thicker than normal,
J I have found the following to allay this craving :
3 Tr. cinchonae comp 5 iv.
Tr. capsici 3 ss.
Tr. nuc. vomicae 3 ij.
M. A teaspoonful every two or three hours.
PHLEGMONOUS GASTKITIS. 237
and its substance oedematous and very friable. Tiie submucous tissue is
distended by, and infiltrated with fibrin and pus, which not infrequently
accumulate in large quantities in the muscular tissue as well. The entire
mucous coat is, in rare instances, very much thinned and undermined by
the purulent accumulation which perforates it at different points ; the
small openings thus formed give exit to the pus from the spongy, irregular
shaped cavities, or "abscesses,'' lying beneath. The mucous surface is
reddened in patches, or is of a deep purple color ; sometimes it is gangren-
ous. If the peritoneal coat is involved it presents the usual appearance of
acute peritonitis. The abscesses in the sab-mucous tissue tend to open
into the cavity of the stomach, although they may perforate externally and
be discharged into the peritoneal cavity. In circumscribed phlegmonous
gastritis these pus cavities may be the starting-point of ulcers of the
stomach.
Etiology. — Phlegmonous gastritis is a very rare disease, usually occurring
between the ages of twenty and forty years. It may occur idiopathically in
previously healthy persons, without any assignable cause, or it may be
secondary to pysemia, septicaemia, puerperal fever, typhus fever, and
diphtheria.
Symptoms. — Phlegmonous gastritis is ushered in by a distinct chill, fol-
lowed or accompanied by intense pain and tenderness over the region of
the stomach. Complete anorexia is an early symptom, and is accompanied
by intense and constant thirst ; there is persistent vomiting, which increases
in severity with the advance of the disease ; the ejected matters are some-
times purulent, but usually consist of a dark colored, bitter fluid. The
pain increases in severity until it becomes as severe as in peritonitis. The
temperature may reach 104° or 106° ¥. When the disease has reached
its climax there is great depression and exhaustion ; the patient is anxious
and fretful, not infrequently passing into active delirium, but, whether
the latter is present or not, typhoid symptoms with low muttering delirium,
jaundice, stupor, and collapse are rapidly developed, and the patient passes
into a state of coma and dies.
Differential Diagnosis. — The diagnosis of phlegmonous gastritis is only
made by exclusion ; it often passes unrecognized during life.
Prognosis. — The prognosis is always unfavorable. The majority die dur-
ing the first week. When it is circumscribed its duration may be pro-
longed to two or three weeks. Its only complications are secondary
abscesses in other organs (as the liver) and peritonitis. When primary,
the disease reaches a fatal termination either from peritonitis or from
exhaustion with typhoid symptoms.
Treatment. — When phlegmonous gastritis is secondary the primary dis-
ease will demand attention; in all cases the treatment is merely palliative ;
stimulants are indicated very early, and the sufferings of the patient must
be relieved by morphia hypodermically.
238 DISEASES OF THE DIGESTIVE SYSTEM.
aASTEIC DYSPEPSIA.
Dyspepsia and indigestion are terms used to indicate a train of symp-
toms caused by a functional derangement of the digestive processes. When
these derangements are confined to the stomach they constitute gastric
dyspepsia.
Morbid Anatomy. — Strictly speaking, gastric dyspepsia has no morbid
anatomy. If it has continued for a long time the walls of the stomach
may be found thinned, the mucous membrane atrophied, and many of the
gastric tubules shrunken and in a state of fatty degeneration. Not infre-
quently the tubular structure of the stomach is replaced by a fibro-nucle-
ated tissue. After death the power of self-digestion in such a stomach is
markedly diminished or entirely lost. It is often met with as a part of
senile decay.
Etiology. — Dyspepsia- is often an inherited condition and accompanies
the changes of advancing age. There is no affection in which individual
idiosyncrasies are so strongly marked. Its etiology can best be considered
under the following heads : —
First : — A class of cases in which there is a deficiency in the quantity of
gastric Juice secreted. Such deficiency often occurs in those disordered
states of the blood which precede the onset of acute diseases. It occurs in
enfeebled conditions, as the result of exhausting discharges, venereal
excesses, masturbation, leucorrhcea and phthisis, and from the excessive
use of narcotics, the tannin of tea, and the nicotine of tobacco.
Second : — There is a class of cases in which there is an excess in the gas-
tric secretion. This is most apt to occur in those suffering with chronic
hepatic and cerebral diseases and in gouty subjects. It is sometimes
changed in quality and in quantity in young persons who have grown
rapidly, and in females at the menopause.
Third: — There is a class of cases in which the gastric secretion is
changed in quality. This occurs with ulcer and cancer of the stomach,
gout, rheumatism, disease of the kidneys, uterus, and gall bladder. A
lithic-acid diathesis is said to cause a change in the quality of the gas-
tric juice.
Fowtli : — There is a form of gastric dyspepsia due to impaired motion
of the stomach, which may be the result of its adhesion to neighbor-
ing parts, to an omental hernia dragging it out of its normal position,
to cicatrices and new growths at its pyloric extremity, to thickening of its
walls, or to a weak, flabby, enfeebled condition of its muscular coat,
and to pressure on the stomach from tight lacing and from positions
assumed by shoemakers, needlewomen, writers, etc.
Fifth .'—Mental emotion, prolonged mental labor, and anxiety rather
than continuous and regular brain work, cause dyspepsia ; in such cases it
is the sudden arrest of the digestive functions, especially after eating too
much, which is the main etiological factor. Organic cerebral disease and
GASTRIC DYSPEPSIA. 239
pressure on, or disease of one or both pneumogastrics act in the same
way.
Sixth : — Deficient or excessive physical labor may be a cause of dyspepsia.
"Walking immediately after a full meal is a prolific cause of this variety, ex-
amples of which are frequently met with in letter-carriers.
Seventh: — Improper diet is a common cause of dyspepsia. It may arise from
an excess of starchy materials, as potatoes ; or from deficiency of meats. Un-
der improper diet may be included decomposing food, impure water, badly
cooked food, too rapid eating, the food not being sufficiently masticated, or
taken at too short intervals and irregularly. Articles of food that may be
suited to one climate, season, or age may in another be wholly indigestible
and cause dyspepsia.
Symptoms. — The symptoms of dyspepsia are a series of phenomena which
vary not only in different individuals, but in the same individual at differ-
ent times ; the most constant is an abnormal appetite : it may be lost, in-
creased, or perverted. There is a weight, dull pain, and a sense of burning
in the epigastrium after ingestion of food, accompanied by flatulence, heart-
burn, gastralgia, constipation or diarrhoea, a dull headache, languor, de-
pression of spirits and irritability of temper. Indiscretion in eating or drink-
ing, and exercise or exposure in dyspeptic subjects are apt to bring on an at-
tack of sick headache. There is frequently a bitter taste in the mouth,
bilious vomiting and sluggish bowels ; this is called a bilious attack. If
these symptoms immediately follow the taking of food, it is called "inges-
tive dyspepsia," or " morbid sensibility of the stomach." In some dyspep-
tics the breath and faeces have a very offensive odor.
Pyrosis, which is the chief symptom in another class of cases, is the
regurgitation into the mouth of a large amount of thin, watery, saline fluid,
preceded by a sense of constriction and pain in the epigastrium. This fluid
consists mainly of saliva. Sometimes there is not only a feeling of oppres-
sion in the thorax, but a severe pain is referred to the heart, accompanied
by palpitation and dyspnoea. In such cases the patient is very apt to im-
agine he has heart-disease.
Accompanying some cases there is vertigo, ringing in the ears, spots
before the eyes, and other sensations which together have been called
"stomachic vertigo." These patients hear a buzzing sound and feel as if a
vapor were enveloping them; they grow pale, and grasp for support through
fear of falling. When in any case the "indigestion" has lasted a long
time, chronic gastric catarrh will almost always be developed, and evidences
of mal-nutrition show themselves by anaemia, premature old age, corruga-
tion of the nails, caries of the teeth, etc. At other times, the patient will
suffer from dyspnoea, with a short, dry cough and occasional paroxysms of
an asthmatic character. The skin becomes sallow, dry and rough, while
various eruptions appear on it, and the abnormal contents of the urine show
that the functions of the kidneys are disturbed. Often in long standing
dyspepsia in females there will be a feeble pulse, leucorrhoea, and irregu-
larities in the menstrual functions. There is no characteristic change in the
appearance of the tongue ; in one case it is white and heavily coated, in
;^40 DISEASES OF THE DIGESTIVE SYSTEM.
another it is clean, large and indented. The urine often contains oxalate
of lime C'oxaluria"). After the oxalates disappear, lithates may appear
for a time, soon to be followed by normal urine.
Differential Diagnosis. — The phenomena of dyspepsia closely resemble those
of chronic gastric catarrh. Their differential diagnosis has already been con-
sidered. Acidity from hypersecretion may be confounded with acidity from
fermentation, and stomachal may be confounded with cerebral vertigo.
The following are the principal points in their differential diagnosis : pain
in acidity irora. hypersecretion, either immediately follows the taking of food,
and is accompanied by " heartburn," or, quite as often, it is felt most when
the stomach is empty, and is relieved by taking food ; but the pain from
fermentation due to obstruction to movements of, or to chronic inflammatory
processes in, the stomach comes on some time after eating, and is more a
sense of weight or fulness in the epigastrium than pain. It is never pres-
ent during the intervals between taking food. Vomiting is rare in acidity
from fermentation, but if it does occur the ejected materials will contain
organic acids, torulae and sarcinae ; while with hypersecretion, vomiting is
a common symptom, and very frequently there is an excess of hydrochloric
acid in the matter vomited. The constitutional symptoms, mental depres-
sion, and emaciation, the sallow skin, etc., are much more marked in dys-
pepsia with fermentation than in dyspepsia with hypersecretion. In case of
acid stomach from fermentation, flatulence is very common, while it rarely
occurs with acidity from hypersecretion. The urine is alkaline or neutral
in acidity from fermentation, while it is always acid with hypersecretion.
Lastly, acidity from fermentation has a history of some cause or causes
which interfere with digestion ; while hypersecretion is usually a reflex
symptom, or occurs with cancer or ulcer of the stomach.
With vertigo or dizziness from stomachal causes there is a history of indi-
gestion, and it usually occurs in middle life ; while in cerebral vertigo, the
individual is beyond middle life, and there will be no history of difficult or
impaired digestion. Vertigo from stomachal causes occurs during an attack
of indigestion, or after some particular kind of food has been taken. Cer-
ebral vertigo occurs wholly independent of the state of the stomach. Con-
sciousness is never lost, nor are the special senses, — sight alone excepted, —
involved in stomachal vertigo ; while ringing in the ears, temporary deaf-
ness, and often complete loss of consciousness occur in an attack of cerebral
vertigo. A person suffering with stomach vertigo knows that the apparent
motion of the surrounding objects is unreal ; — while a patient with cerebral
vertigo believes the apparent movement of the objects to be real.
Prognosis. — The prognosis varies with the etiology. Dyspepsia in most
cases can be cured, but the cure depends for the most part on the will of
the patient. The only danger is that the conditions induced by dyspepsia
may predispose to organic diseases in other organs, as the lungs or kidneys,
and that it may lead to a condition of melancholia.
Treatment— First, if possible, remove the cause. When the gastric juice
is deficient in quantity, hydrochloric acid and pepsin are indicated. In
these cases, also, the vegetable bitters are especially beneficial ; indeed, in
CANCEE OF THE STOMACH. 241
most cases of dyspepsia they are valuable adjuvants to the other remedies.
Tea and tobacco are always to be avoided ; alcoholic stimulants in moderate
quantities may sometimes be combined with the vegetable bitters with ad-
vantage. When acid risings occur after ingestion of food, and there are
actual evidences of active fermentation, the sulphite of soda, creosote and
the alkalies, after meals, are of service. A course of saline waters will be
found, in such instances, to aid the other remedies.
When there is great irritahility of the stomach bismuth acts almost as a
specific, and should be given in twenty-grain doses before eating. If there
is pain in the epigastrium the local application of heat by means of the
hot-water bag will relieve. Dyspeptics should never wear corsets or belts
about the abdomen ; they should retire and rise early, and eat slowly,
masticating their food thoroughly. The meals should be small and taken
at stated intervals, and should be free from hydrocarbons. No mental or
physical work should be performed directly after or before eating. Horse-
back-riding and walking in the open air should be insisted upon. A
change of scene and climate works rapid cures in many instances. Dyspep-
tics should take plenty of rest, have their sleeping-rooms well ventilated,
and take a cold sponge-bath morning and evening. The general princi-
ples of treatment in gastric dyspepsia are similar to those given in chronic
gastric catarrh.
CANCER OF THE STOMACH.
The stomach, next to the liver, is the most frequent seat of internal can-
cerous developments ; one-third of all the cases of primary cancer have
their seat in the stomach. The varieties of cancer of the stomach in the
order of their frequency are as follows :
First, scirrJius ; second, medullary j third, colloid ; fourth, villous ;
fifth, melanotic J and lastly epithelial. The last three varieties are exceed-
ingly rare.
Morbid Anatomy. — Cancer has its seat at the pyloric extremity of the
stomach in about three-fifths of the cases. The next favorite seat is the
cardia and the lesser curvature. When it is developed at the pylorus, it
sometimes extends an inch or two into the duodenum ; cancer at the
cardia usually involves the lower part of the oesophagus.
Scirrhus of the stomach first appears as a small, grayish white, opaque
nodule in the submucous tissue, the normal structures of which are en-
closed by the new growth. The fibrous stroma is far in excess of the cell-
element ; it develops rapidly at the exterior of the mass, causing in-
duration and contraction of the surrounding structures. The mass
sometimes extends inward toward the cavity of the stomach, causing
flattened tumors which project into it. The contraction of these nodules
puckers the mucous surface, which becomes immovably fixed upon them,,
and fibrous lines radiating from the growth penetrate the mucous mem-
brane, which first undergoes a slight increase in thickness, and then be-
comes pale from compression of its vessels. The solitary glands are en-
16
243
DISEASES OF THE DIGESTIVE SYSTEM.
Pig. 54.
Cancer of the Pyloric Extremity of the Stomach.
A. Mucous membram of the stomach beyond the seat of the cancerous in-
filtration.
B. Pylorus.
C. Commencement of the Duodenum.
D, B. Vertical sectiort of the cancerous mass.
E, E. Internal surface of the cancerous infiltration encroaching on th£ py-
loric orifice.
F. Small opening in, the cancerous growth at the pyloric extremity.
larged and the gastric tubules are matted together in an indistinguishable
bundle. A dark slough sometimes forms upon its surface and exposes
the cancerous growth, which then ulcerates. The ulceration may extend
so deeply as to destroy
^ ^.^^ff^X^l ( J/ the new growth and
invade the wall of
the stomach under-
neath it, causing ir-
regular cavities,
bounded by a raised
and indurated band
of connective-tissue,
and sometimes open-
ing into the stom-
ach. These poly-
p o i d tumors are
sometimes as large as
a hen's egg and de-
velop upon the can-
cerous mass. The
glands and villi are
the longest to resist
this encroachment of
the cancerous development, the first change in them being an increase in
the number of their epithelial cells. After a time the muscular coat be-
comes fused with the areolar, so that at the seat of the neoplasm they can-
not be distinguished from each other on section of the mass. At other
times the parts affected are hard and fibrous, the stomach walls being so
thickened that the disease is only differentiated from hypertrophy of its
coats, by the glistening, pearly look, and cartilaginous texture of the mass.
After involving the muscular coat, the growth may involve the peritoneal
covering ; local peritonitis establishes adhesions between it and the dia-
phragm, liver, pancreas and spleen.
The lesions which follow the development of scirrhus in the stomach are
as follows :
Dilatation of the stomach is a frequent result of the obstruction at
the pylorus caused by the cancerous development. Less common than
dilatation of the stomach is the gizzard appearance caused by the same con-
traction that shrivelled the mucous membrane, inducing a shrinking of
the whole stomach wall, which sometimes becomes an inch thick, the
cardia and pylorus not infrequently being closely approximated, and the
anterior and posterior stomach walls being almost in juxtaposition.
Chronic gastritis is developed when the new growth attains sufficient
size to cause pressure, and in such cases the mucous membrane presents
the characteristic appearances of that affection.
Perforation of the stomach sometimes occurs, causing a fatal peritonitis ;
a secondary opening may penetrate into the duodenum, liver. Jejunum, or ile-
CANCER OF THE STOMACH. 243
Tim, or through the anterior wall of the abdomen, and thus form an external
opening. In rare instances openings are made into the lungs, pleural cavity,
bronchi, or pericardium. Large branches of the pneumogastric may be
destroyed by the new growths. In five per cent, of the cases of cancer of
the stomach, secondary cancer is developed in other organs. The organ
which is the most frequent seat of this secondary development is the livery
and after the liver the lymphatic glands in the immediate vicinity of the
peritoneum, and various segments of tlie intestine, especially the rectum.
The kidneys, bladder, spleen, pancreas and ovaries may also be the seat
of these secondary developments. The position of the stomach is some-
times changed, the weight of the tumor dragging it into the lower portion
of the abdomen, and there it may be bound to the intestines, bladder,
uterus or ovaries by firm adhesions.
Medullary, or acute cancer of the stomach, commences in the same tis-
sues as scirrhus, in the form of nodules much softer than those of scirrhus.
On section, cancer-juice can be readily expressed from the cut surface
of the cancerous mass ; the proportion of the stroma being much less, and
the cells more abundant. The growth is more vascular, and not infrequently
contains small blood extravasations. It is much more rapid in its de-
velopment than scirrhus, and while proliferation of the epithelial struct-
ure occurs at the periphery, fatty degeneration breaks down the centre,
and it sometimes becomes diffluent. The mucous tissue is rapidly invaded.
Large, spongy, '' fleshy " excrescences project into the cavity of the stomach.
Around the growth, which varies in size from that of a pigeon's ^g^, to that
of an orange, is a transparent ring of tissue infiltrated with cancer, beyond
which the solitary glands are enlarged, and the stomach-follicles degen-
erated. ''Villous" cancer of the stomach is a modification or variety of
medullary cancer. If medullary cancer ulcerates, the slough is thrown
off, and an excavated ulcer is exposed, surrounded by an elevated rim,
from which projects the. cauliflower-like growth, very friable and vascular.
The surface exposed by such ulceration is often very large, even six or
seven inches in diameter.
Colloid or alveolar cancer has the same structure as colloid cancer
occurring in other parts of the body. It appears oftener in the stomach
than elsewhere, but even here \t is rare. There are different opinions as
to its starting point ; some state that it begins in the sub-serous, others in
the submucous tissue. • Eecently a glandular origin has been ascribed to
it, similar to epithelioma of the skin. Wherever commencing, it rarely
appears as nodules, but commonly as an irregular mass of " gum-like "
glistening material, contained in large and distinctly marked alveoli, in
which are embedded polygonal nucleated cells. The walls of the stomach,
the seat of colloid degeneration, are very much thicker than normal. Its
tendency is to spread rapidly over a large surface. The contents of some of
the alveoli are discharged into the stomach, thus giving to its inner sur-
face an irregular, '' honey-comb" appearance.
Etiology. — Cancer of the stomach occurs most frequently between the
ages of forty-five and sixty-five. It is more frequent in males than females.
^'44 DISEASES OF THE DIGESTIVE SYSTEM.
Hereditary predisposition is undoubtedly its most important etiological
factor. Beyond this its etiology is obscure.
Symptoms. — The earliest and most prominent symptom of cancer of the
stomach is anorexia, accompanied by a sense of uneasiness or distention in
the epigastrium, with nausea and vomiting. Pyrosis is often present quite
early. Patients describe the pain as dull, gnawing, or as a tightness or '' sore-
ness " over the stomach ; after a time it becomes lancinating, fixed and
constant ; the locality of the pain does not correspond to the seat of the
cancer ; when the growth has its seat in the lesser curvature, the pain is
referred to the interscapular region ; it is not usually increased by ingestion
of food, and if it is it does not cease at the end of the digestive process ; it
may become constant and severe. These symptoms usually exist before the
appearance of a tumor. During the period of its growth vomiting becomes
frequent. There are three prominent causes of the vomiting : first, from
olstruction. Vomiting from this cause comes on comparatively late ;
when the obstruction is at the cardia it occurs immediately after eating.
If it is situated at or about the pylorus, the food is retained for one or two
hours. Secondly, from irritation. This occurs independent of taking food
and the time of its digestion. Thirdly, from fermentation. This occurs
after a large accumulation of food in the stomach ; and the matters vom-
ited are dark and yeasty, not infrequently containing sarcince ventriculi.
Hiccough, flatulence and constipation are often very annoying, some-
times very distressing symptoms, and emaciation, debility, and the haggard
"cancer countenance," are often present. There is mental depression, anxi-
ety, and the patient is morose or apathetic.
When ulceration of the free surface of the cancerous mass occurs the
most constant symptom is hemorrhage. This may be copious and bright
red in color, but usually the blood is so altered by the gastric Juice, and so
mixed with food, that it is rusty, brown or blackish in color {"coffee
ground" vomit). In the later and larger hemorrhages, the blood may
in part escape by the bowels, and then diarrhoea occurs caused by the
decomposing blood ; the stools have a dark tarry appearance with a very
offensive odor ("melsena"). The yellowish green color of the skin,
usually present, may change to a jaundiced hue, due to pressure of th&
cancerous mass upon the bile ducts.
One may be deceived or puzzled during the course of cancer of the stom»
ach, by a remission of the anorexia, pain, hemorrhage, and vomiting,
so that improvement seems to be taking place and the patient believes
he is recovering ; but in a short time all these symptoms will return
with increased severity and the disease will progress more rapidly than
before.
Again, there is sometimes a febrile reaction — not a definite hectic, but a
symptomatic fever — which appears irregularly during the progress of the
cancer, and which often misleads on account of the belief that the temper-
ature in malignant disease is normal or sub-normal. During the advanced
stage in many cases the tongue becomes covered with aphtha, typhoid
symptoms develop, and death is often preceded by delirium which is fol-
CASrCER OF THE STOMACH. 245
lowed by coma. The urine is scanty, high colored, and of a high specific
gravity. It is loaded with urates, and deposits a pink sediment regarded
by some as a diagnostic symptom.
Physical Signs. — By palpation a tumor is discovered — sometimes large,
hard, irregular and nodulated ; sometimes small, deep-seated and elastic.
In the former case it is easy, in the latter very difficult of recognition.
If the cancer is situated at the cardiac extremity of the stomach, no
tumor will be felt. The tumor is usually movable, except when ad-
hesions have formed between it and the adjacent tissues. If the can-
cer is at the pyloric extremity of the stomach the tumor is usually
situated in the median line ; it may, however, be felt at the lower part of
the epigastric region, in the right hypochondrium, at, or just above the
line of the umbilicus, or it may be far over on the left side. It may receive
and transmit the impulse of the aorta, that is, become a pulsating tumor.
The epigastric region is prominent, hard, resisting and tender. It is im-
portant during the examination to have the patient distend his stomach by
drinking one or two tumblers of carbonated water.
Percussion over the tumor elicits circumscribed dulness with a tympa-
nitic, or a peculiar hollow quality ; light percussion may give absolute
flatness, when forcible percussion gives a tympanitic resonance.
Auscultation gives negative, results.
Differential Diagnosis. — Cancer of the stomach may be mistaken for gas-
tric ulcer, abdominal aneurism, cancer of the left lobe of the liver, and for
chronic gastric catarrh toith licBmatemesis ; the latter is considered under
Chronic Gastritis. It is hardly possible after a careful study of a case to
mistake cancer of the stomach for gastric dyspepsia, or to confound a can-
cerous tumor at the pylorus with an ovarian tumor.
Ulcer of the stomach occurs most in young adults, especially females,
while cancer is seldom met with in persons under forty. In cancer there
is usually a history of hereditary cancer; while ulcer of the stomach is
usually associated with anaemia, chlorosis, prolonged lactation, or pro-
longed compression of the stomach, as in the case of shoemakers and sew-
ing-girls. The pain in cancer is continuous, and described as lancinating ;
while in ulcer the pain is intermittent, greatly increased by taking food,
often referred to the lower dorsal vertebrae, and described as "gnawing"
or burning. Hcematemesis, in cancer, has a sooty or ^' coffee-ground^^
appearance, is small in amount and appears late in the disease ; while in
ulcer it is bright red arterial blood, is profuse, and appears as an early symp-
tom. Vomiting in cancer does not relieve the pain, is not very severe
and comes on late ; but in ulcer it is severe, comes on early, and affords
temporary relief from the pain. The cancerous cachexia and debility are
present early and steadily progress in cancer ; while in ulcer there may be
pallor, but no characteristic cachexia. The presence of an epigastric tumor
establishes the diagnosis of cancer.
An anenrismal tumor is smooth and ovoid ; a cancerous tumor is hard
and irregular. An expansive, dilating impulse is given to the hand on
palpating an aneurismal tumor ; but in cancer this impulse is lifting in
346 DISEASES OE THE DIGESTIVE SYSTEM.
character. In aneurism there is constant pain in the back corresponding
to the position of the tumor, which is absent in cancer. There is a change
in the femoral pulse in aneurism, which is not present in cancer. The gas-
tric symptoms, the cachexia and the debility of cancer are not present in
aneurism.
Prognosis. — The prognosis in cancer is always unfavorable. Its shortest
duration is seven weeks, and its longest three and one-half years, the aver-
age duration being one year. Early vomiting, with hsematemesis, great
and sudden emaciation, and complete anorexia, are especially unfavorable
symptoms. The important complications of cancer of the stomach are the
development of secondary cancer in other organs, peritonitis, — independent
of, or with perforation, — pleurisy and pneumonia, pericarditis, endocardi-
tis and fatty heart, tuberculosis, coagula in the sinuses of tbe dura ma-
ter, phlegmasia dolens, non-cancerous ulcerations in the rectum and
colon, ascites and general anasarca. Death may occur from hemorrhage,
peritonitis, exhaustion, marasmus, and from complications.
Treatment. ^The treatment is altogether palliative. The indications are
to make the patient comfortable by relieving pain and vomiting. The diet
may be determined by the experience of each patient. In the majority of
cases alcoholic stimulants in moderation are beneficial. When the pain be-
comes severe, morphia may be administered hypodermically. If at any
time the stomach becomes overloaded, its contents may be carefully re-
moved by means of a stomach pump. The constipation, which is often ob-
stinate, is best overcome by aloes ; the flatulence and painful eructations by
sulphite of soda or oil of cajeput. During the whole course of cancer,
subnitrate of bismuth may be administered, its combination with soda,
conium, and stramonium being highly recommended by English physicians.
Some assert that arsenic is efjfective in retarding the cancerous growth, and
that its administration with iodine and carbolic acid may arrest its devel-
opment. My experience does not confirm this statement. If the stomach
entirely rejects food, rectal alimentation may be resorted to.
ULCER OF THE STOMACH.
Statistics show that gastric ulcers, or cicatrices caused by ulcers, are found
in three out of every hundred cases of diseases of the stomach. They may
be classed as follows :
I. Superficial Ulcer, or Hemorrhagic V. The Typhoid Ulcer.
Erosion. YI. The Variolous Ulcer.
II. Follicular Ulcer. Yli. The DijjMlieritic Ulcer.
III. The Chronic, Round, or Perfora- VIII. The Syphilitic Ulcer.
ting Ulcer. IX. The Tutercular Ulcer.
IV. The Typhus Ulcer. X. The Cancerous Ulcer.
The first two have already been considered.
The specific ulcers Vi^hich receive their names from the diseases in which
ULCER OF THE STOMACH.
247
they occur as occasional patliological lesions, will be considered in connec-
tion with the history of those diseases.
The chronic, round, perforating ulcer is l^y far the most frequent form
of gastric ulcer, and is the one indicated when the unqualified term, ulcer
of the stomach, is used.
Morbid Anatomy. — Chronic perforating ulcers most frequently occupy
the posterior wall of the stomach near its pyloric extremity. They var}^
in size from half an inch to two or three inches in diameter ; an ulcer
one-half inch in diameter may exhibit all the clinical characteristics of
one of large size. These ulcers are at first circular or elliptical in form ;
occasionally they become irregular when two or more are fused together.
When oblong they have their axis either parallel with, or transverse to
the axis of the stomach ; sometimes they form a zone about the pyloric
end of the stomach. The large ulcers are formed by the fusion of several
small ones. They begin in the mucous membrane of the stomach ; their
boundary is nearly vertical, smooth and sharp, so that now and then at a
post-mortem the mucous membrane will present an appearance as if a cir-
cular piece had been " punched out " with a sharp instrument. There is
no evidence of an inflammatory process.
The loss of substance may involve only the
mucous layer, or it may extend to the sub-
mucous tissue, or penetrate deeper and in-
volve the muscular and peritoneal coats ;
as it extends, smaller and less regular cir-
cles are formed, gradually diminishing in
diameter, a small opening in the muscular
coat, or a mere point upon the peritoneum,
being the apex of the conical or "funnel-
shaped" excavation. As the ulcer spreads
transversely in the course of the vessels, this ^^^
"step-like," bevelled appearance becomes pejorating uicei of "the stomach.
more and more marked. The tissues around ^ mvcovk surface
the ulcer are sometimes normal, especially ^- ^^^^g'&^lLS^-^c'^^^"' ""
when the mucous membrane alone is in-
volved ; at other times the mucous layer encircling the base of the ulcer is
thickened and indurated. The mucous membrane in the vicinity of an
ulcer is sometimes the seat of a circumscribed chronic catarrh ; but more
often chronic catarrh involves the whole gastric mucous membrane.
The variations from these usual pathological appearances consist, /rs^f, in a
mass of black blood adh.ering to the base of the ulcer ; secondly, in petechial
extravasations around the injected margin of the ulcer ; thirdly, in the villous
or "polypoid" vegetations springing up from the mucous membrane sur-
rounding the base of the ulcer ; a.ndfotirtI/ly, in suppuration in the coats of
the stomach with subsequent suppurative pylephlebitis. The progressive in-
crease in the depth of the ulcer, which is part of its natural history, would
alwaj'^s lead to perforation and discharge of the contents of the stomach into
the peritoneal cavity, were it not for the establishment of a local jierifonitis
248 DISEASES OF THE DIGESTIVE SYSTEM.
which causes the corresponding portion of the stomach to hecome adherent
to the adjacent parts. These adhesions may join it to the pancreas, liver, me'
sentery or spleen.
The number of ulcers which may be found in a stomach varies from one
to six ; as a rule there is but one. Gastric ulcers, if not large or deep,
may heal without producing deformity of the stomach. If they are large
or deep, the resulting cicatrix, by its contraction, causes deformity of the
stomach. When the mucous and submucous tissues are alone involved,
the loss of substance is replaced by new connective-tissue, which does not
contract ; the resulting cicatrix is merely a white spot, with little or no
puckering. The usual process of repair in deep ulcers is that of a local in-
flammation with lymph exudation. The connective-tissue formed at the
base and around the ulcer contracts, and there remains a central, hard
mass from which radiate bands of connective-tissue into the adjacent
mucous membrane. The contraction of this cicatricial tissue may cause a
stricture at the pylorus, or, if the ulcer extends around the central portion
of the stomach, may give it an " hour-glass " shape. When there is steno-
sis at the pyloric orifice, the stomach is dilated and the walls are thickened
in one subject and thinned in another.
Ulcers may extend by degeneration of the newly-formed tissue. With
the extension of the ulcers, some of the larger vessels (as the superior py-
loric) may become involved, and extensive hemorrhage result ; usually, a
"protective thrombosis " prevents this accident. Hemorrhages, the result
of intense passive hyperaemia, or of erosion of small vessels, are of little con-
sequence compared with those which result from the opening of vessels of
large size or of the organs with which the stomach becomes adherent. In
this way the portal vein, and the splenic, pancreatic and hepatic arteries
have been pierced. Perforation of the stomach in gastric ulcer occurs
only in about one-eighth of all the cases. Though the posterior surface
of the stomach is the more frequent seat of these ulcers, the liability to
perforation is greatest when the ulcers are situated in its anterior wall.
If perforation and escape of the contents of the stomach take place into
the peritoneal cavity a general, rapidly fatal peritonitis immediately fol-
lows ; when adhesions prevent the contents of the stomach from escaping
into the peritoneal cavity, a local peritonitis is developed and an abscess
may be formed in the neighborhood of the ulcer, which abscess may com-
municate with the pleural cavity, duodenum, colon, or gall-bladder.'
' Etiology. — Ulcer of the stomach occurs in females oftener than in males,
the proportion being more than two to one. The liability to it is greatest
between the ages of fourteen and thirty, although no age is exempt ; it has
been found in the new-born babe and in the octogenarian. Angemia an^
I Many theories have been advanced in regard to the pathogenesis of gastric ulcers ; the following are
the principal ones : perf orating ulcers may be the result of an inflammatory process, a sequel, oftentimes,
of chronic gastritis. Eokitansky attributes them to congestion, extravasation, and subsequent necrosis of
the tissue. Virchow maintains that embolism or a venous stasis deprives ai portion of the stomach of its
vascular supply, and that the stomach-tissue thus deprived of its nutrition, is acted upon by the gastric
juice as dead tissue ; as a result, there is a loss of substance and the formation of ulcers. He compares the
funnel or cone-shaped appearance of the ulcer to embolic infarctions elsewhere, the capillaries always ram^
jfying outwards from the main trunk.
ULCER OF THE STOMACH. 249
cUorosis are the two great predisposing causes. Chronic and phlegmonous
gastritis, cirrhosis of the liver, and obstruction of the gall-ducts may lead
to ulcer of the stomach by inducing obstruction in the vessels of the walls
of the stomach. Ulcer may resalt from an habitual stooping position, as in
milliners, seamstresses, and shoemakers, or may come from the constant
striking of the shuttle of the weaver against the epigastrium. Miliary
aneurisms in the gastric walls may cause gastric ulcers. Such ulcers are
most frequently met with in connection with a cirrhotic kidney. It may
occur without any recognized cause.
Symptoms, — The symptoms of gastric ulcer are sometimes obscure, at
others well marked.
Pain is one of its constant symptoms : at first it is dull and heavy ;
then it becomes burning and gnawing, causing a sickening sensation quite
distinct from nausea. It usually comes on soon after the ingestion of
food, and lasts during the entire period of stomach digestion ; occasionally
it is not present until an hour or so after eating. It is circumscribed to a
spot rarely larger than a silver dollar, is accompanied by tenderness on
dee]p pressure, and its intensity is usually greatest just above the umbili-
cus. The "dorsal" pain of gastric ulcer was first recognized by Cruveil-
hier. It comes on some weeks or months after the pain in the epigas-
trium ; it is located at the eighth or ninth dorsal vertebra, and is constant,
although it may sometimes alternate with the epigastric pain. In a few
cases the pain is paroxysmal ; there are intervals of freedom from pain, fol-
lowed by severe attacks, resembling those of neuralgia. Eelief from the
pain of gastric ulcer is frequently obtained by a recumbent posture ; this
happens when the ulcer has its seat on the anterior wall of the stomach.
Nausea, vomiting or regurgitation of food may accompany the pain ;
in some instances there is pyrosis, or " water brash ; *' usually the vomit-
ing occurs when the pain is most severe. The matter vomited consists,
first, of the food taken into the stomach, which has a strong acid re-
action ; later it is mingled with bile. The vomiting temporarily relieves
the pain. After a time these dyspeptic symptoms are complicated by
haematemesis, which may be regarded as essential to its diagnosis. In a
few cases there is no vomiting. Some will vomit several times in the
twenty-four hours, others once a day, and others every two or three days.
As small bleedings do not cause vomiting, and as attention is rarely
paid to the stools at this period, the exact date of the first hemorrhage
is usually unknown. The symptoms which attend the haematemesis are
a sense of unusual fulness in the stomach, accompanied by a feeling of
faintness ; the face is blanched, nausea exists for a varying period, and this
is followed by vomiting of partially coagulated blood, which is so bright
as to leave no doubt of its arterial origin. In rare instances the first hem-
orrhage causes distention of the stomach, s3Ticope and painless collapse,
followed by death. Sometimes the blood vomited has a dark, grumous
appearance, looking like coffee-grounds. In young females the hemor-
rhage is usually preceded by a diminution or stoppage of the menses.
Preceding and accompanying the hsematemesis there are usually dyspeptic
250 DISEASES OF THE DIGESTIVE SYSTEM.
symptoms similar to those of gastric dyspepsia. Cachexia is a late symp-
tom, the appetite is rarely impaired, sometimes it is even increased ; great
debility and extreme anaemia result from the recurring hemorrhages. The
face assumes an earthy pallor ; when the pain is intense it is '^ drawn "
and haggard, which by some is regarded as characteristic of ulcer of the
stomach. Perforation of the stomach is attended by the symptoms of
rapidly developed and extensive peritonitis. Pain in the right shoulder is
a prominent symptom if an ulcer of the stomach involves the under sur-
face of the liver. If cicatrization of a gastric ulcer takes place without
adhesions or stricture all the above symj)toms remit and complete recovery
follows; if adhesions or stricture remain dyspepsia and cardialgia may con-
tinue for the remainder of the patient's life. Obstinate constipation is the
rule in ulcer of the stomach, but hemorrhage may cause diarrhoea.
The blood gives to the dejections a dark color and a "tarry" consist-
ence, a condition called '^melsena." The ovl\j physical sign oi gdL&tvia
ulcer is extreme tenderness on firm pressure over the epigastric and
dorsal regions.
Differential Diagnosis. — The diagnosis in a typical case of ulcer of the
stomach is not difficult ; in the more obscure cases it may be mistaken
for cancer of the stomach, hepatic colic, the second stage of cirrhosis,
cardialgia, and chronic gastric catarrh with hcematemesis. The diag-
nosis of cancer of the stomach, hepatic colic, and the second stage of
cirrhosis are considered under these headings (q. v.).
In neuroses causing cardialgia, there will be a history of neuralgia in
other parts of the body or a well-marked history of hysteria. The
pain of cardialgia is not excited or increased by the introduction of
food into the stomach, but often comes on when, the stomach is empty ;
while in ulcer the pain is associated with ingestion of food. In cardialgia
pressure over the epigastrium and the ingestion of food relieve the
pain ; the reverse is the case in ulcer. Again, cardialgia is relieved by
the constant current and Faradization, which increase rather than
relieve the pain of gastric ulcer. Dyspeptic and gastric disturbances
are constantly present in ulcer ; while these are absent in the intervals
between the paroxysms of neurotic cardialgia. Haematemesis never occurs
in cardialgia.
In chronic gastritis with hemorrhage there is the history of disease
of the liver, heart, lungs or kidneys ; while in gastric ulcer there is
usually no such history. The pain in gastritis is not so intense or
of the same character as in ulcer of the stomach. A coated tongue,
great thirst, malaise, and pyrexia are prominent in cases of chronic
gastritis, and absent in ulcer. The vomiting in chronic gastritis comes
on in the morning, and the matter vomited is stringy mucus, some-
times streaked with blood ; while in ulcer the attacks of vomiting usually
follow the taking of fluids or solids, and the blood is vomited in consider-
able quantities.
Prognosis. — More than one half of the cases of ulcer of the stomach re-
cover. The average duration cannot be determined. Some terminate
ULCER OF THE STOMACH. 251
fatally in a few weeks, otliers continue for a long period. In the pro-
tracted cases, the symptoms are probably due to the existence of more
than one ulcer. Most of the cases that recover continue for more than a
year. The prognosis is bad where ulcer occurs in the aged and in feeble
women.
The complications of gastric ulcer are chlorosis and hysteria ; thoracic
complications, such as pneumonia, bronchitis, pulmonary tubercle, acute
pleurisy, and empyema ; abdominal, such as suppurative pylephlebitis and
peritonitis. Death occurs from hemorrhage four times as often in the
male as in the female. Exhaustion, either from pain or from vomiting
or from starvation, causes death in 5 per cent, of the cases. Perforation,
with peritonitis or without it, occurs in about 13 per cent, of all the cases.
The liability to perforation is greatest in the female between the ages of
fifteen and thirty ; while in the male the liability is greatest about the
fortieth year. Cicatrization of an ulcer at the pyloric extremity of the
stomach is usually followed by dilatation of the stomach.
Treatment. — The most important thing to be accomplished in the treat-
ment of gastric ulcer is to give rest to the stomach. To this end the patient
must be kept in led, and if possible should be restricted to a milk diet.
From a tablespoonful to a teacupful may be given at intervals of two hours
during the day and night. When milk is refused, digested beef-juice may
be given in its stead ; all vegetables, tea, coffee, starchy food and fruits
must be prohibited. If all kinds of food are rejected, rectal alimentation
must be practised, four ounces of defibrinized blood (containing four grains
of chloral to prevent its decomposition) may be thrown into the rectum
every six hours.
The remedial agents which have been found most useful in gastric
"ulcers are the sub-nitrate of bismuth, in twenty-grain doses, four times
a day, sulphite of soda, oxalate of cerium, and hydrocyanic acid.
Half a grain of nitrate of silver, three times a day, seems to exert a bene-
ficial effect on gastric ulcers of long standing, as well as on the accompany-
ing gastric cntarrh. Several observers claim that arsenic retards the spread
of gastric ulcers ; my experience does not confirm this observation. If the
pain is severe, and there is no hemorrhage, warm poultices may be applied
to the epigastrium ; but morphia hypodermically is far more reliable for
the relief of pain, and may be used at regular intervals with benefit. Hypo-
dermic injections of ergotin, and ice-bags to the epigastrium, will usually
check the hemorrhages. The flatulence, which is often very distress-
ing, may be mitigated by sulphite of soda, carbolic acid, or the alka-
lies. Constipation when present is relieved by ox-gall enemata, or saline
mineral waters, the latter being especially useful when there are acid eruc-
tations. When the patient will bear it, castor-oil is a safe and efficient
laxative. Stimulants must never be given by the stomach. They may be
given by enemata in emergencies.
Eest in bed and a restricted diet should be enforced for at least three
months. Then, if the symptoms indicate that cicatrization is well es-
tablished, maccaroni, potatoes, stale bread and cocoa may be allowed ; still
252 DISEASES OE THE DIGESTIYE SYSTEM.
later oysters, soft eggs, and sago. The patient must not return to an
ordinary mixed diet for at least six months. The anaemia which follows
gastric ulcer must be overcome by fresh air, moderate exercise, iron, and
quinine. It must be remembered that the higher the nutrition is carried,
the more rapid and complete will be the repair of the ulcer. This end
must be had constantly in view in the management of these cases. The
establishment of nitric acid issues, and the employment of moxcB over
the abdomen or epigastrium, as recommended by some, are of doubtful
service, either for the relief of pain, or to hasten the healing of the ulcer.
JSTEUROSES OF THE STOMACH.
These are comparatively rare independent of a well-marked neuralgic
diathesis. They are known as nervous gastralgia, or cardialgia, and as
erytliism of the stomach. They have no distinct pathological lesions.
Etiology. — Neuroses of the stomach are met with most frequently in
females, and occur especially in those with an hereditary neurotic predis-
position. Exhaustion, anaemia, and chlorosis, especially when accompanied
by depressing influences, as grief, fear, anxiety, or great intellectual effort,
play a most important part in its etiology. In the same way exhaustion
from hemorrhage, insufficient food, venereal excess and masturbation will
induce it. Central nervous diseases and disease of the pneumogastrics or
sympathetic will sometimes cause it. The excessive use of tea or coffee has
been cited as a cause, but those cases where some particular article of diet,
as milk, brings on attacks of pain in the stomach, are not true neuroses.
Reflex irritation caused by painful affections of the teeth, ear, kidneys,
testicles, ovaries and disturbances in the alimentary canal, as hemorrhoids,
constipation, worms and hernia, has been regarded as a cause of gastralgia.
Diseases and displacement of the uterus, accompanied by disturbance of its
functions, will very frequently give rise to attacks of cardialgia.
Hysteria and hypochondriasis are its two most frequent causes ; statistics
show that of 360 cases of these two diseases only 30 were free from gas-
tralgia. Malarial gastralgia is accompanied by othei^ forms of malarial
neuralgiae.
Symptoms. — Gastralgia usually begins with a sense of distention and
tightness in the epigastrium, followed by a severe and agonizing pain,
which will be described differently by different patients. In many in-
stances the pain shoots through to the back. During an attack the abdomen
is sometimes distended and rigid, sometim.es flattened and retracted. The
pain is often so severe that the heart's action becomes irregular, the ex-
tremities cold, the face pinched, and there is a tendency to syncope ; in
rare instances convulsions occur. The pain is relieved by firm pressure
over the epigastrium, by the constant current, and by Faradization ; the
duration of these attacks is not at all regular, sometimes lasting only a few
minutes, at other times an hour or two, generally terminating with gaseous
eructations, or the ejection of an acid or an alkaline fluid. Sometimes be-
fore the first attack there will be complete anorexia. Vomiting, preceded
HiEMATEMESIS. 253
by nausea, may be a part of an attack, and, though very severe, it does not
depress the patient. Between the attacks, which occur at intervals of days
or weeks, regularly or irregularly, the digestive functions are normal.
Differential Diagnosis. — Neurotic cardialgia may be mistaken for ulcer of
the stomach, which has already been considered.
Prognosis. — This depends upon the cause ; cardialgia may continue for
years and not endanger or shorten life.
Treatment. — In the treatment of this affection, tonics are always indi-
cated. Iron, arsenic, nitrate of silver, and oxide of zinc maybe tried alter-
nately. For relief when pain is intense, morphia may be given hypoder-
matically. Great care must be exercised not to repeat the hypodermatic too
frequently, for this class of patients readily become addicted to the use of
opium. Obstinate and pi'otracted cases sometimes yield quickly to the
constant current or to Faradization.
HJEMATEMESIS.
Hasmatemesis, or hlood vomiting, is a symjotom in a variety of diseases ;
it varies in amount and frequency with the morbid conditions which in-
duce it. Eupture of a blood-vessel is one of its essential conditions.
Etiology. — I. Injury to the mucous tissue of the stomach by traumatism
or poisons.
II. Diseases of the wall of the stomach, associated with diseased condi-
tions of the blood-vessels.
III. Obstruction to the portal circulation, as in cirrhosis, acute yellow
atrophy, aneurism of the hepatic artery and tumors compressing the vena
portae ; gastric hemorrhage may remotely be produced by obstruction in
the portal tissue, the result of cardiac and pulmonary diseases ("nut-
meg liver ").
IV. Blood poisoning may cause hfematemesis, as scurvy, yellow, ty|)hus,
and relapsing fevers, snake-bites, and cholera. It also occurs in patients
with the '* hemorrhagic diathesis," and in " bleeders," or those affected
■with limmophila.
V. Cancer and ulcer of the stomach cause it.
VI. Passive hyperemia, stoppage of menses in the female, and the sud-
den arrest of hemorrhoidal discharges, are supposed to cause ha3matemesis
by suddenly raising the blood-pressure in the portal system.
VII. Finally, this symptom appears nearly three times as often in females
as in males, and usually between the ages of twenty and forty years.
Symptoms.— In hsematemesis, if the hemorrhage is profuse, the patient
experiences a sense of heat and distention in the epigastrium, with nausea
and vomiting ; he becomes pallid, and the surface cold and clammy, as
the blood rushes up in a full stream through the mouth and nose, or is
thrown up by successive acts of vomiting. When the blood comes up with
a sudden gush, some portion of it may enter the larynx and excite cough-
ing, and then it may appear to be coughed up. The appearance of the
blood differs according to the length of time it has been acted upon by
254 DISEASES OF THE DIGESTIVE SYSTEM.
the gastric jaice. If it is vomited in large quantities immediately after the
bleeding has occurred, it will be partly fluid and partly coagulated ; but
if it has been retained in the stomach for a considerable time, it will be
fluid and have a black, or brownish-black appearance, with an acid reac-
tion.
Differential Diagnosis. — Hsematemesis may be confounded with hcBmopty-
5i5 or "blood-spitting."
Hcemoptysis is preceded by bronchial or pulmonary symptoms, and
hsematemesis by gastric symptoms. Haemoptysis is preceded or accom-
panied by a sense of constriction across the chest, by dyspnoea and cough ;
while before hsematemesis, there is nausea, with oppression and distention
felt in the epigastrium. If cough is associated, it follows the expulsion
of blood. Blood is coughed up in mouthfuls, bright red, frothy, alkaline
and mingled with sputa in haemoptysis ; while it is vomited more or less
profusely, is dark colored, mixed with food, coagulated, and often acid in
hsematemesis. In haemoptysis there is a sense of " trickling " behind the
sternum, and for a few days after the hemorrhage, small blood-spittings ;
and a physical examination of the chest readily determines the origin of
the hemorrhage and establishes a diagnosis.
Prognosis. — Haematemesis, though a grave symptom, does not often
directly cause death ; the prognosis is determined by the diseased condi-
tions with which it occurs. Hsematemesis from cirrhosis of the liver or
ulcers is always more dangerous than from any other conditions.
Treatment. — During the hemorrhage the patient must be kept absolutely
quiet, in a horizontal position. Ice should be taken freely, and ice-bags
applied to the epigastrium. Morphine and ergotin may be hypodermically
administered, and the patient sustained by rectal alimentation. Astrin-
gents given by the stomach usually do more harm than good, and should
not be employed. In severe cases the head must be kept low and brandy
may be given by the rectum. If there is evidence of heart-failure, brandy
and digitaline may be given hypodermically. After the hemorrhage ceases
great care must be exercised in the diet of the patient ; milk is the only
nutritive article that should be allowed for the first week. The conditions
which cause the hemorrhage must receive their appropriate treatment.
DILATATION OF THE STOMACH.
Morbid Anatomy. — A dilated stomach is much larger than normal ; in
one instance it was found capable of containing ninety pounds of fluid ; it
may be either uniformly dilated, or there may be dilated, circumscribed
pouches corresponding to ulceration or erosion of its walls. When stenosis
at the pylorus exists, the walls of the stomach are first hypertrophied, and
then a muscular paralysis is followed by atrophy, thinning of its walls,
and dilatation of its cavity, which is usually to the left and upwards.
The muscular coat may be so stretched and thinned as sometimes to be
scarcely traceable ; this is more frequently the case when the dilatation is
independent of stenosis. In some few instances fatty degeneration of the
DILATATION" OF THE STOMACH. 255
muscular coat has been found, and with it the rugse of the mucous coat
have disappeared, and the mucous membrane has become j)ale and thin.
Etiology. — Dilatation results^rs^
from pyloric stenosis, and this may . ^
be caused by cancerous or non- \ \-- — ^""""^^v
malignant ulceration, by the effects j \ \
of corrosire poisons (acute gas- y — ^-^c ^ \ \
tritis), by thickening from chronic j^^^N^— k-^Vj 1 t, \
and phlegmonous gastritis, and '\\ j 1
from fibroid indurations of the \^ . y
pylorus. Whether spasm of the ^"v^ \^r y
pylorus is sufficient to cause dila- ^^-, ■ ""^ ^--''
tatiou or not, is as yet undecided. " ~ ■"'
Secondly, dilatation of the stomach '^'^' ^^'
, T, 7 , ,. „ ji Diagram Illustrating Dilatation of the stomach.
may becaused by oc»,sfrz American Clinical Lectures, page 221.
326 DISEASES OF THE DIGESTIVE SYSTEM.
tonitis is met with most frequently in early life, and cancerous peritonitis
between the ages of forty and sixty-five.
Symptoms. — The symptoms of acute peritonitis vary with its extent,
severity, and the causes which produce it. If it is the result of intestinal
perforation, its onset will be marked by excessive pain over the whole ab-
domen. In infectious peritonitis, the first symptom will be a severe chill.
Peritonitis resulting from the extension of an already existing visceral in-
flammation begins with local and gradually increasing pain. All varieties
of acute peritonitis from whatever cause are ushered in hj pain as one of
the earliest symptoms. The pain may be local or diffuse. In severe cases,
if local at first, it becomes diffuse in a few hours. It is described as a.
cutting, burning pain, aggravated by pressure and by movements of the
abdomen. The more sudden the onset, the more intense the pain. In some
cases, the weight of the bedclothes cannot be borne. The pain causes the
patient to remain motionless, he lies on his back, with the knees drawn
up, the breathing is wholly thoracic, the respirations are rapid and super-
ficial, and the face, by its pallid, drawn and anxious look, is almost
diagnostic of the disease. In most cases, the pain is at first paroxys-
mal.
If the peritonitis is general the abdomen soon becomes distended and tym-
panitic, the tympanitis increasing as the disease advances. At the onset of
acute peritonitis, the abdominal muscles are rigid and contracted ; after
this tonic rigidity they relax and allow of abdominal • distention. Some-
times the distention is so great that the diaphragm is pushed up as far as
the third or fourth rib, the lungs are compressed, and the heart, liver and
spleen are displaced. In local acute peritonitis, the tympanitis is usually
slight ; in diffused it is excessive and increases the pain and causes dysp-
noea, the respirations often being increased to forty or sixty per minute.
As the intestines become distended with gas, percussion elicits a tympa-
nitic note over the whole abdominal cavity. If there is a rapid effusion of
serum, it will gravitate to the most dependent portion of the peritoneal
cavity and an abnormal area of dulness will mark its position, the line of
which will change with a change in the position of the patient. If a large
amount of coagulable lymph is poured out over that portion of the perito-
neum which covers the liver or spleen, a distinct fremitus may be com-
municated to the hand as it passes over the hepatic and splenic regions,
accompanied by distinctly audible friction sounds.
The temperature in acute peritonitis has no typical range ; it may not
rise above the normal. In most cases it ranges from 102 to 103° F. ; it is
of the remittent type, being lowest in the morning. If recovery takes
place, it gradually falls to normal. In fatal cases it may fall below the
normal during the period of collapse. The pulse is accelerated, often reach-
ing 140 per minute. For hours before a fatal issue it may beat 200 per
minute. It is small, hard and wiry in character, and when very rapid is'
hardly perceptible at the wrist. In exceptional cases it is tolerably full and
strong, and does not rise to more than 90 beats per minute.
Vomiting is a prominent symptom ; if that portion of the i)eritoneum
PERiToisriTis. 327
coTering the stomach is first involved, it precedes all other symptoms. It
usually comes on about the second day ; the vomited matters at first con-
sist of the contents of the stomach, later they are a mucus mingled with
a spinach-green material, which by some is regarded as characteristic.
Whenever stercoraceous vomiting occurs in peritonitis, it is evidence of
intestinal obstruction, such an obstruction being the cause or the result of
the peritonitis. Total paresis of the lower bowel in rare instances may
cause stercoraceous vomiting when the muscular wall of the intestine
above is still active. Sometimes there is constant nausea without vomit-
ing ; hiccough and gaseous eructations indicate that the diaphragmatic
portion of the peritoneum is involved. The tongue is covered with a
thick coating, and anorexia is present from the onset. Constipation due
to paralysis of the muscular coat of the intestine is the rule, especially
in the early stage of peritonitis. Yet diarrhoea may not only occur during
the later stages of the disease, but it may exist throughout its entire course.
In puerperal peritonitis there is usually watery diarrhoea, and diarrhoea is
often present in the peritonitis of children.
The tirine is, scanty and deposits urates ; " scalding " frequently occurs,
and if the peritoneal covering of tlie bladder is involved there may be
retention of urine or painful micturition. The tendency to heart failure
and to collapse is one of the most striking characteristics of acute peritonitis.
In all varieties it must be remembered that the disease rarely runs a typical
course ; even pain may be absent. A sudden collapse attended by a soft,
feeble pulse and brown tongue, quickly terminating in death, may be fol-
lowed by an autopsy which shows the intestines matted together by recent
inflammatory products. When peritonitis follows intestinal perforation, all
the symptoms from the onset are severe. The face quickly becomes haggard,
drawn, and dejected; the eyes are sunken and surrounded by dark
purple rings ; the nose and cheeks are pinched, the lips are blue,
the upper one being lifted and tightly drawn across the teeth,
the voice becomes feeble, or the patient speaks in a husky whisper,
the extremities are cold and covered with a clammy perspiration, the
radial pulse is hardly perceptible, the respirations assume the type known
as '' Cheyne-Stokes " respiration, general cyanosis supervenes and death is
reached within forty-eight hours. Sometimes death occurs within three
or four hours from the shock of the perforation. The mind is usually
clear throughout the entire course of the disease ; in infectious peritonitis
loss of consciousness, apathy, or delirium may precede death by a few
hours. The pulse and the amount of cyanosis are measures of the heart
failure. In cases where there is a large amount of fluid effusion the j^ain
subsides with the occurrence of the effusion, and this sometimes leads to a
mistake in prognosis on account of the supposed subsidence of the peri-
tonitis. In suppurative peritonitis the pain is not infrequently absent, but
typhoid symptoms are present from the onset, delirium is the rule rather
than the exception, recurring rigors are common, the fever increases
toward evening, and the pulse becomes very rapid. Occasionally in typhli-
tis, gastric ulcer, and intestinal perforation, the shock of the perforation,
328 DISEASES OP THE DIGESTIVE SYSTEM.
or the feeling as if something had suddenly burst, or been torn within the
abdomen, is distinctly appreciated by the patient.
Local or circumscribed peritonitis usually pursues a sub-acute rather than
an acute course. Chronic peritonitis (non-tubercular and non-cancerous)
is usually the sequela of an acute attack. If convalescence is not established
during the first week of an acute general peritonitis, the character of the
inflammation changes and it becomes chronic. Rigors alternate with irregu-
lar sweats, and a steady increase in the size of the abdomen marks the pas-
sage from an acute to a chronic peritonitis. There is rapid loss of flesh and
strength, and a marked diminution in the general vital powers. The face
assumes the haggard, drawn look so often found with chronic abdominal
disease. The intense pain of the acute attack subsides, and a " dull ache "
with more or less tenderness remains. The pain assumes a colicky character
and not infrequently is increased by taking food. The abdominal muscles
remain rigid and tense. The temperature ranges from 99° to 104° F. The
pulse continues rapid and feeble. There is anorexia and progressive ex-
haustion ; diarrhoea alternates with constipation. Fluid accumulates in
the peritoneal cavity, sufficient in some cases to cause dyspnoea. The
thickenings and adhesions which develop may so interfere with the ve-
nous return that oedema, thrombosis and albuminuria may result. In
latent general chronic peritonitis there may be large ascitic accumulations
accompanied by abdominal tenderness, loss of appetite and progressive
ansemia. The pulse is small and rapid, the vomiting is persistent, and with
the accompanying diarrhoea exhausts the patient. Eecurring attacks oi
acute local peritonitis hasten the fatal issue.
In tubercular peritonitis the pain is paroxysmal in character. Its onset
is often sudden, attended by fever and well-marked constitutional disturb-
ance, the pulse is rapid and feeble, there is nausea, vomiting and diarrhoea.
The tongue is heavily coated, thirst is intense, and there is rapid loss of flesh
and strength. The skin becomes harsh and dry. Typhoid symptoms appear
early, fluids gradually accumulate in the peritoneal cavity and the patient
dies of asthenia. Redness and oedema about the umbilicus are regarded as
characteristic of tubercular peritonitis. In some cases the pain is so slight
as to amount only to a sense of tension and fulness in the abdomen ; and
yet there may be a large effusion into the peritoneal cavity. The tongue
becomes red and shining, the stomach is irritable ; hectic fever is accom-
panied by prof nse sweats during sleep, and the abdomen has a doughy feel.
Some cases are unattended by ascites, and knots of intestine embedded in
firm hard masses are felt in the region of the umbilicus. Friction sounds
may be heard over these masses. Tubercular peritonitis may have for its
chief and only symptoms, ascites, anasmia, and the evidences of geneial
tuberculosis ; its progress is interrupted, now there is marked improvement
and cessation of all the abdominal symptoms, and then there follows a period
when death seems imminent. As a rule, there is moderate fever and slight
pain, with considerable ascites. The mesenteric glands are usually en-
larged.
Cancerous peritonitis is attended by the same local symptoms as tuber-
PERiToisriTis. 329
cular. Sometimes a tumor may be felt, especially in the region of the omen-
tum and mesentery. There is always ascites ; the fluid collects giadually,
and often in very large quantities ; constipation is more frequent than diar-
rhoea, and death is often the result of intestinal obstruction. In some cases
the abdomen is very sensitive, and paroxysms of colicky pains are not in-
frequent. The temperature rarely reaches 100° F. If the i)eritonitis has
extended from the stomach, liver or intestine, the symptoms of the primary
disease will have been well defined before the develojjment of the peritoni-
tis. At any period in the course of cancerous peritonitis all the symptoms
of acute general peritonitis are liable to be developed. The diagnosis rests
on the presence of a gradually increasing tumor and the cancerous cachexia.
Differential Diagnosis. — Peritonitis may be mistaken for colic, intestinal
obstruction (without peritonitis), enteritis, abdominal neuralgia, hysteria,
rheumatism of the abdominal muscles, renal and biliary colics, and supjM-
rative cellulitis of the abdominal walls. The ascites of chronic peritonitis
may be mistaken for that of the last stages of cirrhosis of the liver. The
differential diagnosis of colic, intestinal obstruction, and enteritis has al-
ready been given.
The pain in abdominal neuralgia simulates that produced by a
tightly drawn cord about the abdomen, and follows the course of
the genito-crural nerve. There is tenderness on pressure only at the
point of exit of the nerve from the spine. There is no tympanitis, no asci-
tes, no rise of temperature, or acceleration of the pulse, and no signs of
collapse. The muscular rigidity of commencing peritonitis is absent.
In hysteria, the patient is ready to complain of increased pain before the
hand touches the abdomen, yet the firmest pressure does not increase the
pain if the attention of the patient is engaged. The pulse, temperature, and
signs of collapse of peritonitis are absent, the countenance is not that of peri-
tonitis, and there is present the globus hystericus, and the attack is followed
by the passage of a large quantity of watery, straw-colored urine.
In rheumatism of the abdominal muscles, the pain and tenderness are
most intense at the origin and insertion of the muscles. There is no rise of
temperature, no vomiting, and no signs of collapse ; the pulse is normal,
and there will be a history of acute or sub-acute articular rheumatism.
In the passage of a gall-stone, and in renal colic, the patient throws him-
self about in excruciating agony, and the pain is referred to the region of the
common bile-duct, or to the course of the ureter. In the passage of a gall-
stone, it is paroxysmal in character, and will shoot back from the margin of
the ribs over the gall-bladder to the spinal column. If it continues twenty-
four hours, the patient becomes jaundiced. In renal colic the pain radiates
from the kidney along the ureter to the testicle, which is retracted. Both
are accompanied by characteristic changes in the urine or fgeces, neither is
attended by rise of temperature or great acceleration of pulse, and there is no
tympanitis or tenderness on firm pressure in either.
Suppuration of the abdominal parietes is at first difficult to distinguish
from peritonitis, but after the first two days the superficial swelling and the
absence of the constitutional symptoms of peritonitis establish the diagnosis.
330 DISEASES OF THE DIGESTIVE SYSTEM,
Prognosis. — Acute general peritonitis is a very fatal disease. Its average-
duration is from four to eight days ; death may occur in a few hours, or be
delayed two or three weeks. The prognosis in any case is to a great extent
determined by its cause ; it is most unfavorable when it results from perfora-
tion, intestinal obstruction, or sepsis. General puerperal peritonitis is almost
always fatal. The presence of typhoid symptoms, a very rapid and feeble
pulse, cold extremities, with the other symptoms of impending collapse, in-
dicate an unfavorable termination. Peritonitis from rupture of an organ is al-
ways fatal. The prognosis is favorable when the peritonitis is due to extension
of inflammation from a viscus. When the pain and vomiting cease, the tym-
panitis subsides, the pulse diminishes in frequency, the temperature reaches
the normal, and the patient is able to turn in bed, a favorable termination
is to be expected. Chronic diffuse peritonitis in children, unless purulent,
usually terminates in recovery. Tubercular peritonitis, after weeks and
months of anaemia and exhaustion, terminates in death. The same is true
of carcinomatous peritonitis. Death in acute peritonitis may result from
shock, from asthenia with typhoid symptoms, and from exhaustion. Among
its sequelae are collections of pus, stenosis or complete obstruction of the-
intestine, pyaemia, and septicsemia. Permanent Jaundice may result from
narrowing of the bile duct by the contraction of new tissue formations in
the transverse fissure.
Treatment. — Acute peritonitis is a severe, rapidly progressive, and dan-
gerous inflammation, and on this account has always been treated heroic-
ally. Formerly patients with acute peritonitis were subjected to excessive
bleedings, tartar emetic was administered in nauseating doses, and to prolong
the effects of the bleeding, and as an adjunct to these calomel was given
for its specific effect. At the same time many physicians of recog-
nized authority were eager to obtain the purgative effects of cathartics, and
for this purpose recommended and administered large doses of drastic pur-
gatives. Local bleeding by leeches is often of great service in local perito-
nitis, but it should be resorted to only at the very onset of the attack in the
strong and robust. Tartar emetic and calomel, so highly regarded as anti-
plastics, have fallen into disuse. While acute peritonitis is progressing the
bowels cannot be moved, and no benefit would result if they were ; so that
under no circumstance should there be an attempt at purgation.
The plan of treatment which I have followed for years — a plan which
gains in favor with me with every new experience — is the opium plan. Prof.
Alonzo Clark first developed this plan and brought it to the notice of the
profession. The details of it are as follows : — as soon as the unmistak-
able symptoins of peritonitis are developed, administer at one dose from
two to five grains of opium or one-half to one grain of morphine. The exact
quantity in each case is to be determined by the condition of the patient ; the
rule is to bring the patient as soon as possible fully under the influence of the
drug. In the treatment of this disease, it will be observed how greatly pain
and inflammation modify the effects of this powerful drug. I have adminis-
tered to patients with peritonitis four grains of opium every two hours for
twenty-four hours, and then have obtained only a moderate effect of the
PERITONITIS. 331
drug. The point wliicli must be reached in its administration is moderate
narcotism, in whicli stale the patient must be kept, not only until all pain
and tenderness have subsided, but until the pulse has reached its normal
standard and the tympanitis has entirely subsided. The question arises :
what are the indications which are to govern the administration of each
dose of opium ? One must be prepared at the commencement of the treat-
ment of a case of peritonitis, according to this plan, to be present and de-
cide upon the quantity of opium to be given at each dose, until the patient
has fully convalesced. It cannot be trusted to attendants, however intelli-
gent they may be. As the patient is brought fully under the influence of the
opiate, it will be noticed that the entire surface of the body becomes bathed
in a profuse perspiration. In twenty-four hours a rash, due to the opium,
will make its appearance on the surface and neck ; this is accompanied by
an itching of the surface and a constant disposition to rub the nose. The
pupils become contracted, the eyes suffused, the countenance assumes a dull
expression, and there is a constant irresistible disposition to sleep. The
pulse becomes lessened in frequency and force, and the respirations, which,
before the administration of the opium, may have ranged from 40 to 60
in a minute, become less and less frequent as the patient comes fully under
its influence, until they are only twelve in a minute. Xow the greatest care
is to be exercised in the administration of the opium ; the patient is in the
condition in which it is desirable to keep him. By holding him in this
state of semi-narcotism, all will be accomplished that can be by the opium
plan of treatment, and with the respiration at twelve per minute the patient
is perfectly safe. The amount of sleep is not to be taken into account, but
the profoundness of the slumber is of great importance. If it is found dif-
ficult to arouse the patient, the administration of the opium must be stopped
until he can be easily aroused. If by mistake or negligence the patient be-
comes fully narcotized, the respirations will sometimes diminish in fre-
quency to seven or even five in a minute. In this extremity, if the admin-
istration of opium be stopped, the patient will usually rally from its effects
after a few hours ; but avoid extremes, endeavor to keep the patient in a
quiet sleep, not profound, but one from which he can be easily aroused.
When the pulse begins to diminish in frequency and becomes fuller, one
may be certain that he is controlling the peritonitis, and as it is controlled
the patient will become more and more susceptible to the influence of the
opium. Slowness of respiration and absence of pain cannot be relied on as
sure indications that the opium is controlling the inflammatory action ; but
a diminution in the frequency of the pulse, and a subsidence of the tympa-
nitis are sure indications that the peritonitis is arrested, and that ultimate
recovery is probable. In most cases, if an acute peritonitis does not depend
for its exciting cause upon the escape of intestinal gases into the peritoneal
cavity, or upon complete intestinal obstruction, the inflammatory action
can be controlled within forty-eight hours from the commencement of the
attack by adopting, within twelve hours, this plan of treatment. It must,
however, be continued four or five days longer, for there is still danger of
a renewal of the inflammation. As the condition of the j)atient demands
333 DISEASES OF THE DIGESTIVE SYSTEM.
less opium, the dose may be diminished, or the interval between the doses
lengthened. A safe rule by which to be guided is that, so long as any
tympanitis exists, the opium should be continued.
When convalescence is fully established, one should not be too anxious to
overcome the constipation which usually exists, for a free, spontaneous
movement of the bowels generally follows a complete subsidence of the
peritonitis. Wait at least a week for this result before administering a ca-
thartic, and then, if necessary, employ one mild in its action, such as cas-
tor-oil. Warm poultices over the abdomen are usually the only local appli-
cation which I have employed. It is claimed by some that cold compresses
have a much more beneficial effect than warm applications. My experience
leads me to doubt the utility of the former, while the latter are far safer,
and I believe equally efficacious. It has been stated that when the peritoni-
tis becomes general, excessive gaseous distention of the intestines occurs,
and this distention greatly increases the danger to the patient ; under such
circumstances I have recently resorted to minute puncturing of the dis-
tended intestine with a hypodermic or a very small aspirating needle, and
have thus relieved the intestinal distention by allowing the gas to escape.
By so doing, not only is the tension of the peritoneum (which becomes an
exciting cause of the peritonitis) relieved, but the principal obstruction to
the respiration is removed, and thus cyanosis is diminished. Immediate
and marked relief is afforded by such a procedure, and as thus far I have
had no bad results follow, I am disposed to resort to it in all cases where the
abdomen becomes excessively distended and tympanitic. I remember one
case in which the gaseous distention was excessive, and the peritonitis was
supposed to be due to strangulation of a portion of intestine from old peri-
toneal adhesions, where the relief of the distended intestine by puncture
was soon followed by a removal of the intestinal obstruction and the rapid
recovery of the patient. From this circumstance I can readily understand
how a portion of intestine that was partially constricted by a band of ad-
hesion might become completely obstructed at the point of stricture by a
rapid gaseous distention of the intestine above the point of constriction, and
the relief of the intestinal distention by puncture would very likely liberate
the constricted portion and thus overcome the strangulation, and so, per-
haps, save the life of the patient.
The necessity of absolute quiet, and of the frequent administration of nour-
ishment and sometimes of stimulants, in small quantities, to this class of
patients, is apparent. Preceding and during the stage of plastic exudation,
large doses of quinine are beneficial ; but little nutriment should be admin-
istered, and that only in a fluid and a highly condensed form. Cracked ice
may be given to relieve the thirst, and, if there are signs of asthenia, iced
champagne or brandy should be given in small doses. If hiccough is dis-
tressing, it should be relieved temporarily by the inhalation of chloroform.
Vomiting is sometimes allayed by carbonated water, cracked ice and cham-
pagne, or hydrocyanic acid. Turpentine, as an injection and employed lo-
cally as an embrocation, will sometimes relieve the tympanitis. With the
asthenic form of peritonitis, a stimulating plan of treatment should be em-
ASCITES. 333
ployed with the opium. In puerperal peritonitis, great attention should be
paid to the condition of the uterus and its aj^pendages. Chronic peritonitis
is treated by local applications of iodine and mercury, and by the internal
use of iodide of potassium. Its products may be removed by tapi3ing. The
nutrition of the patient must be carried to the highest point. Tubercular
peritonitis demands small doses of opium, warm anodyne applications, and
the administration of tonics, cod-liver oil especially. The treatment of can-
cerous peritonitis is purely symptomatic ; nausea and attacks of diarrhoea
and constipation must be promptly relieved. Narcotics may be given for
the sleeplessness. Concerning the prophylactic and sanitary treatment of
puerperal peritonitis, the reader is referred to obstetrical works.
ASCITES.
(Abdominal Dropsy.)
Ascites is a local dropsy, — an accumulation of serum in the peritoneal
cavity. It has also been called peritoneal dropsy, dropsy of the abdomen,
and hydro-peritoneum. The circumstances under which it occurs are
similar to those which allow of general dropsy — viz. : obstruction to the
capillary or lymphatic circulation of the peritoneum, a diminished amount
of albumen in the blood, and degenerations of the peritoneum. Those
hydrsemic conditions which accompany exhausting chronic diseases, espe-
cially diseases of the kidneys, will induce it. One or several of these con-
ditions may be present in the same case.
Morbid Anatomy. — The amount of fluid present in ascites may vary from
a few ounces to four or five gallons. In consistency it may be viscid or
watery. It is usually of a liglit straw color, having a faint greenish opal-
escent tint. It may be opaque and dark, from admixture of blood. With
disease of the lymphatics it is milky and opalescent. Sometimes it does not
differ in appearance from pure water. It is alkaline in reaction, and may
contain albumen, blood, fibrin, fibrinogen, bile-pigments, kreatin, kreatin-
in, lymph flocculi, and bile acids. Albuminate of soda, leucocytes and pus
cells are its occasional ingredients. The endothelia of the peritoneum are
turbid, thick, and in vai-ious stages of fatty degeneration. The sub-serous
tissue is thickened, and the whole membrane has the look and feel of being
water-logged. The blood changes that cause it consist chiefly in a diminu-
tion of albumen and an increase of water. Compression, dislocation, and
diminished function of the abdominal viscera are the results of the ascitic
accumulation.
Etiology. — Ascites may be a late symptom of general dropsy. In most
other instances it results from damming back of the blood in the portal
tributaries, from pressure on the portal vein — either from hepatic and
abdominal tumors, or from a diseased condition of the liver substance —
as in cirrhosis, waxy degeneration, abscess, hepatic atrophy, portal throm-
bosis, enlarged lymphatics in the transverse fissure, and the constrictions
due to perihepatitis. These all mechanically impede the blood current in
334 DISEASES OP THE DIGESTIVE SYSTEM,
the portal vessels. Diseases of the heart or lungs which interfere with the
normal flow of the blood from the cavae will induce it in connection with
genera] dropsy ; — under this head are included tricuspid obstruction and
insufficiency, chronic bronchitis and emphysema, fibrous phthisis, and cer-
tain forms of mediastinal tumors. Anaemia, hydraemia, chlorosis, malarial
cachexia, purpura, chronic arsenical poisoning, scurvy and chronic Bright's
disease, j)roducing hydraemia— and old age or great exhaustion without
structural disease — lead to what is often called asthenic ascites or cachectic
dropsy. Peritoneal dropsy not infrequently accompanies extensive degen-
eration of the peritoneum, such as tubercle and carcinoma. Finally, ascites
may occur from unknown causes — from taking cold, after suppression of the
menses, after the sudden disappearance of acute and chronic cutaneous
eruptions and ulcers, and perhaps from atmospheric causes.' It has been
suggested that malignant disease of the ovaries and other pelvic organs, and
of the mesenteric and retro-peritoneal glands, obstructs the capillaries and
the lymphatic orifices, increasing the functional activity of the endothelia,
and thus induces ascites.^
Symptoms. — The first sign of ascites is a gradual increase in the size of
the abdomen. The enlargement in simple ascites takes place without pain,
tenderness, or local subjective symptoms. There is a feeling of fulness,
and the patient is rendered uncomfortable by pressure of the fluid. The
respiratory movements are interfered with, and dyspnoea soon results.
The functions of the stomach may be disturbed, and there may be vomit-
ing, anorexia, and perhaps hsematemesis. Flatulence and diarrhoea are
frequently present, but when the accumulation of fluid is large it produces
colicky pains, and often obstinate constipation. All these symptoms are
relieved as soon as the fluid is removed. Gradually the dyspnoea increases,
the patient walks with difficulty, with the legs spread widely apart ; the
urinary secretion is diminished from the pressure on the kidneys and renal
"vessels. The recumbent posture greatly aggravates the dyspnoea. The
skin and mucous membranes become dry ; the liver and pelvic viscera are
displaced ; the heart and lungs are pushed upward, and the skin over the
abdomen becomes tense and shining. The umbilicus is bulged out in the
form of a globular tumor. The superficial veins are enlarged and tortuous.
If the inguinal canal is open, fluid may pass into the scrotum ; and ex-
cessive ascites, by pressure on the vena cava, causes oedema of the feet and
legs. In hepatic diseases the fluid is chiefly confined to the abdomen, but
in cardiac and pulmonary dropsies the fluid accumulates first about the feet
and extends upward, and the abdominal dropsy is then a part of a general
anasarca. In hepatic dropsies the extremities emaciate while the abdomen
enlarges ; the skin has a muddy jaundiced hue, and the patient becomes
exhausted and apathetic. Jaundice, uraemia, delirium, convulsions, coma,
and cholaemia are prominent symptoms as death approaches.
Physical Signs. — The physical examination of the abdomen is most im-
portant in the diagnosis of ascites.
Inspection. — The abdomen, if distended with fluid, presents the appear-
1 Wagner, Gen. Path., pp. 234-5. ^ Oppolzer.
ASCITES. 335
ance of a globular or dome-like tumor, the false ribs are elevated and
pressed out, and the superficial veins are visible and prominent. The cir-
cumferential measurement of the abdomen will often be three times as
great as normal. If the effusion is moderate, the shape of the abdomen
changes with a change of the position of the patient : it broadens when he
lies on his back, and when he stands the enlargement will be confined to
the lower portion. The fluid always gravitates to the most dependent
portion.
Palpation. — Fluctuation is obtained when the level of the fluid is above
the pelvic brim. To obtain the wave most distinctly place the patient on
his back, place the flat of the hand on one side of the broadened abdomen,
and with the other hand give one smart tap at a point opposite ; che im-
pulse of the blow will be felt by the palm of the hand.
Percussion. — There "will be flatness below the level of the fluid, and
tympanitic resonance above. The line of dulness changes with the
change of position, and accurately measures the amount of fluid. When
only a small amount of fluid is present the physical signs of its presence are
commonly obtained by placing the patient in the " knee-elbow " position.
Differential Diagnosis. — Ascites may be mistaken for ovarian dropsy, dis-
tended bladder, pregnancy, hydatid cysts of the liver, and enlargement of
the spleen. It is imjDortant in making a differential diagnosis between
ascites and ovarian dropsy to have a perfect history of the case. The ab-
dominal enlargement in ascites is uniform, in ovarian dropsy it is irregu-
lar. Ascites, however slight, begins at the most dependent portion of the
abdomen, while ovarian dropsy begins in one of the iliac fossae and gradu-
allv extends upwards toward the umbilicus. With every change of posi-
tion, in ascites, the line of dulness changes ; a large ovarian cyst is to be
recognized by its fixed position and non-gravitation of its fluid. In ascites
there is fluctuation on palpation ; in ovarian dropsy, fluctuation is absent
or localized. The abdomen is usually tympanitic above the level of the
fluid and flat below in ascites, while in ovarian tumor there is often a tym-
panitic percussion sound at the most dependent portion of the abdominal
cavity. In ovarian dropsy the outline of the cyst is generally appreciable,
except in very large tumors where the peculiar form of the cyst may be
lost, but a rectal or vaginal exploration will generally at once remove all
doubts. In ascites there will generally be a history of liver, heart, or
kidney disease, and the uterine organs and functions will be normal. On
tapping the abdomen a serous fluid will be withdrawn in ascites ; in ovarian
tumors, it will be a dark, highly albuminous fluid and contain granular
non-nucleated cells, supposed to be characteristic.
A distended and sacculated bladder may be mistaken for dropsy, but the
introduction of' the catheter will decide the question.
Pregnancy will afford ballottement, placental bruit, the sounds of the
foetal heart, and will be accompanied by distinct mammary changes. The
uterine tumor can be distinctly mapped out, and a vaginal examination
combined with external palpation will rarely fail to make a differential
diagnosis between it and ascites.
336 DISEASES OF THE DIGESTIVE SYSTEM.
An hydatid cyst of the liver produces flatness undeviating in area, which
gradually extends from above downwards, and seldom reaches the pelvic
brim. Hydatids produce hydatid fremitus on percussion, which is charac-
teristic. Again, on withdrawal of the fluid, a miscroscopical examination
will often discover the booklets of the echinococci.
Enlargement of the spleen is unsymmetrical ; the tumor is fixed, there is
no tympanitis, no fluctuation, and the boundaries of the enlarged organ
can be mapped out on palpation and percussion. Usually the nofch at the
anterior border of the spleen is so distinct that it at once indicates the
gland.
Prognosis. — The prognosis depends upon the conditions under which the
ascites occurs ; if it is dependent upon organic disease of the liver, heart,
or kidney, the prognosis is unfavorable, but when it is not dependent upon
structural visceral lesions, e.g., idiopathic and anaemic ascites, the prog-
nosis is good. The ascitic accumulation may take place rapidly, or weeks
or months may elapse before the cavity of the abdomen ia distended. The
average duration of hepatic ascites is about six months. So long as the
cause remains, the fluid will accumulate. Ascites may terminate in re-
covery by the spontaneous or mechanical removal of the fluid, or by the
removal of its cause, or it may terminate in death, from complications, as
peritonitis, albuminuria or heart-failure, or from pure slow asthenia.
Treatment. — The first and most important thing in the treatment of
ascites is to discover the cause, and either to remove or palliate it. In
most cases the treatment merges into the treatment of the diseased condi-
tions which produce it. In all cases the diet should be highly nutritious
and concentrated ; as little fluid as possible should be taken. The contin-
ued use of powerful diuretics and hydragogue cathartics usually does harm.
They weaken the patient and often favor rather than retard the
ascitic accumulation. Elaterium is the most efficient drastic cathartic,
the potash salts, nitre, squills and juniper are the most efficient diuretics.
Jaborandi has recently been much employed for the removal of dropsical
accumulations. In most cases these accumulations can be rapidly removed
by this drug, but my own experience leads me to the conclusion that it
hastens rather than retards the fatal issue. Hot-air baths should never be
employed for the removal of ascitic accumulations.
Paracentesis abdominis will have to be resorted to sooner or later in these
cases, but the rule is to postpone it as long as possible. I am, however,
in favor of tapping before the accumulated fluid has caused pressure
upon the viscera. I am convinced that whenever fluid accumulation takes
place in the peritoneal cavity, tapping should be promptly resorted to,
unless the cause can be removed by mild cathartics or non-stimulating
diuretics ; and the number of recoveries and the prolongations of life
which have followed this course in my experience cause me unequivocally
to recommend it in preference to the prolonged use of those remedial
measures which increase the discharges from the skin, kidneys and bowels.
In a large number of cases, improvement of the patient's general health by
tonics, of which quinine, iron and cod-liver oil are the best, is followed by
ACTIVE HYPERyEMIA OF THE LIVER. 337
subsidence of the dropsy, and its return is also prevented for a long time
after its removal by tapping.
DISEASES OF THE LIVER.
Diseases of the liver may be classified under the following heads :
I, Hypercemta : — III. Degenerations : —
a. Active or Fluxion, . Amyloid or Lardaceou8»
h. Passive or Congestion. Fatty.
II. Inflammations : — Pigmentary.
a. Interstitial Hejjatitis or Atrophy.
Cirrhosis. IV. iVew Growths: —
b. Circumscrihed Hepatitis or Cancer.
Abscess. Giimmata.
c. Diffused HejMtitis or Acute Hydatids.
Yellow Atrophy. ^ Tubercle.
Perihepatitis, Local or Gen- V. Diseases of the Gall Ducts
eral. and Gall Bladder.
Pylephlebitis, Adhesive and Sup- VI. Jaundice, Hepatogenous and
purative. Hematogenous.
VII. Functional Derangements.
ACTIVE HYPEREMIA OF THE LIVER.
Active hyperaemia of the liver is an abnormal determination of blood
to the organ. It may be acute or chronic.
Morbid Anatomy. — A liver that is the seat of active hyperaemia is more
or less enlarged in all directions. Its color varies from a light to a dark red'.
It has a firmer feel than normal, although its consistency is really dimin-
ished. The organ is heavier and smoother than normal, its surface present-
ing a peculiar shining appearance.
On section, its substance shows a uniform red color, blood flows freely
over its cut surface, from the arteries and capillaries which are dilated and
sometimes tortuous. When the hyperemia is intense, the glandular sub-
stance of the organ is compressed and there may be evidences of sub-peri-
toneal effusion. So intense may be the hyperaemia that hemorrhagic soften-
ing and apoplectic extravasation result, and isolated clots or an unbroken
layer of coagulated blood may be found under its serous covering.
In chronic hyper mmia the liver is often found in a state of partial fatty
degeneration, somewhat softened, and of a light red or yellow color. In
rare instances, chronic hyperaemia may lead to induration and incipient
cirrhosis. In the severer types abscesses may be found, and the infiltration
of a substance resembling albumen has in some cases advanced so far as to
give distinct colloid degeneration. In syphilitic new-born children, active
hepatic hyperaemia is sometimes found associated with a peculiar plastic
23
338 DISEASES OF THE DIGESTIVE SYSTEM.
exudation. It is important to remember that the normal hepatic hyper-
semia temporarily developed after hearty meals or the free use of stimulants
may be mistaken for active hypersemia. Both acute and chronic hyper-
semia of the liver may be associated with catarrh of the bile ducts.
Etiology. — There is a normal functional hyperaemia of the liver induced
by an unusually large meal, or one very rich in hydrocarbons, or by the
free use of wines : this hypersemia is due to increased blood pressure in the
vena portge ; it becomes abnormal in those who daily indulge in eating to
excess, especially if they lead sedentary lives. If the liver-tissue, which
supports the walls of the capillary vessels, becomes relaxed, there will be an
abnormal afflux of blood to the organ. This is the case in traumatic
hypergemia, where a blow over the viscus causes a localized fluxion. Any
inflammation or growth causing softening of the parenchyma will induce it.
The action of drugs, spices and alcohol is best explained on this basis. In-
tense hepatic hypergemia may be caused by miasmatic influences, malaria,
and other blood-poisons. Under the latter head is included a peculiar
active hyperaemia which occurs in the livers of syphilitic children, and in
secondary syphilis of adults. High temperature undoubtedly gives rise to
active hepatic hyperfemia, especially when it is associated either with acute
or chronic malarial infection, Vaso-motor disturbances may undoubtedly
lead to active hepatic hyperaemia. It sometimes occurs during and after
pregnancy from some unknown cause ; also before the establishment of the
menses, and during the menopause. Capillary embolism may cause local-
ized hepatic hyperaemia.
Symptoms. — Active hypergemia of the liver is usually attended by a sense
of weight and constriction in the right hypochondrium, with some tender-
ness on pressure under the free border of the ribs. In active malarial
hypergemia, there is also gastro-intestinal catarrh, nausea, vomiting, diar-
Thoea, and slight jaundice. There is a bitter taste in the mouth, loss of
.■appetite, coated tongue, drowsiness and apathy. Headache is frequent, and
ihe patient complains of pain shooting up the right side to the right
;shoulder. This pain is due to pressure on the phrenic nerve, and is more
intense after meals and when lying on the left side. A sense of dizziness
tcomes on when the patient assumes any other position than on the back or
right side. It is more or less increased by pressure upward against the
liver. In severe cases of malarial hyperaemia, or when it is associated with
extensive blood changes, such as scurvy, the symptoms are often masked by
those of the condition with which it occurs.
Physical Signs. — Inspection in severe cases may show bulging of the
right hypochondrium, and loss of motion of the lower ribs on the right side.
On jpalpation the liver is found enlarged and smooth, and its free
border is felt below the ribs ; firm pressure against its under surface causes
pain.
Percussion. — The area of hepatic dulness is increased in every direction,
but more vertically than laterally.
DiiFerential Diagnosis. — A severe active hyperaemia may be mistaken for
circumscj'ihed hepatitis with abscess. In circumscribed hepatitis there is
PASSIVE HYPEREMIA OF THE LIVER. 339
acceleration of the pulse, rigors followed by a slight rise of temperature,
and localized pain. Kecurring cliills and sweats indicate the formation of
pus. In abscess the hepatic enlargement is irregular, while in active
hypersemia it is uniform. If the case is seen early, and the enlargement is
carefully followed, in hyperaemia it will be seen to take place rapidly, while
in abscess it will be slow. The hepatic enlargement from active hyperaemia
may be distinguished from displacement of the liver downwards, by the
fact that, although its free border may extend far below the free border of
the ribs, the normal area of hepatic dulness is not increased.
Prognosis.— Active hyperaemia generally subsides as rapidly as it occurs.
The only danger is that the causes which produce it may be continued,
and lead to some form of hepatic degeneration.
Treatment. — The main indication in the treatment of this condition is to
remove its cause. When high living and alcoholic stimulants cause it, re-
strict the diet and stop the alcohol. When it occurs from prolonged high
temperature, or from malarial influences, a change of residence is the only
remedy. An excess of blood in the liver may be temporarily removed by
saline or mercurial purges, by taraxacum or podophyllum ; their action will
be increased by the application of one or two leeches about the anus. In
active malarial hyperemia, the mercurial purges and leeches may be followed
by full doses of quinine. Turpentine stupes may be applied over a very
tender liver. When there is gastro-intestinal catarrh with diarrhoea,
chloride of ammonium and ipecacuanha will be found of service. In those
who have a predisposition to active hepatic hyperaemia, the daily use of
mineral waters will be found of service.
PASSIVE HTPEE^MIA OF THE LIVEK.
Passive or mechanical hepatic hyperaemia (''congestion of the liver")
consists in an excess of blood, chiefly in the portal veins, with a slowed
current.
Morbid Anatomy. — A congested liver, in its early stage, is larger, heavier
and darker in color than the normal liver, the extent of the increase in size
corresponding to the degree of the congestion. The capsule may be
stretched tightly over the enlarged organ, and present a shining appear-
ance. The consistency of the organ is increased, frequently amounting to
a stony hardness.
On section, the cut surface appears mottled, rarely uniformly red in
color ; the small dark spots seen upon its cut surface are the enlarged and
thickened veins in the centre of the liver lobules, and as the return of
blood by these veins is impeded, the surrounding cells undergo atrophy,
and a granular pigment is deposited about the vence centrales. This change
in color is made more apparent by a deposit of fat globules in the periphery
of the lobules, which causes a dirty white ring around the dark central
spot. Occasionally there are yellowish spots about the central vein due
either to a catarrh in, or obstruction of the bile ducts, or to distention
340
DISEASES OF THE DIGESTIVE SYSTEM.
of the minute ramifications of the portal vein.
In the advanced stage of
hepatic congestion,
the liver is diminish-
ed in size and has a
peculiar hard feel.
On section, it presents
the char acteristic
''nutmeg" appear-
ance, which has been
called the red granu-
lar liver. The proc-
esses which were es-
tablished in the ear-
lier stage of the con-
gestion, and the new
conn ective -tissue
which has been de-
veloped in the inter-
lobular spaces, dimin-
ish the parenchyma
of the organ.' The
rootlets of the central
vein become dilated
and hypertrophied
and crowd upon the
liver cells ; thus the
central spot spreads nearly to the periphery of the lobules. Atrophy of
the cells grouped around the central vein occurs, and a soft pultaceous
mass, in which appear new vessels, takes their place. The cells at the
periphery are in a state of fatty infiltration, and connective-tissue passing
inward from the interlobular spaces produces the contracted, stony hard
liver. In connection with these changes in the liver, the mucous mem-
brane of the stomach is usually the seat of chronic catarrh, and the spleen
is enlarged.
Etiology. — The causes of hepatic congestion are mainly included under
the head of impeded venous return. Heart disease is the most fre-
quent cause of such obstruction. The damming back of the blood in the
hepatic veins is the necessary result of tricuspid insufficiency, and of right
heart failure. When right ventricular hypertrophy fails to compensate for
valvular lesions in the left heart, or when disease of the lungs, as emphyse-
ma and chronic pleurisy, obstructs the blood current in the pulmonary artery
so that the right ventricle is unable to empty itself, engorgement of the
hepatic veins necessarily follows. The absence of valves in these veins,
and the fact that they cannot collapse, favor this result. In the same
way enfeebled heart power, occurring in the course of exhausting diseases,
causes congestion of the liver. Habitual constipation and a sedentary
1 Atrophy is chronic congestion with, dilatation of the central vessels and their radicles.
Pig. 68.
Passive Hepatic Hypersemia.
Section of liver shoiving a single lobule.
A. Central vein of lobule.
B. Area of congestion. — Vessels filled with blood, crowding the hepatic
cells.
C. Atrophied liver cells.
B. CommeruAng fatty infiltration of cells in peripheral zone, x 350.
PASSIVE HYPERiEMIA OF THE LIVER. 341
mode of life, either singly or combined, may produce it. The sudden
suppression of long-continued hemorrhages, as menorrhagia, or bleed-
ing hemorrhoids, may lead to passive hypergemia of the liver. A large
mediastinal tumor, such as a thoracic aneurism, may also produce it by
pressure on the cava.
Symptoms. — As there is usually some derangement in the circulation of
the thoracic organs, the early symptoms are very apt to be confounded with
those of cardiac or pulmonary disease. But soon slight jaundice follows
the headache, drowsiness and apathy, and it lacks the i^eculiar greenish
hue of that which sometimes accompanies the cyanosis of long-standing
heart disease. Gastric catarrh will usually attend these symptoms, marked
by loss of appetite, nausea, and vomiting. In the "India Liver" there is
anaemia, and soon a cachexia is developed. The skin is dry and harsh.
Later, hemorrhoids appear, and after a paroxysm of dyspnoea and cyanosis
the hepatic dulness is markedly increased. In severe cases haematemesis
may occur. If congestion has reached the stage of induration, the gastric
symptoms become greatly aggravated, and tympanitis, gastric hemorrhage,
and general dropsy occur, 'i'he bowels become constipated, and the faeces
clay-colored. The urine is scanty, high-colored, and usually presents traces
of albumen ; it is loaded with lithates. These patients finally become
irritable, and are subject to fits of palpitation and irregularities of the
pulse.
Physical Signs. — Inspection may show slight bulging of the right hypo-
chondrium and some restriction in the movements of the lower portion of
the right thoracic walls.
Palpation. — In its early stage, the free border of the liver is readily felt
below the margin of the ribs ; it is smooth and tender. Later the organ
is diminished in size, but its free margin can still be felt, and is hard and
uneven.
Percussion. — At its commencement the normal hepatic dulness is in-
creased in every direction, and firm percussion elicits pain. In advanced
cases the area of hepatic dulness is uniformly diminished. It is always
important to subject the chest to a thorough physical examination to deter-
mine the presence or absence of pulmonary or cardiac disease.
Differential Diagnosis. — Congestion of the liver may be so masked by the
primary disease which produces it, that it will be overlooked, but it will
rarely be confounded with any other form of hepatic disease.
Prognosis. — The prognosis depends upon the condition which causes it.
If constipation and a sedentary life cause it, the prognosis is favorable. In
chronic pleurisy and emphysema it can only partially be relieved. When it
is associated with extreme cardiac disease, recovery is impossible and re-
lief is only temporary.
Treatment. — When the symptoms which attend congestion of the liver
are urgent, a mercurial purge or a brisk saline cathartic with the applica-
tion of a few leeches about the anus will give relief. If the symptoms are
not urgent, a mild laxative followed by a course of mineral waters will
be beneficial. If the gastric symptoms are severe leeches may be applied
342 DISEASES OF THE DIGESTIVE SYSTEM.
over the stomach. The diet must be as free from carbo-hydrates as is
compatible with nutrition. Nitro-muriatic acid internally and externally
is recommended by English and East Indian physicians. Chloride of am-
monium and iodide of potassium are often advantageous, reducing the
enlarged organs. In some cases of extensive cardiac disease, mineral
waters are not well home; and although digitalis will relieve the conges-
tion, it is apt to interfere with digestion. Each case is peculiar and requires
its special treatment, which at best is only palliative.
INTERSTITIAL HEPATITIS.
Interstitial hepatitis is an inflammation of the connective-tissue of the
liver. It has been variously named sclerosis of the liver, cirrhosis, the
"gin-drinker's" liver, the "hob-nailed" liver, granular, and gouty liver.
Cirrhosis of the liver, the name most commonly used, was first applied by ,
Laennec. It means yellow, referring to the color, and not to the consis-
tence of the organ.
Morbid Anatomy. — The anatomical changes in interstitial hepatitis begin
in the connective-tissue covering the smaller twigs of the vena portae, and
gradually extend to its larger branches. The hyperplastic process consists
in the formation of a soft, red, pulpy or gelatinous mass, which makes its
appearance first in the portal canals. This mass consists of an immense
number of small round cells, which soon undergo fibrilization and form
new connective-tissue. The new tissue contracts ; this contraction may
be limited, or it may involve the whole organ. In the latter case, both
stages — namely, the stage of enlargement due to the hyperplasia, and the
stage of diminution in size, the result of connective- tissue contraction —
may exist in the same liver at the same time. The new tissue, contract-
ing, presses on the portal capillaries and liver-cells, and gradually en-
croaches on the intra-lobular structures, causing atrophy and disappearance
of the cells at the periphery of the lobules, while those at the centre un-
dergo fatty change, the result of defective nutrition. Sometimes the cells
at the periphery undergo fatty change before they atrophy. The bile-ducts
and hepatic capillaries suffer from compression, and the cells around the
central vein are bile-stained.
In the first stage of cirrhosis, the liver is slightly enlarged, noticeably in
the vertical direction ; it is resistant and hard to the feel, the edges are
rounded and smooth, and the capsule becomes opaque and thickened. Upon
the capsule are numerous small flattened projections, which are, however,
not sufficiently prominent to destroy the smoothness. In the first stage the
liver is uniformly enlarged and hypersemic. In the second stage it is
smaller than normal, the left lobe usually being but a caudal-like append-
age to the right, which is nearly globular in shape. The whole organ
presents a hob-nailed appearance, and is hard, rough, leathery and granu-
lar. The serous covering assumes a dull gray color, and fibrous bands bind
the organ to the adjacent parts, especially to the diaphragm. In syphilitic
cirrhosis these changes are in patches, which are large and well defined.
INTERSTITIAL HEPATITIS.
343
On section the liver-tissue, during the first stage, is extremely hyper-
gemic. The new cell growth around the branches of the portal vein and be-
tween the lobules has a pulpy, fleshy look. In the second stage, the liver
gives a cartilaginous feel to
the knife, and the capsule
is thickened and resistant.
The cut surface presents a
yellow, mottled appearance,
the mottling being due to
three changes : first, the
non-vascular fibrinous
bands, which are of a slate
color ; second, the obstruc-
tion of the bile ducts inter-
fering with the outflow of
bile, and the centres of the
atrophied cells becoming
pigmented ; third, the cells
at the periphery of the lobes
becoming the seat of fatty
degeneration. The n e w-
formed connective-tissue is
filled with an abundance of
round cells, formerly called
nuclei ; they are now known
as lymphatic corpuscles, and
are probably emigrated leu-
cocytes. The smaller
branches of the portal vein
are shrunken and twisted,
and in extreme cases new
capillaries are developed,
which communicate with both hepatic and portal vessels. Again, a whole
lobule may have disappeared and its place be occupied by connective-tissue.
The bile-ducts have their commencing I'ootlets destroyed and their mucous
membrane tumefied. In cases of long-standing cirrhosis, the gall-bladder
will be found bound to the adjacent parts by adhesions, and its walls are
thick and tough ; while the spleen is enlarged, softened and congested.
The gross appearance of the liver in cirrhosis may vary in different cases,
but the anatomical lesions are the same in all.
There is a form of this disease which has been called liijpertropliic
cirrhosis, because the liver is markedly increased in size, sometimes reach-
ing six or seven pounds in weight ; but the fibroid change, the yellow
staining, the atrophy of liver-cells, and the fatty change at the periphery of
the lobule, are the same as in the ordinary variety, the only difference being
a marked increase in the size of the liver.
As a result of the compression and obliteration of the branches of the
D
Fig. 69.
Interstitial Hepatitis.
Section of liver in advanced cirrhosis, as shown . by low mag-
nifyiiig power.
A, A, A. Bands of connective-tissue.
B, B, B. Brunches of portal vein.
C, C\ C. Hepatic ducts.
D, I). Newly fanned connective-tissue.
E, E, E. Lobules, separated by the advancing cirrhosis.
F, F. Lobules nearly obliterated, x 40.
S4:4
DISEASES OF THE DIGESTIVE SYSTEM.
portal and hepatic vein from the new connective-tissue in the advanced
stage of cirrhosis, a chronic venous congestion occurs in those viscera
which empty their blood into the portal vein. The spleen, stomach and
intestines consequently be-
come the seat of chronic ve-
nous congestion. The result
of this is, that with cirrhosis
of the liver we find an en-
larged spleen, and a chronic
gastric and intestinal catarrh.
If the portal obstruction is
very great, there will be trans-
udation of serum from the
vessels of the peritoneum into
the peritoneal cavity, causing
ascites.
Etiology. — The chief cause
of cirrhosis is the intemperate
use of alcohol. Alcohol is
most rapidly absorbed when
the stomach is empty. When
it is taken in a concentrated
form without food it acts as
a direct irritant to the hepatic
circulation. If this irritation
is long continued interstitial
hepatitis is the result. Those
who take alcohol before break-
fast as well as through the day are almost certain to develop cirrhosis of
the liver. Those who partake freely and daily of highly seasoned food,
even though they may not use alcohol, are also liable to develop this
disease, especially if they reside in hot climates. Syphilis, gout and rheu-
matism cause it. Gout, especially starting from faulty liver digestion, is
liable to develop cirrhosis. Malarial hyperaemia, if long continued, may
lead to it. Extension of inflammation from the capsule of Glisson may
develop cirrhosis. It may also occur without any assignable cause.
Symptoms. — The early symptoms of interstitial hepatitis are those of
hepatic congestion. Following the dull pain and tenderness in the hepatic
region, the dyspncBa, apathy, headache, nausea and furred tongue, there
is loss of appetite, especially for meats. The individual has a desire for
food, but after a few mouthfuls the sense of hunger gives place to loathing;
this occurs most frequently at breakfast. Diarrhoea alternates with con-
stipation, and distressing attacks of retching, especially on waking in the
morning, are followed by intestinal pain and flatulence. As the dyspepti3
symptoms increase, slight jaundice appears, but it is never very marked,
for although the bile secretion is diminished, there is no obstruction to its
passage into the intestine. Hemorrhoids are early signs of obstructed
Pig. to.
Interstitial Hepatitis.
Same tissue as in last illustration, more highly magnified.
A, A. A. Conrifctive.-tissue of ajm'tal canal, containing, B, B,
Hepatic dvcts; C, C, Portal veins; and D, D, Hepatic ar-
E. Atrophied hepatic cells in periphery of a lobtde.
F. Infiltration of round cells— the commencement of the new con-
nective-tissue growth, x 300.
INTERSTITIAL HEPATITIS. 345
portal circulation and are a very constant accompaniment of cirrhosis, and,
with the gastric symptoms, are the earliest indications of obstruction to the
portal circulation. If cirrhosis has been induced by the excessive use of
alcohol, a craving for alcohol persists. Attacks of vertigo and occasional
slight elevations of temperature with emaciation and cachexia mark the
end of its first stage. The dingy hne of the surface, which was early
present, disapj)ears, and the skin gradually assumes an earthy pallor, rarely
tinged with yellow. The increase in the hepatic symptoms and the severe
pain and tenderness over the hepatic region, which are sometimes present,
are due to intercurrent attacks of perihepatitis.
At the commencement of the second stage gastritis is established as a
result of the mechanical obstruction to the capillary circulation of the
mucous membrane of the stomach, and is marked by acidity, nausea, and
often by vomiting after taking food, in consequence of which emaciation,
weakness, and depression of spirits occur ; venous stigni.*/.ta may now appear
on the cheeks. The obstruction of the vessels of the gastric mucous mem-
brane is often so great that haematemesis occurs, and although the patient
may experience temporary relief after the first bleeding, the hemorrhage
will recur, and may be the direct cause of death. Intestinal hemorrhage
occasionally occurs from the same cause. If there is persistent diarrhoea
during this stage, it indicates that there is gastro-intestinal catarrh. Tym-
panitis, as well as intestinal catarrh, usually precedes the occurrence of
ascites, which is slow and insidious in its advent, and so masked by the
preceding tympanitic distention that it is often difficult to determine the
exact time of its occurrence. It will usually be noticed that, before the
appearance of the ascites, the abdominal veins, especially of the right side,
are distended, sometimes enormously.
Ascites is sometimes absent in advanced stages of cirrhosis. When
this happens, any or all of the following conditions may exist to ac-
count for its absence : first, during the contraction of the new connective-
tissue, the branches of the vena portfe sometimes remain patent. Second,
the hemorrhoidal branches of the inferior mesenteric may inosculate with
the internal iliac. Third, the veins of the colon and duodenum may
anastomose with the left renal vein. Fourth, the phrenic vein may com-
municate with some of the more superficial branches of the vena portge.
Fifth, new vessels may be formed in the adhesions which bind the liver to
the adjacent parts, and thus relieve the obstructed portal circulation.
Sixth, the portal and hepatic vessels may anastomose sufficiently within
the liver to relieve the portal obstruction. Seventh, branches of the vena
porta, which are distributed on the under surface of the diaphragm, and
on the inner surface of the abdominal parietes, may anastomose with the
internal mammary and epigastric veins, and thus assist in returning the
blood to the right auricle. When the internal mammary in its turn be-
comes engorged, there is a dark bluish mass surrounding the umbilicus,
due to distention of the cutaneous veins, and called the "caput Medum "
When ascites is once developed it progressively increases. By its pressure
dyspnoea and often pulmonary oedema are developed, and the gastric de-
346 DISEASES OF THE DIGESTIVE SYSTEM.
rangements are so increased that rapid emaciation quickly follows its
accumulation. (Edema, beginning in the feet, gradually extends upward.
Fluid drawn from the abdominal cavity is of a pale amber color, highly
albuminous, and of a specific gravity varying from 1.010 to 1.020 ; it is not
turbid, and contains no inflammatory products. Slight jaundice may ap-
pear with the ascites, but if excessive is due to pressure on the ducts, either
from connective-tissue indurations or from enlarged lymphatics in the trans-
verse fissure, which obstruct the outflow from the bile ducts. The mind is
usually clear to the last, but sometimes the patient will pass into a state
of complete stupor, which is preceded by delirium and active cerebral
symptoms. At first, it seems plausible to ascribe the cerebral symptoms
to cholaemia, but I have found the jaundice in inverse proportion to the
cerebral symptoms. Cholaemia may occur in cirrhosis, and then, of course,
exhibits its peculiar train of symptoms ; but I think the more reasonable
view is the one that ascribes the delirium, coma, and other cerebral symp-
toms which come on late in this disease, to alcohol. The stools in cirrhosis
are characteristic. They are clay-colored in the centre ; surrounding this
there is a dull pinkish ring, and around this a slaty gray ring tinged with
mucus. The urine is scanty and very dark colored ; in one-third of the-
cases it contains albumen. Bile pigment is present in the urine when
jaundice exists. The urine is rich in urates, and a pinkish sediment of
lithates is very common.
Physical Signs. — Inspectio7i, in the early stage of cirrhosis, may show a
slight loss of motion over the lower portion of the right side. In a few in-
stances the faint outline of the liver margin is seen below the free border of
the ribs.
Palpatio?!. — The surface of the liver is smooth, or finely granular; the
edges are round ; on firm pressure there is a marked tenderness, and more
or less resistance.
Percussion. — The area of hepatic dulness is somewhat increased in the
early stage (especially over the right lobe) in a vertical direction, and so,
too, is the area of splenic dulness.
Inspection, in the advanced stage, shows enlargement of the superficial
veins of the abdomen, chiefly on the right side, and the caput Medusm is
often visible. There is usually more or less ascites, and the face and sur-
face of the body are clay-colored, often tinged with yellow.
Palpation is best performed when the patient is lying on the left side,
and if the surface of the liver can be felt, it will be uneven and hob-nailed,
with sharp, firm edges.
Percussion gives a diminished area of hepatic dulness, and the left lobe
of the liver may be so small that the line of hepatic dulness will not extend
to the left of the median line. Persistent tympanitic percussion is present
above the line of the fluid, and flatness below. The spleen is markedly en-
larged, and the splenic dulness extends below the free border of the ribs.
Differential Diagnosis. — The early stage of cirrhosis may be mistaken for
fafty or waxy degeneration of the liver. In fatty liver, the enlargement be-
gins without localized pain, and there is no sense of constriction or dys-
INTERSTITIAL HEPATITIS. 347
pepsia, so constantly present in the early stage of cirrhosis. In fatty
liver, the skin is of a light yellow color, is greasy, and has a velvety
feel ; in cirrhosis, it is of a dingy hue, wrinkled, and rough. There is a
history of high living, and of a sedentary life, or of some phthisical com-
plication with fatty liver ; while in cirrhosis, a history of excessive spirit-
drinking, gout, rheumatism or syphilis is elicited. The liver is doughy and
painless in fatty degeneration, while it is hard, resistant and tender in cir-
rhosis. The tendency in fatty liver is to obesity, while emaciation is rarely
absent in cirrhosis. Ascites is never an attendant of fatty liver.
Waxy liver is accompanied by a history of syphilis, prolonged suppura-
tion, or disease of bones ; the face is pale and pufPy, the urine is increased
in quantity and of low specific gravity. Pressure over the liver gives no pain,
and the surface of the organ is smooth, and its free edges sharp and well
defined. These symptoms readily distinguish it from cirrhosis.
The advanced stage of cirrhosis may be confounded with chronic peri-
tonitis, of a tubercular or cancerous origin, with gastric ulcer, with adhe-
sive pylephlebitis, chronic or brown atrophy of the liver, multilocular hy-
datids, gummata and cancer.
Gastric symptoms are prominent in cirrhosis, and absent \n peritonitis.
The ascitic fluid of cirrhosis is albuminous, while in chronic peritonitis it
contains inflammatory products. The countenance has a clay-colored or
jaundiced hue in cirrhosis ; in peritonitis, it is pale and anxious. The liver
is diminished and the spleen increased in size in cirrhosis. The abdo-
men is excessively tender in chronic peritonitis, and the fluid accumulates
more rapidly than in cirrhosis.
A history of drinking, dyspepsia, haematemesis and emaciation may sug-
gest ulcer of the stomach ; but if it is remembered that tympanitis, asci-
tes, hemorrhoids, clay-colored faeces, dark, scanty urine, a small and hob-
nailed liver, and an enlarged spleen are present in cirrhosis, and absent in
ulcer of the stomach, the differential diagnosis is readily made.
In cancer of the liver, the nodules are very much larger than in cirrho-
sis. Ascites and enlarged spleen, if present in cancer, occur late, when the
large size of the liver leaves no doubt in the diagnosis. The liver is exces-
sively painful and tender on pressure, and there are marked exacerbations
of the pain. A cancerous cachexia, with an almost chlorotic hue, exists in
cancer. These, with the history of the case, and perhaps the presence of
cancer in other organs, are sufficient for its diagnosis.
Hepatic phlebitis may give symptoms identical with those of cirrhosis.
The most important diagnostic point is, that in hepatic phlebitis the as-
citic fluid accumulates very rapidly, and after paracentesis returns more
quickly than in cirrhosis. Jaundice occurs early and rapidly deepens, and
the stools are dark-brown and semi-fluid in phlebitis. The points of dif-
ferential diagnosis between the other diseases which have been named and
cirrhosis, will be considered under the head of those diseases.
Prognosis. — The prognosis will be determined by the stage of the cirrhosis.
In its early stage its progress may be arrested, but Avhen the stage of contrac-
tion is reached, the disease is progressive, and the prognosis is exceedingly
348 DISEASES OF THE DIGESTIVE SYSTEM.
unfavorable. A fatal result occurs in all cases. Its course is a chronic one,
and though death has occurred in three months from the time the liver be-
gan to be diminished in size, I have usually found a year and a half to be
its average duration. Complicating diseases influence the prognosis. Hem-
orrhage from the intestine and from the hemorrhoidal veins may be so great
as to exhaust the patient, and render him too feeble to resist the inroads of
the disease. This class of patients are especially liable to develop the cir-
rhotic form of Bright's disease. Delirium tremens, pleurisy, and pneumo-
nia sometimes complicate it. Death may result from exhaustion due to
faulty nutrition, from the large fluid accumulation, from repeated and pro-
fuse hemorrhages, and from wasting diarrhrea. Intercurrent pulmonary or
cardiac disease, peritonitis, or delirium tremens may be the direct cause of
death. Those cirrhotic patients live the longest who have large dropsical
accumulations, the dropsy disappearing and recurring.
Treatment— Cirrhosis, in its early stages, should be treated in the same
way as active hepatic hypersemia. In alcohol drinkers, all spirituous
liquors must be abstained from, and the patients must be placed on a nutri-
tious, though restricted diet, from which all irritating ingesta are excluded,
and alkaline waters should be freely taken. If the hepatic congestion is
intense, leeches to the anus, mercurial purges, and nitro-muriatie acid will
be found of temporary service. The importance of a restricted diet, and
the free use of saline waters in this stage of the disease cannot be over-
estimated. Cod-liver oil is indicated in this stage. After the stage of
contraction is reached, the treatment can only be palliative. The most
important thing to be accomplished now, is to improve nutrition, and to
relieve urgent and troublesome symptoms. Mineral acids combined with
vegetable tonics, such as dilute nitric acid and calumbo assist stomach
digestion ; creosote and sulphite of sodium are of service when acid fermen-
tation is a distressing symptom. Mineral waters should be discontinued
during this stage. If constipation exists, the bowels may be regulated with
rhubarb combined with small doses of ipecacuanha. Cod-liver oil should
be constantly taken by this class of patients. Care must be taken not to
suddenly check diarrhoea, or hemorrhages, but if they become exhausting
opium may be cautiously given.
Ascites and general dropsy are the most troublesome symptoms in
this stage of cirrhosis. When it becomes imperative to remove the
dropsy, it may be attempted through the skin, kidneys and intes-
tines, or it may be removed by tapping. If the patient is too feeble
to employ drastic purges and hydragogue cathartics, diuretics and di-
aphoretics may be resorted to. The condition of the intestinal tract, as
well as the strength of the patient, will determine whether elaterium, or
any of the other drastic cathartics can be employed. It must be remem-
bered that they may excite acute gastric and intestinal catarrh. Diuretics
(as squills and digitalis) are more efficient in this than in any other form
of dropsy. If the kidneys and renal vessels are compressed by the fluid, diu-
retics will have little effect. Its removal must not be delayed too long, for
the strength of the patient may be so diminished that after the removal of
CIRCUMSCKIBED SUPPURATIVE HEPATITIS. 349
a large quantity of fluid fatal collapse may occur. When, however, reme-
dial measures fail and dyspncea becomes troublesome, paracentesis abdo-
minis should always be resorted to. The mechanical removal of the fluid
may be effected either by the aspirator or trochar. After its removal, the
hob-nailed surface of the liver may cause peritonitis by the constant irrita-
tion produced by the respiratory movements. There are few cases where
tapping has been frequently performed, in which after death a moderate
amount of chronic peritonitis is not found. The ascites will return sooner
or later after paracentesis ; but when tapping is only required at sufficiently
long intervals for the patient to recuperate between the tappings, and the
amount of fluid gradually diminishes, or becomes stationary, the case will
continue for years. '
CIRCUMSCRIBED SUPPURATIVE HEPATITIS.
Abscess of the liver is an acute circumscribed hepatitis which results in
irregular areas of suppuration, the liver-tissue surrounding the points of
suppuration remaining normal.
Morbid Anatomy. — In a certain proportion of cases circumscribed hepati-
tis has its origin in an infarction. The emboli which produce these infarc-
tions are, in most instances, stamped with pyemic infection or are necro-
tic ; they may vary in number from two or three to a dozen. Immedi-
ately around the inflamed spots the liver substance is normal or in a state
1 Fatti/ Hypertrophic Cirrhosis-— In Le Progy^es Medical [No. 9, 1883, p. 163, etc.] is an account of a dis-
ease whose name— fatty hj'pertrophic cirrhosis— was given by Sabourin. It is claimed to be a new variety
of hepatic disease, which has a special clinical history, that develops regularly and which usually allows of
a positive diagnosis. Its anatomical changes were first noticed by Cornil ; and Hanot, Lancereaus, Du-
pout and Renan have contributed to its literature. Autopsical examinations first led to clinical obser-
vations. At the post-mortems of many who were supposed to liave hypertrophic cirrhosis, the liver pre.
eented the yellow color of fatty degeneration, and was soft and flabby. In simple hypertrophic cirrhosis
the liver is hard and brown, often very dark. In fatty hypertrophic cirrhosis the liver is very thick, so
that the whole organ is like a cube. Sabourin dwells particularly on this. There are no granulations upon
its surface. Glisson's capsule, sometimes thickened from perihepatitis, is smooth and so transparent that
through it can be seen opaline-looking new connective-tissue inclosing yellow parenchyma. It differs from
ordinary fatty liver, in that we find no new tissue formations between the lobules. Upon' section the
hepatic parenchyma seems made up of fatty nodules, usually circular, smaller or larger than the normal
liver lobules, and almost completely inclosed by new tissue. The latter has sometimes induced absorption
of the proper glandular elements. With a low power there is an appearance like the sub-cutaneous adipose
tissue; cirrhotic bands inclose collections of fat-cells. These groups of fat-cells are hepatic lobules. The
fatcells are merely enormous oil-globules. The granulo-fatty degeneration peculiar to typhoid jaundice is
absent. The new growth originates in the porta! spaces ; the portal vessels and bile-ducts being sur-
rounded by compact fibrous tissue whence radiate bands to the central and sub-lobular veins. The sub-
lobular veins may undergo entire obliteration ; but they are always occluded more than any other vessels.
The biliary passages are only secondarily attacked. It is the vascular apparatus which is most involved in
fatty hypertrophic cirrhosis. Sclerotic renal chansres also coexist. The symptoms are divisible into two
periods. The^r.sY, or latent period, is often overlooked or misunderstood. But when the seco?id stage sets
in there will be abdominal pain, weight in the hypochondrinm, nausea, vomiting, anorexia, attacks of
vertigo, nocturnal delirium or hallucinations, hyperesthesia of the limbs and then fever. Now a diagnosis
is easily reached. There is oedema of the extremities and face, great depression, profuse sweats, and
often signs of a sub-acute peritonitis. Sooner or later there is slight jaundice or a tendency to hemorrhages
This resembles " typhoid jaundice '" (acute yellow atrophy). But the jaundice lasts longer and the symp-
toms exacerbate and re-unite. No flesh is lost. The patients are usually lat. The abdominal fat renders
physical signs m^. Late, there maybe abundant blood-stained expectoration. The second period lasts
four to fi/e weeks. There are, however, deceptive intervals of apparent recovery. Nearly all the patients
are subjects of alcoholismus, and this, with the frequent tubercular complication, is a great diagnostic
point. The pror/nosis is very bad. The treatment of this disease is palliative, expectant— none of the
many theories advanced has, as yet, been accepted or been free from illogical deductions. All we can say
is that fatty hypertrophic cirrhosis is not an hybrid disease— it lias a special place.
350
DISEASES OF THE DIGESTIVE SYSTEM.
of intense congestion, and corresponding to them on the surface of the
liver are found brownish-red elevated patches from an inch to an inch and
a half in diameter, and of firm consistence. Their most frequent seat is
the posterior portion of the right lobe. They may be single or multiple.
Soon after the development of the infarction purulent inflammation is estab-
lished. In the centre of the mass the liver cells undergo albuminoid infil-
tration, become larger, degenerate, and pus is formed. As the process
advances small cavities containing pus are developed. These may en-
large into one large abscess or remain separate. If abscesses result from
other causes than pyaemia,
the process does not follow
the lobular course, but begins
by small exudations of lymph
and pus, which soon coalesce
and become surrounded by a
membraneous wall. The cavity
of the abscess varies in size
from that of a hazel-nut to
one capable of containing two
or three quarts. Their con-
tents are usually pale yellow
pus ; but when the suppu-
rating process has broken
through the wall of some
vessel, then the contents are rust colored and have a granular appearance.
If the process involves the bile-ducts the pus has a greenish or ochre-color.
Avariety of changes take place in these purulent collections ; as they grow
older, their walls may become smooth, and the encysted pus gradually
become absorbed, or undergo cheesy or calcareous degeneration. If absorp-
tion takes place, a cicatrix deeply indented on the exterior of the liver
marks the place where the abscess approached the surface, and within its
substance cicatricial tissue indicates its exact seat. In other cases, no lining
membrane is produced around the purulent collection. As the inflamma-
tion extends, a necrotic process is established which extends to the surface
of the liver, and the abscess opens externally. This process may pierce the
peritoneum, causing a fatal peritonitis ; but this is of rare occurrence, for
adhesions are formed which bind the diaphragm and adjacent organs to
the liver ; or the abscesses may open into the pleural cavity, the right
lung, or the stomach. In rare instances the two large venous trunks, the
vena portse and inferior cava may be pierced. Frequently the abscess
ruptures externally, through the adhesions formed between the surface of
the liver and the abdominal walls. The intestines, the gall-bladder,
or the pericardium may be perforated by the abscess. Again, the pus
may burrow in the cellular tissue, and discharge itself at some point at
the lower part of the trunk. At the autopsy the liver may be found irreg-
ularly enlarged, often attaining an immense size. The capsule is opaque
and thickened, and on its surface are elevated flat spots varying in color
Fig. n.
Circumscribed Suppurative Hepatitis.
Sketch shmving the cut surface of a portion of the left lobe of the
liver, the seat ofmvltipl'e abscesses. The open mouths of the di-
vided hepatic veins are also shown.
CIRCUMSCKIBED SUPPURATIVE HEPATITIS. 351
from dark red to yellow. Adhesions generally exist between it and the
adjacent parts, and a layer of lymph frequently envelops the entire organ.
The whole liver is hypertemic. Evidences of perforation, in any of the
directions which have been mentioned, may be present.
On section, a dark fluid oozes from the congested surface, and the
interior of the abscess may exhibit any of the changes above described.
Near an abscess the coats of the veins, especially the portal, are thickened,
and their interior is often filled with a shaggy, fibrinous deposit.
Etiology. — Pya^mic infarction must be regarded as a frequent cause of
hepatic abscess, especially when associated with injuries to the cranial
bones. Phlebitis, with the formation of thrombi leading to suppurative
inflammation, the result of operations on the intestines (as for prolapsus ani,
hemorrhoids, and strangulated hernia) and any intestinal traumatism, may
give rise to abscess of the liver. Hot climates and miasmatic influences
favor, if they do not cause, suppurative hepatitis. In hot climates dysen-
tery, particularly the epidemic form, is frequently accompanied or followed
by hepatic abscess, so that dysentery has come to be regarded as one of the
causes of abscess of the liver. Hepatic abscess sometimes accompanies
ulceration of the stomach and of the intestine, especially of the colon.
Ulceration of the gall-bladder and of the appendix vermiformis, perityphlitis,
pyelitis, ulcerative endocarditis, and cancer of the stomach or of the parts
near the liver are often associated with hepatic abscess. Worms, calculi, or
other obstructions of the ductus communis, causing inflammation of the
hepatic ducts, sometimes lead to ulceration, and this ulcerative process is
often followed by abscess. The prevailing tendency of modern pathology
is to ascribe hepatic abscess to an infective embolus, from a preceding
phlebitis, and the attempt has been made to trace back all the causes above
named to such a primary cause, though, in many, direct proof is im]3ossi-
ble. Abscess of the liver may also be the result of inflammation of the bile-
ducts and of the veins of the liver ; and, finally, it may be developed
without any recognizable cause.
Symptoms. — An abscess of the liver of considerable size may exist with-
out there being local or constitutional symptoms to point to its existence.
A patient may have fever, gradually become emaciated, and finally die
from exhaustion, without a single objective symptom of abscess, and yet a
post-mortem examination will reveal a large central hepatic abscess. Again,
symptoms of intermittent fever, associated with gastric and intestinal
catarrh, may be all that, with the greatest care, can be elicited, when, in
fact, a large abscess is developing in the liver. When abscess is associated
with dysentery the difficulty is often increased ; for chills and rigors,
enlargement of the liver, and pain may all be attendants of dysentery with-
out abscess. Again, in pyaemia, when metastatic abscesses in the liver are
especially liable to develop, the recurring chills, the sweats, the pyrexia,
and the jaundice, are all part of the history of the pysemia, so that in many
cases we are compelled to rely almost exclusively on the' physical signs for
a diagnosis of abscess of the liver. Such cases of hepatic abscess are fre-
quently overlooked. •
352 DISEASES OF THE DIGESTIVE SYSTEM.
Usually the development of hepatic abscess is indicated by well-de-
fined symptoms. A slight feeling of chilliness, sometimes a distinct chill,
is followed by dull pain and weight in the right hypochondrium, the pain
often radiating to the tip of the right shoulder ; the chilly sensations recur,
and resemble those of a slight attack of ague. The pain increases, and
IS aggravated by position and pressure. The tongue is brown and
furred, there is loss of appetite, slight nausea, and often vomiting, which
is bilious in character. The bowels are at one time constipated, at an-
other there is a bilious diarrhoea.
The respirations are hurried and shortened, either because of slight lo-
calized pleurisy, which so often accompanies hepatic abscess, or because a
long inspiration increases the pressure on the liver, and thus causes pain.
With the dyspnoea there is a short dry cough resembling that of pleurisy ;
the skin rarely changes color. With the formation of the abscess there is
a distinct exacerbation of symptoms : hectic, rigors, and recurring night
sweats occur ; the gastric symptoms become urgent, and there is persistent
and profuse vomiting. The pain becomes sharp, lancinating and localized,
and indicates the direction of the future perforation. The temperature
rises to 103° or 104° F., sometimes reaching 106° F. The pulse is accel-
erated, generally keeping pace with the temperature. Exhaustion and
emaciation are rapidly developed, and as the disease advances, typhoid
symptoms may supervene. If the situation of the abscess is such that
portal obstruction results, hemorrhoids, ascites and oedema of the extremi-
ties occur, though peritonitis may be suspected in those cases where there
is ascites. As the abscess advances toward the surface of the liver, attacks
of perihepatitis are apt to cause severe exacerbations of pain, and the hepatic
tenderness becomes excessive. Toward the end delirium. Jactitation, som-
nolence, and coma may develop. The urine is scanty, high-colored, and
contains an abnormal amount of urates, often causing a considerable pink-
ish deposit.
Hepatic abscesses may be discharged (as has been stated) in a variety of
ways. When an external opening is to occur, the skin becomes tense,
red, shining, and oedematous at some point over the hepatic region ; fluc-
tuation can be detected, and becomes more and more marked as the ab-
scess advances toward the surface. In some cases the heart impulse is
transmitted to the abdominal walls by the intervening tumor. When the
cavity of the peritoneum is perforated, signs of local or general peritonitis
are developed, marked by rapidly developed tympanitis, intense and sud-
den collapse. When an opening occurs into the stomach, severe gastric
symptoms are developed, accompanied by purulent vomiting and purulent
stools. A sudden diminution in the size of the hepatic tumor, the sub-
sidence of the pain and of the urgent symptoms, indicate that the intes-
tine or biliary passage has suffered perforation. Symptoms of localized
pneumonic inflammation in the right lower lobe precede the opening of
an hepatic abscess into a bronchus. The expectoration suddenly becomes
purulent and mixed with blood, serum, and shreds of disintegrated lung-
tissue ; the breath becomes offensive, there is cessation of pain, and sub-
CIKCUMSCRIBED SUPPURATIVE HEPATITIS. 353
sidence of the hepatic enlargement. Eecovery in such cases is rare unless
the abscess is a small one, the patient usually dying of exhaustion from long-
continued suppuration. When the pleural cavity communicates with the
abscess, the symptoms of pleuritic effusion and empyema are well defined,
and when, in this case, an external opening is to occur, the evidences of
it are the same as those of empyema. Almost immediate death follows per-
foration of the pericardial sac by an hepatic abscess. Absorption of the
fluid contents of an hepatic abscess, and the development of cicatricial tis-
sue, followed by gradual diminution in the size of the liver, are of rare
occurrence.
Physical Signs. — Inspection. If the abscess is large, inspection will show
a bulging of the right hypochondriac region, reaching nearly to the um-
bilicus. The respiratory movements on the right side are restricted, and
the respirations are accelerated. If the abscess is to open externally, there
is a flattened, defined bulging near the free border of the ribs, between
the intercostal spaces.
Palpation. — The liver is enlarged and has an uneven feel, especially
when the abscesses are multiple and superficial. The pain, localized in
the case of a single abscess, is increased and diffused in multiple abscesses
by pressure. Fluctuation is a valuable sign, but cannot always be de-
tected. When it can be, a ring of abnormal hardness surrounds the spot.
Palpation should be made from before backward ; if a single large abscess
exists, its outline may be well defined.
Percussion. — The area of hepatic dulness is always more or less in-
creased. If the abscesses are multiple, it may be increased in all direc-
tions ; but if there is only one large abscess, the area of dulness will
correspond to the direction of enlargement, which may be upward or
downward ; by its direction we are able to determine the probable mode
of the termination of the abscess.
Differential Diagnosis. — The readiness with which the diagnosis of ab-
scess of the liver may be made will depend upon its size and situation ;
small abscesses can only be suspected. Abscess of the liver may be mis-
taken for hydatids of the liver, cancer, localized pleurisy, intercostal neu-
ralgia, abscess of the abdominal ivalls, enlarged gall-bladder, perihepatitis,
suppurative pylephlebitis, a.r\d active hyper cemia ot the liver.
Hydatids occur most frequently in those living in northern climates,
and abscesses most in those who live, or have lived, in hot climates. Hyda-
tid tumors run a chronic course, and are slow in growth ; while abscess
is usually a rapid and acute disease. Accompanying hydatids there is no
pain, rigors, hectic, or sweats ; but these are important symptoms in abscess.
Gastric disturbances and a rapidly developing cachexia are prominent in
abscess, and absent in hydatids. In some cases of hydatid tumor the hyda-
tid "thrill" or fremitus can be detected ; it is never present in abscess.
With the exploring trochar the liquid in the one will be found to be pus, in
the other a clear saline fluid containing booklets of the echinococci.
Cancer of the liver is generally associated with cancer of the stomach,
breast, or some other organ, primary cancer of the liver being very rare.
23
354 DISEASES OF THE DIGESTIVE SYSTEM.
In cancer, the hepatic enlargement is slower than in abscess, and there is
usually a more or less marked cancerous cachexia. Suppurative fever, chills,
hectic, and sweating are present in abscess, and absent in cancer. The temper-
ature in cancer is normal or sub-normal, and jaundice, if present, is persist-
ent. Ascites is common in cancer, and rarely present in abscess. In can-
cer, palpation discovers scattered nodular masses, which rarely fluctuate ;
while in abscess a large fluctuating tumor can usually be made out. The
exploring needle withdraws pus from an abscess, while blood follows the
puncture of a cancer nodule.
Pleurisy on the rigid side can usually be readily distinguished from ab-
scess of the liver by the physical signs alone. The grazing friction sound
accompanies loss of vocal fremitus ; the dulness on percussion, the feeble
respiratory murmur, and the crepitant friction sound decide the question.
Intercostal neuralgia occurs most frequently in women with a neuralgic
history. The pain is located in the region of the sixth, seventh, and eighth
intercostal spaces, and the three points of tenderness are almost diagnostic.
When the pain of abscess becomes as excruciating as that of neuralgia, in-
spection, palpation, and percussion will all reveal well-marked enlargement
of the liver. Gastric disturbances, chills and profuse sweats are prominent
signs of abscess, and are absent in intercostal neuralgia.
In abscess of the abdominal walls, there is no history of pyaemia, dysentery,
or internal ulceration, which so often precede an hepatic abscess. In he-
patic abscess the line of dulness is well marked, and corresponds in outline to
the hepatic area ; while in abscess of the abdominal walls the line of dulness is
ill defined, and does not follow the hepatic outline. A tense, shining, oedem-
atous skin, and superficial tenderness and hardness appear early in abscess
of the abdominal walls. The signs of pus formation are early in abscess or
the abdominal wall, and very late in abscess of the liver, if they appear at
all. The respiratory movements cause an upward and downward motion
in the tumor of an hepatic abscess ; while an abscess of the abdominal wall
will remain stationary during the respiratory acts.
' An enlarged gall-bladder will usually be accompanied by a history of bil-
iary colic. The presence of a pear-shaped, movable, fluctuating tumor, oc-
cupying the normal position of the gall-bladder, a history of Jaundice, and
the absence of constitutional symptoms indicate enlarged gall-bladder ;
while the tumor in abscess of the liver is broader, less movable, less globu-
lar in shape, and is attended by chills and sweats.
Prognosis. — The majority of abscesses of the liver terminate fatally. Py-
aemic abscesses are generally mviltiple ; their average duration is three
months ; I have known death to occur within three weeks after the com-
mencement, and I have known them to be prolonged over a period of two
years. In abscess from other causes than pysemia, the prognosis is favora-
ble whenever there are no indications of an opening into the pericardium,
peritoneum, or pleural cavity. When an hepatic abscess complicates a severe
attack of dysentery, the prognosis is unfavorable. Their duration is shorter,
and the prognosis is better when they open externally ; their next most
favorable termination is when they open into a bronchus, or into the intes-
CIRCUMSCRIBED SUPPURATIVE HEPATITIS. 355
tinal canal. Pyaemia and dysentery often cause death when the accompany-
ing abscess is too recent to have induced it. Exhaustion from suppuration
may cause death, especially when accompanied by intestinal catarrh. Peri-
tonitis, 23eri carditis, pneumonia, and empyema sometimes cause the fatal
result.
Treatment. — When multiple abscesses occur, antiseptics have been pro-
posed, but there is no evidence that they arrest the progress, or diminish
the severity of the suppurative process. When supjDurative hepatitis can
be recognized early, it should be treated according to the rules which have
been given for the management of acute hepatic liypereemia. Local blood-
letting by leeches may be employed when the symptoms are localized and
well defined ; and mercurial purges may be given at the onset, in combina-
tion with large doses of quinine, but they should be discontinued when sup-
puration is established. We rarely have an opportunity to carry out the
preventive treatment, for the abscess is formed before the patient seeks
medical advice. When pus has formed, and the locality of the abscess can
be determined, aspiration should be performed. If the withdrawal of the
pus is followed by decided signs of improvement, the aspiration may be
repeated at intervals indicated by the amount and effects of the purulent
accumulation. Few cases, however, will be permanently benefited by aspira-
tion. I question very much if those cases reported cured by one or two
aspirations were true hepatic abscesses. The dysentery and the gastro~in-
testinal catarrh, which are so often attendants of hepatic abscess, are best
treated with large doses of ipecacuanha ; a fuller description of this method
of treatment will be found under the head of dysentery.
The question of operative interference is one which it is often difficult
to decide. Strong opinions have been given for and against it. On the
one hand, it is claimed that if a free opening is not made, death may result
from exhaustion produced by large purulent accumulations, or the abscess
may open into the peritoneal cavity, pericardial sac, or pleura, and thus
cause death. The process is a progressive one, and each day more and more
of hepatic tissue will be involved, and thus diminish the chances of recov-
ery. On the other hand, those who oppose opening the abscess say that
peritonitis and the entrance of air may result from it, that the ribs are more
liable to become eroded, and the surrounding tissue to become gangrenous,
when an opening is made. Some regard it as highly dangerous to pass an
instrument into the liver, claiming that it may excite a suppurative process
in healthy liver-tissue. All these objections are removed if Lister's
method is employed. If no adhesions have formed between the liver and
the abdominal walls, they should be established by caustics, and then the sac
may be opened ; if it is very large, all of the pus should not be allowed to
escape at once. It is always safest to open the sac by means of caustics, using
the knife to divide the superficial tissues. The abscess should be opened as
soon as possible. When hepatic abscesses open into the bronchi, colon or
gall-bladder, absolute rest must be insisted upon. In all cases, during con-
valescence, absolute rest and a careful regimen must be maintained for
months. The diet throughout the whole course of the disease should bo
356
DISEASES OF THE DIGESTIVE SYSTEM.
the most nutritious, and stimulants should be freely given. The impor-
tance of sustaining the patient in every possible way is apparent.
DIFFUSE PARENCHYMATOUS HEPATITIS.
This disease, also called acute yellow atrophy and malignant jaundice,
has been regarded as a '* passive degeneration," the metamorphosis being
more rapid than in any other gland structure in the body. Some think it
due to bilious liquefication ox polycholia, and that it is a general disease —
like typhoid fever or cerebro-spinal meningitis — with a local lesion. The
more recent views are that acute yellow atrophy is a diffuse inflammation of
the whole hepatic structure, where the inflammatory changes are so rapid as
to lead to disintegration and complete destruction of the liver cells and sub-
sequent atrophy. Whether it is an exudative process, or one in which there
first occurs albuminoid infiltration of the hepatic cells, and then molecular
change, is still a disputed question, but the more reasonable view is that it
comes from albuminoid infiltration, irregular cloudy swelling of the cells,
and subsequent softening of the hepatic tissue.
Morbid Anatomy, — It is seldom that one sees a liver that is the seat of
diffuse hepatitis until after the process is completed, but the few that have
been studied present the evidences of having been the seat of an intense
congestive and exudative process. The liver lobules have a dark gray
muddy ring at the periphery, due to granular degeneration or albuminoid
swelling of the peripheral cells, while the liver structure immediately sur-
rounding the central vein is normal. The latter is, however, soon involved,
and in place of liver cells there are fat and pigment granules, with traces of
leucin and tyrosin. All outline of lobular
structure disappears, the capillaries are
intensely engorged, and the bile-ducts
become more or less completely closed,
owing to the compression which they
suffer from peripheral exudation. Thus
the bile formed between the central vein
and the exterior of the lobule has no
mode of escape, except through the cen-
tral vein. The liver is diminished in size,
sometimes to two-thirds of its normal size;
in the early stage the organ is supposed
to be very slightly enlarged. The diminu^
tion is most marked in the right lobe.
It is so soft that it folds upon itself, and
takes any shape and position from the
pressure of the adjacent organs. At the
post-mortem, the body will be emaciated,
the skin A^ery much discolored, and ecchymotic spots will often be found
scattered over the surface.
TJie capsule is loose, freely movable, very much wrinkled, and opaque or
Fig. 78.
Cells, etc.
from an hepatic lobule in Acute
Yellow Atrophy.
A, A. Hepatic cells filled with granvlar detritus,
zvith obscuration of nuclei and cell walls.
B. A group of atrophied cells.
C. Cells with fatty infiltration.
D, E. Pigment granules^ with blood and ty-
rosin crystals, x 300.
DIFFUSE PARESrCHYMATOUS HEPATITIS. 357
yellowish in appearance. The parenchyma is soft, flabby, and brittle, and
varies in color from a bright yellow to a yellow-red.
On section, when the disease is far advanced, the color of the cut sur-
face is of a rhubarb red, the outlines of the lobules are lost, and only a
detritus of granular matter is left. The blood is darker and thicker than
normal and coagulates imperfectly. It may contain leucin and traces
of urea. If the organ be set aside for a while it becomes covered with crys-
tals of leucin and tyrosin.
The heart is jaundiced, fatty and pultaceous.
The spleen is enlarged and softened, and leucin is found in it. The gall-
bladder is empty, or contains a small amount of pale bile or mucus.
The Tcidneys are slightly enlarged, and in most cases are in a state of
acute fatty degeneration. Hemorrhages from the surface of the mucous
membrane of the stomach and intestines are common. Occasionally there
is softening of the central portion of the cerebral substance, and staining
of the meninges. The serous cavities contain fluid, often bloody, and in
rare instances nearly every organ in the body is blood stained and has
leucin and tyrosin in its tissues.
Etiology. — Acute yellow atrophy is a rare form of disease. Its causes are
regarded by some as constitutional, by others as due to a peculiar miasm.
Two-thirds of the cases occur in pregnant females, between the ages of
twenty and thirty. The supposed predisposing causes are sex, pregnancy,
chronic alcoholism, syphilis, malaria, sexual excess, and a prolonged course
of mercurials. But with our present knowledge, it is difficult to say
whether these are really predisposing causes, or that the acute yellow
atrophy is an intercurrent accident. Among the exciting causes may be
named mental emotion, great grief, or fear. It is doubtful if obstruction
of the bile-ducts alone can excite acute yellow atrophy ; some are inclined
to regard malaria as an exciting cause, rather than a predisjDOsing one.
While its etiology is still so obscure, the history of its development leads to
the conclusion that a malarial poisoning is present in a large proportion of
cases.
Symptoms. — The symptoms of the early stage of acute yellow atrophy
usually pass unnoticed, for they are not in themselves distinctive. When
the disease is slow in its advent, loss of appetite, occasional vomiting, a
furred tongue, slight headache, and a sense of fulness in the right hypo-
chondrium may be the only symptoms for the first week. Jaundice may
precede it for a week or two. In cases where its advent is sudden, it will
be ushered in by constant vomiting and great prostration. In either case
during its early stage the temperature will be raised only a degree or two,
and the pulse but slightly accelerated. A condition of despondency is often
present, there are wandering pains simulating rheumatism, and a sense of
great depression. Delirium and convulsions may be the only ushering-in
symptoms. After from three to five days, the characteristic symptoms of
the disease are developed ; of these jaundice is the earliest and most con-
stant, it is progressive and never very intense, first affecting the upper half
of the body. The rise in temperature and increased pulse-rate which
858 DISEASES OF THE DIGESTIVE SYSTEM.
marked its premonitory stage disappear, and now even a retarded pulse
and sub-normal temperature may exist. In a few instances, after the first
twenty-four hours, the temperature ranges from 100° to 101° E. during the
whole course of the disease. The vomited material consists of mucus
tinged with bile ; later it assumes the nature of black vomit, similar to that
in yellow fever, the color being due to gastric capillary hemorrhage. There
is intense pain in the epigastiic and right hypochondriac regions, which is
increased by firm pressure over the liver. In the stage of coma, the liepatic
tenderness is so great that pressing the liver up against the diaphragm may
rouse the patient. At first the cerebral symptoms are those of mental de-
pression and slight headache, which rapidly increases in severity ; this,
later, gives place to wild delirium, jactitation, and convulsions. Twitch-
ings of the voluntary muscles of the head and neck (trismus) mark the
convulsive stage of the disease. These spasms usually follow the vomiting,
but in cases where the disease runs a rapid course, typhoid symptoms
make their appearance, sordes collect on the teeth, while low muttering
delirium, subsultus, muscular tremors, and partial stupor precede the
convulsions. The convulsions are epileptiform, and are sometimes ushered
in by a peculiar shrill cry.
During the period of nervous excitement, the pulse undergoes remark-
able changes. It may rapidly rise to 120, 130, or even 140 beats in a
minute, falling in moments of calm to 80 or 90, the temperature remain-
ing unchanged. The breathing during the convulsions is interrupted
or stertorous, and a peculiar groaning noise is heard with each inspira-
tion ; the expirations are prolonged and puffing. Whether the convulsions
have been preceded by typhoid symptoms or not, the patient gradually be-
comes more and more tranquil, passes into stupor, and finally into deep
coma, from which he cannot be aroused. The discharges from the
bowels and bladder are either passed involuntarily or retained. The
pupils are normal or slightly dilated, and respond to light slowly. The
breathing becomes sighing, the pulse reaches 140 to 150, and grows shorter
and shorter until death occurs. The skin during the progress of the disease
has become more or less deeply jaundiced, ecchymotic and petechial spots
sometimes appear on the surface, and there may be hemorrhages from the
stomach, nose, intestine, uterus, and kidneys. In pregnant females abor-
tion is likely to occur before death. The fceces are firm, clay-colored, and
often blood-stained. The urine is acid and dark in color, is not quite
up to the normal amount, and often contains albumen and blood ; urea
and uric acid have totally disappeared, the sulphates and phosphates are
diminished in quantity, and leucin and tyrosin are found in their place.
The duration of the disease varies from one to three weeks.
Physical Signs. — Palpation elicits extreme tenderness over the epigas-
trium and right hypochondrium.
Percussion. — The area of hepatic dulness rapidly diminishes from day
to day, and as the liver decreases in size it is displaced backward, so that
there is no well-defined area of hepatic dulness in front. As the liver
diminishes in size the spleen enlarges.
DIFFUSE PARENCHYMATOUS HEPATITIS. 359
Differential Diagnosis. — Diffuse parenchymatous hepatitis may be mis-
taken for yellow fever, pymnia, typhoid fever, and the bilious remittent
variety of pernicious fever.
In acute yellow atrophy, the liver is diminishing in size from day to
day, while in yellotu fever it is steadily increasing. The spleen is increased
in size in acute yellow atrophy, and is unchanged in yellow fever. T!io
urine in yellow atrophy is acid throughout, and contains leucin and tyro-
sin ; while as soon as jaundice appears in yellow fever the urine becomes
alkaline. Yellow fever is ushered in by a distinct chill, while yellow
atrophy of the liver rarely begins with a chill. The pulse, in severe forms
of yellow fever, is gaseous in character and is rarely over 110, while in
acute atrophy the juilse may reach 140 or 150 per minute. The stools are
dark and fluid in yellow fever, and firm and clay-colored in acute atrophy.
Pymmia is ushered in by distinct chills. The chills in pyaemia are
followed by irregular rigors and exhausting sweats, which do not occur in
acute atrophy. In pyasmia there is diarrhoea, and in acute yellow atrophy
the stools are firm and clay-colored. In pyaemia there is a peculiar sweet
sickish breath, which is absent in acute atrophy. Evidences of multiple
abscesses, especially in the lungs, soon follow the sweats of pyaemia ; these
do not occur in acute atrophy. The presence of leucin and tyrosin and
the absence of urea, with the other urinary symptoms of acute atrophy,
are in marked contrast with the normal urine of pyaemia. Physical
(hepatic) signs are negative in pyaemia, while a daily diminishing area of
hepatic dulness is usually present in acute yellow atrophy.
Typhoid fever has nearly the same premonitory symptoms as acute
yellow atrophy, but the steady rise in temperature with the typical morn-
ing and evening exacerbations and remissions during the first week, are in
marked contrast with the continual low temperature of acute atrophy.
The delirium is wandering in typhoid, and wild in acute yellow atrophy.
The characteristic *' rose rash " ajDpears about the seventh day of typhoid
fever. Diarrhoea is the rule in typhoid fever, while constipation and clay-
colored faeces are the rule in acute atrophy. In typhoid, the urine is
simply diminished in amount, and the urea is increased, while in acute
yellow atrophy the urea is greatly diminished in quantity, and often com-
pletely absent, and the other (mentioned) urinary changes are present. In
typhoid fever the liver is slightly enlarged, while in acute yellow atrophy it
is markedly diminished in size.
The " iilious remittent " form of pernicious fever very closely re-
sembles in its symptoms acute atrophy of the liver. The severe sudden
chill, rapid rise in temperature to 105° or 107°, the sweating, and the re-
mission in pernicious'fever are all, however, absent in acute atrophy. Eree
pigment exists in the blood in bilious fever, and is absent in atrophy.
Jaundice is a late symptom of pernicious fever, but occurs early in acute
atrophy. The liver is markedly enlarged in pernicious fever, and as
markedly diminished in size in acute yellow atrophy. Poisoning from
phosphorus can only be diagnosticated from acute yellow atrophy when we
know the drug has been taken.
360 DISEASES OF THE DIGESTIVE SYSTEM.
Prognosis. — This is exceedingly unfavorable, and those cases where a cure
has been reported are in the doubtful list. The average duration is one
week, the extreme limits being twelve hours and four weeks. Cholsemia
and urgemia, by inducing the cerebral symptoms which have been referred
to, may be the direct cause of death. Peritonitis and hemorrhages from
the stomach and bowels are also frequent causes of death.
Treatment. — All plans of treatment have thus far failed either to arrest
the progress, or to diminish the fatal tendency of this disease. It has
been preferred, in the early stages, to administer drastic purges, and apply
leeches over the region of the liver and about the anus, and in the robust
and plethoric to practice venesection ; there is, however, no evidence that
these measures have any controlling influence over the disease. Pregnant
females should be placed in pleasant apartments, with cheerful surround-
ings. When the pain over the liver is intense, leeches and hot fomenta-
tions over the hepatic region, with morphine hypodermically, will afford
relief. When the cerebral symptoms develop, chloric ether, in drachm
doses every hour will often quiet the wildest delirium. Hemorrhages from
the mucous surfaces can usually be checked by astringents and cold. Bis-
muth or strychnia will sometimes relieve the vomiting. Bi-carbonate of
soda in ten grain doses every hour has been given with apparent benefit.
PEEIHEPATITIS.
Perihepatitis is an inflammation of the capsule of the liver. It is im-
portant to remember that the liver has two envelopes, the outer, the serous
covering which is part of the peritoneum, and an inner, its true fibrous
covering, the capsule of Glisson.
Morbid Anatomy. — A liver which has been the seat of perihepatitis is
diminished in size, except when it is complicated by those diseases of the
organ which give rise to enlargement. The capsule is thickened, the thick-
ening varying from a few lines to half an inch ; it is more or less firmly
adherent to the colon, stomach, diaphragm, and abdominal walls. In
syphilitic perihepatitis, Glisson's capsule is hard and leathery and has a
granular appearance. Sometimes the capsule is so thickened and con-
tracted in the transverse fissure of the liver as to obstruct the portal vein
and hepatic duct. The liver substance usually remains normal, being only
slightly compressed on the surface of the organ, corresponding to the fur-
rows between the larger lobules. In " perihepatitis syphilitica " prolonga-
tions of new connective-tissue will penetrate the parenchyma, and the out-
lines of the lobules will be indistinct. This condition is called induration.
Slight atrophy of the parenchyma may occur at points corresponding to
the circumscribed capsular thickening. The coats of the hepatic veins
may be thickened and the bile-ducts dilated. The gall-bladder is some-
times displaced by the contraction of the new tissue, and the ductus
communis may be partially occluded by fibrous bands. Perihepatitis is
usually accompanied by pleurisy in the lower part of the right pleural
cavity.
PERIHEPATITIS, 361
Etiology. — Exposure to cold, when the liver is in a state of active hy-
persemia, is the most frequent cause of perihepatitis. Blows over the
hepatic region often excite it, and it may come from an extension of in-
flammation from the peritoneum or from the right pleura. In all in-
flammatory forms of hepatic disease and during the development of new
growths, perihepatitis is of frequent occurrence. Syphilis is a very com-
mon cause.
Symptoms.— It is often ushered in by a chill, followed by a slight rise
in temperature and a corresponding increase in the pulse rate. The pulse is
tense and wiry in character ; pain in the hepatic region is its most constant
symptom, and is increased by pressure, by a full inspiration, by coughing,
and by lying on the right side. Jaundice is rare, but when the new tissue
compresses the common duct it may be developed. A dry, hacking cough
is rarely absent. New tissue developments in the transverse flssure may
cause suflBcient obstruction to the portal vein to produce ascites. From
obstructions of the common duct, under similar circumstances, gall-stones
may form and be found in the faeces.
Physical Signs. — On palpation the liver will be found intensely tender,
slight pressure causing severe pain. It may be diminished in size, its
edges lobulated, rounded, smooth and harsh.
Percussion. — The area of hepatic dulness is somewhat smaller than
normal.
Auscultation. — In the early stage there is sometimes heard over the liver
a rubbing sound, like the friction sound in pleurisy.
Differential Diagnosis. — Perihepatitis may be confounded with intercos-
tal neuralgia of the right side, with pleurisy, and with abscess of the
liver.
In intercostal neuralgia there is usually a neuralgic history and three
diagnostic points of tenderness : — -first, at the exit of the nerve from the
spinal canal ; second, midway between the sternum and the spine ; third,
just at the edge of the sternum. The pain is usually confined to the sixth,
seventh and eighth intercostal spaces. In perihepatitis there is generally
e§'w«? tenderness over the whole hepatic region, and pressure up under the
ribs increases the pain. Elevation of temperature, increase in the pulse-
rate, and the history of a chill are all absent in intercostal neuralgia.
In pleurisy, the pain is located under the right nipple. The pain is
lower down in perihepatitis, and pressure up under the ribs will cause a
marked increase in its severity. The dyspncea is more urgent in pleurisy
and the cough has a teasing, hacking character. With the advent of plas-
tic exudation in pleurisy, there is diminished vocal fremitus, dulness on
percussion, feeble respiratory murmur, and a *' sticky "crepitating friction-
sound.
Perihepatitis often accompanies abscess of the liver, and then the dif-
ferential diagnosis is difficult. In abscess there are hectic, rigors, and re-
curring sweats ; while in perihepatitis there is but one chill, and that at the
commencement. The temperature in abscess is 103° and 105°, while it is
lower, rarely above 101° F., in perihepatitis. Urgent gastric symptoms.
362 DISEASES OF THE DIGESTIVE SYSTEM.
profuse and persistent bilious vomiting, are marked in abscess of the
liver, and absent i n perihepatitis. In abscess there is a rapidly developing
cachexi.1, which does not exist in perihepatitis. In abscess, distinct fluctua-
tion on palpation is often present, while it never occurs in perihepatitis.
Percussion in abscess shows an area of hepatic dulness either uniformly
increased, or increased in one direction, while the area of hepatic dulness
is never increased in perihepatitis.
Prognosis. — The prognosis in perihepatitis is good ; it is influenced, how-
ever, by the disease which it accompanies. The chief danger is that
repeated attacks will lead to ''induration" or compression of the portal
vein, and subsequent atrophy of the liver. In the latter case, all the
symptoms of cirrhosis will follow. When obstruction to the ductus
communis is sufficient to cause jaundice, the prognosis, is unfavorable.
Treatment. — Rest in the recumbent posture is essential to the successful
treatment of this disease. The severe pain which usually attends it can
be relieved by hypodermic injections of morphia and the application of
leeches over the hepatic region. Warm anodyne poultices should be ap-
plied after the leeches. In those cases where there is active hepatic hy-
persemia, a mercurial or saline purge is indicated, unless general peritonitis
exist. In all cases the diet should be non-stimulating and nutritious, and
an individual who has once had perihepatitis should abstain from all forms
of alcoholic stimulants.
PYLEPHLEBITIS.
PylephleUtis is an inflammation of the portal vein, accompanied by
coagulation of its contents. Under this term are now included all cases
of ''portal thrombosis,-*' whether the thrombosis is preceded, followed, or
unattended by an inflammatory process. It is of two varieties, adhesive
and siippiirative. In adhesive pylephlebitis there is more or less extensive
obliteration of the veins ; in suppurative, the thrombus which forms in
the vein becomes a centre of purulent accumulation. When the unquali-
fied term pylephlebitis is used, the adhesive variety is always indicated.
' Morbid Anatomy. — In adhesive pylephlebitis the coats of the portal veins
become thickened and their calibre is diminished, fibrin collects upon the
constricted portion, and thus thrombi are formed. Sometimes the coagu-
lum forms before any recognizable change in the coats of the vein has
occurred. When this happens, the process may commence in a small branch
and extend to the main trunk, or a single spot in a large branch may be
the point where blood first coagulates. In either case, obliteration of the
vein is the result. The wall of the vein is the seat of hyperplasia,
adhesion of its two surfaces occurs, and as a result the vein is obliterated
and a fibro-cellular cord alone remains. As a rule the liver is smaller in
size than normal, and may exhibit on its surface cicatricial contraction,
showing the lines of the obliterated vein.
On section, coagula may be found in all stages of formation.
Tlie spleen is usually found much enlarged. The abdominal cavity is
PYLEPHLEBITIS. 363
often filled with fluid, and the superficial abdominal veins on the right
side are enlarged and tortuous. The gall-hladder is usually found full of
greenish bile.
Etiology. — Certain blood conditions predispose to adhesive pylephlebitis,
and chief among these are acute septic and malarial poisons. The most
common and direct cause is narrowing of the trunk of the portal vein, from
contraction of cicatricial tissue in the transverse fissure of the liver, or from
pressure of enlarged lymphatic glands, tumors of the pancreas, omentum,
or stomach : — hence cirrhosis plays the most important part. Blows, in-
juries to the walls of the vein, and inflammation of the tissue immediately
about it, act as direct causes. The secondary causes are an extension of
inflammation from inflamed hemorrhoidal tumors, from the umbilical phle-
bitis of the new-born, from severe local inflammation of the intes-
tine, from extension of inflammation from the mesentery to the mesenteric
vein, from a peculiar form of phlebitis called "gouty," and from a chronic
inflammation excited by pressure of gall-stones.
Symptoms. — When the main trunk of the portal vein or its larger branches
are not involved, the disease cannot be recognized. But when they are exten-
sively involved, fluid rapidly accumulates in the peritoneal cavity, and after
withdrawal it quickly reaccumulates. This is an important point in the
diagnosis. The veins of the abdomen, and often those of the thorax, be-
come enlarged, tortuous and promirnent ; at the same time hemorrhoids,
which often attain immense size and become yery painful, are developed.
The spleen enlarges so rapidly in some cases that the extent of the enlarge-
ment can be determined each day. Profuse and exhausting vomiting, with
hsematemesis, is common, and diarrhoea, with frequent discharges of fluid
blood from the bowels, marks the advanced stage. Gastro-intestinal hem-
orrhages and epistaxis may lead to fatal syncope. In the majority of cases
its course is rapid ; — if it is slow in its development, it gives rise to precisely
the same symptoms as those of the latter stage of cirrhosis of the liver. Jaun-
dice is never a prominent symptom. If it does occur, it is usually due to
a complicating catarrh of the bile-ducts.
Physical Signs. — Inspection o^ndi palpation will give the evidences of fluid
in the abdominal cavity, and the superficial veins will be markedly enlarged
and cord-like.
Percussion. — The normal area of the hepatic dulness is diminished, un-
less waxy degeneration or some other disease of the liv^r precedes its devel-
opment. The spleen is enlarged in all cases.
Differential Diagnosis. — C'irrJwsis is the only disease which would be liable
to be confounded with pylephlebitis. In the advanced stage, it is impossi-
ble to make a differential diagnosis. The previous history of the patient is
important : — in cirrhosis it is one of chronic alcoholismus, gout, rheuma-
tism, or syphilis, none of which can be regarded as causes of pylephlebitis.
Cirrhosis is much slower in its development than pylephlebitis. The ab-
dominal dropsy accumulates rapidly in pylephlebitis, while in cirrhosis it
accumulates slowly, and does not return quickly after paracentesis. The
stools in cirrhosis are firm and clay-colored. The urine contains abundant
364 DISEASES OF THE DIGESTIVE SYSTEM.
urates in cirrhosis ; these are absent in pylephlebitis. Persistent tympani-
tis precedes the ascites of cirrhosis, and is absent in pylephlebitis.
Prognosis. — The prognosis is unfavorable. Death may result from as-
phyxia, from gastric and intestinal hemorrhage, and from exhausting
diarrhoea.
Treatment. — Medication avails little in this disease ; the treatment is al-
together palliative. The diarrhoea and hemorrhage should be checked with
vegetable astringents. If dyspnoea becomes urgent, on account of the large
accumulation of the fluid in the abdominal cavity, paracentesis should be
performed. The food should be highly nutritious, and taken in small quan-
tities, at short intervals.
SIJPPUEATIVE PYLEPHLEBITIS.
Suppurative inflammation of the portal vein is always a secondary disease,
and leads to the formation of small hepatic abscesses.
Morbid Anatomy.— The wall of the vein is the seat of the inflammatory
process; it becomes thickened, and its cavity is filled with a puriform
fluid, coagulated blood, or a stratified thrombus. The primary seat of the
process may be the trunk of the vein before it enters the liver. It may
extend to the smaller branches, and from them to the liver substance. If
coagula occupy the venous twigs as well as the trunk of the vein, it is com-
mon for the puriform infiltration to take place only in them, while a firm
€lot obstructs the main channel. When the veins near the surface of the
liver are the seat of suppurative pylephlebitis, extension of the process from
the sheath of the vessels to the adjacent parenchyma gives rise to small ab-
scesses. The liver becomes enlarged and softened, and circumscribed col-
lections of pus are visible underneath its capsule.
On section, the calibre of the vena portse is seen enlarged and gaping ;
the wall is thickened. Its contents vary : sometimes it only contains pus;
at others, fibrinous matter and small coagula of blood are mixed in the
purulent fluid. Abscesses are found along the course of the larger portal
veins, and the smaller branches often terminate in larger collections of pus.
If pieces of thrombi have been swept into the blood current, infarctions are
found in all stages, from reddish-brown clots to purulent masses. The
spleen is usually found enlarged, and of a dark purplish color.
Etiology. — The chief causes are ulceration and inflammatory processes in
the abdominal cavity. Typhlitis, perityphlitis and ulceration of the vermi-
form appendix sometimes induce it. Diseases of the rectum, as recto-ure-
thral fistulse and suppurating hemorrhoidal tumors, chronic peritonitis, ab-
scess of the spleen, suppurating mesenteric glands, diseases of the mesen-
tery which have pus as their product, and diseases of the bile ducts, such
as inflammation, ulceration and perforation, especially when caused by im-
pacted gall-stones, often excite suppuration in the portal vein. Severe
blows over the region of the liver have been followed by pylephlebitis.
^Suppurative gastritis may be followed by it.
Sjrmptoms. — The symptoms of this disease are usually well marked. Pain
SUPPURATIVE PYLEPHLEBITIS. 365
is the first and most constant symptom. The location of the pain varies in
different cases ; it is generally most intense about the umbilicus and right
hypochondriac region, just to the right of and below the xiphoid cartilage.
Frequently it is felt below the spleen, and again it seems to come from, or
extend to, the region about the caecum. The pain is burning in character,
and accompanied by slight tympanitis and tenderness. With the pain the
temperature is elevated, the pulse-rate increased, and soon a more or less
prolonged rigor occurs, during which the temperature will rise to 101°,
102° F., or even higher. After this comes a profuse and exhausting sweat.
The rigors and sweats continue for two or three days, and may occur so
regularly in the morning or evening as to suggest the presence of some form
of malarial fever ; usually, however, the chills are irregular. Slight jaun-
dice, gradually deepening, but never very intense, is soon present, and
sometimes assumes a greenish tint. The pulse is gradually increased in
frequency, reaching in some cases 130 per minute. The spleen increases
in size daily, and is quite tender to pressure. The appearance of the patient
is that of one suffering from some grave form of disease. He becomes
greatly emaciated, and there is more or less profuse diarrhoea, often contain-
ing blood. Hgematemesis and bilious vomiting are frequently present, and
as the disease advances the fever assumes a hectic type, with signs of gen-
eral peritonitis, accompanied by painful tympanitis and obstinate vomiting.
Ascites, if present, is slight. Petechiee appear upon the surface, and aph-
thae develop in the mouth. Typhoid symptoms usually come on toward
the close, with low, muttering delirium, subsultus, somnolence, and fatal
coma. The mind may be clear to the last, the patient dying in an ex-
tremely emaciated condition. In this disease there sometimes occur dis-
tinct remissions at the end of the first week, but this must not mislead one,
for exhausting rigors and sweats will soon follow and lead to a fatal result.
The iirine is scanty, non-albuminous, and usually contains bile pig-
ment.
Physical Signs. — By palpation and percussion both liver and spleen are
found uniformly enlarged, and very tender, but the spleen is relatively
much more enlarged than the liver.
Differential Diagnosis. — Suppurative inflammation of the portal vein may
be mistaken for adhesive pylephlebitis, for malarial fever, abscess of the
liver, and catarrh of the bile-ducts.
In suppurative pylephlebitis severe pain, rigors and sweats usher in
the disease, and recur irregularly throughout its course ; these never mark
the advent of the adhesive variety. A large amount of fluid accumulates
rapidly in the abdominal cavity in adhesive pylephlebitis, and it rarely, if
ever, occurs in suppurative. Jaundice is the rule in suppurative pylephle-
bitis, and the exception in adhesive. The liver is smaller than normal in
adhesive, and larger than normal, and tender, in suppurative. The spleen
is enlarged in both diseases, but it is excessively tender in the suppurative
form.
In malarial fever the rigors and sweats follow a definite order, while
in suppurative pylephlebitis they occur irregularly. There is no pain in
366 DISEASES OP THE DIGESTIVE SYSTEM.
malaria, while in suppurative pylephlebitis it is diffused over the hepatic,
umbilical and splenic regions.
Diarrhoea rarely occurs in abscess of the liver, and if present it is of
short duration, often alternating with constipation, when the stools are
firm and clay-colored ; while profuse diarrhoea exists from the commence-
ment in suppurative pylephlebitis. Jaundice is rare in hepatic abscess,
and of common occurrence in suppurative pylephlebitis. Fluctuation is
often present in abscess of the liver, and never in suppurative pylephle-
bitis.
In catarrh of the hile-ducts slight fever soon gives place to a normal
temperature and a slow pulse, while there is a high temperature and rapid
pulse throughout the course of suppurative pylephlebitis.
Prognosis. — Nearly all the cases of suppurative pylephlebitis are fatal.
Its duration varies from one or two weeks to one or two months, the aver-
age being about one month. Death may occur from diarrhoea, from hem-
orrhage, from exhaustion, and from the intense gastric catarrh which may
complicate the disease.
Treatment. — We are powerless to arrest this disease ; and its treatment is
altogether palliative. Morphia hypodermatically is the only reliable means
of relieving the pain which is so distressing. Diarrhoea is a part of its
natural history, and all the resisting power of the patient is required to
withstand the exhaustion and cachexia which it produces. Although
quinine has no controlling power over the disease, it may be used as an
antipyretic and stimulant, and should be freely administered in connection
with stimulants and a most nutritious diet.
AMYLOID DEGENEEATION.
The most common degenerations of the liver are the amyloid and the
fatty.
Amyloid, waxy or lardaceous degeneration of the liver, is never a pri-
mary disease. It is one of the painless enlargements of the liver.
Morbid Anatomy. — The degenerative process begins in the walls of the
capillaries and small arteries, very rarely in the veins. Various theories
have been advanced concerning the nature of this degeneration ; some
claim that it depends upon blood changes, and refer to the connection
between waxy change and syphilis in support of their views. Others main-
tain that, the alkalinity of the blood being diminished, the normal relation-
ship between its other constituents is disturbed, and as a consequence
amyloid material or " dealhalized fibrin ■' is deposited ; that the process
is not one of simple infiltration. In detail the changes are as follows :
— the capillaries are stretched and consequently have their diameter
increased ; their walls then become thickened by infiltration or deposit, so
that their channel is narrowed or wholly occluded. The material depos-
ited is a substance resembling albumen in its reaction ; it is nitrogenous,
homogeneous, and translucent, with a dull, shining surface. Its reaction
AMYLOID DEGENEEATION".
367
is characteristic, a watery solution of iodine changing it to a deep red-
brown color, which gradually passes off ; if before it entirely disappears a
drop of concentrated sulphuric acid is poured over it, a violet or deep blue-
black color results. The change in the capillary walls is rapidly followed
by a similar one in the walls of the arterioles ; all the coats of the smaller
arteries are involved simultaneously, the most marked change, however, be-
ing in their muscular coat. The amyloid change in the liver always begins
in the radicles, midway between the centre and the periphery of the
hepatic lobules. An extension of the infiltration to the adjacent liver-
cells causes thera to enlarge, become irregular in outline, and coalesce in
masses; finally a whole lobule becomes involved. This enlargement, the
increased lateral pressure, and the diminution of the lumen of the vessels,
cause a decrease in the blood supply, and this leads to atrophy of the liver-
cells. The liver is uniformly enlarged, sometimes to such an extent as to
nearly fill the abdominal cavity. It is stony hard, non-elastic, heavier
than normal, its specific gravity is increased, and its edges are sharp and
well defined. The capsule is tense, shining, and has a gray " waxy" look.
In some rare cases enlarged lymphatics are found in its transverse fissure,
and then jaundice may be present.
On section, the liver cuts with a '' creaking" sound, like bacon (hence
its name lardaceous), and
the cut surface has a
*' cheese yellow," or dull
gray, glistening appearance.
The whole or a part of the
liver may be involved. If
the whole liver has under-
gone amyloid degeneration,
the cut surface presents a
homogeneous appearance,
and either the outline of
the lobules is lost or they
are seen to be enlarged and
irregular ; sometimes a
" yellow rim " can be traced
at their periphery, due to
fatty change. The micro-
scope shows the lobules to be
increased in size ; the liver
cells at the periphery of
the lobules are infiltrated
with small spherules of fat ;
midway between the sur-
face and centre of the lobule there is a zone of amyloid matter, and in
some instances there is a pigment deposit in the zone just about the vena
centralis. We have, then ; first, the fatty zone at the periphery of the
lobules ; secondly, the waxy intermediate zone ; and, thirdly, the pig-^
Pig. 73.
Amyloid Degeneration.
Section of a Lobule of the Liver in amyloid degeneration.
A. Central vein of the lobule.
B. Normal htpaiic cells.
C. Pigmented cells.
D. Commencement of the amyloid change,
E. Waxy zone— the hepatic cells completely changed. At F,
cells are shown containing fat. x 350.
368
DISEASES OF THE DIGESTIVE SYSTEM.
Fig. 74.
Diagram showing the three Intralobular Zones.
V. Small branch of Pm'tal Vein.
A. Hepatic Artery.
D. Bile Duct.
The three vessels are s^irrounded by fibrous connective-
tissue., a prolongation of Glisson's capsule, and alto-
gether constitute the elements of the Portal Caned.
ment zone around the central vein. The liver cells lose their polygonal
outline,' and become irregular oval
or circular in shape. Their cell- walls
cannot be traced, but merge into
the neighboring mass of amyloid
material. The contents of the cell
are atrophied, nuclei are not visi-
ble, though occasionally a nucleus
of one cell stands out enlarged and
shining. A semi-transparent ho-
mogeneous mass fills the cell, caus-
ing it to present the appearance of
''waxy scales." Fatty degenera-
tion frequently coexists with amy-
loid change. The liver will then
partake of the characters of both
waxy and fatty change. Cirrhosis
or simple atrophy may precede, or
be associated with waxy degenera-
tion, and syphilitic nodules and
cicatrices from " perihepatitis sy-
philitica " may exist in a liver
which has subsequently undergone waxy degeneration. The Mdneys
undergo amyloid degeneration. The spleen is enlarged, firm and waxy ;
the lymphatics generally, and the gastro-intestinal mucous membrane may
also become the seat of the amyloid change.
Etiology. — Seventy-five per cent, of the cases of waxy liver occur in males
between twenty and fifty years of age. Syphilis is its chief cause. Pro-
longed suppuration and chronic diseases of bone are also prominent causes.
Caries, necrosis, especially when the larger Joints are involved, rickets, dys-
entery, chronic intestinal ulceration, and sometimes chronic pyelitis are
reckoned among the morbid conditions which predispose to it. A scrofu-
lous diathesis, prolonged exposure to malaria, and a cancerous cachexia are
among the rarer conditions under which amyloid degeneration is devel-
oped.
Symptoms. — Its advent is never well defined, occurring as it does with
diseases which are prone to cause anaemia and wasting of the body ; its sub-
jective symptoms are at first very obscure. There is no pyrexia accompany-
ing it. The patient has a sense of weight, fulness, and constriction in the
right hypochondrium, never amounting to pain, the sensation being rather
one of discomfort. Jaundice and ascites are not part of the natural his-
tory of amyloid liver. When jaundice is present, it is due either to an
intercurrent catarrh of the bile-ducts, or to pressure from the enlarged
lymphatics in the transverse fissure. Ascitic accumulations result from
complicating peritonitis or from the pressure of enlarged glands in the trans-
verse fissure. Late in the disease, diarrhoea and vomiting are induced by
1 Quite recently Cornil, in examining many specimens, found no change in the hepatic cells.
AMYLOID DEGENERATIOlSr. 369
the slightest irregularities in diet, on account of the implication of the
gastro-intestinal tract in the amyloid change. On an examination of the
blood of one who has suffered from waxy degeneration of the liver, the
proportion of white blood globules will be found increased. The skin has
a pale, "waxy "look, and oftentimes exhales a peculiar odor. Early in
the disease the faeces are firm, and pale in color, because of absence of bile ;
later, when the so-called ''waxy diarrhoea" sets in, there are pale mucous
stools, sometimes having a dysenteric odor. The urine is increased in.
amount, is of a pale lemon-yellow color, low specific gravity, averaging
about 1.010, and contains albumen. The amount of the albumen increases
as the disease progresses ; epithelial and large hyaline casts are present.
Anasarca may occur in the advanced stage of the disease, with general
dropsy.
Physical Signs. — Inspection in the advanced stage of the disease shows
bulging of the hepatic and splenic regions. The sharp edge of the liver
will be found projecting belov/ the free border of the ribs, with a firm, hard,
resistant feel and a smooth surface. The spleen is increased sometimes to
three times its normal size, and is resistant.
Percussion. — The areas of hepatic and splenic dulness are increased
equally in all directions.
Differential Diagnosis. — "Waxy liver may be confounded with the first
stage of cirrhosis, which has already been referred to, and also with
fatty liver, the diagnosis of which is considered in the history of that
disease.
Prognosis. — The prognosis is unfavorable ; the disease is progressive and
fatal, and we can only hope to arrest its progress when it occurs with syph-
ilis. Its exact duration cannot be estimated, since its beginning is so ob-
scure. It is usually slow in its development, and extends over a period of
many months and sometimes years. Among its most frequent complica-
tions are diarrhoea, purulent peritonitis, perihepatitis, fatty and waxy
kidney, dysentery, pulmonary oedema, pneumonia, and pulmonary gan-
grene. Death may result from exhaustion due to faulty nutrition or diar-
rhoea, from general dropsy, and from urgemia or other complicating
diseases.
Treatment. — The first indication for treatment is to be found in its causa-
tion. If it is developed in connection with disease of the bones, the diseased
bones should be removed, and prolonged suppuration arrested. If syphilis
exist, antisyphilitic measures are indicated. In phthisis, empyema, and
other similar diseases, attention, must be directed to the primary disease.
Alkalies have been administered, on the ground that the amyloid material
is "dealkalized fibrin," and that with the suppurative process a large quan-
tity of alkalies pass rapidly out of the system. When once the amyloid
process is well-established, the diet should consist largely of meat; sugars
and starch should, be avoided. Alcoholic stimulants may be taken in mod-
eration. The climate, clothing, and general hygienic surroundings of the
patient are important. Tonics, and iron combined with some preparation,
of iodine are indicated in all cases. But when a history of syphilis is clearly
24
370 DISEASES OF THE DIGESTIVE SYSTEM.
elicited, then iodide of potassium may be given in large doses, with the
hope of arresting the progress of the disease. Alkalies, chiefly potassic salts,
are in great repute among the advocates of the ''alkaline treatment," and
they can be given without fear of injury in nearly every case. It is claimed
by some that ammonium chloride produces the most beneficial effects, but
my own experience does not sustain the strong statements that have been
made regarding it. The mineral waters are too exhausting for this class of
patients, and, although they may give temporary relief, should not be used
in its treatment. External applications, such as iodine ointments, and
nitro-muriatic acid baths, have been used, but without any markedly favor-
able results. If ursemic symptoms develop, measures for their relief should
be promptly instituted. Drastic purges, however, must not be employed,
for the condition of the gastro-intestinal tract contra-indicates their use.
CHEOlSriC ATROPHY OF THE LIVEE.
The term "atrophy" includes all those forms of hepatic disease in which
there is a diminution in the size of the liver, due to decrease in either the
number or the size of the hepatic cells. Strictly speaking there are six
varieties of hepatic atrophy, viz.: — acute yellow atrophy, induration
atrophy, from repeated attacks of perihepatitis, cirrhosis, atrophy from
long continued Jiypermmia, atrophy from adhesive pylephleMtis, and chronic
atrophy. All these varieties have already been considered under their
proper head, except the one termed chronic atrophy. The liver in chronic
atrophy may have a brown or red color ; hence the term chronic brown or red
atrophy. The pathological processes which lead to it are similar to those
which take, place in atrophy of any gland tissue.
Morbid Anatomy. — Chronic atrophy may be partial or general. The
liver is smaller than normal, and its diminution in size is uniform. Some-
times its weight is decreased to twenty-four ounces. It is flabby and
tenacious, its edges are thickened, its capsule is smooth, of normal thick-
ness, and free from adhesions. Sometimes it is shrivelled, but never
~" hob-nailed " or lobulated. In partial atrophy, there are often large de-
pressions on the surface, the result of the pressure of neighboring organs,
or of tight lacing, or the wearing of belts tightly about the waist. A large
quantity of thin blood flows from its cut surface, which has a uniform
brown-red or mottled appearance. The sections of the larger portal vessels
gape. The outline of the lobules is obliterated. The portal vein and
its branches are enlarged, the walls assume a yellow-red color, the fibrous
sheath, derived from Glisson's capsule, is thickened, and its finest ramifica-
tions end in blind pouches or club-shaped extremities near the periphery of
the lobule. The capillaries are usually filled with pigment granules.
Sometimes the hepatic vein is involved, but never to the same degree as
the portal. The bile ducts are either empty or contain a small amount of
pale, turbid fluid, having traces of albumen. By the microscope the gran-
ular contents and nuclei of the hepatic cells will be found to have dis-
AMYLOID DEGENERATION".
371
^^f .%^'^J
t-A
Fig. 75.
Chronic Atrophy.
Section of portion of a Lobule.
A. Hepatic cells, shrivelled and pigmented, with disap-
pearance of nvclei.
B. Cells containing fat spherules.
C. Pigmented capillaries, x 300.
appeared. The cell walls will be indented and shrivelled^ and often
pigment granules, traces of bile
coloring matter, or little fatty-
spherules will be seen occupy-
ing their place. When the
atrophy is partial, these morbid
changes will be found to exist
underneath the depressions on
the surface, where pressure has
been long continued. The
spleen is usually enlarged, but
only slightly. The gastro-in-
testinal mucous membrane is
the seat of catarrh, and some-
times there are punctate hem-
orrhages beneath its mucous
surface.
Etiology. — The causes of par-
tial chronic red atrophy are tight lacing and pressure from peritoneal
effusions and from abdominal tumors. It may also be caused by extensive
adhesions to adjacent organs. General atrophy may be due to the con-
traction of the new connective-tissue developed in the substance and on the
surface of the organ, and to chronic malarial infection.
Symptoms. — The symptoms closely resemble those of cirrhosis of the
liver. There is loss of appetite, furred tongue, a sense of weight in the
right hypochondrium, accompanied by the train of symptoms which attend
chronic gastritis. There is profuse and exhausting diarrhoea alternating
with constipation, hemorrhoidal tumors, hsematemesis, intestinal hemor-
rhages, tympanitis, ascites and emaciation, — all which may be present in
interstitial hej)atitis.
Physical Signs. — Palpation. If the surface of the liver can be reached,
it will be found smooth and I'esistant.
Percussio7i. — The area of hepatic dulness will be diminished in every
direction.
Differential Diagnosis. — The differential diagnosis between chronic red
atrophy and cirrhosis of the liver is always difficult. In cirrhosis there
will be the history of spirit drinking, of gout or rheumatism ; none of
which will form a part of the history of chronic atrophy. In cirrhosis,
slight jaundice is common, to ward the end of the disease ; it never exists
in uncomplicated red atrophy. Venous stigmata, which are so often
met with on the cheeks in cirrhosis of the liver, are absent in chronic
atrophy. Diarrhcea is not so common or persistent in cirrhosis as in
atrophy. The urine in cirrhosis is high colored and contains albumen, bile
pigment, and lithates ; while in atrophy it is pale, and bile pigment is
rarely present. In cirrhosis the liver is hob-nailed and rough on palpa-
tion, while in atrophy it is smooth on its surface.
Prognosis. — Recovery from chronic red atrophy never occurs. Death
372
DISEASES OF THE DIGESTIVE SYSTEM.
may result from exhaustion due to the diarrhoea, from haematemesis or in-
testinal hemorrhages, and from general dropsy.
Treatment.^Little can be accomplished in the treatment of this disease
except to alleyiate suffering and prolong life ; it is incurable. When the
ascites causes dyspnoea it must be removed by mechanical means.
FATTY LIVER.
Fatty degeneration of the liver occurs either as a fatty infiltratmi or
as a metamorphosis of the albuminous elements of liver-tissue into fat. It
is one of the painless enlargements of the liver.
Temporary fatty infiltration of the liver is a physiological state which
occurs after the ingestion of food rich in hydrocarbons.
Morbid Anatomy. — In fatty infiltration, the liver is increased in size and
has a peculiar flattened appearance. Its surface is smooth and presents a
pale brown or light yellow color, according to the degree of infiltration ;
its borders are smooth and rounded, and it has a doughy, flabby feel, and
pits on pressure. Its capsule is tense, shining, and transparent ; enlarged
tortuous vessels are frequently seen traversing it.
On section the organ cuts readily, and the warmed knife blade is coated
with oil globules ; little blood flows from the cut surface. In the early
stage it presents a reticulated, mottled appearance, of a dull yellow color.
This appearance is due to the rim of fat globules around the periphery of
the acini, while the parts immediately about the central vein are intensely
congested and pigmented. In
the latter stage, the whole
surface presents a homogene-
ous bright "■ butter yellow '^
color, and fat cells are found
occupying the centre of the
lobule. Amyloid degeneration
and fatty infiltration may be
found in the same organ.
With the microscope the lobules
will be found enlarged, and
the cells at their periphery are
rounded, larger than normal,
and filled with fat globules.
These fat globules vary in size,
sometimes a single oil drop
occupies the entire cell space,
the clouded nucleus and gland-
ular contents being pressed up
At first
Fig. 76.
Fatty Infiltration .
Section of a Portal Canal and portion of three Lobules.
A, A, A. Connective-tissve of Portal Canal.
B. Branch of Portal Vein.
C. Eeiyatic Artery.
B, Hepatic Buct.
E. Periphery of a Lobule, in ^ohich small fat globules oaainst the cell Wall
are seen in the liver-cells. to
F. Same as LJ, tvith increased amoimt qfinflltration. _ -fchc Capillaries near the Central
G. Periphery of a third Lobule, in ivhich the lesion is _ ^
still further advanced. x28o. vcm are distended, and the
cells about the vein are infiltrated with fat to a slight extent ; later on
FATTY LIVEE.
373
the capillaries are compressed and the cell filled with pigment granules.
Pigment deposit and fatty infiltration are not often found in the same
cell. When the cell-wall remains intact, and the accumulation of fat is very-
great, the outline of the cell is uneven. The proportion of fat has ranged
as high as seventy-eight per cent, when the liver was freed of water, and
consisted of olein and margarin, with slight traces of cholesterin and
sugar.
Etiology. — Fatty Infiltration. — As has been stated, an exaggeration of the
normal physiological processes will lead to a pathological accumulation of fat
in the liver. Thus we find it in those eating largely and exercising little,
especially if the food taken is rich in hydrocarbons, and if alcoholic stimu-
lants are freely used at the same time. The obese and the gourmand are
always subject to this disease. Females are more liable than males to fatty
infiltration of the liver. Fatty infiltration occurs most frequently at the
middle period of life, when the time of active physical exertion is past. A
warm and moist climate predisposes to it, especially when one or more of
the above-named causes are in operation. Pulmonary phthisis is often ac-
companied by fatty infiltration of the liver, the deficient respiratory power
causing imperfect oxidation. Extensive crippling of the lung from any
cause may lead to it. In the new-born the liver sometimes contains an
abnormal quantity of fat, and there is undoubtedly an hereditary predispo-
ition to it in some families.
Fatty Metamorphosis, or true fatty degeneration, may occur at circum-
scribed spots in the liver, about cancer-nodules, pathological new forma-
tions, and in advanced stages of cirrhosis, chronic atrophy, and amyloid
degeneration. It may be uniform throughout
the whole liver, as a result of poisoning from
phosphorus, antimony, arsenic, ether, and
chloroform, or from blood-changes in typhoid,
yellow, and puerperal fevers, in small pox,
scarlatina, pyaemia, and any disease where an
extremely high temperature is sustained for a
considerable period. There is a similar form
of degeneration, due to the altered state of
the blood, in old age.
Symptoms. — The symptoms of fatty liver,
with few exceptions, are decidedly negative.
The fatty accumulation, though not enough
to cause sufficient obstruction to the portal
circulation, to lead to ascites or splenic en-
largement, is sufficient to give rise to gastric
symptoms, such as dyspepsia, flatulence, and
loss of appetite. There being no inter-
ference with the formation and outflow of
the bile, neither jaundice nor changes in the
color of the faeces occur. As the disease progresses the enlargement of the
liver may cause a sense of fulness in the right hypochondrium, never.
Fig. 77.
Fatty degeneration.
Section showing part of a Lobule in a
case of poisoning by phosphorous.
A. Hepatic cells showing the granvlar
chavqe of true fatty degeneration.
X 3.50.
B. Capillaries.
■374 DISEASES OF THE DIGESTIVE SYSTEM.
however, attended with pain. The slightest indiscretion causes an attack
of gastric catarrh and diarrhoea, whicli persists long after the removal of
the cause. The patient is anaemic and moody, and there is a general loss
of muscular power, with a disposition to sleep. The blood is hydrsemic.
The skin is sometimes shining, always ''velvety" to the feel, and often
pasty and smooth, like that of a wax figure. The integument all over the
body feels smooth, velvety, and flabby. Dyspnoea results as much from the
weakness and anaemia, as from pressure of the enlarged liver. When symp-
toms of acholia, due to the altered state of the blood, are attended by absence
of bile in the intestinal tract, rapid anaemia, exhaustion, delirium and col-
lapse occur, and extensive fatty metamorphosis is then usually associated
with some other hepatic degeneration. The faeces are usually normal in color
and the bowels are irregular and constipated ; in the highest grades of fatty
metamorphosis they are pale and clay-colored, and attacks of diarrhoea are
frequent. The urine is pale, non-albuminous, and of a low specific gravity.
Physical Signs. — Palpation. The rounded smooth edges of a uniformly
enlarged liver are readily felt below the border of the ribs ; the organ has
a doughy, soft feel. When fatty degeneration occurs with waxy or colloid
disease, the liver is diminished or is of normal size and smooth.
Percussion. — The area of hepatic dulness is increased in all directions,
the increase being mainly downward and forward.
Differential Diagnosis. — Fatty and waxy degeneration are frequently
mistaken for each other. In ivaxy liver a history of syphilis, prolonged
suppuration, or disease of bones will be elicited ; in fatty liver there is a
history of alcoholism, prolonged wasting disease, or one of high living and
sedentary habits. In waxy liver, the skin is pale, dry, and has a peculiar
odor resembling that of indigo ; in fatty liver the skin shines with fat,
and has a velvety feel. The blood is hydraemic in fatty liver, and is leu-
kaemic in waxy liver. The urinary symptoms in both are distinct : in
waxy liver the urine is often increased in amount, is albuminous, and con-
tains casts ; in fatty liver it is normal. In waxy liver the faeces are early
deficient in bile and pale in color ; in fatty liver they are normal until
an advanced stage of the disease is reached. A waxy liver is hard ; a fatty
liver is soft and flabby. A waxy liver may become much larger than a
fatty liver, and its edges are sharply defined ; w^hile in fatty liver they are
smooth and rounded. With a waxy liver the spleen is enlarged, but with
fatty liver it is normal in size.
Prognosis. — Fatty infiltration of the liver is not a grave form of disease.
There is danger only when fatty degeneration of liver-tissue occurs.
Death may result from fatty heart, pulmonary cedema, acholia, apo-
plexy, the exhausting diarrhoea, and from the complications already re-
ferred to.
Treatment. — When the diet, mode of life, or climate is the main element
in its causation, the indications for treatment are simple. A restricted
diet, with no fat or sugar, and with regular daily exercise in the open air
will, in most cases, increase the patient's strength and lessen the size of
the liver. Care must be taken not to stop alcoholic stimulants too suddenly.
PIGMENT DEGENERATION.
S7L
for fatty heart may co-exist. They must be decreased gradually. In all
cases, a residence in an elevated temperate region, free from marshes, is im-
portant. The vegetable bitters combined with alkalies will aid in restor-
ing the appetite when it is lost. Iron should be administered in the form
of the carbonates and lactates. Ehubarb and aloes will best relieve the
constipation, and vegetable astringents control the diarrhcea. In syphilis,
iodide of potassium is of service. In the fatty liver of phthisis, nothing can
be expected from treatment so long as the phthisis is progressive.
PIGMENT DEGENEEATION.
The pigment or melanotic liver is that form of hepatic degeneration in
which there is an abnormal deposit in the liver of pigment derived from
the coloring matter of the blood. In pigmentation there must be prima-
rily a fault in the circulation or in the blood-vessels ; usually it is the re-
sult of slowing of the blood curi'ent. The red corpuscles either pass
through the walls entire, or liberate the haemoglobin, which then transudes
the capillary vessels. The blood from
the spleen, loaded with pigment,
passes into the portal vein, is carried
through the interlobular veins, then
into the veins just within the periph-
ery of the lobule. Haamoglobin re-
maining in the portal capillaries soon
breaks up into haematoidin and, ac-
cording to some, into melanin, though
we are inclined to-day to regard me-
lanin as altered haematoidin. This
haematoidin is first yellowish, later it
consists either of brownish-black
granules or crystals of an intensely
black color. Both haematoidin and
melanin remain unaltered when once
formed. Pigmentation of the liver
is confined to the vascular system.
Extensive capillary stagnation with
a large amount of pigment matter oc-
cluding the vessels gives rise to atrophy of the cellular structure.
Morbid Anatomy. — The liver is at first enlarged from congestion and
the capsule is smooth and tense ; afterward the organ becomes smaller
than normal and atrophies, its color being much deeper than in the ear-
lier stage and its edges sharply defined.
On section, in the first stage, dark blood flows from the congested paren-
chyma. If the cut surface presents a mottled appearance there is a steel-
gray or black ring around, and slightly encroaching on, each lobule, shad-
ing off toward the central vein. In congestion of the liver pigmentation
Fig. 78.
Pigmentary Degeneration.
Section of an Hepatic Lobule frcnn a case of per-
nicious fever.
A. Central veifi of the lobule.
B. Longitudinal section of a small hepatic duct.
C. Vessels containing small pigment grannies in
great numbers. The pigmentation in this case
was pretty general throughout the intralobular-
capillaries. x 250.
376
DISEASES OF THE DIGESTIVE SYSTEM.
commences about the central yein, and gradually diminishes toward the
periphery of the lobule. If the surface is uniform it presents a color which
resembles ''graphite," a blackened gray color having a slight lustre, and
the pigment deposit is seen to have reached the central vein. Occasionally
spots of extravasation are found scattered throughout the organ. On sec-
tion of an atrophied " pigment livefr " the whole cut surface is black, and all
trace of the lobules is frequently lost. A micro scojncal examination shows
the capillaries, not only portal but hepatic, filled with granules or crystals,
either throughout their entire extent or in isolated patches. The hepatic
cells contain no pigment, but are filled
with oily or amyloid material, or some-
times with dark-colored bile. Leucin
has often been found in the parenchy-
ma of a pigmented liver. In an
"atrophied" liver, the lobules and
cells are shrunken, and the capillary
system is a mass of pigment. The
spleen is softened and usually enlarged,
never smaller than normal, and is
more extensively pigmented than the
liver. In some cases of pigment liver,
there are evidences of hemorrhages
into the various serous cavities. In
connection with pigment degeneration
of the liver, pigmentation may occur
in all the organs of the body.
Etiology. — Malarial infection is the
only known cause of melanotic liver,
but whether a large amount or peculiar
Tcind of malarial poison is necessary for its development has not as yet
been determined.
Symptoms. — Frequently those who have had extensive pigment deposits
va. all the organs of the body, have given during life no symptoms to indi-
cate their presence. The first efPectof extensive pigmentation of the liver is
an abnormal secretion of bile. The liver is enlarged and tender to press-
ure. The skin in the milder forms is ash-colored, and in severer forms it
is of a dark-bronze hue. There may be slight jaundice. There is gastro-
intestinal catarrh with nausea, loss of appetite, flatulence, painful tympa-
nitis, vomiting, and diarrhoea which may pass into dysentery. In severe
cases, hemorrhage from the gastro-intestinal mucous membrane and from
the kidney occurs, attended by exacerbations and remissions correspond-
ing to febrile exacerbations and remissions. There is I'apid emaciation
and extreme exhaustion with giddiness, headache, and ringing in the ears.
Occasionally the vertigo comes on so suddenly that the patient falls to the
ground without the least warning. Active delirium is often followed by
profound coma. The urine and fseces are passed involuntarily during the
period of stupor. Coma is the most frequent termination of the cerebral
c-
Fig. 79.
Pigment Degeneration.
Section of the same tissue as preceding cut, show-
ing the centime of a lobule more highly magnified.
A. Central vein of the lobule.
B, B. Strongly pigmented capillaries.
C, C. Hepatic cells infiltrated with fat. x 450.
CANCEE OF THE LIVEE. 377
variety of pigment liver. In severe cases which terminate in recovery there
is often temporary loss of memory.
Physical Signs. — Inspection shows the ashy-gray, jaundiced, or brown
colored skin.
Palpation. — The surface of the liver is smooth, and in the first stage the
organ is larger, softer, and more tender than normal. In the second stage
it is small and hard.
Percussimi. — In the early stage the area of hepatic dulness is increased;
in the later stage it is uniformly diminished.
Differential Diagnosis. — The liability of confounding pigment degenera-
tion with other diseases of the liver is not so great as is the difficulty of
recognizing its existence. If, in intense malarial infection, cerebral or
urinary symptoms come on suddenly with hemorrhages from the mucous
surfaces, a bronzed hue of the skin, and the physical changes in the size of
the liver already referred to, pigmentation of the liver may be suspected ;
and if, in addition to these, pigment matter is found in the blood, the
diagnosis will be established.
Prognosis. — The prognosis is favorable if the patient can be removed
from the source of malarial infection. The elements which render the
prognosis unfavorable are severe cerebral and renal symptoms combined
with signs of extensive portal obstruction. Death may occur from exhaus-
tion due to the diarrhoea, dysentery, or intestinal hemorrhage.
Treatment. — The preventive treatment corresponds to the preventive
treatment of malarial fever. When the disease is once established, the
chief indication is to administer large doses of quinine. The symptoms in
all varieties of the disease remit as soon as the individual is brought fully
under the influence of this drug. Purges act unfavorably. If the cere-
bral symptoms are urgent, ammonia may be combined with quinine.
Preparations of iron and a change of residence to a non-malarial district
are essential to its successful management. The diet should be of the most
nutritious character and non-stimulating.
CAlSrCER OF THE LIVEE.
Cancer of the liver may be either primary or secondary. It is secondary
to cancer of the stomach in one-half of the cases. It has been estimated
that one out of every one hundred persons has cancer of the liver. The
varieties of cancer met with in the liver are scirrhus, medullary, melanotic,
and colloid cancer. Infiltrated cancer without any change whatever in the
form of the organ has been found.
Scirrhus is usually primary, while medullary is almost always second-
ary. Scirrhus makes its appearance first as rounded masses. These masses
increase rapidly and soon attain their full size, which varies from that of a pea
to that of an orange ; they then remain stationary for a time until the fibrous
tissue contracts. The number of these nodules varies inversely with their
size. Scirrhus developments usually commence in the interlobular spaces
and gradually extend toward the centre of the lobule. As the liver-cells
378 DISEASES OF THE DIGESTIVE SYSTEM.
are being crowded upon, the portal capillaries disappear, while the hepatic
vessels enlarge and ramify in the cancerous mass as a new and peculiar
vascular net-work. The neighboring lymphatic glands may also become
infiltrated with cancer, and often exert sufficient pressure upon the bile-
ducts to obstruct the outflow of the bile. The cancerous growth sometimes
involves the walls of the portal vein, and, extending in the direction of the
capillary terminations, fills up their channel. The bile-ducts also may be
obstructed, distended, or ruptured. With these changes, the centre of the
cancer-nodule becomes harder and harder ; or by shutting off its own
nutrition, the interior of the nodule becomes fatty, while the periphery is
soft and vascular. The obliteration of the capillaries at the exterior of the
mass shuts off the nutrition of the adjacent liver-cells, and this induces
fatty degeneration. The theory of the development of medullary cancer
(the implantation theory, as it is called) is that cancer-cells pass through
the lymphatics, or blood-vessels, and reaching the interlobular spaces
become the starting points of the cancer development. This theory has
received much attention, and experiments seem to warrant our adopting it
as one method, at least, in which cancer may develop.
Medtdlary cancer is simply a modification of scirrhus. Rapidity of de-
velopment is the distinguishing pathological difference, — the line between
the two forms often being arbitrarily drawn, for scirrhus may pass into
medullary, and vice versa.
Melanotic cancer of the liver is also of rapid growth. The nodules,
though very numerous, are small in size. The cancer-cells have a deposit
at their centre of yellow, brown or blackish pigment, the " granite " look-
ing spot shading off toward the periphery. Its course is the same as in
other varieties of hepatic cancer.
Colloid cancer is of rare occurrence in the liver, appearing only as a
degenerated form of scirrhus or medullary cancer. If either of these forms
undergoes mucoid or colloid degeneration, a gelatinous, gray, tenacious
fluid takes the place of the cancer-juice, while the fibrous framework be-
comes more distinctly alveolar. Melanotic sarcoma has been found ; it
often pursues as malignant a course as true carcinoma.
Morbid Anatomy. — In scirrhus cancer the liver is increased in si^e,
the right lobe being usually most affected. Sometimes it is so much en-
larged as to fill the abdominal cavity. In color it is darker than normal,
and it is increased in weight, sometimes reaching twenty pounds. Upon
its surface are nodules, hard, elastic, rarely fluctuating, and umbilicated at
their centres. Occasionally, there are no nodules on the surface, the can-
cerous developments being confined to the interior of the organ. The cap-
sule of the liver is thickened and sometimes the seat of cancerous develop-
ment. Adhesions connecting it to the adjacent parts are the result of
intercurrent local peritonitis.
On section, if the degeneration is advanced, the liver cuts hard, and
creaks like cartilage under the knife. The cut surface is seen studded with
nodules, the diameters of which vary from one-eighth of an inch to four
inches. Between the nodules the liver- tissue is sometimes congested, and
CAKCER OF THE LIVEE.
379
of a dark red color, or it is atrophied. The nodules increase in density from
their centre outward, or have a central cavity filled with fatty granules.
On pressing them, more or less cancer-juice exudes according to the density
of the tumor. The color of the tumor varies from a glistening dirty white
to a deep red, according as the vascular net-work is meagre or abundant.
If there has been obstruction to the bile ducts the parenchyma will be of a
bright yellow color. Evidences of extravasation from distended vessels may
be found throughout the liver-tissue and often in the interior of the can-
cerous growth.
Under the microscope, a cancer nodule will be found to consist of a fibrous
framework or '* stroma " in which are cancer-cells and cancer-juice. In
Pig. 80.
Cancer of the Liver.
Section showing part of a canceroiis nodule with the contiguous hepatic tissue.
A . Connective-tissue of a portal canal in which the nodule was developed.
B. Hepatic duct in lakgitudinal section.
C. Hepatic artery.
D. Stroma of cancer.
E. Alveoli of the same filled with " cancer. cells. "
F. Empty alveoli.
G. Periphery of an hepatic lobule hordenng on the career, infiltrated at HH.
I. Infltratian of connective-tissue with same, x 300.
scirrhus the fibrous stroma is greatly in excess of the other elements. The
cancer-juice contains a large amount of fine granular matter, nucleated
cells and distinct free nuclei. The cells are of large size and irregular,
and the nuclei and nucleoli are often multiple and very distinct. The
walls of the capillary vessels in the tumor are thin, and their calibre large.
A ring of liver cells at the margin of the cancer-nodule exhibits well-
marked degeneration.
380 DISEASES OE THE DIGESTIVE SYSTEM.
Medullary Cancer. — The gross appearances of the liver are the same
as in soirrhus, except that the nodules are fewer and larger. They are
very soft and fluctuating, and frequently the more advanced tumors
have ruptured through the peritoneal envelope of the liver. In this
variety the cancer nodules are often lobulated. Those which occupy the
surface of tlie liver project as large irregular tumors.
On section large nodular masses of curdy-white homogeneous matter re-
sembling foetal brain-substance are found scattered throughout the liver-
tissue. Between the cancer nodules the liver substance is more or less in-
tensely congested. Dark red hemorrhagic spots are seen scattered over its
cut surface.
On a microscopic examination a small amount of fibrous stroma is found
containing a very large number of cells. The cells are much larger than
in scirrhus, though the same in kind, and they are the seat of more fatty
degeneration.
Melanotic Cancer. — In common with the morbid appearance of all can-
cerous developments, we find, besides, that the liver is nodular and very
dark.
On section the surface presents a peculiar mottled appearance resembling
granite, and there are numerous small nodules studding the whole gland.
On pressure a dark fluid flows from the cancerous mass, varying in color
from a gray-brown to a deep black.
A microscopical examination shows a stroma varying in amount and
color. Sometimes it is colorless, sometimes very dark. The degree of
vascularity has wide ranges ; the cells at certain spots in the liver often dis-
appear and only a peculiar pigment color remains.
Colloid Degeneration. — The surface of the liver in this form of cancer
differs from the other varieties in that it is smooth with large lobulations.
Under the microscope the cancerous mass is made up of large and spherical
alveoli with thin walls. The alveoli contain mucoid or colloid matter,
with fatty material and a few epithelial cells.
Etiology. — The causation of primary hepatic cancer is unknown ; in
most instances there exists an hereditary predisposition. It is a disease of
middle life, occurring oftenest between the ages of forty and sixty-five.
Medullary cancer of the liver, especially when secondary, is sometimes met
■with in early life, even as early as the fourth year. It occurs equally among
males and females. Some have dated its development from some great
mental emotion or strain, others from the receipt of a blow upon the right
hypochondrium. Cancer of the liver is often secondary to cancer of the
stomach, mamma, ovary, uterus, pancreas, brain, or portal vein. Clinical
exp3rience indicates that extirpation of external cancerous masses is very
apt to be followed by cancer of the liver.
Symptoms, — The early symptoms of hepatic cancer are obscure. The
more superficial its development, the more marked are the symptoms and
the easier the diagnosis. It will be noticed that the individual is gradually
losing flesh and strength, he complains of a sense of weight and fullness in
the right hypochondrium, he is anaemic, and the surface assumes a doughy
CANCER OF THE LIVER.
381
hue ; with these there may be pain localized over the hepatic region, or
shooting up toward the right shoulder, and sometimes to the back. The
pain soon becomes lancinating in character, and is localized at some point
over the liver which is tender to pressure. There is loss of appetite, flatu-
lence, nausea, vomiting, and constipation alternating with diarrhoea. Tlie
vomiting is often profuse and persistent. There is progressive emaciation,
and the skin assumes an earthy pallor. Jaundice is present in one-half of
the cases, and is due either to compression of the bile ducts or to intercur-
rent catarrh of the ducts, and when once developed it is permanent. Asci-
tes occurs more frequently than jaundice ; the accumulation at first is in-
considerable in amount and increases slowly. It is due to compression of
the portal vein by the cancerous tumor or by enlarged glands in the trans-
verse fissure, or to chronic peritonitis. (Edema of the feet comes on late.
The temperature is normal or sub-normaL Dyspnoea may become an
urgent symptom in the advanced stage of hepatic cancer. The cervical
and inguinal glands may be enlarged. Hemorrhages from the stomach,
intestines, mouth, and vagina, with petechial and ecchymotic spots, are
sometimes accompaniments of hepatic cancer. It is to be remembered that
hepatic cancer may run its entire course without pain, without jaundice
and without ascites. In medullary cancer, loss of flesh and the peculiar
cancer countenance may not appear until the end of the case. The fseces
are normal at first, later they are firm and clay-colored. The fluid stools
of cancer diarrhoea contain no bile. The urine is scanty and high-colored.
Deposits of lithates and of bile pigment are rarely absent.
Physical Signs. — Inspection. There may be a perceptible bulging in the
right hypochondrium and the outlines
of large nodules may be visible.
Palpation discloses an enlarged and
irregularly shaped liver, tender to
pressure. Hard, smooth nodules are
felt over its surface, which rarely
fluctuate. If the nodules are um-
bilicated it establishes the diagnosis
of cancer. In colloid cancer of the
liver, and when the cancerous devel-
opment is central, no nodules will be
felt.
Percussion. — The area of hepatic
dulness is irregularly increased and
marked by an irregular line of flatness
below the free border of the ribs.
Auscultation. — A friction sound,
caused by the rubbing of the rough-
ened peritoneal surfaces, is sometimes
heard.
Differential Diagnosis. — Cancer of
the liver may be mistaken for hydatids
Fig. 81.
Diagram sh(nvi?7ff enlargements of the Liver as
determined by percussion.
A, A. Line of diaphrag7n.
B, B. Lower border of costal cartilages.
C. Dotted tine enlargpnent upivard.
D. Shaded area indicating successive and in-
creasing enlargements.
IS. Lower edge of Liver in Cancer, Leukamia
and Adenoma.
382 DISEASES OF THE DIGESTIVE SYSTEM.
of the liver, abscess of the liver, luaxy degeneration with gummata, cancer
of the stomach, and an enlarged gall-hladder.
In hydatids there are no gastric or severe constitutional symptoms.
Cancer of the liver is rapid in its development, rarely exceeding one year
in duration, while hydatids are of slow growth, lasting from four to eight
years. Gastro-intestinal hemorrhages are common in cancer, and do not
occur in hydatids. Pain is a prominent symptom in cancer ; hydatid
tumors are painless. In cancer the nodules are hard, tender, and firm ;
hydatid tumors are large, soft, smooth and elastic, and can be freely manip-
ulated without pain. The peculiar hydatid fremitus is sometimes obtained
by percussing a hydatid tumor. In hydatids (with an exploring trochar) a
saline fluid containing the booklets of the echinococci may be withdrawn,
which will decide the diagnosis.
In waxy degeneration of the liver, there is a history of syphilis, pro-
longed suppuration, or disease of bone ; and in cancer an hereditary cancerous
history, or the evidences of carcinoma elsewhere. The progress of waxy liver
is slow; that of cancer is rapid. A waxy liver is painless, while pain in
cancer is constant. In waxy liver the spleen is markedly enlarged ; in cancer
it is normal in size, unless it is the seat of cancer infiltration. Jaundice and
ascites are rare in waxy degeneration, and frequent in cancer.
In cancer of the stomach gastric symptoms are urgent and appear
much earlier than in cancer of the liver. In cancer of the stomach there
is usually coSee-ground vomiting and cancer-cells in the ejected matter.
In cancer of the stomach the pain and gastric symptoms are aggravated
after ingestion of food, while in hepatic cancer the pain and gastric symp-
toms are constant. In cancer of the liver in thin subjects, immovable
nodulated tumors may be felt by pressing up under the ribs ; while in
gastric cancer a single tumor which is movable, and changes its posi-
tion as the stomach is full or empty, is usually felt. In hepatic cancer
there is absolute dulness over the tumor ; while in cancer of the stomach
the percussion note has a peculiar tympanitic quality.
Cancer of the right hidney, impaction of fceces, and various alterations
in the size of the healthy liver will not long confuse one if the symptoms
and physical signs are carefully analyzed.
Prognosis. — Cancer of the liver is a fatal disease. The average duration
is about one year. Medullary cancer runs its course in from two weeks to
four months. The duration of all varieties will be influenced by the pres-
ence or absence of complications. Death may result from exhaustion,
from the cancerous cachexia, dropsy, diarrhoea, dysentery and hemorrhages,
or from peritonitis, pneumonia or pulmonary cedema.
Treatment. — All varieties of cancer of the liver are incurable, hence the
absurdity of all the so called curative measures. The diet should be nu-
tritious, and care should be exercised not to overfeed this class of patients.
Easily assimilated preparations of iron are often of service. Diarrhoea, if
present, may be checked by such remedies as gallic acid, lead, and opium.
The operation of paracentesis should be delayed as long as possible. In
the advanced stage of the disease alcoholic stimulants are often necessary
GWJMMY TUMOE OF THE LIVER. 3b3
and beneficial. In the great majority of cases tlie principal ofiice of the
physician is to relieve pain, and morphia is our most reliable remedy for
this purpose ; it should be given in sufficient quantities to keep the patient
comfortable .
GUMMY TUMOR OF THE LIVER.
This form of new growth is perhaps the most characteristic lesion of con-
stitutional syphilis. Some writers group these tumors under the head of
syphilitic disease of the liver. Those forms of perihepatitis, cirrhosis, and
amyloid degeneration which are of evident syphilitic origin, I have preferred
to describe in connection with the other corresponding forms, giving at the
same time the few differences due to the syphilitic causation.
Morbid Anatomy. — The syphilitic nodules, gummy tumors, or " gum-
mata " appear first as small masses of reddish-gray, pulpy, vascular tissue,
scattered throughout the liver. Their point of origin I believe to be the
wall of the capillaries, — the cells and nuclei of the " syphiloma" being due
to the growth of the nuclei of the capillaries. The mass is composed of
highly organized granulation-tissue, and is usually spherical in shape. The
liver may be enlarged, or may retain its normal size, according to the ex-
tent of the waxy change which usually accompanies the development of
the gummata. Diminution of its size is due to perihepatitis causing re-
traction. Under these circumstances the organ is lobulated, and deep,
whitish furrows indent it, the result of cicatricial contractions. Fibroid
nodules occasionally lie in these cicatrices. The bulgings are soft and smooth
to the touch. The capsule is firm and opaque, and the seat of fibroid thick-
ening, and is frequently bound to surrounding parts by adhesions.
On section there will be found scattered through the liver rounded
masses varying in size from a pea to an orange, yellowish-white in color,
either surrounded by congested parenchyma, or as isolated spots in the
midst of an infiltrated homogeneous grayish-red mass. They may be en-
capsulated, a layer of translucent fibrous-tissue surrounding them and
shading off imperceptibly into the surrounding liver-tissue. Brown spots
in the tumors correspond to obstructed bile-ducts. The liver parenchyma,
between the nodules, undergoes various changes : at one time it is con-
gested and hypertrophied, at another it is atrophied and undergoes fatty
degeneration. In well-marked cases there are two zones, an outer, red and
fleshy, and an inner, dry, grayish and firm. Again, nothing may remain
of a previous gumma but a shrivelled cicatrix.
A microscopical examination of a fully developed gummy tumor reveals
three jorocesses -.—first, at the periphery, there is a vascular mass of gran-
ulation-tissue, embedded in which are cells bearing a striking resem-
blance to white blood globules, and some larger nucleated ones. Sec-
ondly, just beneath this zone is found a fibro-nucleated mass, the fibril-
lations being very dense and cicatricial. Thirdly, in the centre of the mass
are found fat-granules and broken-down cells, with occasional traces of
cholesterin, and sometimes faint evidences of fibrillar tissue. Cheesy and
calcareous masses are also sometimes found in the centre of the gumma.
384 DISEASES OF THE DIGESTIVE SYSTEM.
Etiology. — As has been stated, gummata are the most characteristic of
the lesions of internal syphilis. They are met with under no other condi-
tions.
Symptoms. — The subjective symptoms of hepatic gummata are few and
inconstant. At a post-mortem, a liver may be found studded with gummy
tumors, when no symptoms referable to the liver were present during life.
There is generally a history of increasing debility, and a feeling of press-
ure, tightness, and dull pain in the region of the liver. Sometimes the pain
is severe and localized, at other times it is dull and diffused over the whole
hepatic region. The pain in one case is constant, in another intermittent.
If jaundice exists, it is due to the pressure either of the gummata or of an
enlarged lymphatic. The temperature is normal, and the pulse-rate is but
slightly increased. Ascites may result from pressure on the portal vein, or
from chronic peritonitis, which oftea complicates its development. Both
jaundice and ascites are not present until the liver has become very much
enlarged. The symptoms which are present in the advanced stage of this
disease, such as diarrhoea, loss of appetite, vomiting, hemorrhoids, gastric
and intestinal hemorrhage, are due rather to the accompanying hepatic de-
generation than to the gummata.
Physical Signs. — Palpation may show the liver to be enlarged or normal
in size ; a moderate increase in size is the rule. The organ has smooth
lobules upon its surface between which run deep fissures. The lobulations
are soft and elastic, never fluctuating.
Percussion. — The area of dulness is increased and its outline is irregular
below the free border of the ribs. The area of spleen-dulness in the ma-
jority of cases is slightly increased.
Differential Diagnosis. — Gummata of the liver may be mistaken for can-
cer, and if the liver is diminished in size, for syphilitic cirrhosis. The
differential diagnosis of both has been considered.
Prognosis. — Gummata of the liver rarely directly destroy life. The prog-
nosis is unfavorable when ascites, gastro-intestinal hemorrhage, persist-
ent diarrhoea, or a marked cachexia exists. Complicating diseases also influ-
ence the prognosis ; amyloid degeneration of the spleen and kidneys is a bad
complication. The most frequent intercurrent lung diseases are pleurisy,
pneumonia, pulmonary oedema, and chronic bronchitis. Death occurs from
exhaustion due to the syphilitic marasmus, from diarrhoea, dysentery, and
dropsy. Pneumonia and pulmonary oedema often cause it, and sometimes
cholsemia, with its peculiar symptoms, ends in coma and death.
Treatment. — The treatment of this afl'ection resolves itself into the treat-
ment of syphilis. As it is a tertiary symptom, our main reliance is on large
doses of the iodide of potassium combined with mercurial inunctions. With
these iron and cod-liver oil should be constantly taken, and the patient
should be placed under the best hygiene. The diet should be nutritious
and non-stimulating. Opium combined with nitric acid will always con-
trol the diarrhoea if it becomes exhausting.
HYDATIDS OF THE LIVEB. 385
HYDATIDS OF THE LIVER.
Hydatid tumors are cysts due to the development in the liver of the em-
bryos of the tcenia ecMnococcus ; these embryos are called "echinococci,"
their development '' hydatids" ; they are usually single, and for more than
two or three to be present in the same liver is a phenomenal event.
Morbid Anatomy. — An ovum of taenia echinococcus, either during masti-
cation or from the action of the digestive juices, has the envelope containing
the echinococcus removed, and then by its booklets it bores its way from
the stomach or intestine into the liver. It there becomes encysted: the
cyst consists of an external laminated cuticular layer and an internal par-
enchymatous lining. From the internal layer numerous little heads bud
forth in the form of vesicles, and these, the '^ daughter vesicles," in turn
bear a second crop, the " grand-daugh-
ter cells," the mother-sac meanwhile
enlarging, partly from the increase in the
number of the vesicles, and partly from
its own secretion, which is clear and wa-
tery. As these successive generations of
vesicles appear, broods of immature tae-
nia C'scolices ") in the form of a gray-
ish granular layer, are developed first
upon the internal surface of the mother
sac and then upon that of the other
cysts, in the order of age. While the
younger vesicles cling to the parent-
walls, the larger and older ones become
, , , Ti^ir 82
detached, and float m the mterior of ' "
, , I • 11 1 • ; Sketch from an Hydatid Tumor showing the tntd-
the continually enlargmg parent-sac. ding vesicles.
Proliferation of connective-tissue upon the exterior of the sac resulting
from the inflammatory process excited by the pressure of a foreign body,
develops a fibrous capsule closely connected with the adjacent liver par-
enchyma ; this is supplied with blood by the hepatic and portal capilla-
ries.
During its enlargement the hydatid tumor loses its spherical shape and
becomes indented. As it increases in size, the fibrous capsule becomes
thickened, rough and cartilaginous ; sometimes it undergoes ossification.
The echinococci may be destroyed by the bile which enters the cysts when
the bile-ducts are opened, or by the inflammation which is established be-
tween the connective tissue capsule and the wall of the true sac, causing
a grayish oily material of variable consistence to be developed. The clear
fluid in the cavity of the hydatid becomes cloudy, then opaque, while all
traces of the vesicles disappear, and at last only a few booklets of the echi-
nococci remain. This is a process of fatty degeneration. Sometimes
the formation of vesicles is so rapid that their number is beyond all pro-
portion to the fluid, and then they die and collapse, undergoing no degen-
35
386 DISEASES OF THE DIGESTIVE SYSTEM.
erative process ; again, when neither of these terminations is reached, tha
hydatid tumor may continue to increase in size until finally it bursts into
the adjacent cavities.
The most frequent rupture is into the right pleural cavity. The hyda-
tid tumor, by its pressure upon the diaphragm, causes it to become thin,
and to rise upward, sometimes as high as the second rib. Finally the
diaphragm ruptures and the sac is discharged into the pleural cavity, or
when the pleural surfaces become adherent the tumor ruptures into the
lung-tissue or bronchi. These tumors sometimes rupture into the perito-
neal cavity, and peritonitis results, or the stomach or intestinal canal may
communicate by a small aperture with the hydatid sac. A communication
is sometimes established between the bile-ducts and the hydatid tumor, and
the ducts become filled with the contents of the hydatid mass ; the ductus
communis may become obstructed by a large hydatid vesicle. Another
mode of termination is by an intense inflammatory action, causing sup-
puration of the liver-tissue in the vicinity of a ruptured hydatid tumor,
which consequently is filled with coagulated blood and pus ; more rarely
a gangrenous process may be established in it.
The liver is irregularly enlarged and displaced. The increase in size
varies with that of the projecting cysts, which are sometimes large enough
to fill the abdominal, and a portion of the thoracic, cavity. The bulging
is globular if the cyst is simple and is situated in the right lobe of the
liver. The tumor is elastic and often fluctuating. A uniform enlarge-
ment of the liver results from a centrally located hydatid. The capsule
covering the cyst is thickened, and adhesions often bind the liver to the
surrounding parts.
071 sectio7i, the liver-tissue in the vicinity of the tumor is found com-
pressed and atrophied, or congested and hypertrophied. The mother-sac is
commonly the size of a foetal head. The true cyst wall is a gelatinous, whitish,
semi-transparent membrane, containing the hydatid fluid, floating in which
are vesicles from the size of a millet-seed to that of an egg, and varying
in number from hundreds to thousands. On the inner walls of the larger
ones, and on that of the parent-sac, are younger vesicles about the size of a
pin's head. On the inner side of the sac are also found patches of white
granular matter. The cysts may be found filled with atrophied and shriv-
elled vesicles embedded in a debris consisting of fat-granules, cholesterin,
haemaglobin, and bile. Its consistency varies : sometimes it is liquid and
watery, then semi-fluid, gelatinous, or like a thick paste ; at other times
only a few booklets remain in this gray, putty-like mass. The cyst may
contain blood or pus.
A microscopical examination shows the sac of the hydatid to be a gela-
tinous mass made up of concentric hyaline lamellas. The scolices are from
1-75 to 1-225 of an inch in length ; the head is furnished with four suckers
and a proboscis, about which are sicMe-sliapecl liooklets in number from
twenty-five to fifty. The body is striped longitudinally and transversely,
and has a groove between it and the head, which latter, being usually re-
tracted into the body, causes the animal to look somewhat like an in-
HYDATIDS OF THE LIVES.
387
dented rubber ball, the hooks fringing the depression.
clear or slightly opalescent, it has a
specific gi'avity of 1010 to 1015, is
usually neutral in reaction, and is
non-albuminous. It is chiefly water
containing chloride of sodium.
Etiology. — The essential cause of
the development of hydatids is the
entrance into the stomach, or intes-
tines, of tlie taenia echinococcus. If
they remain in the intestine they be-
come tape-worms ; when they pass
into the liver they develop hydatids.
Hydatids are chiefly met with be-
The fluid is
i?iG. 83.
Hj'datids of the Liver.
A. Head of echinococcus from an hydatid tumor. — B.
tween the ages of thirty and fifty. E. Fmc/ment' of capsule of ' hydatid tunwr, showing
,,^^ ■ T -1 n T Tin itsiamell(B.—F. Gei-ms. x 200.
Ihey are rare m childhood and old
age. They are most common among the poor and filthy, and in cold
climates. It is estimated that one out of every six of the inhabitants of
Iceland has hydatids of the liver. Dogs, sheep, pigs, cats, and rats are
subject to tapeworms, and as the ova of these parasites are discharged in
the excrements of these animals, they can only gain entrance into the
human stomach through polluted drinking-water, or the most filthy prac-
tices.
Symptoms. — If an hydatid tumor is deeply seated and of small size, it gives
rise to no symptoms and cannot be recognized. A large hydatid tumor
will cause sufficient functional disturbance by its pressure to be easily
recognized. The patient may first see or feel a tumor in the region of the
liver, and have a sense of weight and dragging in the right hypochon-
driiim. Symptoms of pressure of the tumor on adjacent organs are the
first, and often the only ones which attract attention. Dyspnosa, a dry
hacking cough, and bronchial catarrh may result from the upward press-
ure of the tumor. When the heart is displaced by the tumor, there is
palpitation ; and when the stomach is encroached upon there is vomiting,
dyspeptic symptoms and emaciation. When the portal vein or vena cava
is pressed upon by the hydatid tumor, ascites, jaundice and hemorrhoids
may result. When the hydatid compresses the bile duct, or when there is
intercurrent catarrh of the ducts, or when they have become obstructed by
the hydatid vesicles, jaundice sets in and absence of bile in the freces is
noted. A large vesicle may, in passing the duct, give every symptom
of gall-stone colic, and thus be confounded with it.
When the pleura is perforated, the symptoms of acute pleurisy are devel-
oped, and in most cases the cavity is rapidly filled with pus containing
hydatid vesicles. Peritonitis may result from spontaneous or traumatic
rupture of an hydatid cyst. The opening into the stomach or intestines
being usually very small, it is rarely attended either by peritonitis or sec-
ondary abscess ; when a cyst is evacuated in this way the case usually ter-
minates in recovery. When shreds of hydatid vesicles and echinococci are
388 DISEASES OF THE DIGESTIVE SYSTEM.
found in the urine, it indicates that the rupture has taken place into the
urinary passages. When the hydatid tumor is to discharge itself through
the abdominal parietes, redness of the skin, tenderness, pain, and fluctua-
tion will precede its discharge. If, in a patient who is known to have
hydatids of the liver, there is pain, elevation of pulse and temperature,
extreme sensitiveness over the hepatic region with a peculiar friction sound
on auscultation, it may be suspected that inflammation in and around the
sac has occurred. In such case abscess may be excluded by the absence of
rigors and sweats.
Finally, the growth of an hydatid of the liver is in rare cases attended
with pain caused by its pressure. The feeces are normal unless jaundice
exists, in which case they are firm and clay-colored. The urine is generally
normal, but if pus or albumen is found in it, pyelitis exists as a result of
the pressure of the tumor on the renal vein.
Physical Signs. — Inspection may show a distinct bulging in the right
hypochondrium, which has the appearance of a globular elevation over the
right or left lobe of the liver. The ribs often project, and respiratory
movements on the right side are interfered with.
Palpation discovers an enlarged liver, elastic to the touch when the
tumor is deeply seated ; when it is superficial, fluctuation may be detected.
The tumor is smooth, but if two, three or more cysts exist, the liver will
have a lobulated outline below the free border of the ribs.
Percussion. — The normal area of hepatic dulness is increased in some
one direction. When the tumor is superficial, the hydatid thrill or "fre-
mitus " is elicited by firm percussion. This sign, peculiar to hydatids of
the liver, is elicited in the following manner : place three fingers, slightly
separated, firmly over the most prominent part of the tumor ; give a sharp
blow upon the middle one, and a vibration or fremitus will be communicated
to the other two.
Differential Diagnosis. — Hydatids of the liver may be mistaken for cancer ^
abscess, abdominal aneurism, enlarged gall-Madder, pleurisy, rarely multi-
locular hydatids, and a cyst of the right Tcidney. In aMominal aneurism
there will be severe and constant pain in the back ; the tumor is soft,
doughy, and compressible, has an '^^ expansive" pulsation and is immov-
able, while an hydatid tumor moves up and down with the respiratory
movements and fluctuates. A "bruit" synchronous with the heart and
often double will be heard over an aneurism, while neither of these is
ever present in hydatids. The femoral pulse will be altered in an abdom-
inal aneurism, but normal in hydatids of the liver.
When di, pendulous hydatid cyst is attached to the liver by a pedicle, we
may readily mistake it for an enlarged gall-bladder. An enlarged gall-
bladder is usually preceded by jaundice, biliary colic, or symptoms ol
catarrh of the ducts, while an hydatid has no such previous history. On.
palpation it will be found that an hydatid does not correspond exactly to
the position of the gall-bladder. The gall-bladder is pear-shaped and evades
manipulation or pressure, while an hydatid tumor is globular and readily
manipulated.
HYJOATIDS OF THE LIVER. 389
When hydatids extend into the pleural cavity so as to be mistaken for
pleurisy, the heart will be displaced much more than ever occurs in pleu-
risy. Percussion in pleurisy marks out a line of dulness which is trans-
. verse when the patient is erect, and which changes with his position, while
in hydatids the upper limit of dulness is irregular and stationary, being
lower near the median line of the body than toward the axilla. This is
an important point. In hydatids the lower edge of the liver is below
the free border of the ribs and rises and falls with the respiration ; in
pleurisy the liver occupies nearly its normal position and is station-
ary.
In a cyst of the rigid kidney, there is the history of a growth from below
upward, while in hydatids the tumor grows from above downward. In
cystic kidney the colon lies in front of the tumor, while in hydatids of the
liver the colon is behind the tumor. An hydatid of the liver rises and falls
with respiration, while a cyst of the kidney is motionless. In hydatids of
the liver, an exploring needle will withdraw a non-albuminous, salty fluid,
containing booklets of the ecbinococci, while from a cyst of the kidney it
will withdraw an albuminous fluid with chlorides and perhaps pus.
Prognosis. — Hydatids are dangerous in proportion to their size and the
direction of their growth ; if they cease to enlarge, they may be regarded as
harmless. Their average duration is about four years. They have been
known to exist twenty-five years. If they rupture into the pleura, lung,
peritoneum, pericardium, or through the abdominal walls, the prognosis is
unfavorable. When the discharge takes place into the intestines, stomach,
or bronchi, the prognosis is favorable. Death occurs from exhaustion caused
by the pressure of a very large hydatid, rarely from that caused by ascites
through pressure on the vena cava. Suppuration of the cyst, or an abscess
developed secondarily to phlebitis may induce fatal exhaustion. Any one
of the pulmonary complications referred to may cause death. A fatal result
has, in some few cases, followed hemorrhage from the sac through an ex-
ternal opening. Peritonitis, pericarditis, and uraemia are infrequent causes
of death, and when the pulmonary artery is plugged, when the vena cava
is opened, or when a large vesicle is lodged in a bronchus, asphyxia is the
immediate cause of death.
Treatment. — Prophylactic measures consist in preventing the drinking-
warter from being contaminated by the evacuations of animals, and in not al-
lowing dogs to feed upon the offal of sheep. Chloride of sodium and iodide
of potassium have been proposed as internal remedies to destroy the echino-
cocci. The chief solid ingredient of hydatid fluid is chloride of sodium,
but no trace of iodide of potassium has ever been found in the fluid after
the administration has been continued for months.
If the tumor is of large size, and is still increasing in size, operative inter-
ference is necessary. Select the point where the hydatid tumor is most
prominent, and puncture with a fine aspirating needle. The dangers which
have been feared in this procedure are peritonitis, and the entrance of air
into the peritoneal cavity. Peritonitis maybe avoided by pressing the parts
about the puncture firmly against the tumor as the aspirating needle is
390 DISEASES OF THE DIGESTIVE SYSTEM.
withdrawn, so that no fluid can escape into the peritoneal cavity. All dan-
ger of the entrance of air is obviated if a small aspirating needle is used ; all
of the fluid should not be withdrawn from the cyst at the first aspiration.
It is important to enjoin absolute rest after the operation for two or three
days ; febrile symptoms and pain will follow the withdrawal of the fluid,
and the tumor will decrease in size ; usually a second puncture will be re-
quired. It is not essential to wait for adhesions to form between the tumor
and abdominal wall, though it is much safer if they exist.
Where simple puncture is not sufficient to destroy the echinococci, iodine
or bile may be injected into the cavity of the sac. When the fluid with-
drawn is pus, or when the symptoms are indicative of a suppurating cavity,
it is best to establish adhesions by caustics. Vienna paste is to be preferred
for this purpose, and the same precautions are to be exercised as in the
opening of an hepatic abscess. Puncture of the cyst by insulated needles, —
electrolysis,— has been claimed to be very successful in those cases where it
has been resorted to, but it seems to me that it is the puncture, rather than
the electric influence, which produced the favorable result claimed for it.
Never hesitate to aspirate an hydatid tumor when it is well developed and
elevated above the level of the abdominal walls ; the nearer the cyst is to
the surface, the better the result of the aspiration.
MULTILOCULAR HYDATIDS.
Multilocular hydatids in their pathology are similar to the ordinary hyd-
atid, except that in the one case a cyst is formed, and in the other it is
wanting.
Morbid Anatomy. — The liver is enlarged, the right lobe being out of all
proportion to the rest of the organ ; it is hard, and sometimes has a carti-
laginous feel. There are large nodules on its surface, the tumors often
being as large as a child's head. The capsule is thickened and opaque over
the tumor, and adhesions may be formed with surrounding parts.
On sectio7i a tumor is usually found embedded in the right lobe, varying
in size from that of an orange to a cocoanut, with a reticulated surface.
The stroma is connective-tissue, dull-yellow in color, and the spaces are
rounded, oval, or caudate, from the size of a ]3in's head to that of a pea,
usually communicating with one another by small apertures, and contain-
ing a clear or semi-transparent gelatinous substance. The stroma gener-
ally contains some hepatic parenchyma, which, at the periphery of the
mass, is dark-colored from pigment deposit, and nearer the centre is in a
state of partial or complete fatty degeneration. In the centre of the mass
is usually found a large spot of suppuration, varying in size, or a cavity
filled with a light-brown fluid or a greenish fetid pus. This cavity is well
defined, having a wall whose lining membrane is sacculated at points, with
openings into neighboring cavities. This membrane frequently has clus-
ters of hydatid vesicles upon it. The surface cavities are much smaller
than the central one, and are strung along like "strings of pearls," com-
pressing and occluding the branches of all the vessels of the liver at the
MULTILOCULAR HYDATIDS. 391
point whence the growth develops. The rest of the liver is congested or
hjpertrophied.
Microscopically, the gelatinous contents in one of the alveoli ai-e found to
be made up of the laminated structure of the vesicle and containing echi-
nococci with their circlets of booklets ; it is rare, however, to find perfect
"scolices." The cyst-wall may exhibit calcareous, fatty, or pigmentary
degeneration. Between the cysts small globules, consisting of calcare-
ous matter, are sometimes found, and also granular and crystalline haema-
toidin. The spleen is usually enlarged.
Etiology. — The etiology of multilocular hydatids is the same as that of
a single hydatid tumor. When the ova of the taenia reach the liver, the ques-
tion arises: what is it that causes the peculiar alveolar or colloid arrange-
ment of the vesicles ? This has been variously explained : some claim that
when the embryo enters either the lymphatics, blood-vessels, or bile-ducts,
the growth extends along the channels of either system, since it cannot ex-
tend concentrically because of the exterior pressure. I am inclined to
agree with those who think that when a cyst-wall is developed around the
embryo and no connective-tissue encapsulates the cyst, it can grow in all
directions. Their development is yet obscure.
Symptoms. — The insidious apjDroacli and slow progression which mark
the course of single hydatid tumors are present here. The effects of pressure
may be shown by vomiting and dyspepsia when the stomach is encroached
upon ; constipation and difficulty in defecating when the intestines are
pressed upon ; and ascites, cedema, hemorrhoids, and enlarged spleen,
when the portal trunk or vena cava is compressed. There are no subjective
signs. When suppuration occurs there will be a slight rise in temperature,
increased frequency in the pulse, and other symptoms which attend the
formation of pus in the liver. G-astro-intestinal hemorrhages, and hemor-
rhages from mucous surfaces rarely occur. When the bile-ducts are in-
volved, jaundice is the first, or an early symptom ; the jaundice gradually
deepens and is persistent. The faeces are clay-colored.
Physical Signs. — Palpation shows the liver early enlarged, having slight
elevations^ with a smooth feel. Later it is hard, resistant, nodular, and
uneven. The tumors are confined to the right lobe, or, at least, are best
marked there.
Percussion. — The area of hepatic dulness, in the region of the right lobe
especially, is increased, and the spleen is enlarged with multilocular hyda-
tids. There is neither fluctuation nor the " hydatid thrill."
Differential Diagnosis. — When the bile-ducts are involved a diagnosis may
be made by exclusion ; in other cases, the affection is liable to be con-
founded with cancer, cirrhosis, and nodular (syphilitic) loaxy liver.
In cancer of the liver there is a history of a gradually developing ca-
chexia and lancinating, almost constant, pain, with evidences of cancer else-
where, or an hereditary tendency ; while in multilocular hydatids there are
no constitutional symptoms and no pain, the hepatic region merely being
tender. The duration of cancer is rarely more than a year, while the de-
velopment of multilocular hydatids is protracted to two or three years. A
392 DISEASES OF THE DIGESTIVE SYSTEM.
cancer nodule, on palpation, is usually umbilicated and soft at the centre ;
while a multilocular hydatid is smooth and elastic. An exploring trochar
will remove all doubt.
In cirrhosis of the liver there is a history either of alcohol drinking,
rheumatism, gout, or syphilis ; in multilocular hydatids no such history
necessarily exists. In cirrhosis the liver is smaller than normal and hob-
nailed ; in multilocular hydatids it is enlarged and the nodules are of a
larger size. Ascites is common in cirrhosis ; while it is rare in hydatids.
In a nodular waxy liver there is a well-marked history of syphilis ; there
is a complicating diarrhoea, albuminuria, and the characteristic waxy
cachexia, which are absent in multilocular hydatids.
An hydatid tumor can only be diagnosticated from multilocular hydatids
by the exploring trochar. The fluid in multilocular hydatids contains pus
in varying quantities, a few booklets of the echinococci, and numerous
small vesicles ; while that from an ordinary hydatid is nearly pure water,
containing the booklets and 2ifeiv vesicles. In many instances the hydatid
thrill is present in a single hydatid tumor, but never present in multilocu-
lar hydatids.
Prognosis. — In those cases in which the jaundice is intense, the disease
may run its course in six months ; in other cases, the course is as pro-
longed as in single hydatids. Peritonitis is a frequent complication, and
amyloid degeneration of the liver may also occur with it. Death results
from the exhaustion due to the suppuration or from the complicating peri-
tonitis.
Treatment. — There is no medicinal treatment which can in any way affect
the course of this disease ; and operative interference has thus far proved
unsuccessful. This class of patients must be sustained during the exhaus-
tion of the supervening suppuration. The pain, if severe, may be relieved
by hypodermatics of morphia.
TUBEECULOSIS OF THE LIVER.
Tubercle of the liver is always secondary to tubercle elsewhere. Though
rare, it is probably more common than is usually supposed, from the fact
that hepatic tubercle is always microscopic.
Morbid Anatomy.— The liver is slightly but uniformly enlarged in size.
On close inspection the surface is seen to be irregularly elevated and de-
pressed, and looks and feels, in this respect, like the surface of an orange.
On section the liver cuts hard, the parenchyma being tense and tough.
The tissue is pale and yellow, resembling a fatty liver. The bile-ducts at
points are expanded, the walls being thinned. They contain a turbid fluid
mainly composed of mucus and bile. There are also small cavities filled
with pus and bile. When the tubercle has undergone retrograde metamor-
phosis, small gray masses the size of a pin's head are seen, and, also, " yellow
tubercle " or larger yellow masses the size of a pea; these changes are usually
best marked just beneath the capsule.
A microscopic examination shows miliary tubercles scattered between the
JAUNDICE. 393
lobules. When, as a result of obliteration of blood-vessels, tubercles under-
go fatty degeneration, the so-called "yellow tubercle" is the product.
Etiology.— Hepatic tubercle occurs as part of acute miliary tuberculosis,
and is secondary to tubercle in the lungs, peritoneum, spleen, and lym-
phatics.
Symptoms.— There are no symptoms indicative of hepatic tuberculosis,
independent of those of genera] tuberculosis. '
JAUNDICE.
Jaundice is a yellow discoloration of the skin, due to the presence of bile
or blood pigment. There are two varieties, hepatogenous or obstructive
jaundice, and hematogenous or non-obstructive.
Hepatogenous Jaundice is the more common variety, and is caused by
the absorption of bile, its passage into the ductus communis or intestine
being prevented by some mechanical obstruction.
Hematogenous Jaundice results, probably, from a change in the blood,
whereby its coloring matter is set free in excess.
Morbid Anatomy of hepatogenous Jaundice. In a normal state, the liver-
cells are constantly manufacturing bile, which flows along the bile-ducts
into the ductus communis. The cause of its outward flow is the vis a tergo, —
the secretion of the bile in the hepatic cells, — for there are no muscular
fibres except in the larger bile-ducts ; the respiratory movements also assist
slightly in its outward flow. When from any causes the bile cannot enter
the common duct or the duodenum, the small ducts and then the hepatic
cells become overfull and distended. In consequence of this increased
pressure, bile passes through the wall of the smaller ducts into the blood-
vessels and lymph channels. If the normal tension of the capillary system
in the liver is diminished, then the passage of bile through the walls of the
vessels is favored and Jaundice results. Bile pigment with serum exudes
and stains the tissues, even the bones, the teeth and pathological new forma-
tions. In both hepatogenous and hematogenous Jaundice, the staining occurs
in the same way.
Hematogenous Jaundice. — In health the bile pigment is formed within
the liver, by transformation of the coloring matter of the blood, and after
it has been poured into the intestine, it is partly absorbed by the blood and
appears, after another change, as one of the coloring matters of the urine.
Under abnormal conditions, and as the result of processes that are not fully
understood, coloring matter is either set free in excess or is not excreted
with the bile, and is then deposited in the tissues producing Jaundice. As
this variety of Jaundice is thought to have its origin in morbid conditions
of the blood, it is called hematogenous.
The anatomical lesions which are associated with hematogenous Jaundice
have already been considered in connection with the history of the different
hepatic affections in which it occurs.
' Lymphatic formations, simple cysts, dermoid cysts, erectile cavernous tumors, and benign fibrous
growths occur in the liver, but are only of pathological Interest.
394 DISEASES OF THE DIGESTIVE SYSTEM.
Etiology. — The causes of hepatogenous jaundice may be included under
three heads :
I. Thoso which obstruct the larger hepatic ducts.
II. Those which obstruct the hepatic radicles.
III. Those which diminish capillary tension.
Those obstructions of the larger hepatic duct which have their seat within
the duct are :
(1) Inflammations of, or inflammatory exudations from, the lining mem-
brane of the duct, that which accompanies duodenal catarrh being the most
frequent, (2) Biliary calculi. (3) Inspissated bile and mucus. (4) Hydatid
vesicles. (5) Distomata. (6) Foreign bodies from the intestinal canal, such
as stones of fruits and round worms. (7) Congenital occlusion, or plugging
of the duct. (8) Cicatrices from ulcers on the mucous membrane of the
duct. (9) Carcinomatous growths from the lining membrane of the ducts.
The causes which obstruct the duct by external pressure, are •
(1) Contraction from perihepatitis, or from inflammation of thehepatico-
duodenal ligament. (2) Tumors of the pyloric extremity of the stomach,
of the head of the pancreas, and of the kidney. (3) Pressure from a preg-
nant uterus, from ovarian and fibroid tumors, from omental tumors, and
from large impaction of faeces. (4) Enlarged lymphatic glands in the trans-
verse fissure from waxy, cancerous, or tubercular change, abdominal aneu-
rism, and the new tissue in hypertrophic cirrhosis of the liver..
Slight hepatogenous jaundice may be caused by compression or oblitera-
tion of the hepatic radicles, such as occurs in cirrhosis and the other atro-
phies of the liver, in active and passive hypersemia, in hydatid tumors and
multilocular hydatids, in cancerous and syphilitic tumors, in abscess of the
liver, in adhesive pylephlebitis, and perhaps in acute yellow atro]3hy.
Finally, the bile may be prevented from entering the intestine in its normal
amount when capillary tension is diminished. This may occur in severe
right diaphragmatic pleurisy, in perihepatitis, in thrombosis of the trunk
or of the larger branches of the vena portae, and in exhausting hemorrhage
from the radicles of the portal vein.
The causes of hematogenous jaundice are fevers, especially yellow, typhus,
typhoid, and the malarial fevers. It is often an attendant of pyaemia, puer-
peral fever, septicaemia, and suppurative pylephlebitis. The poison of
snake-bites, phosphorus, mercury, copper, antimony, and the excessive
use of ether and chloroform may cause it. Pneumonia, probably by its
action on resiDiration, and ulcerative endocarditis induce it ; it may follow
a fright, a fit of anger, great anxiety, or cerebral concussion. A long con-
tinued hepatogenous jaundice may lead to a hematogenous jaundice ; and
it is yet undecided whether the icterus in yellow atrophy belongs to the
first or second named group.
DiflFerential Diagnosis. — Hematogenous jaundice accompanies acute in-
fectious fevers and other conditions of blood poison, while hepatogenous
jaundice can be traced to some mechanical interference with the outflow
of the bile. The yellow staining is slight in hematogenous jaundice ;
while the discolorization in hepatogenous jaundice is more intense and may
CATAREH OF THE BILE-DUCTS. 395
appear suddenly without constitutional disturbances. A feeble and irreg-
ular heart-action> a small pulse, and a tendency to hemorrhages attend
hematogenous jaundice; while an unimpaired heart-action, a slow pulse, and
a low temperature mark the development of hepatogenous jaundice. There
is great itching of the surface in hepatogenous jaundice which is absent in
the hematogenous variety. The faeces are dark in hematogenous jaundice,
and white or clay-colored in hepatogenous. The urine is albuminous, con-
tains a small amount of bile pigment, and deposits a sediment of uric acid
in the hematogenous variety, while it is rarely albuminous in hepatogenous
jaundice and contains bile-pigment in considerable amouAt, the quantity
varying with the intensity of the jaundice.
DISEASES OF THE GALL-BLADDER AND GALL-DUCTS
will be considered under the following heads :
I. Catarrhal Inflammation of tJie III. Cancer of the Gall-Bladder.
Biliary Passages. IV. Enlargement of the Gall-Blad-
II. Exudative Inflammation of the der.
Biliary Passages {croupous V. Gall Stories.
or diphtheritic).
CATAERH OF THE BILE-DUCTS.
Morbid Anatomy. — Catarrhal inflammation of the mucous membrane of
the larger bile-ducts, the ductus communis, and the gall-bladder is similar
to that of other mucous surfaces. There is hyper^emia followed by an ab-
normal secretion of mucus and muco-pus which more or less obstructs the
outflow of bile. The catarrhal process usually begins in the duodenum
and extends inward, and in severe cases may be so rapid that pus will be
the product of the inflammation, in which case the deeper tissues are in-
volved and numerous little ulcers may form, and Avhen the duct is perfo-
rated by them, cavities of varying sizes, resembling small abscesses, result.
When the catarrh becomes chronic the deeper tissues are infiltrated, caus-
ing thickening and induration of the ducts from the consequent obstruction
to the exit of the bile. Dilatations occur at points along the bile ducts ;
these dilatations often become very large and occasionally form cysts ; at
other times the alternate dilatations and constrictions give the appearance
of a string of beads. The lymphatics often become involved, and their en-
largement gives a nodular appearance to the mucous membrane. Ulcera-
tive processes are more frequent in chronic catarrh of the bile passages
than in acute. The liver is uniformly enlarged and its margins are firm
and sharp.
On section, its substance presents a mottled appearance, resembling a
nutmeg, and varies in color from a deep yellow to an olive green. The
color is deeper at the centre of a lobule and shades oif toward its periphery.
The gall-ducts commonly have their mucous membrane pale and covered
with a. thick, purulent mucus ; and plugs of mucus and epithelial debris
396 DISEASES OP THE DIGESTIVE SYSTEM.
are found in them, most frequently near or at the opening of the duct into
the duodenum. The gall-bladder is enlarged, and the cystic and common
ducts often attain immense size ; in one case this diameter reached an inch
and a half.
In chronic catarrh the liver is normal or diminished in size, and is soft,
flabby and shrivelled.
On section it is greenish-black in color, the hepatic ducts are dilated,
forming cysts, and little points of ulceration are formed on the mucous
surface of the duct, often extending into the adjacent parenchyma which
is atrophied. The ramifications of the vena portse are compressed by the
ducts, and thickened bile may cause these ducts to present the appearance
of a dark brown tube. The gall-bladder is enlarged in size, and sometimes
there are spots of ulceration upon its walls which may also undergo cal-
careous changes.
Etiology. — The most frequent cause of biliary catarrh is extension of a
gastro-duodenal catarrh. Most of the structural diseases of the liver may
lead to or be attended by catarrhal inflammation of the bile ducts. Thoracic
disease where the venous return is impeded (as in cardiac valvular lesions
and emphysema) may cause catarrh of the biliary passages. General blood
diseases, syphilis and pyaemia prominently, and mineral poisons, phos-
phorus, and perhaps arsenic, cause it. A gouty diathesis causes or pre-
disposes to a catarrh of the biliary passages, just as it does to catarrhal
inflammations of the mucous membranes elsewhere in the body — bronchitis,
for instance. Foreign bodies, as calculi and parasites, in the bile passages
may cause biliary catarrh. Exposure to cold and an altered condition of
the bile may induce it.
Symptoms. — The subjective symptoms of biliary catarrh are at first obscure.
It is usually preceded by the symptoms of gastro-duodenal catarrh, and
hence for a few days there will be loss of appetite, furred tongue, flatulence,
nausea and vomiting. There is also some pain and tenderness in the epi-
gastrium, and in most cases the temperature will be slightly raised, and the
pulse accelerated. The bowels are constipated, unless it is accompanied
by extensive intestinal catarrh, when diarrhoea will be present. The fsecal
discharges are of a light clay color and contain no bile. The urine is of a
dark green color, and contains bile pigment. The liver is enlarged and
tender, especially over the region of the gall-bladder. The absence of
bile from the intestine favors gaseous distention of the bowel. The
sclerotic becomes yellow, and gradually the entire surface assumes a yellow
hue. The temperature falls to normal and the pulse is slowed. As the
jaundice deepens, there is a noticeable loss of strength, the patient becomes
apathetic and disposed to sleep during the day. There is headache, vertigo,
and great depression of spirits ; itching of the surface becomes exceedingly
troublesome.
All these symptoms remit, the appetite returns, and the fseces and urine
return to their normal color ; or the catarrh becomes chronic and continues
for months, the jaundice deepening, exhaustion and emaciation becoming
extreme. Then gastric and intestinal hemorrhages frequently occur, and
CATAEBH OF THE BILE DUCTS. 397
ascites may be followed by general anasarca ; coma closes the scene. The
last stage of chronic catarrh is accompanied by evidences of atrophy of the
liver.
Physical Signs. — Inspection reveals a jaundiced condition of the skin
and conjunctivae, and perhaps a bulging in the right hypochondrium.
Falpation discovers an enlarged, smooth and tender liver. The gall-
bladder is enlarged, and sometimes there is a pear-shaped fluctuating tumor
at its anterior margin. The gall-bladder is tender on firm pressure. Late
in chronic catarrh the liver is diminished in size.
Percussion shows a uniform increase in the area of hepatic dulness,
which, however, in chronic disease may be normal or diminished.
Differential Diagnosis.— This condition may be mistaken for suppurative
pylephlebitis and exudative inflammations of the ducts. The former has
already been considered, the latter will be considered under exudative in-
flammations.
Prognosis. — This is good ; catarrh of the bile ducts is not a dangerous
disease. The jaundice usually continues from three to five weeks, but
sometimes it continues for months. The prognosis is rendered unfavorable
when oft-repeated biliary catarrhs lead to permanent closure of the ducts
and atrophy of the liver. Catarrh of the bile-ducts may be complicated
by peritonitis, pleurisy, pneumonia, dysentery, suppurative hepatitis, or
acholia. Death then results from exhaustion, from faulty nutrition, or
dropsy, from intercurrent diseases, rupture of the ducts, or with brain
symptoms — " acholia."
Treatment. — It should be remembered that the jaundice is only a symp-
tom, and requires no treatment. The treatment of this catarrh is mostly
symptomatic ; it is usually self-limiting and will subside without remedial
measures. If the hepatic pain is severe, leeches followed by an anodyne
poultice over the points of greatest tenderness will usually relieve it. When
the bowels are constipated, " blue-pill," or a saline purgative is first de-
manded, after which old cider or tamarinds will regulate the bowels for the
remainder of the attack ; nitro-muriatic acid acts favorably in most cases.
If there is diarrhoea, ipecacuanha or Dover's powder will readily control it.
When the urinary secretion is much diminished the salts of potash in com-
bination with diaphoretics may be administered. The diet throughout
should contain no carbo-hydrates ; the food should consist principally of
lean or prepared meats, vegetables, and skimmed milk.
When there is a gouty diathesis, colchicum and iodide of potassium are
often of service. In a syphilitic diathesis, chloride of ammonium and the
bi-chloride of mercury are indicated. Emetics rather aggravate the gastric
intestinal catarrh than cause the expulsion of a hypothetical plug in the
common duct, and should not be administered. Finally, if the hepatic
parenchyma become involved, a tonic and diuretic plan, similar to that
adopted in cirrhosis, may be adopted. The use of mineral waters must be
determined by the influence which they exert on each patient ; in some
cases increased appetite results, while in others they seem to hasten the
wasting process.
398 DISEASES OF THE DIGESTIVE SYSTEM.
EXUDATIVE INFLAMMATIOlsr OF BILIAEY PASSAGES.
Under the head of exudative inflammation of the biliary passages I in-
clude both a croupous and Si diphtheritic process. Both are rare and seldom
recognizable during life.
Morbid Anatomy.— The commencement of croupous inflammation is the
same as catarrh ; but the inflammatory product is fibrinous.
In diphtheritic inflammation, the deeper tissues of the walls of the gall-
bladder and bile-ducts are involved, and large gray sloughs, more firmly
adherent than in croupous inflammation, are formed upon their walls. The
liver is usually enlarged.
On section the ducts within the liver are seen clogged with inspissated
bile, and occasionally there are abscesses. When constriction and occlu-
sion of the ducts exist, they become dilated behind the narrowed portion,
and resemble cysts, containing a pale yellow fluid with loose coagula floating
in it. The gall-bladder is sometimes filled with a gray- white liquid, neutral,
albuminous, and sometimes containing leucin ; at other times the liquid is
purulent, or thick and dark like tar. On the mucous membrane of the
gall-bladder and common duct is a yellowish- white fibrinous layer, varying
in thickness and tenacity, having all the anatomical characteristics of a
diphtheritic exudation. The walls of the gall-bladder and larger ducts are
thickened and sometimes ulcerated. The ulceration may lead to perfora-
tion and fistulous openings. Adhesions sometimes bind the gall-bladder
to the surrounding parts. If the diphtheritic process extends to the venous
coats pylephlebitis may result ; sometimes the bile-ducts open into branches
of the ,vena portse.
Etiology. — These inflammations occur with typhus and typhoid fevers,
cholera, diphtheria, pyaemia, septicaemia, bilious fever, and from the
irritation produced by biliary calculi.
Symptoms. — The first symptom of exudative inflammation of the biliary
passages is a sense of constriction in the right hypochohdrium. This is soon
followed by pain, increased by pressure in the region of the gall-bladder,
and vomiting. There are active febrile symptoms, but these are usually
not marked. If ulceration of the ducts or implication of the branches
of the portal vein occurs, then chills, sweats, and the other symptoms of
pygemic abscesses of the liver result, or the symptoms of pylephlebitis are
developed. When an opening into the peritoneal cavity occurs, rapidly
fatal peritonitis is the result. If there is no obstruction to the outflow of
bile, neither jaundice nor alteration in the color of the stools will be
present.
Physical Signs. — Inspection may show a slight elevation of the free border
of the ribs.
Palpation discovers a pear-shaped, tender, movable tumor at the nor-
mal site of the gall-bladder. Slight pressure over it gives pain.
Percussion. — The area of liver dulness is normal or slightly increased ;
over the enlarged gall-bladder the percussion note is dull and somewhat
tympanitic in character.
CANCER OF THE GALL-BLADDER. 399
DiiFerential Diagnosis. — Exudative inflammation of the bile-ducts may be
mistaken for simple Mliary catarrh. The points which will aid in a di-
agnosis are the occurrence of intense pain, actiye febrile symptoms, and a
careful study of the etiology of each case.
Prognosis. — This is determined by the disease which it accompanies.
It usually terminates in death.
Treatment. — Absolute rest is important. To relieve the pain leeches may
be applied over the tumor, followed by poultices and, later, by counter-
irritation. The diet and saline purgatives should be the same as in sim-
ple catarrh, unless the primary disease contraindicates their use. If symp-
toms of pus formation are present, quinine may be given in large doses
a.nd tonics are indicated. If the tumor becomes large, so that there is
danger of its rupture, it may be aspirated, the same rules being observed
as in hydatids and abscess.
CANCER OF THE GALL-BLADDEE.
Cancer of the gall-bladder is usually associated with cancer of the liver
substance, and is often the primary seat of the development of scirrhus
or medullary cancer of the liver.
Morbid Anatomy. — The gall-bladder is enlarged, nodular and adher-
ent to the surrounding parts ; sometimes there are spots of ulceration on
its surface, and there may be fistulse from the gall-bladder to the intestine.
On section its wall is found thickened, and the cavity sometimes filled with
a cancerous mass in which are embedded numerous concretions.
Etiology. — This is the same as that of cancer of the liver. It is often
secondary to cancer of the stomach. Concretions are so often found that
some have ascribed its development to gall-stones.
Symptoms. — The subjective symptoms are few : none are constant except
the gastric derangement and the paroxysms of lancinating pain ; vomiting
is common and severe, because of the pressure of the tumor on the py-
lorus. Jaundice may be present when the common duct is involved.
While the tumors often increase very rapidly, the cancerous cachexia and
emaciation are slow in their development. In some cases the symptoms
undergo marked exacerbations and remissions. Swelling of the glands in
the inguinal and axillary regions may occur.
Physical Signs. — Palpation will discover over the site of the gall-bladder
a hard, nodular and immovable tumor. It is tender, and sometimes fluctu-
ates at the centre.
Percussion shows an increase in the area of hepatic dulness below the free
border of the ribs.
ENLARGED GALL-BLADDER.
Dropsy of the gall-bladder is a term used to include those cases where,
on account of some obstruction, bile is prevented from entering the nat-
ural reservoir, and an increased secretion from its mucous surface leads to
its distention.
400 DISEASES OF THE DIGESTIVE SYSTEM,
Morbid Anatomy. — The gall-bladder is found enlarged, sometimes reach-
ing the size of a cocoa-nut. The walls are thickened, at some parts more
than at others, and occasionally sacculations render its outlines uneven.
The cystic wall is often tense, and now and then plates of calcareous matter
are found upon it. On opening it there may be a discharge of gas from its
interior, but more commonly a curdy white fluid fills its cavity. This fluid
contains whitish flakes of albuminous matter resembling synovial fluid ;
it may contain bile, and then it is dark and viscid. On close examination
the mucous surface resembles a serous membrane, and the muscular fibres
of its wall are attenuated and wide apart. Later on, the fluid contents of
the cavity may disappear, and only a mass of pultaceous matter remains.
When the obstruction has been near the opening into the duodenum, the
ductus communis and the cystic duct are dilated and their walls thick-
ened.
Etiology. — Hydrops cystidis fellm, as it is sometimes called, may be caused
by a catarrhal, croupous, or diphtheritic inflammation of the cystic duct,
which obstructs the passage of bile into the intestine. Plugging of the
common or cystic duct, or of the neck of the gall-bladder, by a calculus,
may cause dropsy of the gall-bladder. Multilocular hydatids or hydatid
cysts may plug the cystic duct and induce it. Pressure by tumors outside
of the duct, as enlarged glands in chronic peritonitis, aneurisms, impacted
faeces, and cancerous growths of the adjacent parts, occasionally leads to it.
Symptoms. — When the cystic duct alone is pressed upon or in some way
plugged, there are few subjective symptoms. The patient may notice a
bulging in the hepatic region, which steadily increases, and is accompanied
by pain, nausea, vomiting, loss of appetite, and constipation. But the color
of the skin, urine, and faeces exhibits no change. If a calculus is the cause
of the obstruction, there is usually a history of " bilious colic," and if
abdominal tumors press upon the cystic duct there will be the physical
evidences of their existence.
Physical Signs. — Inspection msij reveal a globular tumor near the rectus
muscle, at the free border of the ribs. Palpation discovers at the normal
site of the gall-bladder a pear-shaped, extremely movable tumor, which is
elastic and rarely fluctuating. When the ductus communis is obstructed,
jaundice is a prominent symptom, and the other symptoms which have been
described under " catarrh of the bile-ducts " are present. Occasionally the
tumor suddenly disappears, the stools become dark, and the skin regains
its normal color. This denotes that the obstruction, which is, then com-
monly a calculus, has been temporarily removed. When external openings
are formed, or rupture into the peritoneal cavity occurs, there are, in the
latter case, evidences of a rapidly developed peritonitis, and, in the former,
a remission of symptoms with a biliary fistula discharging externally.
Differential Diagnosis. — Dropsy of the gall-bladder may be mistaken for
abscess, hydatids, and medullary cancer of the liver. In medullary cancer,
there is, in nine-tenths of the cases, an hereditary predisposition or a his-
tory of cancer of the stomach or heart ; while in dropsy of the gall-bladder
we get a history of previous biliary catarrh, or of the passage of gall-stones
GALL-STONES.
401
In cancer, the constitutional symptoms and cachexia are marked, while
persistent gastric symptoms, ascites and. hemorrhages from mucous surfaces
are absent in enlarged gall-bladder. Cancer growths are slow, and precede
jaundice if it exists, while a gall-bladder enlarges rapidly, and follows jaun-
dice. Palpation, in cancer, discovers a nodular, uneven, immovable mass be-
low the free border of the ribs. An enlarged gall-bladder gives rise to a
smooth, pear-shaped, elastic, or fluctuating tumor, which is movable and
projects below the free border of the ribs in the direction of the gall-bladder.
Prognosis. — This varies with the cause. When inflammatory products or
gall-stones induce the dilatation, it is better than when it is due to external
pressure ; it is always attended with more or less danger.
Treatment. — The treatment, when it is the result of catarrhal inflamma-
tion of the ducts, has already been considered. When it is due to the pres-
ence of gall-stones, the treatment appropriate to such conditions is indica-
ted. If the enlargement is very great and shows no indications of becoming
stationary or diminishing in size, aspiration should be practised.
GALL-STOl^ES.
When bile is retained in the gall-bladder for a long time it decomposes,
and the chelate of soda and other bile salts, with cholesterin, globules of
bile-resin, and granules are precipitated. These materials combine to form
concretions, which are called Mliary calculi. Catarrh of the gall-bladder
always accompanies this retention and decomposition of bile.
Morbid Anatomy. — The number of gall-
stones varies : single calculi are rare ; eight
thousand were found in one case. Their
usual number is about thirty. Their size
varies from that of a pin's head to that of
a goose Qgg. In shape they are originally
spherical, ovoid, or pear-shaped ; but when ^ Ufe^^^^^^^Jr^W'l!'] A
there are many and they lie in contact
with one another for a long time, they
have numerous facets developed on their
surface; six, or even twelve are some-
times found on a single calculus. Warty
or '^ mulberry" calculi are occasionally
met with ; solid or hollow casts of the
larger bile ducts, and those which resemble
rhomboidal crystals, and the star-like cal- ,,,^,j. f,,
culi with blunt points are rare forms of Imii'lil'.'! i^^?^ i>
gall-stones. These calculi are commonly
of a light-brown or greenish-yellow color ; Fig. 84.
they may be white, green, blue, red,
black. The specific gravity of fresh calculi
Oj. Sketch of a ftall-Uadder fitted With biliary
calculi. This bladder contained 260
gall-stones. At B are single calculi
1 i..r>^ I'l ^■^^/^ n, shoiuing fttcets.
IS about 1.02, and it may reach 1 09, so that
they will not float in water.
26
In most cases a fresh biliary calculus can be
402
DISEASES OF THE DIGESTIVE SYSTEM.
crushed between the fingers. Gall-stones may form in the smallest radicle
of the hepatic duct.
On section a biliary calculus will rarely be found liomogeneous through-
out. Its substance, if it breaks down like clay, consists of cholesterin and
lime. If it has a saponaceous fracture, it consists of bile-resin and choles-
terin. The i7igredients of biliary calculi are cholesterin, the coloring
matter of the bile, bile resin, lime salts, mucus, epithelium, biliary acids,
margarin and traces of iron. A gall-stone usually has a nucleus, an
external crust, and an intermediate
portion. The nucleus may be
formed of crystals of cholesterin,
cholate of lime, mucus, a distoma,
blood-clot, round worm or foreign
body. Most nuclei are formed of
casts of the hepatic ducts. Some-
times small calculi form the nu-
clei of larger ones, and in very rare
instances multiple nuclei are ob-
FiG.85. served. The external crust varies
Section of a large Gall-stone, showing successivelayers. in thicknCSS at difEercnt points, and
^' fJ^^SoTsfze^''^'™'''^'''^' Portion.-c. Nu. jg distinguished from the interme-
diate portion by its color ; it is
commonly composed of cholesterin, and its color is due to a mixture of
cholesterin and biliary pigment ; carbonate of lime gives a rough, whitish
crust. The intermediate structure usually consists of crystalline radia-
tions of cholesterin, which substance forms about eighty per cent, of all
gall-stones. In this radiation can be seen evi-
dences of a lamellar deposit, and sometimes,
when there is no radiation, the layers are concen-
tric, like those of an onion. Again, light layers
of cholesterin alternate with deeper ones of pig-
ment ; gall-stones are rarely found to undergo a
process of erosion or disintegration.
The gall-bladder may be normal, or enlarged
and sacculated, and is often adherent to the in-
testine, abdominal wall, and adjacent organs. Its -piG. 86.
walls are thickened, and there are evidences of a crystals of dwiestenn from gaiu
s, showi
local or general catarrh ; late in the disease there pS, 'SZi^cmmerZaS-
may be fibroid contraction and calcareous degen- ^ ^°°"
eration in the cystic walls. Ulceration of the walls is frequently found in
a bladder distended with calculi. When a gall-stone becomes impacted
near the entrance of the ductus communis into the duodenum, the duct
may become enormously dilated, and have its walls thickened, hyper-
trophied, or calcareously degenerated.
When the ulcerative process extends through the walls of the gall-blad-
der or of the larger ducts, we may have openings externally through the
abdominal walls, usually about the umbilicus, called ''biliary fistulas/'
GALL-STONES. 403
These fistulous openings may lead from the gall-bladder or ductus com-
munis to the duodenum, stomach, colon, right ureter, trunk of vena portae,
pleura, or vagina. When calculi are found in the smaller ducts, they may
excite abscess of the liver, local fatty degeneration, inflammation of the
ducts or pylephlebitis. Either by rupture into the cavity, or by extension
of inflammation, peritonitis may be caused by the presence of gall-stones.
'They may also excite ulceration and gangrene of the intestines, and there
are rare cases where gall-stones, having escaped into the intestines, have
caused death by intestinal obstruction.
Etiology. — Gall-stones may be formed at any period of life, but are most
frequent after thirty-five. A sedentary, physically inactive life is a great
factor in their etiology, and I regard the greater prevalence of calculi in
women than in men as due to their less active mode of life. Those who
have to pass the greater part of their lives in bed, and prisoners who are
confined in cells for a long time, are especially liable to the formation of
gall-stones. A diet over-rich in fats, animal food, or alcoholic beverages,
predisposes to the formation of biliary calculi. Cancerous growths in the
liver and gall-bladder, catarrh of the gall-bladder, and in fact any morbid
condition interfering with the excretion of bile and favoring its retention
in the gall-bladder, predispose to the development of calculi. I have been
able in a few cases to make out an hereditary predisposition to the forma-
tion of gall-stones. The menstrual epoch seems to have some peculiar
influence upon their formation.
Symptoms. — Small gall-stones,— ''gravel," — in the hepatic ducts may cause
hepatic congestion, but without enlargement of the liver, and give rise to
dull pain, a sense of weight and constriction in the right hypochondrium,
with nausea and the other symptoms of gastric disturbance. Jaundice in
these cases is of rare occurrence. When the hepatic and larger ducts are
occluded, the liver becomes enlarged, and there is jaundice, sharp pains,
colic, and sometimes rigors and sweats. If the hepatic duct is closed, the
gall-bladder is normal in size. Fatal rupture of the ductus hepaticus
sometimes, though rarely, is the result of the impaction of a calculus in it.
When small calculi are formed within the gall-bladder, they often cause
no inconvenience ; when they reach a large size they excite inflammation,
which may ultimately cause closure of the neck of the gall-bladder. When
the gall-bladder contains a large number of calculi, violent physical exer-
tion causes pain, which disappears during rest. Sometimes the patient may
actually "feel something rolling around " in the vicinity of the gall-blad-
der, which on a physical examination is found enlarged, more or less
tender, hard, and nodulated, and by a stethoscopic examination gives to
the ear the impression of a number of pebbles being grated together in
water.
If biliary calculi in this situation cause perforation of the gall-bladder,
a fatal peritonitis follows, or a biliary fistula may be formed between the
gall-bladder and the stomach, which will be attended by sudden intense
pain, with obstinate vomiting ; sometimes one or more calculi are found in
•^16 vomited matter. The vomiting of a gall-stone cannot be accounted for
404 DISEASES OF THE DIGESTIVE SYSTEM.
on the ground of reversed peristaltic action after the stone has passed the
ductus communis into the duodenum. Again, when calculi are formed in
the gall-bladder, a fistulous opening into the duodenum may occur, followed
by vomiting and signs of a local peritonitis, or of intestinal hemorrhage
and haamatemesis. An opening from the bladder into the colon is exceed-
ingly rare, for the colon is very movable. The symptoms which attend
such a perforation are obscure. The gall-bladder may open into the pelvis
of the right kidney, and then biliary concretions will be voided in the
urine. There is an instance on record where, during pregnancy, a com-
munication was made between the gall-bladder and the uterus, the discharge
of the calculi taking place at the birth of the infant. If an opening from
the gall-bladder into the vena portse occurs, symptoms of pytemia will de-
velop very rapidly. If perforation of the left pleural cavity occurs, fatal
pleurisy will result. A single, rarely a double, fistulous canal may connect
the gall-bladder with the external surface ; the opening is usually near the
umbilicus, and may discharge for months. It may cicatrize, and form a
mass of fibrous induration ; or abscesses may form when a large calculus
plugs the fistula formed by previous perforation. If perforation occurs,
recovery is most frequent when an external opening is established.
When a gall-stone has by any means entered the intestinal canal, it may
be voided j^er anum or it may lead to an intestinal obstruction, ulceration,
or gangrene of the intestine. Obstruction in the common duct may be
temporary or permanent. If temporary there is no Jaundice ; if the
obstruction is complete and is continued for twenty-four hours. Jaundice is
added to the other symptoms ; this Jaundice increases and is persistent
when the obstruction is permanent.
Biliary colic, or the passage of gall-stones, is the name applied to the pe-
culiar and severely painful symptoms produced by the passage of one or
more calculi along some one of the larger biliary ducts. Usually after a
hearty meal, or after some Jolting exercise, as horseback riding, the patient
is suddenly seized with a severe pain in the epigastrium, which is increased
by change of position or pressure. Sometimes slight rigors, nausea, eruc-
tations, and attacks of yawning precede the colic. The pain is paroxysmal,
and has its seat at a point where a line from the right nipple to the anterior
superior spinous process of the left ilium crosses the free margin of the
ribs. It radiates backward and upward, often as far back as the right
shoulder, and may extend over both hypochondriac regions. It has been
described by patients as boring, tearing, piercing, or lancinating. It is
often so agonizing that patients will roll about the floor or bed, double
themselves up, and groan with the pain. The face is pale and covered with
cold sweat, and the pulse is very small. The abdominal muscles are rigid,
and pressure greatly augments the pain. Vomiting, hiccough, a distended
and tympanitic abdomen are often present during an attack, and a weak or
feeble subject may faint, or pass into convulsions, which are epileptiform
in character. Fatal syncope has occurred during an attack of gall-stone
colic. After a few hours, sometimes a day, of exhausting and intense pain,
the patient experiences sudden relief, and the pain entirely disappears;
GALL-STONES. 405
often the pain remits, but does not cease until tlie calculus enters the du-
odenum ; an exacerbation occurs at the moment the calculus enters the in-
testinal canal. Jaundice is often present, but not until the attack has con-
tinued for twenty-four hours. During the colic, the gall-bladder is very
sensitive to pressure ; during and after the attack, the patient is very much
exhausted, and shows great lassitude. When jaundice is present the fseces
are clay-colored, and the bowels are apt to be constipated. After the at-
tack, gall-stones may be found in the fseces. It is to be remembered that
fresh gall-stones are slightly heavier than water. The urine, if jaundice
exists, contains bile-pigment and is mahogany in color; after the colic, it
deposits lithates and lithic acid.
Diflferential Diagnosis. — Gall-stone colic may be mistaken for cardialgia,
intestinal and renal Colic. Cardialgia may be mistaken for biliary colic
when there is no jaundice present. In cardialgia, pain comes on immedi-
ately after eating; gall-stone colic has no necessary connection with taking
food. In cardialgia, the symptoms are referred to the epigastrium alone,
while in biliary colic the pain shoots to the right shoulder and back. In
cardialgiaj the pain gradually diminishes ; in biliary colic it suddenly
ceases. In gall-stone colic, the presence of a gall-stone in the fseces is
pathognomonic.
in intestinal colic, the pain begins at the umbilicus, and radiates over
the abdomen ; in gall-stone colic it has its seat at the free border of
the ribs, and shoots to the back and upward to the right siioulder. In in-
testinal colic, pressure relieves the pain ; in gall-stone colic it aggravates it.
In intestinal colic, the pain is intermittent ; in gall-stone colic it is con-
stant, though paroxysmal. In intestinal colic, jaundice is never present,
while it may exist in biliary colic. Intestinal colic accompanies or is fol-
lowed by diarrhoea ; in gall-stone colic, the fseces are firm and may be clay-
colored.
With renal colic, the pain shoots from the region of the affected kidney
to the inner part of the thigh and end of the penis, and the testicle is
retracted ; in gall-stone colic, the direction of the pain is upward and back-
ward. In renal colic there is a constant desire to micturate. There is no
urinary disturbance in biliary colic. In renal colic, after the cessation of
pain, pus, blood and epithelium are found in the urine ; after gall-stone
colic, bile-pigment is found in the urine. Jaundice and clay-colored stools
frequently containing gall-stones may be present in biliary colic ; they are
all absent m renal colic. The gall-bladder is very tender after biliary colic ;
while there may be dull pains in the region of the loins after the passage of
a renal calculus.
Cancer of the head of the pancreas may readily be mistaken for gall-stones
in the common duct.
Prognosis. — The sudden and unexpected terminations and varied conse-
quences due to the formation of a gall-stone, render it impossible to
give any rule for the prognosis. When a large stone, without facets,
has been voided, in any manner, from the bile passages, the prognosis is
better than when small facetted calculi are found. Oft-repeated at-
406 DISEASES OF THE DIGESTIVE SYSTEM.
tacks of biliary colic are bad. Catarrhal and exudative inflammations of
the bile passages are frequent accompaniments of gall-stones, and pulmon-
ary gangrene, empyema and pneumonia may sometimes complicate. Though
it is not necessarily a fatal disease, death may result from peritonitis, ulcer-
ation, gangrene or obstruction of the intestines, pyaemia, pylephlebitis, ab-
scess of the liver, from exhaustion or from the escape of bile through an
external opening. Death may occur during an attack of colic, from un-
explained causes.
Treatment— An attack of biliary colic demands that attention be given,
first, to the pain : this is relieved best by opium, or morphine, which should
be given hypodermically or per rectum, when it is not possible to give it
by the mouth. At the same time put the patient in a tepid bath, or
wrap warm cloths about the abdomen. In mild cases, and when opium is
contra-indicated, belladonna will be sufficient, in connection with anodyne
fomentations over the region of the gall-bladder. Inhalations of chloro-
form or ether may be employed to relieve the severity of the spasm. The
application of two or three leeches over the gall-bladder is often followed
by relief, and diminishes the enhances of inflammation of the bile-ducts.
Large draughts of warm water, containing bicarbonate of soda, often re-
lieve the pain at the onset of the attack. If the patient shows signs of
collapse, stimulants, ammonia and brandy should be administered.
A patient who has passed gall-stones must be put on a restricted diet :
wines or fats should be prohibited ; exercise in the open air, and an
entire change in the mode of life are important. Mineral waters, whether
by giving an alkaline bile or by an increase in the amount secreted, cause
the number of gall-stones to diminish, and also allow them to be passed
with less pain. A prolonged course of alkaline mineral water has been
found the best remedy against the formation of gall-stones. Ether, tur-
pentine, chloroform and hydrate of chloral have been proposed as specifics,
it being thought that they have the power of dissolving the gall-stones.
FUNCTIONAL DERANGEMENTS OF THE LIVER.
The terms biliousness and torpid liver ' were more frequently used
twenty years ago than now. Many indeed have denied that any such con-
ditions exist, but there is undoubtedly a variety of symptoms (such as
constipation, yellow and itching skin, dark urine, headache, lassitude,
furred tongue, bitter taste in the mouth, etc., etc.), which can properly
be classed as functional derangement of the liver. Writers describe ten
varieties, I shall only briefly consider those which are the most common.
In these functional hepatic derangements there are no morbid appearances
in the organ itself to account for the symptoms.
Etiology. — Functional derangement of the liver may be due to struct-
ural diseases (e. g., cirrhosis, abscess, and acute yellow atrophy), to dyspep-
sia, both gastric and intestinal, to atony of the bowels, to obstructive diseases
of the heart and lungs, to the specific fevers, malaria especially, to faulty
diet, the food being too rich in hydrocarbons, to the daily use of alcoholic
FUNCTIONAL DERANGEMENTS OF THE LIVER. 407
beverages, especially ales and sweet wines and liquors (not from whiskey,
brandy or gin, unless in the form of a hot toddy or sweet punch), to badly
ventilated, hot, and moist apartments, sedentary habits, a deficient supply
of oxygen, a warm climate (India, for instance), and finally to anxiety and
prolonged mental labor. In many cases the tendency to " liver complaint "
is inherited ; the children of the diabetic or gouty are very prone to func-
tional derangements of the liver.
Symptoms. — Few cases are exactly alike. The prominent symptoms
which usually first attract the patient's attention are anorexia, a bitter
taste in the mouth (due to taurocholic acid in the blood), flatulency,
"acidity" and pyrosis.' The tongue is large, pale, and flabby, with inden-
tations of the teeth along its edges. It may be white, showing elongated
papillae-like villi. The faeces are pale, unless they have remained long in
the large bowel, when they are blackish. Constipation and diarrhoea may
alternate. When bile is in excess the faeces are semi-fluid and contain more
bile than normal. It is a question whether melaena ever occurs as a sole
vesult of hepatic derangement, but hemorrhoids are very common. There
is often a sense of weight, fulness, tightness, burning, or even actual pain
over the liver. Those who suffer from functional derangement of the liver
may become very fat, or they may emaciate rapidly. Emaciation results
either from deficient production of bile or from derangement of the glyco-
genic function of the liver. Bile may saturate the texture of the body for
months, and yet no symptoms of blood poisoning occur so long as the
eliminating function of the kidneys is not impaired.
A deficient elimination of cholesterin may give rise to " biliousness,"
and thus be a part of functional derangement of the liver. ^ " Cholester-
gemia " is said to be associated with obstinate constipation, and Dr. Murchi-
son regards this as "torpor of the liver," or at least one, and a frequent,
form of it. Lithates and pigments deposited in the urine should al-
ways be regarded as signs of functional derangement of the liver arising
from causes sometimes temporary and sometimes permanent. Murchison
says " lithuria, like glycosuria, must be classed as a functional derangement
of the liver," and he calls the antecedent morbid blood state litlimmia. In
many, who by heredity are predisposed to "liver troubles," the liver is
capable of performing its healthy functions only under the most favorable
circumstances, and functional derangement is at once induced by articles
of diet which most persons can easily digest.
" Gouty dyspepsia," "latent gout," suppressed, anomalous or irregular
gout, are terms which in many instances should be dismissed, and "func-
tional derangement of the liver " substituted for them, for the symptoms
which have been ascribed to them occur in those who neither inherit nor
• The functions of a healthy liverare. fir»t. sanguinification ; second, the re-combination of albuminous
matter derived f r om the food and tissues ; Hard, the formation of urea and lithic acid, both of which are
afterward eliminated by the kidneys ; fourth, the secretion of bile, most of which is reabsorbed ; fifth, the
glycogenic function. Among the most constant results of functional hepatic derangement is imperfect
formation of urea evidenced by the deposit of lithic acid or lithates in the urine. When a great part of the
liver has been destroyed by disease the urea is lessened or disappears from the urine. Destructive
nitrogenous metamorphosis is unquestionalily an impoitant function of the liver.
a Virchow'8 Archiv. Bd. 65, p. 410. 1875.
408 DISEASES OF THE DIGESTIVE SYSTEM.
ever have shown any gouty tendencies/ Biliary calculi (cholesterin and
bile-pigment) may result from hepatic derangement. Frerichs regards
the coincidence of gall-stones and urinary calculi in the same individ-
ual as purely accidental. Since the kidneys eliminate certain products
of the liver, renal derangements may be a consequence of faulty hepatic
digestion. Hence Murchison places lithfemia among the chief causes of
Bright's disease of the kidneys.^ Many suppose that albuminuria may be
induced by functional derangement of the liver, independent of any mor-
bid kidney change, and this accords with the modern theories of albu-
minuria.
After the functions of a liver have been interfered with for some time,
the structure of the liver is very liable to become diseased. Fatty liver and
cirrhosis are common sequelae, and their causes are closely allied to func-
tional derangement of the liver. ^ Senile decay (sometimes premature),
fatty, calcareous and atheromatous arterial changes are very frequently
direct sequelae of functional hepatic derangement. It is questionable
whether the rheumatic hyperinosis is due to non-destruction of fibrin in
the liver, as Murchison would have us believe. But the anaemia of this
cachexia is undoubtedly often due to it.
Symptoms. — Those who suffer from torpor of the liver complain of lassi-
tude, drowsiness, pain in the limbs, dull pain in the right hypochondrmm
often shooting up the right side to the shoulder, and not infrequently of
sciatica and lumbago. Circumscribed patches of skin, usually on the ex-
tremities, often become hot and burning. Headache, usually frontal, is
very common, and when induced by indiscretions in diet it is called " bil-
ious " or " sick headache," and the patient states that he has had another
^'bilious attack." Dizziness, dim vision, and muscae volitantes are fre-
quent results of over-eating in those whose livers are functionally deranged.
Convulsions, paresis and cramps in the legs are rare, but they may occur.
Melancholia, insomnia, hypochondriasis, irritability of temper, and moodi-
ness are consequences of deranged liver-function. The term '^ bilious
temperament " has passed into common use. In some cases there are car-
diac palpitations, an irritable, irregular or even intermittent pulse, cold
extremities, and slight lividity or cyanosis, and, according to Sir James
Paget, venous thrombosis may result from functional derangement of the
liver. Paget and Murchison regard lithaemia, i. e., functional derange-
ment of the liver, as causing acute urethritis (non-specific) in many in-
stances.*
After prolonged hepatic derangement psoriasis, lichen, eczema, lepra,
urticaria, boils, carbuncles, pigment-spots (popularly called liver spots),
and pruritus are liable to appear. Frequently the same individual will
within a year have three or four of the above-named skin diseases as a
direct result of functional derangement of the liver.
1 Gout is one result of lithsemia ; and urinary calculi are frequently but an exhibition of functional de-
rangement of the liver.
2 Clin. Lee. Dis. Liver, pp. 572-573.
* Trousseau describes a chronic gouty hepatitis that comes under this head.
•* British Med. Journal, 1875, i. 70L
FUNCTIONAL DERANGEMENTS OF THE LIVEE. 409
The diagnosis is made by a consideration of the conditions and habits of
life of the patient, the sequence of symptoms, its long duration, inter-
rupted by "acute bilious attacks," and by the exclusion of structural
hepatic and kidney disease.
The prognosis depends on the cause : if due to diet, a cure can be easily
effected if the individual obeys instructions ; if hereditary, a definite prog-
nosis should never be given.
Treatment, — The treatment in the main is dietetic and hygienic ; all
starchy and saccharine substances should be avoided or taken in small
quantities. Wines and ales should be wholly discarded. Fresh air, sea-
air especially, and moderate exercise, attention to the cutaneous functions,
and abandonment of severe mental work should be recommended. Min-
eral waters (Hunyadi Janos and Pullna especially) should be freely drunk
at all times. Kochelle, Glauber's and Epsom salts are beneficial. The
bowels should always be kept freely opened. Alkalies, especially the car-
bonate of soda, are always of service. Chlorine, bromine and iodine are
useful in some cases, and the bromide of potash is highly beneficial
when combined with ammonium chloride. The mineral acids are apt to
do more harm than good, although in works on materia medica the nitro-
muriatic acid is said to be almost a specific for torpor of the liver. ^ Acetic
extract of colchicum is indicated in gouty and rheumatic subjects. Tar-
axacum was formerly thought to have a powerful effect on the liver ; its
only action is that of a cathartic.
Mercury, in the form of bhie pill, is more efficacious in affording tem-
porary relief in the so-called bilious attacks than any other drug. It is
denied by many that mercury is a cholagogue ; still there are few who do
not recommend " blue-mass " in functional hepatic disturbances, and
although experimental therapeusis shows that mercury simply increases the
biliary secretion by acting on the upper portion of the small intestine, yet
there must be some action of mercury now unknown, which makes it the
most reliable drug in functional derangement of the liver. It is suggested
that by promoting or in some way influencing the disintegration of albu-
men the liver is relieved, and thus the effects of an overtasked or naturally
feeble organ are overcome. A dose of calomel at night, followed in the
morning by a saline purge, relieves both the hepatic and urinary symptoms.
Podophyllum (^ gr. of the resin) given with cannabis indica or henbane is
by many thought equal to mercury. Tonics and opium are to be expressly
forbidden ; iron does positive harm.
' Prof. Rutherford states that in dogs it has no effect upon the bile secretion.
410 DISEASES OF THE DIGESTIVE SYSTEM.
DISEASES OF THE PANCREAS.
Diseases of the pancreas are almost always secondary to, or associated
with, disease of neighboring organs ; I shall briefly consider them under the
following heads :
I. Acute and Chronic Pancreatitis. IV. Cysts of the Pancreas.
II. Degenerations, Fatty and Waxy. V. Calculi and Parasites.
III. Morbid Groiuths :~Cancer, Tubercle, Sarcoma, and Gummata.
ACUTE PAI^CKEATITIS.
This is a rare affection, and is chiefly of interest from a pathological
standpoint.
Morbid Anatomy. — The pancreas is enlarged, hyperaemic and firmer than
normal. When the hyperemia is intense, small hemorrhages occur in its
substance. In febrile diseases the whole organ is seen to have undergone
diffuse parenchymatous changes. In suppurative pancreatitis there i&
either a diffuse infiltration of pus, or numerous small abscesses are
formed. In some instances the surrounding connective-tissue and lym-
phatic glands are involved and the pancreas is surrounded by pus. Pus
may form in the ducts, acini, or the cellular tissue. Pancreatic abscesses
may open into the stomach, peritoneal cavity, duodenum, or externally.
Etiology. — This is obscure ; it may possibly be caused by acute alcoholis-
mus and by blows over the organ. It occurs more frequently in men than
in women. Acute tuberculosis, typhoid fever, pyaemia, septicaemia, and
parotitis (from metastasis) are sometimes followed by it.
Symptoms. — These are obscure and variable, the most constant is colicky
or deep-seated dull pain over the pancreas, shooting to the back and shoul-
der. Fever, dyspnoea, anorexia, and vomiting of a thin, viscid fluid, some-
times containing bile, are nearly always present. There is great thirst and
restlessness. The pulse is rapid, the pain is greatly increased by firm press-
ure over the pancreas, and symptoms of collapse are often present. There
is marked anxiety and depression from its onset. The bowels are consti-
pated. In some cases of metastatic pancreatitis the stools are watery and
like saliva. In these cases diarrhoea is generally present.
Differential Diagnosis. — Hepatic diseases are excluded by the absence of
jaundice. But it is frequently impossible to exclude acute gastritis or duo-
denitis except by the site and distribution of the pain, and by the presence
of fever and the irregular heart-action.
Prognosis. — It usually terminates in death after a very rapid course. It
may become chronic, terminating in abscess or induration.
Treatment. — Rest, a mild, fluid diet, and anodynes are the only means to
be employed in its treatment. The eflficacy of ice or poultices over the
epigastrium is questionable.
CHRONIC PANCREATITIS. 411
CHRONIC PANCEEATITIS.
MorMd Anatomy. — The changes are identical with cirrhotic processes
elsewhere, e. g., in the liver and spleen. This process may lead to complete
disappearance of the gland substance or to closure of the duct and the con-
sequent formation of cysts. The head of the gland is most involved in the
cirrhotic process. Interstitial hemorrhages may occur, or little cysts may
stud the gland. Adhesions generally bind the organ to the adjacent parts.
In chronic su]3purative pancreatitis the pus may infiltrate the gland, or
there may be one or more small abscesses. The contents of the latter may
become cheesy or calcareous.
Etiology. — The causes are similar to those of cirrhosis of the liver ; — cal-
culi, the pressure of an adjacent tumor, or extension of inflammation from
adjacent parts, especially ulcers of the stomach and duodenum. It may be
associated with syphilitic infection.
Symptoms. — The only symptoms that could lead to a diagnosis are fatty
stools, intercurrent mellituria, neuralgic pains, and the presence of a trans-
verse tumor in the epigastrium. Abdominal dropsy and signs of intestinal
obstruction may be caused by the pressure of the hard gland which acts as
an abdominal tumor. A peculiar cachexia is usually present.
FATTY DEGENEEATION.
Two forms are recognized :
I. Fatty infiltration of the connective-tissue investing the gland and sur-
rounding the acini, where the new growth of fat-tissue causes atrophy and
disappearance of the gland cells by its pressure. The whole gland may
look like a mass of fat with only a central canal.
II. Fatty degeneration affects the gland cells and ultimately destroys
them ; the acinous structure is preserved in the midst of a soft, flaccid and
wasted gland. A more or less abundant fatty emulsion is found in the
ducts.
Etiology. — The first form occurs in general obesity and in chronic alco-
holismus. The second is due to the same causes, and a^so to heart disease
or obstruction to the outflow of the pancreatic secretion.
WAXY DEaENEEATION.
The vessels of the pancreas and the cells of the acini may exhibit amy-
loid change. This is the rarest disease of the pancreas.
CANCER OF THE PANCREAS.
This is the most frequent form of primary disease of the pancreas. In
one hundred cases of cancer the pancreas was found involved in five.
Scirrhus is the most frequent variety of cancer found here. Pancre-
412 DISEASES OF THE DIGESTIVE SYSTEM.
atic cancer tends to involve adjacent organs ; the bile-duct and left
ureter may be pressed upon and obstructed, and the mass may com-
press the splenic or superior mesenteric vessels, the vena portge, the in-
ferior cava, or even the aorta. The cancer may ulcerate into neighboring
structures. The canal of Wirsung may be obstructed, and then cysts will
form.
Etiology. — It occurs chiefly in men after the fortieth year ; further than
this little can be said.
Symptoms. — -The symptoms are varied, because the neighboring organs
are so frequently and extensively involved. Neuralgic and paroxysmal
pain, is an important symptom. The presence of a tumor with enlarge-
ment of the adjacent lymphatic glands is essential for a diagnosis. Vom-
iting, jaundice, dyspepsia, dropsy, oedema of the feet, — all may be present.
Sometimes the stools may be fatty. There may be constipation or diarrhoea,
or the two may alternate. The general symptoms are those of anaemia.
Differential Diagnosis. — A pancreatic cancerous tumor may pulsate and
have a bruit conducted from the aorta, and therein simulate aortic aneu-
rism.
Prognosis. — Cancer of the pancreas usually causes death within a year.
The treatment is symptomatic.
Small-celled Sarcoma usually occurs as a melanotic tumor. It is very
rare, and clinically indistinguishable from carcinoma.
Tuberculosis of the pancreas, secondary to that of the lungs and peri-
toneum, develops in the connective-tissue between the acini. Caseous
nodules are oftener met with than diffuse miliary tubercles. It is denied
that the pancreas ever is involved in acute miliary tuberculosis.
Syphilitic Gummata are usually found in connection with syphilitic in-
terstitial pancreatitis. They have been described by Eostan and Rokitansky.
It is believed that more frequent examinations of the gland would reveal a
larger number of gummata.
CYSTS IN THE PANCEEAS.
Cysts in the pancreas are due to retention of the pancreatic secretion,
from obstruction of the duct by calculi, or from external pressure of tumors.
Hemorrhagic cysts are very rarely found. When the duct is closed near
its mouth, the canal and its branches look like a bunch of currants. Atro-
phy and cirrhosis of the gland may result from these cysts, which at first
contain a normal secretion which afterward becomes purulent, hemorrhagic,
or albuminous. Hgematoidin crystals, lime-salts and urea have been found
in these cysts. The cyst-walls thicken from connective-tissue develop-
ments.
Etiology. — Any tumor, either of the pancreas itself or of neighboring
parts, calculi, cirrhosis of the pancreas, or angular displacements of the
pancreas may cause it.
Symptoms. — The only symptom is the discovery of a smooth lobulated tu-
mor in the region of the pancreas.
HYPEREMIA OF THE SPLEEN". 4-13
CALCULI OF THE PANCEEAS.
Calculi of the pancreas are usually gray-white, rounded masses of car-
bonate or phosphate of lime. They are situated anywhere in the pancreas,
are either free or embedded, vary in size from microscopic dust to a walnut,
and also vary in number, but rarely exceed fifteen or twenty. Laminated
protein concretions are described by Virchow.
Etiology. — Anomalies in the pancreatic juice itself, catarrh of the ducts,
and retention cysts are the most frequent causes.
Symptoms. — There will be no symptoms except when interstitial inflam-
mation is excited, or the common duct is pressed on so as to cause jaundice.
Round worms have been found in the pancreas.
DISEASES OF THE SPLEEN.
Diseases of the spleen will be considered in the following order :
I. Hyper wmia. IV. Degenerations, Waxy or
II. Inflammation, or Splenitis, includ- Sago-spleen.
ing EmhoUsm and Infarction. V. Morbid Growths.
III. Hypertrophy, or Chronic Enlarge- YI. Parasites,
ment.
HYPEREMIA.
Splenic hypersemia may be active or passive.
Morbid Anatomy. — The accumulation of blood in the vessels and inter-
vascular spaces of the spleen, causes, the enlargement which occurs in
hypersemia ; the organ may be increased to five or six times its normal size
and yet retain its normal shape. Its color is darker than normal, its cap-
sule is usually tense and shining, and its consistency is often diminished,
being sometimes as soft as pulp. A microscopic examination shows no new
elements in the spleen, only an increase in the number of its normal ones.
Etiology. — A physiological congestion of the spleen takes place after every
meal. A pathological engorgement occurs : (1) when there is any ob-
struction to the venous flow from the spleen, as happens in certain cardiac,
hepatic, and pulmonary diseases ; (2) in the acute infectious diseases, such
as typhus, malarial fevers, and pyaemia ; (3) at the menstrual epoch, de-
pending upon an abnormality of menstruation ; (4) as the result of inju-
ries and inflammation, when the hypersemia will be circumscribed.
Symptoms. — The symptoms of simple hypersemia of the spleen are usually
not well marked ; the patient may complain of a sense of weight in the
left hypochondrium and more or less tenderness on pressure over the
splenic region. Palpation and percussion will discover a tumor in this
region of greater or less size ; this tumor extends obliquely downward to-
ward the umbilicus, rises and falls with each respiratory movement, and
has the outline of the spleen, with the characteristic notches on its lower
rounded edge. The pale and anaemic appearance often met with in those
414 DISEASES OF THE DIGESTIVE SYSTEM.
having splenic hypersemia is dne to the overloading of the spleen with
blood at the expense of the rest of the body, rather than to any change in
the composition of the blood.
Prognosis. — The prognosis is good, although in certain rare cases death
has occurred from rupture of the distended organ.
Treatment. — The treatment is directed rather to the disease which gives
rise to the hyperaemia than to the condition itself. Quinine in large doses
has been found in most instances to remove the splenic congestion and
relieve the accompanying symptoms.
IlSrFLAMMATIO]!^ OF THE SPLEEIST.
{Splenitis.)
Primary splenitis is exceedingly rare ; it is generally due to injury, em-
bolism, or infarction, especially when occurring with pyaemia or septic
diseases. It may occur in connection with morbid growths and abscesses
in the spleen. There is a condition of the spleen resembling cirrhosis of
the liver, called by some chronic or interstitial splenitis.
Morbid Anatomy. — The anatomical arrangement of the splenic arteries
renders the spleen a favorable seat of metastatic inflammation. In acute
splenitis a part or all of the organ may be attacked ; the involved portions
are congested and swollen; and the peritoneum over them is injected and
covered with a fibrinous exudation. The spleen is of a deep purplish color
and friable, being broken down as easily as coagulated blood. When a
hemorrhagic infarction is formed in the spleen, it is usually without rupt-
ure of the blood-vessels, and is encircled by a zone of sero-hemorrhagic
infiltration. These infarcts are at first of a brownish red color and of a
firm consistency ; later, they become dirty yellow in color, and either under-
go fatty degeneration and become absorbed, or remain as cheesy and
calcareous masses ; or, lastly, the infarctions soften and abscesses form,
wliich are single or multiple, sometimes fusing together, and again in-
creasing by peripheral extension.
In a few instances these abscesses are found incapsulated in a proliferation
of connective-tissue, but in most cases this is not the case ; the connective-
tissr.e breaks and a large sac is formed filled with pus ; as much as thirty
pounds have been found in one of these sacs. At last the capsule becomes
mvoWed, perisplenitis is set up, and, adhesions having formed between the
spleen and adjacent parts, the abscess may open into some adjacent organ,
as the stomach and colon, into the thorax or abdominal cavity, or an
external fistulous opening may be formed. Localized suppurative inflam-
mation of the small Malpighian bodies in the spleen has been found to occur
in typhus and other fevers.
" Necrotic splenic softening " may occur from an infarction caused by
atheroma and endocarditis : here the latter is not ulcerative. In these
cases the lymph-cells in the fibrinous reticulum of the clot become fatty,
and then they mass themselves into spheres of fat-crystals. The whole
infarction softens and becomes a fatty, pulpy mass. The capsule over such
INFLAMMATION OF THE SPLEEN. 415
a spot is villous and appears covered with vegetations. A gangrenous con-
dition of the left lower lobe of the lung has been caused by such a form of
metastatic splenitis ; with the intense engorgement which accompanies
acute splenitis, hemorrhage into the organ may occur, the capsule may
be ruptured, and a fatal peritonitis may be induced.
Chronic splenitis is the result of long-continued splenic congestion. The
spleen is of a brownish-red or slate color, its capsule is thickened, and
covered with very firm vegetations and new connective-tissue formations,
which are highly vascular. The organ is more or less pigmented, owing
to the pigmentary deposit in tlie endothelia of the veins. This whole proc-
ess is analogous to that which occurs in cirrhosis of the liver, except
that a spleen which is the seat of interstitial inflammation is larger than
normal.
Etiology. — It is very doubtful whether idiopathic splenitis ever occurs.
Blows and severe muscular exercise are said to have caused it. Splenitis
is usually metastatic, the embolic plug, the result of endocarditis and
valvular disease, most often having its origin in the left heart, although it
may be induced by thrombotic changes in the aorta. Earely the embolus
comes from the lungs, having passed through the pulmonary vein and left
heart. In pyaemia and its allied states hemorrhagic infarctions of the sj^leen
are of frequent occurrence, and a similar condition has been noticed in
Bright's disease and in the infectious diseases. Extension of inflammation,
especially the result of ulcerative changes in the stomach, is an occasional
cause of acute splenitis.
Symptoms. — These are vague ; often there is nothing except the local
changes to direct attention to the spleen as the seat of disease. There is
no pain, unless the capsule is involved ; if pain is present it will be in-
creased by a full inspiration. There may be hectic fever, but, as splenitis
is secondary to some febrile disease, the fever may be attributed solely to
the latter. There may be a sense of weight and pain in the left hypo-
chondrium, and even shooting pains in the left shoulder and arm.
Vomiting of blood and pus, or the simultaneous passing of blood and pus
with the fgeces is indicative of rupture of a splenic abscess into the stomach;
this, however, is an exceedingly rare event. The recognition of a splenic
abscess will depend upon its attaining a sufficient size to form an appreciable
fluctuating tumor in the splenic region.
Physical Signs.— Inspection will show a marked enlargement in the splenic
region.
Palpation may discover a fluctuating mass. The ''notchings" on the
anterior margin of the spleen are usually readily made out. The mass is
more or less movable, unless adhesions have formed between the splenic
capsule and adjacent parts.
Differential Diagnosis.— Acute splenitis may be mistaken for cancer of
the stomach, disease of the pancreas, or hepatic disease, especially that in-
volving the left lobe of the liver. Ooarian tumors will rarely be con-
founded with it. In stomach diseases the absence of fever, the vomiting,
pain and discomfort dependent on the ingestion of food, the long dura-
416
DISEASES OF THE DIGESTIVE SYSTEM.
tion, and the peculiar haematemesis will readily distinguish them from
acute splenitis.
Cancer, abscess, or cirrhosis of the liver would give physical signs which
could hardly be confounded with those of acute splenitis — the position of
the area of dulness would of itself be sufficient for a diagnosis. The con-
dition of the stools, the urine, and the color of the skin are often sufficient
to lead to a diagnosis of hepatic diseases. If the tumor is of considerable
size, the diagnosis of splenic abscess can always be safely reached by the
aid of the exploring trochar.
Prognosis. — Suppurative splenitis is always a dangerous disease, and is
rarely recovered from, even when an extensive opening is established.
Treatment. — No special treatment is called for unless the pain is severe,
when anodynes and fomentations may be used. When an abscess can be
made out it should be treated in the same manner as an hepatic abscess.
HYPERTKOPHY OF THE SPLEElf.
(Enlarged Spleen.)
Enlargements of the spleen are of two kinds : (1) acute and transient ;
and (2) chronic and permanent. The first class occurs in f fevers, e. g.,
typhoid ; the second from long-continued and repeated congestion, as in
chronic malarial infection.
Morbid Anatomy. — In acute enlargement, the spleen may reach four or
five times its normal size. The capsule becomes thin and tense. The
spleen pulp varies in consistence, and may even be completely diffluent ;
its color varies from a bright pink to a red black. Hemorrhagic foci in-
dependent of embolism may occur. Many lymphoid cells contain one or
more red corpuscles, the latter either being
normal in size or smaller (1-8000 of an
inch). This microscopical appearance is
best marked in typhoid fever.'
Chronic Enlargement of the Spleen. — The
organ is enlarged without any obvious
change in texture ; there is an increase in all
its elements, and it acquires a more or less
fleshy consistency. It sometimes reaches a
very great size, filling the left side of the
abdominal cavity from the ribs to the pelvis;
it may be increased to twenty pounds in
weight. Its normal shape is unchanged and
the notches on its edges are distinctly re-
FiG. 87. tained. In rare cases chronic enlargement
Diagram illustrating the abdominal areas of ii.'i nii„„i-
plrcussiou-duinessin Splenic Enlargement, occurs as a multiple nodular hyperplasia.
1 The color of the spleen in congestive enlargement is always paler than that of the other viscera, on
account of the presence of a larger quantity of white blood corpuscles than are found elsewhere in the
body.
AMYLOID DEGENERATION OF THE SPLEEN". 417
Etiology. — Acute enlargement of the spleen is met with most frequently
in acute infectious diseases. Many regard the accumulation of micrococci
in the spleen and their retention within the splenic protoplasm as a cause
of acute swelling.' Of all the diseases that cause sudden and gi-eat enlarge-
ment of the sj)leen, the most frequent are typhoid and intermittent fevers.
Chronic enlargement of the spleen is frequently associated with cirrhosis
and other chronic affections of the liver, and with chronic cardiac and
pulmonary diseases that induce long-continued or repeated congestion of
the organ. But chronic malarial infection is its most common and constant
cause. Chronic enlargement of the spleen is part of the history of leucocy-
thsemia ; it is never idiopathic. Chronic mercurialism disposes to en-
largement of the spleen.
Symptoms. — Acute enlargement of the spleen is jDart of the history of
acute general diseases ; its natural symptoms are few : pain on pressure,
dyspnoea, and an increased area of splenic dulness are the most constant
and prominent. Chronic enlargement of the spleen is attended by no
symptoms except the physical signs of sjDlenic enlargement.
Treatment. — Quinine and iron are always indicated, but they should be
given alternately and never at the same time; they may be combined with
arsenic and cod-liver oil. In malarial hypertrophy of the spleen the patient
should reside in a non-malarial district. Inunctions of the biniodide of
mercury are strongly recommended by English authorities, but I have
never seen any beneficial results from their use.
AMYLOID DEGENEEATIOlSr OF THE SPLEEl^.
{Sago Spleen.)
s
Waxy or lardaceous degeneration of the spleen, also called the "sago
spleen," is a part of a general cachexia in which other organs are primarily
involved.
Morbid Anatomy. — It occurs in two forms ; in one it is limited to the
Malpighian bodies, in the other it is diffused. In both the organ is en-
larged, rounded and doughy. The capsule is tense, but not thickened, and
is usually smooth and glistening.
On section the first variety presents the appearance of a number of sago
granules, the Malpighian bodies being enlarged to 1-25 or 1-12 of an inch
in diameter, and filled with waxy material which gives the characteristic
reaction with iodine. The corpuscles through which the arteries pass are
involved, but the wall of the in-going vessels may remain normal. The
"adenoid" or "cytogenic" tissue, the lymph-corpuscles, and the capilla-
ries of the spleen are, however, infiltrated with waxy material, massed to-
gether, and channelled by healthy capillaries. The veins near the diseased
Malpighian bodies are sometimes involved. In diffuse lardaceous degenera-
tion, the spleen, on section, is pale, homogeneous, glistening and anaemic ;,
all the vessels, the trabeculse, and capsule are involved.^
Etiology. — The causes of waxy spleen are identical with those of waxy
' MohIct and Birch-Hirschfeld.
2 Rokitansky regards this form as but a later stage of " sago spleen."
26
418 DISEASES OF THE DIGESTIVE SYSTEM.
liver ; it is met with in chronic bronchitis with bronchiectasis, in phthisis,
chronic Bright's disease, chronic peritonitis, cirrhosis of the liver, chronic
alcoholismus, and intermittent fever. Sago spleen frequently accompanies
chronic intestinal catarrh in children. Syphilis is probably its most fre-
quent cause.
Symptoms. — As the liver and intestines are generally involved in the same
change, the waxy cachexia will not be characteristic of splenic changes.
There will be anaBmia, accompanied by a great increase in the area of splenic
dulness. Late in the disease there is usually anorexia, vomiting, and
hemorrhages, but it is not possible to determine to what extent these vari-
ous symptoms depend on the splenic disease.
The diagnosis rests mainly on its etiology.
The prognosis is unfavorable-
Treatment. — It never calls for independent treatment. Niemeyer regards
iodide of iron as the most efficacious drug. Our first efforts should be to
cure or remove the causes or conditions which have led to its development,
and to improve the general condition of the patient by tonics, hygienic
measures, and a carefully regulated, nutritious diet.
MORBID GEOWTHS OF THE SPLEEN.
Cancer of the spleen is very rare ; it may be secondary to cancer of the
stomach, mamma, liver, or brain. When disseminated, it is generally of
the encephaloid variety. It may develop in the hilum by contiguity of can-
cer in the other organs. Secondary isolated growths may be scattered
through its substance, or in many more instances it may be the seat of pri-
mary cancer. In pigment-cancer of the spleen, the organ rapidly enlarges
to nearly double its size ; in other forms it is but slightly enlarged. The
symptoms are obscure and of little clinical importance.
Gummata, or syphilitic tumors of the spleen, are only met with in con-
nection with amyloid changes, and are accompanied by similar develop-
ments in the liver. Syphilis thus shows itself in the spleen in one of four
-ways, — waxy degeneration, gummata, inflammation of the spleen- pulp, or
hypertrophy of the spleen with increase in interstitial tissue. Syphilomata
are of no clinical importance.
Tubercles in the spleen develop in the spleen-pulp. The nodules may be
small and gray, or large, yellow and cheesy. In acute tuberculosis, the
spleen rapidly enlarges as the tubercles develop. Tubercular formations
are very common in young children. Yellow tubercular masses, varying
in size, are frequently found in the spleen in connection with similar form-
ations in other parts of the body ; occasionally they soften and form ab-
scesses. The small splenic vessels are often clogged with lymph and fibrin.
Tubercles of the spleen cannot be recognized during life.
Cysts have been found in the spleen. They are associated with cystic
developments in the liver and omentum.
Hydatids, when occurring in the spleen, usually accompany similar de-
velopments in the liver and peritoneum. The enlargement of the spleen
MOEBID GROWTHS OF THE SPLEEN. 419
may cause a sense of weight in the splenic region, and if the splenic capsule
becomes inflamed their development will be accompanied by sharp pains in
the left side. An hydatid tumor in the spleen usually fluctuates, but it
rarely gives the hydatid fremitus. An exploratory puncture decides its
character.
The prognosis and treatment are the same as in hydatids of the liver.
SECTION III.
DISEASES OP THE HEART, BLOOD-VESSELS AND KIDNEYS.
Diseases of the heart may be classified as follows :
I. Pericarditis. VIII. Cardiac Atrophy.
II. Endocarditis. IX. Cardiac Thrombosis.
III. Valvular Lesions. X. Cardiac Aneurisin.
IV. Cardiac Hypertrophy. XI. Morbid Growths and Parasites.
V. Cardiac Dilatation. XII. Tuberculosis of the Pericardium.
VI. Myocarditis. XIII. Cardiac Neuroses.
VII. Cardiac Degenerations. XIV. Hydro-pericardium.
XV. Pneumo-hydro-perioardium.
PEEICAEDITIS.
The pericardium is a fibro-serous sac ; the fibrous layer is firmly adherent
to the diaphragm and is attached to the large vessels about two inches
above the heart ; it forms a closed sac. The serous layer is in close appo-
sition to the internal surface of the fibrous layer, is reflected from the large
vessels, and completely invests the heart itself. This shut serous sac, when
diseased, behaves in all respects like the pleura. Inflammation of the
pericardium may be acute or chronic. Chronic pericarditis is usually the
sequel of acute.
ACUTE PERICARDITIS.
Acute pericarditis is perhaps more frequently overlooked than any other
acute disease, for its subjective symptoms are rarely, if ever, well marked.
Morbid Anatomy. — At its commencement, the serous surface of the
pericardium becomes more or less reddened, with here and there ecchy-
motic spots of irregular shape. The reddening may be circumscribed about
the roots of the great vessels, or it may involve the whole visceral and
parietal pericardium. The reddening is due to hyperaemia of the sub-
serous capillary vessels. With the redness there are swelling and infil-
tration of its serous and sub-serous tissue. Following the hyperaemia
and infiltration the epithelium desquamates and the membrane loses its
natural glistening appearance. If the inflammatory action is continued,
an exudation is poured out on its free surface : it may consist of but a few
shreds of lymph, or a fibrinous layer may cover the whole of its car-
diac or parietal surface. It varies in thickness from a line to three-fourths
ACUTE PERICARDITIS.
431
of an inch, or even more. This exudation is composed of fibrin, a few pua
cells and detached epithelia ; it causes the free surface of the pericardium
to assume a roughened appearance ; it is this appearance which has given
rise to the expression "hairy heart." When there is only a very small
amount of plastic exudation, it
will usually be confined to that
portion of the pericardium which
covers the blood-vessels.
With or following the plastic
exudation there may be a fluid
effusion which varies in quantity
and in quality. It may be sero-
albuminous, sero-fibrinous, hem-
orrhagic, or purulent. It varies in
quantity from three fluid ounces
to several pints. In most instances
it will be sero-fibrinous in char-
acter ; it is rarely sero-albuminous.
When it is small in amount it will
gravitate to the most dependent
portion of the pericardial sac.
When it is large in quantity, the ^^^ gg
entire pericardial sac is filled, and Diagram illustrating the Morbid Anatomy and Physical
thp adiaCPuf lllUJir fissno oom- Signs of Sero-plastic Pericarditis.
tne aajacent lung-tissue com a. Line of diaphragm.
pressed, and the surfaces of the b. Heart. ^ . ^. ,
r ^ . C Serous effusion into Imver portion of pericardial sac.
membrane have a reticulated or B. Plastic exudation upon both viscerai and parietal
_ . layers of the pericardium.
honey-combed appearance, it is
always turbid from the molecular fibrin suspended in it, and may be
yellow, green, brown, or red in color.
Hemorrhagic pericarditis is rare, except with purpura, scurvy, cancer of
the lung, and tuberculosis. In this variety the line of demarcation between
the false membrane and the pericardium is very indistinct.
Tuberculous pericarditis is attended by the development of tubercles in
the pericardium and in the substance of the heart ; the blood effused forms
ochre-colored masses in the exudate. The exudations and effusions in
pericarditis may all undergo absorption. The serous effusion is removed
rapidly, the hemorrhagic with less facility, the plastic and purulent with
still greater difficulty. The fluid disappears first, then the granular, and
last the coagulated fibrin. The lymph and purulent exudations may
undergo fatty metamorphosis and be absorbed, or remain in a cheesy,
mortar-like mass, and finally become calcareous after the absorption of the
more fluid portion of the degenerated mass. The calcareous material with
connective-tissue formations may form ossified plates upon the surface of
the heart and pericardium.
New connective-tissue formations may take place upon the surface of
the pericardium under the layer of plastic exudation ; if the inflamma-
tory process is continued sufficiently long, these are converted into a firm
422 DISEASES OF THE HEART.
fibrinous mass, causing either a permanent thickening of the pericardium,
or adhesions between its two surfaces. Sometimes these adhesions are by
bands stretching across from one portion to the other ; at others there is
complete agglutination of the two surfaces, and an entire obliteration of the
pericardial cavity ; in either case more or less complete organization takes
place. The adhesions about the base are the most dense. Those at the
apex are drawn out into fibrinous strings.
With infiammatory changes in the visceral pericardium, there will be
more or less inflammatory change developed in the muscular tissue of the
heart immediately beneath the pericardium. If the pericarditis has been
extensive and long continued, the walls of the heart will become weakened ;
indeed, they are somewhat weakened in every attack of pericarditis. The
development of myocarditis will be considered more fully under its appro-
priate head. Dilatation of the cavities of the heart may take place in con-
sequence of the weakened condition of the cardiac walls, and cardiac hy-
pertrophy may be developed as a result of this weakening and dilatation.
Upon post-mortem examination not infrequently smooth, opaque, pearly-
white patches are found upon the external surface of the heart. They are
slightly elevated, variable in size, have irregular sinuous margins, and are
usually located on the anterior surface of the ventricle. As to the nature
of these spots there has been considerable discussion. These " milhy
patches " are, however, nothing more than growths of white, laminated con-
nective-tissue with elastic fibres, immediately beneath the cardiac pericar-
dium, and indicate the previous existence of a localized pericardial inflam-
mation which has been recovered from without adhesions. In rare instances
the two surfaces of the pericardium will become firmly agglutinated through-
out their entire extent, and the pericardial sac will remain completely oblit-
erated, and if attempts are made to separate them the cardiac muscle is
torn. Under such circumstances, the movements of the heart carry with
them the pericardium, and with each cardiac pulsation there is a lifting of
the diaphragm.
Etiology. — Acute pericarditis rarely occurs as a primary affection, but is
usually secondary, or is developed during the course of some other disease. '
It may be produced by injuries to the pericardium, — by extension of inflam-
mation from neighboring organs, as when it occurs with pleuro-pneumonia,
pleurisy, necrosis of the sternum, ribs, rupture of abscesses, etc. It occurs
most frequently in connection with that class of diseases which depend upon
well-recognized blood -changes ; under this head are included pericarditis
which accompanies acute rheumatism, Bright's disease, acute infectious
diseases, as scarlatina, small-pox, typhus and typhoid fever, pneumonia,
tuberculosis, syphilis, chronic alcoholismus, etc. Occasionally it is devel-
oped in connection with scurvy and purpura ; then it is of the hemorrhagic
variety. Cancer of the lung and tuberculosis also cause *' hemorrhagic
pericarditis."
When pericarditis occurs in connection with pyaemia and septic condi-
tions, the effusion is purulent in character and accumulates rapidly. It is
1 A case of " Idiopaihic Pericarditis.'''' Glasgow Med. Journal, Sept., 1878.
ACUTE PERICARDITIS. 423
of most frequent occurrence in connection with acute articular rheumatism,
Bright's disease and pneumonia. Often in rheumatic pericarditis, the ar-
ticular rheumatic development occurs subsequent to the pericarditis. In
rheumatism it is an early, in Bright's disease a late occurrence. Pericar-
ditis occurring in connection with scarlet fever is especially liable to be
overlooked, for its presence is not revealed until a large fluid effusion takes
place.
Symptoms. — The symptoms cf acute pericarditis are rarely well defined.
It is very difficult to give a clear description of the rational symptoms which
attend its development, for it is usually associated with some other affection
whose symptoms tend to obscure those of pericarditis ; more than one-half
of the cases are latent, and come on so insidiously that they would go un-
recognized were it not for the physical signs which attend them.
The two prominent rational symptoms are pain in the precordial region
and cardiac palpitation. The joain is usually confined to the precordial
space ; occasionally it involves the brachial plexus, and extends down the
left arm ; under such circumstances it is probably reflex in character. The
pain may be increased in severity by pressing the left lobe of the liver
against the diaphragm. It varies in severity ; sometimes it is very slight,
again it is of a sharp, lancinating character, and sufficiently severe to de-
mand immediate relief. With the pain there is always more or less cardiac
palpitation, a dry irritable cough, and a sense of constriction over the whole
chest, with more or less dyspnoea ; the intensity of the dyspnsea will vary
with the amount of the fluid effusion. When the effusion is considerable
and there is orthopnoea the patient becomes restless and the countenance
assumes an anxious expression, with a painful look of suffering somewhat
characteristic ; he assumes the half-sitting posture, leaning somewhat
toward the left side. Lying on the back with the head elevated, is the
position usually preferred when the effusion is not large. The face is often
livid.
At first the pulse is full and strong, ranging from 90 to 120 beats in the
minute,— after the fluid effusion has taken place, it becomes feeble, sup-
pressed and sometimes delayed. If the effusion is abundant the pulse has
a tendency to become irregular, and not infrequently intermitting ; it is
always out of proportion to the activity of the heart and strongly dicrotic.
The temperature usually rises one or two degrees,— in some cases it may
rise as high as 10^° F. In fatal cases the temperature falls toward the
close of life, sometimes below normal. Jaundice sometimes occurs and
headache and dizziness are frequently present ; in the severe forms of the
disease there is often delirium, the patient sometimes becoming so furious
as to require restraint ; at other times it is low and muttering. The de-
lirium is often accompanied by delusions, tetanic or clonic spasms, and in
rare cases convulsions occur, rapidly passing into coma and followed by
death. Usually Avhen the fluid effusion takes place, the acuteness of the
symptoms subsides, and the patient experiences a sensation of op23ression
referaljle to the precordium, — he is disinclined to make any movement, for
the least motion of the body gives rise to a sinking sensation with a
424 DISEASES OF THE HEAET.
tendency to syncope. Painful hiccough, accompanies this symptom. The
patient is now constantly in danger of sudden and fatal syncope from press-
ure of the pericardial accumulation upon the heart. Some maintain that
sudden and fatal syncope never occurs in primary pericarditis, but that it
is met with only after several attacks have occurred, and more or less ex-
tensive pericardial adhesions have taken place. This is not necessarily the
case, for whenever large fluid effusions are developed, with the attendant
weakening of the cardiac walls from superficial myocarditis, patients are
constantly in danger from sudden syncope.
The severity of the symptoms in pericarditis corresponds to the intensity
of the inflammation and the amount of the effusion ; if the inflammation
is slight and the effusion moderate, the plastic exudation predominating,
none of these symptoms will be present, and the subjective symptoms will
only serve to attract attention to the heart as the seat of disease.
The subjective symptoms in many cases of pericarditis being so obscure,
often altogether wanting, the physical signs become all important. In fact,
in all cases of acute articular rheumatism, for the first two weeks ifc is an
imperative duty each day to make a careful physical examination of the
heart, especially if its action becomes irritable and the apex-beat is increased
in force. Delirium in acute rheumatism ought at once to direct attention
to the heart. The same care in examination should also be exercised in
Bright's disease when convulsions or coma occur ; and in severe acute infec-
tious disease the heart will often be found implicated.
Physical Signs. — These vary with its different stages. In the early stage
the only sign furnished by inspection and palpation is an irritable, turbulent,
forcible, and sometimes irregular action of the heart.
Palpation gives a friction-fremitus in a few cases. There is no change
in the normal area of precordial dulness.
On auscultation the first positive physical signs of pericarditis are the
pericardial friction sounds. They may be grazing, rubbing, or creaking
in character. These friction sounds may be single or double, and may
accompany the heart sounds or occur independently of them. They are
always superficial in character and are generally restricted to the precordial
space. Their point of maximum intensity is usually at the junction of the
fourth rib with the sternum on the left side ; occasionally they will not be
audible at this point, but will be heard over the large vessels at the base of
the heart ; when this is the case it indicates that only a small extent of the
pericardium is involved, and that the inflammatory changes are confined
to that portion of the pericardium which covers the large vessels. When
absent, as they sometimes are, their absence may be due to softness of the
fibrin, feebleness of heart action, or alteration in, or abnormal position of,
the lungs. Pericardial friction sounds may be increased in intensity by
changing the position of the patient : when the body is thrown forward
-the heart will be brought nearer to the anterior wall of the chest and the
friction sound will be more distinctly audible. These friction sounds will
also be increased in intensity by a full inspiration, for the distended lung
will press the two pericardial surfaces together and thus intensify the rub-
ACUTE PERICARDITIS.
425
bing sounds. In this way a single friction sound may become double.
These sounds are usually of short duration, disappearing after a few hours,
or at most in a few days.
As soon as the stage of effusion is reached and liquid is poured into the
pericardial sac, the friction sounds disappear and another class of physical
signs are developed which mark the effusive stage of pericarditis.
Inspection now shows a diminution in the respiratory movements over
the precordial space, and if the pericardial sac is distended — especially in
children and young persons — there will be arching forward of the precordial
region ; this arching forward may extend from the second to the sixth in-
tercostal space. On lying down the apex-beat often becomes more promi-
nent. This bulged portion does not move with the rest of the thorax in
respiration.
Palpation shows the point of the apex-beat to be raised and carried to the
left of its normal position. This raising of the apex-beat is never actual
— only apparent— for as the fluid accumulates the apex is jDUshed further
back from the anterior wall of the chest, and the portion of the heart that
is nearest to the chest wall appears to strike it and cause an "apex-
beat," which is nearer the base the more fluid there is in the pericardium
■ — a simj)le physical phenomenon dependent upon the " conicity " of the
heart and the pear-shaped sac in which it hangs. The cardiac excitement
and friction-fremitus which might have been j^resent before the effusion
occurred disappear, and if the effusion is large the apex-beat becomes im-
perceptible. Sometimes in extreme pericardial effusion an undulating
impulse is communicated to the hand as it rests on the chest walls, by
the action of the heart in the fluid.
On percussion, if the pericardium is distended with fluid, the area of
precordial dulness is found to be
increased in every direction, espe-
cially laterally and vertically. The
shape of the enlarged area corre-
sponds to the pyramidal form of
the pericardial sac. Eecent experi-
ments prove that the triangular
or pyramidal dulness is not due to
the shape of the pericardial sac,
but to the retraction of the edges
of the lung. In a lateral direc-
tion the precordial dulness may
extend from one nipple to the
other ; it may extend upward as
high as the second or the first rib,
or above the clavicle, and down-
ward somewhat beyond the nor-
mal limits. A small amount of
effusion isdenoted by an increase ^^'^' ^^'
,1 .,,1 „,i ,., Diagram illustrating the Pliysical Signs of Pericarditis
in the width OI the precoraial area when the ijencardial sac is distended with fluid.
426 DISEASES OF THE HEART.
of dulness at the lower portion of the precordial region ; if emphysema
exists the changes in the area of dulness will be less marked.
Upon auscultation an absence of respiratory murmur is noticed over all
that space which is normally occupied by lung tissue, the lungs being
pushed to the right and left by the distended pericardial sac. The friction
sound which may have been present before the occurrence of the effusion
disappears and the heart sounds become feeble or indistinct. In most
cases the fluid disappears rapidly within a week or ten days.
Stage of Absorption. — As recovery takes place and the effusion is absorbed,
the area of precordial dulness decreases and the pericardial surfaces again
come in contact and the friction sound reappears, the heart sounds will be-
come more distinct, the apex will assume its normal position, the cardiac
impulse will regain its normal force, and the respiratory and vocal sounds are-
again heard over the space formerly occupied by the distended pericardium.
If the anatomical changes developed in the substance, and on the surface of
the pericardium, have been extensive, as the two pericardial surfaces come
together they may become firmly adherent and all motion between the
heart and pericardium cease. This condition cannot be recognized by phys-
ical examination — it is only to be inferred from the history of the case.
If one who has had all the symptoms of pericardial effusion which has
been followed by a friction sound that has gradually disappeared, leaving
a slight intermittent action of the heart, suffers on active exertion from a
sense of constriction above the precordial region, it may be inferred that
the two surfaces of the pericardium have become adherent. Pericardial ad-
hesions, whether general or in bands, may undergo absorption, and if a sec-
ond attack of pericarditis is not developed motion between the two surfaces
will be restored, and the only evidence of the disease will be the milky
patches on the pericardial surface found at the autopsy.
Differential Diagnosis. — The existence of pericarditis can never be positive-
ly determined except by its physical signs ; even when attention has been
directed to the heart it is not always easily recognized. Its physical signs may
be confounded with those of endocarditis, pleurisy, and cardiac hypertrophy.
The friction murmurs of pericarditis may be distinguished from endocar-
dial murmurs -.—first, by their superficial character. Second, by their lim-
ited area of diffusion, their maximum area of intensity being over the right
ventricle and the junction of the fourth rib with the sternum ; while endo-
cardial murmurs are audible beyond the pericardial limits to the right and
left, upward along the course of the vessels and sometimes in the back.
Third, the intensity of a pericardial friction sound may be increased or di-
minished by inclining the body of the patient forward or backward, and
it is rendered more distinct by a full inspiration ; whereas endocardial
murmurs are not changed in intensity by a change in the position of the
patient, nor by the period of time of the respiratory movement. Fourth,
pericardial friction sounds are not necessarily synchronous with the heart
sounds and may be double; while endocardial murmurs always pre-
cede, take the place of, or follow heart sounds. Pericardial sounds are
more grating, rubbing or creaking in character than endocardial.
ACUTE PERICAEDITIS. 427
Pericardial friction sounds may be distinguished from the friction
sounds of pleurisy when the j)leurisj occurs over the precordial space, by
directing the patient to hold his breath for a moment ; if the friction
sound is pericardial it will continue during the suspension of the respira-
tory act — if it is pleuritic the friction sound will cease during the arrest of
resjDiration. Occasionally, however, where there is consolidation of the
lung directly over the heart, accompanied by a pleuritic friction, and firm
adhesions having taken place between the two surfaces of the pericardium, a
distinct friction sound may be produced in the pleura by the motion of the
heart. This is of rare occurrence and is hardly to be taken into considera-
tion. In this case the general bodily condition and the state of the pulse
may aid us.
The abnormal area of percussion dulness produced by liypertropliy or
dilatation of the right ventricle very closely resembles that produced by peri-
cardial effusion, and it is often exceedingly difficult to draw a distinct line
between them. There is one point which may be regarded as diagnostic :
that is, in enlargement of the right heart the precordial dulness never ex-
tends to the left beyond the apex-beat, while in pericardial effusion it may
extend one or two inches beyond the apex-beat. The fact that cardiac
dulness extends to the left of the apex-beat proves that there is more or
less fluid in the pericardial sac. The outline of dulness is quadrilateral
in dilatation, and triangular in pericardial effusion. Besides, in cardiac
hypertrophy there is an increase in the force of the apex-beat, and an ab-
normal intensity to the heart sounds ; in pericarditis both will be dimin-
ished in intensity. Pericardial effusion is distinguished from hypertrophy
or dilatation of the left heart by the fact that in left cardiac hyj)ertrophy the
apex- beat is carried downward and to the left, and the area of precordial
dulness is increased in the same direction and not to the right. The
force of the heart's action is greatly increased in left ventricular hypertrophy.
Prognosis. — In most instances pericarditis ends in complete recovery.
The exceptions to this rule are met with almost exclusively in connection
with Bright's disease and septic or pysemic conditions. In connection with
either of these diseases there is always more or less danger ; if it occurs in
connection with pysemia, the danger is very great, for the exudation in
such cases is usually purulent and its absorption can hardly be expected,
although it does occur. A large amount of fluid may compress, and cause
paralysis of the heart, death resulting in a few hours. The nature of the
exudation determines to a great extent the prognosis ; when it is hemor-
rhagic or purulent, the prognosis is bad. Eheumatic pericarditis is rarely
fatal. Occasionally, acute pericarditis passes into chronic, or rather is ac-
companied by a large serous effusion, which disappears slowly, and is es-
pecially liable to be accompanied by relapse, and thus the disease goes on
for months. During its progress the patient suffers from repeated attacks
of extreme dyspnoea ; in rare instances a fatal syncope occurs.
As a result of the long continuance of the fluid effusion the substance of
the heart becomes softened and its muscle undergoes more or less degener-
ation, on account of which its propelling power is diminished, and death
428 DISEASES OF THE HEART,
by oedema of the lungs may occur ; or any sudden effort may result in in-
stant death. This form of subacute or chronic pericarditis is generally as-
sociated with blood changes attended by a loss of red corjDuscles and fibrin,
and must always be regarded as a grave disease. The most frequent
sequelas of acute pericarditis are adhesions of the two surfaces of the peri-
cardium, cardiac dilatation, and hypertrophy. Cardiac dilatation occurs
as the result of the weakening of the cardiac walls from myocarditis. The
hypertrophy of the cardiac walls which follows this dilatation is compensa-
tory. . Occasionally the pericardial exudation is abundant, and extensive
pericardial adhesions take , place at the base of the heart, which, by their
contraction and pressure, interfere with the current of blood through the
coronary arteries, and as a result the nutrition of the heart is impaired and
fatty degeneration of its walls may be developed. The duration of peri-
carditis is from one to three weeks ; some cases end fatally in a few hours
from sudden heart failure.
Treatment. — We have to deal with an inflammation of considerable sever-
ity, yet from our knowledge of its etiology and morbid anatomy we are not
warranted in the use of a single antiphlogistic measure. Blood-letting,
hydragogue cathartics, diuretics and blisters, which at one time were
almost universally employed, are now abandoned ; the tendency is toward
a supporting plan of treatment. As soon as it is discovered that peri-
carditis exists, endeavor to determine its cause, and, if possible, remove it ;
if this is not possible, endeavor to counteract it. If the pericarditis is due
to uraemia, employ those means which favor elimination of urea. If it ac-
companies articular rheumatism it must be treated as a rheumatic affection.
In those acute diseases marked by great depression the occurrence of peri-
carditis is an indication for an increase in stimulants. Under all such cir-
cumstances, especially in connection with septic and pysemic developments,
supporting measures are early called for. The favorite local applications
in its early stage are hot anodyne poultices over the precordial space in con-
nection with the internal administration of opium ; absolute rest in bed
must be enjoined. If the pulse exhibits dicrotism, stimulants in small
quantities may be given.
Opium is the most valuable internal agent. It should never be given in
large doses, but only in sufficient quantities to relieve pain and arrest or al-
lay an irritable action of the heart. The largest doses administered should
be given at night, in order that the patient may secure quiet sleep ; the
heart is more liable to become irritable at night, and the patient usually be-
comes more restless. Great care should be exercised in the administration
of opium ; it should never be carried to semi-narcotism. Chloral is thought
to be equally good, since it does not interfere with secretions ; my expe-
rience is against its use.
The means usually employed for removal of the fluid are hydragogue
cathartics, diuretics and blisters. I am convinced that this plan of treat-
ment will not hasten, but will rather delay the removal of the fluid. Ex-
perience teaches that pericarditis is an inflammation which occurs in the
weak and feeble, and not in the strong and vigorous ; it is met with among
CHRONIC PERICARDITIS. 4:39
the young rather than in healthy persons in the prime of life. In almost
all instances it is associated with those diseases that are especially marked
by a loss of vitality ; consequently all measures that have a tendency to
depress the patient are to be avoided. Blisters are apt to accelerate the
heart's action and should never be applied directly over the precordial
space ; leeches are less painful and more efiBcacious, and may be applied
over the precordial space. The same general rules which were given as
guides in promoting the absorption of the inflammatory product in pleu-
risy are to be followed in the treatment of pericarditis. Iron, stimulants,
and a highly nutritious and readily digestible diet are the most efficient
remedies. Anything which accelerates the heart's action should be
avoided.
The surface of the chest must be carefully protected from changes in tem-
perature ; any exposure incident to a physical examination of the chest must
be carefully avoided. The Germans advocate cold to the precordia ; it is said
to diminish pain and frequency of the heart's action. They direct that an
ice-bag shall be kept over the precordial space until all evidences of peri-
carditis have disappeared.
During the period of convalescence the patient must be very strictly
guarded, for the walls of the heart are in a weakened condition, and
should not be overtaxed. Everything which will have a tendency to
increase the action of the heart must be carefully avoided. Children
should not be allowed to go up and down stairs or to play with other
children during the period of convalescence. Patients convalescing from
pericarditis must be placed under the very best hygienic conditions for two
or three months after the disappearance of the pericardial symptoms.
Sometimes the symptoms which attend a large fluid effusion become very
urgent, and the question presents itself : — shall aspiration of the pericar-
dium be performed ? It has been claimed that little danger attends its per-
formance, but it should never be rashly undertaken. When it is positively
determined that pus is in the pericardium aspiration should be practised.
When the effusion is sero-fibrinous it must be remembered that the urgent
symptoms, for the relief of which aspiration would be resorted to, are usu-
ally of short duration, and patients rarely die from the pressure produced
by the effusion. Whether aspiration shall be performed under .such cir-
cumstances is a question for most careful consideration.'
CHEOlSriC PEEICAEDITIS.
Chronic pericarditis is rare except as a sequela of acute ; occasionally it
may be sub-acute from its commencement. When, after three or four
weeks, acute pericarditis does not terminate in recovery, it becomes chronic.
In some cases of chronic pericarditis the pericardial sac contains several
pounds of fluid. In others firm adhesions form between the pericardial sur-
' In a monograph by Dr. Roberts, who gives an account of sixty cases with twenty-four recoveries
(forty per cent.), he states that the best points to tap are in the fossa between the ensiform and costal
cartilages on the left side, or in the fiftli left interspace near the junction of the sixth rib with its carti-
lage. In Huidenlang's case 1000 c. c. were withdrawn at two tappings and recovery followed. (Archiv. f.
klin. Med. 24, p. 452.) .
430 DISEASES OP THE HEART.
faces, binding them more or less closely to each other ; mingled with these
adhesions are chalky debris and calcareous plates. The adhesions which
form in acute pericarditis are not regarded as a part of the history of
chronic pericarditis. The fibrous changes of chronic pericarditis only
occur when the sub-pericardial tissue is involved. The heart may then be
encased in a calcareous wall, and a fibrous degeneration of the cardiac
muscles result, which may lead to local aneurismal dilatation.
The Symptoms of chronic pericarditis are those which give evidence of
obstructed circulation with signs of enlargement of the heart — there is dysp-
noea sometimes amounting to orthopnoea and uneasiness or a sense of weight
in the precordial region. In some instances this condition is associated
with attacks of angina pectoris. The heart's action is easily disturbed, and
cardiac palpitation is present on slight physical exertion or mental excite-
ment.
The Physical Signs of chronic pericarditis closely resemble those of eccen-
tric cardiac hypertrophy ; in both cases there is increased dulness in the pre-
cordial region, but in pericarditis the apex-beat is indistinct and is raised
above its normal position ; while in hypertrophy the apex-beat is distinct
and is carried downward and to the left of its normal position. A friction
murmur is usually present even when large quantities of fluid are present.
There is no murmur present in hypertrophy. Bulging sometimes occurs,
and there may be fluctuation when the fluid is large in amount. If the
two surfaces of the pericardium are closely agglutinated, and the pericar-
dium is adherent to the costal pleura, so that firm adhesions are formed
between it and the chest wall, there will be more or less depression of the
precordial region — so-called "systolic depression;" — ^the cardiac impulse
will be permanently displaced upwards, and will be unaltered either by
change of posture or by a full inspiration, and there will be an irregular
Jogging motion of the heart during both its systole and diastole. Some-
times there is a depression over the scrobiculus cordis caused by adhesion
of the two layers of the pericardium to each other and to the pleura cover-
ing the diaphragm, and concomitant adhesion of the diaphragm with the
liver.
Although the Diagnosis of chronic pericarditis is always difficult and its
existence is rarely, if ever, positively determined unless there is a large
amount of fluid effusion in the pericardial sac, still, if the symptoms and
physical signs already detailed follow an attack of acute pericarditis, there
is presumptive evidence of its existence.
The Prognosis in this affection, as regards complete recovery, is always
unfavorable, and when it accompanies degeneration of the cardiac walls
and valvular insufficiency life will not be prolonged.
The Treatment consists in limiting physical exercise so as not to overtax
the embarrassed heart ; at the same time to furnish the patient with a
most nutritious but non-stimulating diet, and to administer daily some
preparation of iron. Ccncerning paracentesis, the same rules apply here
as in acute pericarditis. Perhaps the operation will be resorted to in
chronic cases with better success than in acute.
ACUTE EXUDATIVE ENDOCARDITIS.
431
Ein)OOAKDITIS,
Endocarditis is an Inflammation of the endocardium. I shall describe
it under three heads : —
I. Acute Exudative Endocarditis.
11. Ulcerative Endocarditis.
III. Interstitial Endocarditis.
In most instances this disease depends upon a constitutional dyscrasia,
characterized by alterations in the vital, physical, or chemical properties
of the blood. Etiologically, all the different varieties are closely con-
nected ; clinically and pathologically, they are distinct. They cannot be
classified as acute and chronic in the ordinary acceptation of the terms, for
some cases are at no time acute, and even in so-called chronic endocarditis
the changes are but an advanced stage of an acute process.
So-called acute endocarditis is accompanied by a fibro-cellular exudation
into the substance of and underneath the endocardium, causing elevations
of its surface. A better term for this variety is "acute exudative endo-
carditis," it being understood that no exudation occurs on its free surface,
but underneath it. This form may be entirely recovered from, or may
lead to interstitial formative changes.
Acute exudative endocarditis may be
stamped with an ulcerative process,
the result of septic infection, giving
rise to changes known as acute ulcera-
tive endocarditis.
Chronic or interstitial endocarditis
is the form in which the endocardial
and myocardial tissues are involved in
sclerotic or cirrhotic changes, giving /J
rise to the many varieties of valvular
disease. It may be a sequela of the
acute exudative variety, or the inflam-
mation may have been interstitial from
its commencement, for the valvular Fis. 90.
changes due to this form are often ^ -i'^^i^s «i^T>?ri.l^'^T^„^r£?.lJ^^
found in those who never have had a, a
either acute articular rheumatism, or
acute exudative endocarditis, but who are subjects of chronic rheumatism,
syphilis, or gout.
ACUTE EXUDATIVE ENDOCARDITIS
This variety is met with most frequently in connection with acute articu-
lar rheumatism. In adults, the left, and in intra-uterine life the right,
heart is oftenest affected. The process rarely extends beyond the valves
and valvular orifices ; but it may involve the whole or any part of the ven-
tricular or auricular portions of the endocardium.
theritic Endocarditis.
Thickening of the Endocardium on the free
harder of the mitral valve, imth papillary
elevatiom surmounted by fibrinous deposit.
432
DISEASES OP THE HEAET.
Morbid Anatomy. — The endocardium becomes infiltrated with cells, the
process beginning in the layer of flat cells. The new formative cells are
developed in the layer underneath the endocardium. This hyperplasia is
accompanied by softening of the intercellular structure, which is soon de-
stroyed. The endothelial elements take part in the process. The masses
of new cells push out the endocardium, and papillary elevations are formed.
These conical elevations are sur-
rounded in the deeper layers of
the endocardium by a zone of pro-
liferation which is never distinctly
limited, but which exhibits pro-
gressive hyperplasia from the
periphery toward the centre. All
these changes may have taken place
in non-vascular tissue. Where the
capillaries are most numerous a
punctate or aborescent vascularity
is seen, after which the part be-
comes opaque. There is no exu-
dation upon the papillary eleva-
tions, but fibrin from the blood is
deposited on them as on foreign
bodies. These coagula are most
numerous on the surface opposed
to the blood current. They have
a cauliflower-like, bulbous ex-
tremity connected by a constricted
neck with a firm, hard base which
is continuous with the subjacent
tissue. Each mass is covered by a thin hyaline layer. At first these vege-
tations are so small and numerous that the membrane has a granular look.
Later, they enlarge, sometimes to the size of a pea, and have a conical or
raspberry-like shape. They are arranged
on the borders of the aortic valve near
the edge, their seat being determined by
the limit of the vascular net-work. The
bands of tissue passing from the attached
valvular border to the corpus Arantii in
the centre show the granulations most
distinctly. Near the insertion of the
tendons upon the auricular surface of the
mitral valve are irregular wreaths of vege-
tations enclosing attachments of the
chordse tendineae. Friction of the coagula
upon them may excite the vegetations or
of endocarditis at points remote from
the valves. The chordae tendineae may adhere to one another. From
Fig. 91.
Drawing from the previous case showing simUar changes
upoij the Aortic Valves.
A, A. Aortic Valves showing papillae, and fibrimms de-
posit.
Vertical Section of an Aortic Valve in Acute
Endocarditis.
A. Endocardium.
B. Papillary elevation.
C. Fibrinous deposit, x 60.
ACUTE EXUDATIVE ENDOCARDITIS. 433
these adhesions stenosis may result, by the flaps becoming agglutinated
to each other, or regurgitation by their adhering to the heart-walls. As
a result of these changes, new vessels appear in the substance of the mitral
valve or existing ones become more apparent. The more rajiid the course,
the more marked are these changes. The largest vegetations are found
on the valves. Young vegetations are translucent, soft and friable.
UlcerativeEndocarditis. — Ulcerative endocarditis occurs in those diseases
where there is great vital depression. It is oftenest met with in pyaemia,
puerperal fever, scarlatina and diphtheria, ; it has been called "septic,"
"diphtheritic," and " infectious" endocarditis. The margins of the valves
are irregular, but well defined. The edges are swollen and thick, and their
floor is infiltrated with pus. In some cases the apices of the vegetations
which are formed are swept off by the blood-current, and an ulcerated sur-
face is left. If their removal causes great loss of substance, perforation of
the valve may occur. These perforations are sometimes closed or hidden
by a fibrinous exudation. It is claimed that the ulceration or suppuration
of these elevations is the result of granular degeneration ; micrococci and
bacteria are often found in ulcerative endocarditis of a septic or diphtheritic
origin, and have given to it the name of "mycosis endocardii.''^ ' It is more
probable that these minute organisms are developed by the aid of the ulcera-
tive process, rather than that they are the cause of it.
The valvular ulcerations in this form of endocarditis may give rise to
various lesions. If small masses are detached from the cardiac orifices, ei-
ther from deposits on the valves or from ulcerations, and enter the blood-
current, they originate morbid processes in the organs to which they are
carried. It is important to distinguish between the results produced by
displacements into the blood-current of large masses, and those arising from
the entrance of molecular fragments. Masses from the vegetations, or from
the ulcerated valves in ulcerative endocarditis, being stamped with a septic
element, lead to the development of suppurative infarctions in different or-
gans. The size and site of the emboli are important ; they may be so large
as to obstruct vessels of the largest size, as the external iliac. When arte-
ries in the lungs are thus plugged, the result is generally an ischmmia, often
terminating in gangrene. Capillary embolism may occur in a number of
organs simultaneously.
Wlien the cutaneous capillaries are obstructed, ecchymotic spots are
formed, followed by cellulitis. If in cerebral embolism the occluded ves-
sel is large, instantaneous hemiplegia and secondary softening will result ;
if it is very small, softening develops without evidence of obstructed circu-
lation. Infarctions and suppuration of the spleen (sjolenitis, so-called) are
not uncommon. The kidneys may be similarly affected. Septic phenom-
ena are very important. When typhoid symptoms, deep jaundice, and
symptomatic intermittent fever are associated with endocarditis, it estab-
lishes its " ulcerative " character. When the inflammation develops rapidly,
the valves soften, lose their resisting joower, and in time become stretched,,
bulged or torn by the blood- current. A rupture of the mitral valves will
' Jaccoud. Klebs.
28
434 DISEASES OP THE HEART.
open into the auricular, and tliat of the aortic into the yentricular
cavity.
If the blood penetrates a rent in the flap of the valves, the endocardium
is puifed out and a "valvular aneurism" is formed; round or funnel-
shaped aneurismal sacs may project from the valves ; the bottom of one of
these sacs may be perforated, and long, ragged, gray shreds covered vs^ith
fibrin may hang into the ventricular cavity. When the ulceration is situ-
ated in the ventricular wall, the pressure of the blood may bulge out the
heart- wall and give rise to ''partial cardiac aneurism." Communication
between the various heart cavities may thus be established. The results of
both varieties of acute endocarditis will be considered under the head of
''interstitial endocarditis."
Etiology. — Acute exudative endocarditis is rarely if ever idiopathic. It
is closely connected with those diseases and dyscrasiae in which the blood is
altered either in the relative proportion of its constituents or in its phys-
iological elements. Endocarditis is so frequently associated with acute
articular rheumatism, that they are often described as one disease. It is
said to occur in fifty per cent, of all cases, but the statistics of Bellevue
Hospital show that it complicates only thirty- three and one-third per cent.
of the cases. The irritation caused by blood, the salts of which are
changed, or which contains excrementitious products, or a specific poison,
is shown most markedly upon the valvular surface of the endocardium ;
and for this reason the parts most exposed to friction are those which first
and most extensively exhibit its pathological changes,' There is no disease
characterized by a morbid condition of the blood in which endocarditis may
not occur : thus it often complicates the essential fevers, the exanthemata,
diphtheria, Bright's disease, and syphilis. When an individual who is
already suffering from valvular disease of the heart is attacked with acute
rheumatism, the liability to acute endocarditis is much increased. Even
when rheumatism and chorea are absent, acute endocarditis is liable to
occur when valvular disease exists.
Some regard myocarditis, pericarditis, pleurisy and pneumonia as capa-
ble of exciting endocarditis by the extension of the inflammatory process
from the surface of the heart ; this is questionable, but that it can result
from traumatism is possible.^
Wunderlich ranks measles next to rheumatism as a cause of endocarditis.
We must remember that not every " blowing " murmur is indicative of
endocarditis. Bamberger and Niemeyer think that the excited and irregu-
lar action of the heart in children, by inducing irregular tension of the
valves, will bring about a "blowing" sound during acute rheumatism
without endocarditis.
Acute ulcerative endocarditis is met with in pyaemia, puerperal fever,
scarlatina, diphtheria, and it may occur secondarily to a septic inflammatory
process located in any part of the body — " septic endocarditis," It may
1 Charcot records a large number of observations in which endocarditis was developed in patients with
chronic rheumatism, and in which it never assumed an acute form. It thus seems evident that organic
valvular lesions from endocarditis may arise during chronic as well as acute articular rheumatism.
* Bamberger records two traumatic cases.
ACUTE EXUJ)ATiVE EJSJ J)OCATlDITIS. 435
also appear without any obvious cause, — spontaneously, — or in connection
with some siJecific form of inflammatory disease, as croupous pneumonia.
Wicks calls it then arterial pycemia.
Symptoms. — The subjective symptoms of acute exudative endocarditis are
more obscure than those of any other cardiac disease. They are few,
ill-defined, and without any regular order of development ; when the heart-
muscle is not involved the disease cannot be appreciated by a single
rational symptom, for the urgency of the symptoms of the diseases in which
it occurs often masks the few symptoms which attend its development.
But when it is extensive and the muscular tissue of the heart is involved,
palpitation and a sense of discomfort in the precordial region are present,
and there may be attendant dyspnoea and decubitus on the left side. Sel-
dom is the palpitation appreciable to the physician, for the heart may beat
with force and be tumultuous and yet the pulse remain unchanged. At
first the pulse is strong and forcible ; later it becomes rapid, small, feeble,
and irregular ; it is frequent from the onset. As a rule, the force of the
pulse does not correspond to the cardiac activity, for as the heart-muscle
becomes involved, its propelling power is diminished and the pulse becomes
feeble, compressible and sometimes dicrotic. The respirations are accele-
rated and sometimes labored ; there may be paroxysmal dyspnoea, the face
may be flushed, or it may be dusky, pallid, ashy-gray, or even cyanotic.
Sleeplessness and' nocturnal delirium are rare. When the muscular tissue
of the heart is extensively involved, nausea, vomiting, giddiness and syn-
cope may be present, yet slight pain or a ''tightness" is not an infre-
quent symptom when endocarditis occurs in those who have chronic val-
vular disease. The temperature seldom exceeds 103° F.
When in acute ulcerative endocarditis^ a valve ruptures, a typhoid state
rapidly supervenes. The patient is forced to assume the upright j)os-
ture on account of dyspnoea ; cyanosis is sudden and extreme, and the
symptoms of multi]3le embolism ajDpear. The temperature rises to 106°-
107° F. There is jaundice and frequent rigors which with the parox-
ysms of fever simulate the icteric form, of malarial fever. The spleen
becomes enlarged and tender ; the urine is scanty, dark colored, albumi-
nous, and of high specific gravity. Delirium and coma occur in severe cases.
Some cases are marked by nausea, vomiting, and diarrhoea. The frequency
with which this form of endocarditis is associated with pneumonia suggests
the presence of a blood poison of great intensity. Although it rarely occurs
except with septic diseases, yet it may occur late in severe forms of rheu-
matic and traumatic endocarditis or when there has been pre-existing sup-
purative bone-disease.
The symptoms of embolism, are due to the arrest of a detached portion of
the endocardium in some artery. The spleen is much oftener the seat of
such embolisms than the kidney or brain. The occurrence of hemiplegia
with aphasia or of severe cerebral disturbance during the course of an en-
docarditis is indicative of cerebral embolism.
Physical Signs. — Inspection sometimes shows the area of cardiac impulse
greater than normal ; the impulse is irregular and often tumultuous.
436 DISEASES OF THE HEART.
Later the apex-beat and the impulse grow more distinct, but never so sud-
denly or so markedly as in pericarditis. In children the vessels of the neck
may exhibit venous stasis.
Palpation. — At the onset of the disease, the cardiac impulse is more
forceful than normal, and the heart's action is frequently irregular. Some-
times the heart thumps violently against the chest- walls. The force of the
cardiac impulse varies from day to day, being stronger when pain is present.
If, during the disease, there is no increase in the force of the apex-beat, we
infer that the muscular power of the heart is deficient. When acute en-
docarditis supervenes upon long-standing valvular disease, there is alter-
nate increase and diminution in the area and force of the impulse. When
the heart-walls are weakened by myocarditis, or when the endocarditis is it-
self very extensive, the force of the apex-beat is diminished ; an endocar-
dial thrill is often present.
Percussion. — The area of cardiac dulness is normal unless changes at
the valvular orifices retard the outflow of blood from the lungs, and then
the cavities in the right heart become engorged and the area of dulness
will be abnormally increased. But this increase is always slight, except in
those cases where sudden and extreme distention of the heart cavities re-
sults from the presence of masses of fibrin. Extensive myo- or endo-car-
dial inflammation may so weaken the heart that dilatation results, and
then percussion will show marked increase in the area of cardiac dulness.
Auscultation reveals a murmur, or murmurs, over the various cardiac ori-
fices. The fact that valvular disease may have pre-existed makes it impor-
tant to carefully examine the heart at the first visit to one suffering with
acute rheumatism, chorea, Bright's, etc., etc. When hyj)ertrophy and old
valvular disease of the heart exist, the advent of an attack of acute exu-
dative endocarditis generally passes unrecognized and even its presence is
often undetermined. The most important constant sign of endocarditis is
2i systolic murmur, heard with greatest intensity at the apex ; this soft, blow-
ing, or " bellows " murmur may be ventricular or valvular. In all cases,
it is due to roughening or tMchening of the endocardium. It often changes
its point of maximum intensity during the acute period of the disease. It
is developed early, and when one is on the lookout for endocarditis this
will be the first evidence of it. In some instances no murmur is at any
time present.
A mitral murmur alone occurs in fifty per cent, of cases of rheumatic
endocarditis ; it is developed early and is preceded by j^rolongation of the
first sound, a " transition " sound, so to speak, feeble and wavering in char-
acter, extending over the slight interval which normally exists between the
first and second sounds. Other changes, not murmurs, but which precede
them in many cases— are loud, ringing normal sounds ;— muffled first
sound ; — feeble first, intensified second sound ;— doubling of the first sound ;
— "roughening" of the first sound ;— and a "humming" over the right
heart. Complete absence of the heart sounds is a rare but possible ante-
cedent of an endocardial murmur. A mitral murmur, in acute endocar-
ditis, is usually audible over a limited area. It is the exception to hear it
ACUTE EXUDATIVE ENDOCARDITIS. 437
both in front and at the back ; very frequently it is heard most distinctly
over the stom;ich. Wlien the joulmonary circulation is greatly obstructed,
it causes an extra strain on the pulmonary valves and then the second
sound will be accentuated, while the first j^ulmonic sound may be feeble or
absent. A subdued or absent sound shows tension of the artery. Eedu-
plication of the second sound in mitral endocarditis is probably due to the
difference in time occupied by the ventricles in emptying themselves.
A tricuspid murmur occurs in fifty per cent, of the cases of acute mitral
endocarditis : o, pulmonic murmur in about one-third of the cases. They
are superficial and " scratchy" in character, and indicate a relaxed condi-
tion of the vessels and a thin state of the blood. They are never perma-
nent. Mitral endocarditis is accompanied by aortic murmurs in about
sixteen per cent, of the cases, and these murmurs are usually soft and
blowing, but maybe "musical," ''whistling," or " twangy."
In aortic endocarditis the second sound is usually lost over the carotids.
In about twelve per cent, of all cases of acute (rheumatic) endocarditis a
regurgitant murmur will be heard over the tricuspid orifice. Tricusj)id
murmurs are present in fifty per cent, of all cases of recent mitral mur-
murs, in forty per cent, of recent aortic murmurs, and in twenty-five per
cent, of mifcro-aortic murmurs. They are due to an increase in the slight
(normal) insufficiency of the tricuspid valves. Such murmurs are of short
duration, vibrating in character, and heard over the right ventricle. In
children aortic endocarditis is rare ; at this period obstruction at, and re-
gurgitation through, the mitral orifice commonly occur together.
DifFerential Diagnosis. — Acute exudative endocarditis may be mistaken
for pericarditis, and its murmur may be mistaken for that produced by
aortitis or for those friction murmurs that develop during fevers. The
friction-sounds oi pericarditis are superficial and limited to the precordial
space, while those of endocarditis are distant, and each murmur will have
its area of diffusion beyond the precordial space. A pericardial sound is
distinctly a friction, creaking, or rubbing sound, and it has a "to-and-
fro " character, while that of endocarditis is soft and blowing. Endocar-
dial murmurs accompany the heart sounds, while pericardial friction
sounds are not rhythmical with the heart-sounds. The intensity of a peri-
cardial sound is increased when the patient bends forward, at the end of
a full inspiration, or when the stethoscope is pressed firmly over the pre-
cordial region, and in the last instance it becomes "grazing" and "rub-
bing " in character. As soon as effusion occurs in pericarditis, alteration
in the. character of the pulse, increase in the area of precordial dulness, and
the disappearance of adventitious sounds will decide the diagnosis.
Aortitis has many of the symptoms of endocarditis, but in addition the
pulse is more rapid, the respirations are more hurried, and pain is present
in the precordial region, shooting down the spine and increased by motion.
Aortitis is often accompanied by cutaneous hypersesthesia. Acute aortitis
is very rare.'
The functional murmurs which occur in fevers are usually heard only
1 Lebert and Rindfleisch doubt its existence.
438 DISEASES OF THE HEART.
at the base of the heart ; while those of endocarditis are most frequent and
dibiinct at the apex. There are no signs of obstruction present with fe-
brile murmurs, while they are frequent with endocarditis
It is difficult to tell whether a murmur is of old or recent origin. If,
during an attack of rheumatism, a murmur is developed under daily exam-
ination, it indicates acute exudative endocarditis. If a murmur exists
at the first examination, systolic, soft, blowing, and unaccompanied by car-
diac hypertrophy, there is reason to believe that it is due to an acute
endocardial inflammation ; but should it be rough, diastolic, and accom-
panied by cardiac hypertrophy, ,it is probably not due to acute endo-
carditis.
Prognosis. — Acute exudative endocarditis is rarely a direct cause of
death, and is seldom completely recovered from. Acute mitral endocar-
ditis ends in permanent valvular disease in twenty-five per cent, of the
cases. The prognosis is rendered unfavorable when the signs of embolism
or metastasis occur. Sudden splenic enlargement with tenderness, albu-
minuria, or hemiplegia, when accompanied by the physical signs of acute
insufficiency or perforation of a valve, with cyanosis, dyspnoea and disturb-
ance of the cardiac rhythm will render the prognosis bad. All these symp-
toms indicate acute ulcerative endocarditis, so that when the symptoms of
this disease appear during the course of septic diseases, the liability to its oc-
currence must be borne in mind. Typhoid symptoms in acute endocarditis,
render the prognosis unfavorable. In children, bronchitis, lobular pneu-
monia, and intercurrent diarrhoea may cause death. It may result from
acute insufficiency of the heart.
In cardiac aneurism death may result from rupture of the sac, apo-
plexy, or from secondary disease in organs.
Treatment. — The treatment of both varieties of acute endocarditis must
be determined by the conditions under which they occur. The patient
must have absolute rest in bed, in a room whose temperature is never
below 70° to 75° F. The chest should be covered with flannel, and during
the physical examination it should be exposed as little as possible. Some
claim that an ice-bag over the heart during the acute period will arrest or
limit the inflammation, but my own experience does not sustain this state-
ment. In rheumatic endocarditis anti-rheumatic remedies are indicated.
The joints must be kept absolutely at rest in the most comfortable position
and the pain relieved. If the urine is kept alkaline, the liability to endo-
carditis is diminished. To insure rest small doses of opium may be given,
but opium cannot be administered as freely as in pericarditis. The pa-
tient's strength must be sustained by the judicious use of concentrated
nutriment with some preparation of iron.
"When endocarditis, accompanied by typhoid symptoms, occurs with
septic lesions, or when it is of the "ulcerative" variety, alcohol, quinine
and iron must be freely administered ; when it complicates Brighi,'s dis-
ease the rapid elimination of urea must be established. The pain over the
precordium is often relieved by the application of a few leeches. The
(internal) use of mercury, with the external application of blue ointment
INTERSTITIAL ENDOCARDITIS. 439
to "lessen the plasticity of the blood," and even the use of iodide of
potassium — "for the absorption of the fibrinous exudation" — are harmful,
and the theory of their use has no foundation.
ESTTEESTITIAL ENDOCARDITIS.
Kreizing first traced the relationshij) between chronic valvular diseases of
the heart and interstitial endocarditis.
Morbid Anatomy. — Interstitial (or chronic) endocarditis may be a sequela
of the acute, or it may be interstitial from its commencement, and be so
insidiously evolved as to escaj)e notice. Sometimes its lesions are con-
fined to the edges or base of the valves ; at others the entire valve may be
involved.
The affected valves may be thichened, indurated, contracted, adherent,
or degenerated. It is more closely allied to rheumatism, gout, and chronic
interstitial changes in other organs than either of the other varieties ;
no part of the endocardium is exempt from interstitial changes, but the
endocardium over the valves and that at the apex of the left ventricle are
its favorite sites. The mitral valves may become three or four times thicker
than normal. Sometimes their functional activity is unaffected even after
they have undergone extensive ]3athological changes. White, thickened,
oi^aque spots, the results of interstitial endocarditis, are often found irregu-
larly scattered over the internal wall of the heart cavities. When vegeta-
tations are developed in interstitial endocarditis, they differ from those of
the acute form, for they are firmer and less prominent, and rest upon an
indurated base. In, and u.nderneath, the endocardium there is tissue-
increase, and fibrin is deposited on any prominence of the endocardium.
These deposits are of various forms, and may extend for one-half an inch
or more into adjacent vessels or cavities. They are usually globular or
wart-like in form, and are situated on the ventricular surface of the aortic,
and upon the auricular surface of the mitral and tricuspid valves.
A microscopical examination of a cross section of an indurated valve
shows flat cells arranged in irregular layers, having between them a fibrinous
material, which has in it, here and there, a few elastic fibres. The new
formation always originates in the layer of flat cells. These changes are
best marked in the fibrous zone of the valvular orifices, upon the surfaces of
the valves, and in the chordae tendinese. After a time the new tissue be-
comes organized, and contracts, and this contraction is progressive. Gradu-
ally the rigid valves, whose edges are rounded and hard, are drawn together
toward their base, and thus assume a puckered appearance. Similar proc-
esses in the chordae tendinese cause them to hypertrophy, become rigid and
shortened. In this way the valves are diminished in depth, and sometimes
their free edges become approximated to the cardiac walls, so, that exten-
sive valvular insufficiency is the result. This does not always happen ; for
a thickened cartilaginous valve may have so much fibrinous or papillary
groAvth upon it, that the inward current is obstructed and stenosis results
without insufficiency. As this thickening and rigidity increase the mobility
440 DISEASES OF THE HEART.
of the valvular flaps is diminished, and adhesions occur between their
edges, beginning at their base and extending toward their apex. So ad-
herent may they become that all evidences of a valvular outline is lost and
a fibrous diaphragm is stretched across the orifice, having only a small slit
at its centre, looking and feeling like a button- hole, hence the term
" hutton-hole slit." The mitral opening, which normally will admit the
ends of three fingers, may be so narrowed that the end of the little finger
will scarcely pass through it, and the aortic opening may not even admit
a small quill. These retractions and adhesions cause the mitral valves
with their columns and cords, to assume the form of a perforated cone.
Long gelatinous vegetations on the aortic valve sometimes form adhesions
with the aortic walls, and thus a sudden and extensive regurgitation is in-
duced. Insufficiency and stenosis are often found at the same valvular
orifice as the result of the valvular thickening, adhesion, and retraction.
Such changes at the aortic orifice usually occur after middle life, and cause
more thickening, adhesion, and retraction than those at the mitral valve.
In children and early adalt life, the mitral valves are the most frequent seat
of interstitial endocarditis. The tendency of this lowly organized tissue is
to undergo fatty and calcareous changes. The minute patches of fatty de-
generation in the imperfectly organized tissue underneath the endocardium
sometimes form atheromatous masses, containing more or less granular
debris. The endocardium over these patches may be destroyed, or they
may soften, ulcerate, and cause extensive destruction of the valves.
A valvular aneurism may form in the same manner as has been described
in ulcerative endocarditis. The formation of calcareous granules and
plates is a very frequent termination of interstitial endocarditis. The
aortic orifice is the most frequent seat of these calcareous degenerations.
So extensive may this process become that little beads of chalky material
are seen studding the free edges of the valve and even extending into the
cardiac cavities.
"When interstitial endocarditis has its seat in the endocardium of the
heart cavities, it will undergo changes similar to those of the valves, and
the muscular walls of the heart will become the seat of interstitial changes.
As a result the walls of the heart become thin and less resistant than nor-
mal, and depressions occur on its inner surface. The process is a fibrous
overgrowth, which occurs in spots varying in size from one-half an inch to
one inch in diameter. When it extends through the entire heart-wall, the
columns and cords may be so shortened as to cause valvular insufficiency.
If the cardiac walls yield to the internal blood pressure, a well-defined
pouch is produced. This condition is called '' aneurism of the heart," and
is usually situated at the apex of the left ventricle ; the pouch may be as
large as the closed fist, and may communicate with the ventricle by a fun-
nel-shaped or ring-like aperture. The walls of the sac are firm and rigid,
the internal surface is generally smooth, but it may be irregular, in which
case clots adhere to its walls. Cardiac muscular fibres are found in the
walls of the aneurismal sac. Aneurisms at the base and in the interven-
tricular septum may result from the extension of a valvular aneurism.
CAKDIAC MURMURS. 441
These may destroy the septum and establish a communication between the
two ventricles.
Etiology.— As has already been stated, the majority of cases of interstitial
endocarditis are the sequelae of the acute, and the affection is more fre-
quently associated with articular rheumatism than with any other disease.
When it occurs with gout, chronic rheumatism, in alcohol drinkers, or
in the aged, it is interstitial from its onset.
Symptoms. — There are no positive subjective symptoms of interstitial
endocarditis. There may be palpitation and a sense of uneasiness, some-
times amounting to pain, in the pericardium. There may be irregularity
in the action of the heart ; but all of these when taken together are not
sufficient for a diagnosis. It can only be determined by the changes it pro-
duces in the valves and valvular orifices, causing abnormal changes in the
heart-sounds.
The physical signs s^xidi differential diagnosis are those of the murmurs
or valvular disease induced by the chronic interstitial process, and will be
next considered.
The prognosis in interstitial endocarditis will depend upon the seat and
the extent of the valvular lesions which it produces.
CAEDIAC MURMURS AND THEIR RELATIOJSTS TO VALVULAR DISEASE
OF THE HEART.
A cardiac murmur is an adventitious or abnormal sound produced within
the heart or blood-vessels, either by obstruction to the blood-current, an
abnormal direction of the blood-current, or a change in the blood constit-
uents. The study of cardiac murmurs dates from Laennec's discovery of
auscultation, although forms of valvular diseases had been described by
Vieussens as early as 1716. Aortic disease was the form first brought to
notice, from the changes it induced in the radial pulse ; ' John Hunter,
Laennec, and Allan Burns were among the pioneers in this branch of in-
vestigation.''
Corvisart was the first to mention the importance of what we call to-day
the " purring thrill ." ^
Many advocate the " tension theory,^' viz., that an increase in the ten-
1 In Virchow's " Handbuch " Meckel's ess^y of 1756 is given as the first paper on endocardial disease.—
Art. by Friedrichs.
2 The last named supposes " that a reflux current can produce a hissing noise, something like what is
described as audible palpitation in some diseases of tlie heart," 1809.
3 He said : "It probably came from a difficulty experienced by the blood hi going through an orifice
disproportionate to the amount of fluid." Laennec regarded murmurs or '■'■bruits" as due to spasmodic
contraction of the heart or arteries. Corrigan said that murmurs are "the result of the development of
currents — the intrinsic collision of the moving liquid." In 1842 Gendrin established the '■'■friction theory "
^bruits de frottements endocardiaques), and first called attention to the fact that alteration in the con-
stituents of the blood will produce murmurs audible in arteries of medium calibre. Bouillaud describes
a murmur as an " exnggeration of the normal bruit caused by blood friction airainst the segments of the
heart." Chauveau states that a tjrnit de souffle is produced by the vibration of a " reine fiuide " always
formed when blood rushes throui^h a part of the circulatory system actually or relatively dilated. This
veine fluidehas its best development in aiicemia (then called brnit de diable), for the jugular veins do not
collapse and the volume of blood in anaemia is diminished. Chauveau's theory is applicable to anaemic
murmurs, but not to other cardiac murmurs. It is claimed that valve murmurs are produced by collision
of the blood particles against one another ; or that either the liquid alone or the liquids and solids con-
jointly may develop murmurs.
442
DISEASES OF THE HEART.
sion and force can so exaggerate a normal sound as to produce a murmur.
Tins theory has clinical foundation ; for valve lesions may exist, and the
blood current and propulsive force may be so feeble that there is no au-
dible murmur. Spasm of the papillary muscles and chordae tendinese and
vi^eakening of these structures by fatty degeneration are by some regarded
as causes of temporary murmurs.' The same vibration that produces a
murmur may produce an endocardial thrill, called the ''purring thrill."
Far more important than the loudness, pitch or quality of a murmur are
its rhythm, point of maximum intensity, and area of diffusion, all of
which will be considered in connection with the physical signs of each lesion.
At the end of a cardiac diastole all the heart cavities are filling ; just
before the cardiac systole, blood is forced from the lungs and cavse through
the auricles and ventricles, while the mitral and tricuspid valves are pressed
against the ventricular walls, thus offering no obstruction to the blood
current. Should any obstruction exist at either of the auriculo-ventricular
orifices, the blood while passing through the opening will impinge on such
obstruction and cause a presystolic murmur. During a cardiac systole,
the filled ventricles contract and blood is thrown through the arterial
openings, the flaps of whose yalves are pressed against the walls of the
vessels so that no obstruction is offered to the outgoing current. At the
same instant, the auriculo-yentricular valves close their orifices, so that
blood may not flow back into the
auricles. If the semilunar valves
obstruct the outgoing current, or
if the mitral or tricuspid valves do
not wholly close the auriculo-ven-
tricular orifices, then, in the one
case, the blood-current as it passes
over the obstruction at the semi-
lunar orifices, will produce a sys-
tolic murmur, and in the other a
systolic murmur will be produced
by the backward current through
the abnormal opening at the au-
riculo-ventricular orifices. If the
pulmonary and aortic system —
which are filled at the systole —
have back of them a semilunar
valve that does not completely
close that end of the circuit, the blood will regurgitate into the ventricles
during the period of cardiac rest, so that semilunar incompetence causes
a diastolic murmur.
Fig. 93.
Diagram illustrating the mode of producticm of Car-
diac Murmurs in the Left Heart, with the cmidition
qf the valves and cavities. By svhstituting tlie words
Tri cuspid a.7id Pulmonary for Mitral aiid Aortic, the
diagram will illustrate Murmurs occurring in the
Bight Heart.
1 The factors that determine the character of a murmur— its pitch, quality and intensity— are physical,
as the force with which the jet is propelled, and the physical properties of the media of conveyance ; and
they are the same as those which determine the quality of other sounds.
ENDOCARDIAL MURMURS.
443
ENDOCARDIAL MURMURS.
TIME.
SITUATION.
ORIFICE.
NATURE.
Systolic, 1
Basic.
Aortic.
Obstructive.
2
"
Pulmonary.
"
3
Apical.
Mitral.
Regurgitant.
4
"
Tricuspid.
a
Diastolic, 1
Basic.
Aortic.
"
Presystolic, 1
Apical.
Mitral.
Obstructive.
Pulmonary (diastolic) regurgitant murmurs and tricuspid (presystolic) obstructive mur-
murs are so rare, clinically, that they may be disregarded.
The following is the order of relative frequency of cardiac murmurs :
(1) mitral regurgitation ; (2) aortic obstruction ; (3) aortic regurgita-
tion ; (4) mitral obstruction ; (5) tricuspid regurgitation ; (6) tricuspid
obstruction ; (7) pulmonary obstruction ; and (8) pulmonary regurgita-
tion.
The most frequent combinations of murmurs are : (1) aortic obstruction
and regurgitation ; (3) mitral obstruction and regurgitation ; (3) mitral
obstruction and tricuspid regurgitation ; (4) aortic obstruction and mitral
regurgitation ; (5) double valvular disease at aortic and mitral orifices (four
murmurs).
Having appreciated the existence of a cardiac murmur, it is often very
difficult to determine its rhythm. This difficulty may be lessened by re-
membering that the first sound of the heart is synchronous with the carotid
and radial pulse and the apex-beat, and that it may be wholly replaced by
a systolic murmur ; the second sound is, however, almost always heard, for
the pulmonic and aortic valves are rarely diseased at the same time.
After determining the rhythm, pitch, intensity, and quality of a cardiac
murmur, we next find the point of its maximum intensity. Murmurs
arising at the mitral valve are loudest at the apex of the heart, ov just alove
it ; tricuspid murmurs are loudest over the lower part of the sternum ;
pulmonary murmurs, in the second left intercostal space close to the
sternum, and aortic murmurs in the second right intercostal space at the
edge of the sternum.
Valvular diseases, causing murmurs, consist in a condition of the valves
allowing either of regurgitation or obstruction.
Valvular insufficiency results when extensive retraction, perforation, or
partial detachment of the valves prevents them from completely closing
their respective orifices ; or when the chordge tendinese have been rupt-
ured, or calcareous degeneration has made the valves rigid, the backward
current in such conditions giving rise to a regurgitant murmur.
444
DISEASES OF THE HEART.
"When the valves are thickened, retracted, adherent, hypertrophied, or
degenerated, they obstruct the outward current of blood and give rise to
obstructive murmurs.^ Both conditions, viz., stenosis and insufficiency,
are often found co-existing, but
rarely to the same extent. The
lesions which induce these mur-
murs are acute, when they occur
during the course of acute endocar-
ditis, and chronic when they de-
pend upon the presence of some
firm tissue, such as connective,
fibroid, calcareous, or atheromatous
tissue, which alters the form and
impairs the function of the valves.
Both the above varieties may pro-
duce the same murmurs.
Since physical signs are here the
most important factors in diagnosis,
the normal (physical) relation of
the heart must be borne in mind:
the apex of the heart is normally
felt between the fifth and sixth
ribs on the left side, about two
inches below the nipple and one
inch to its sternal side. The highest part of the base of the heart is on a
level with the third costal cartilage. The tricuspid orifice is situated at
the junction of the fourth left costal cartilage with the sternum. The
mitral orifice is to the left of the tricuspid, immediately behind the left
border of the sternum, at the junction of the third costal cartilage with
that bone. The aortic orifice is one-half an inch lower than and to the
right of the pulmonary orifice, behind the sternum on a level with the third
interspace. The tricuspid orifice is the most superficial, then the pulmonary,
next the aortic, and deepest of all the mitral. Eanged from above down-
wards, the pulmonary orifice comes first, then the aortic, then the mitral,
lastly the tricuspid.
Fig. 94.
Diagram showing the Areas of Cardiac Murmurs.
A. Area of Aortic Murmurs; M. 3Iitral ; T. Tri-
cuspid ; P. Pulmonary.
AORTIC OBSTEUCTION, OE STENOSIS.
This is a common cardiac lesion, and is always accompanied by more or
less hypertrophy of the left ventricle.
Morbid Anatomy. — The valves will be found to present some or all of the
changes described in the history of interstitial endocarditis, together with
degenerative changes due to atheromatous, calcareous, fibroid, fatty, or con-
nective-tissue metamorphosis ; they may be covered with thick, warty,
irregular excrescences, that cause loud murmurs and yet do not seriously
1 Some call obstructive murmurs direct ; and regurgitant murmurs indii'ect, from the current that causes
the sound.
AORTIC OBSTRUCTION, OR STENOSIS.
445
Fig. 95.
Vegetations on the Aortic Valves giving
rise to Aortic Obstruction.
obstruct the out-going blood-current. Or the aortic orifice may be almost
completely occluded, and then the extent
of the lesion is measured more by the re-
sulting hypertrophy and its effects on the
systemic circulation, than by the loudness
or harshness of the murmur. The A^alves
are often so rigid that they cannot be
pressed back, and then they present greater
obstruction to the outgoing current than
when vegetations exist ; as the result of
adhesions, the valves may become fused
into a mass, so that they project into the
blood-stream in the form of a funnel, ir-
regular in shape and studded with calcare-
ous nodules. The line of attachment of
the valves to the aorta frequently becomes
obliterated.
Aortic stenosis is frequently accompanied
by atheromatous changes in the aorta, called "Arteritis deformans." As
a result of aortic stenosis, hypertrophy of the left ventricle occurs, which is
gradual in its development and called ''compensatory" hypertrophy, be-
cause it is due to the increased force required to propel the blood through
the constricted orifice. Mitral insufficiency is apt to occur later, either
from extension of the inflammation from the aortic valves, or from forcible
pressure of blood upon the ventricular surface of the mitral flaps. Slight
thickening and roughening of the aortic valves lead to no serious
results.
Etiology. — Aortic stenosis is most frequently met in middle and ad-
vanced life ; the mean age. being forty-seven years, and the extreme limits
twenty to sixty. It is occasionally met with in children under two years
of age. It may be the result of defective aortic development and perhaps
of imperfect development of the trachea, causing imperfect expansion of
the chest.' Interstitial endocarditis of rheumatic origin is its most fre-
quent cause. Chorea and chronic Bright's disease may cause it. Atheroma
or arteritis deformans extending to the valves sometimes gives rise to it.
Increased aortic tension indirectly causes aortic stenosis.^ Men suffer from
aortic stenosis oftener than women, for in them the valves are subject to
greater tension, and hence non-rheumatic aortic valvular disease is common
in men and rare in women. Occupations that involve re^Dcated sudden and
severe muscular effort induce it. In old age, the aortic walls are weak-
ened, and when aortic disease is met with in the young, it is often the
result of premature vascular senility.' Disease of the aortic valves is
1 Guy's Hosp. Reports, S. I., vol. vi., p. 2,35.
2 The coexistence of cardiac valvular disease and cancer is a remarkable coincidence, possibly with a
causal relation.
' Dr. Allbutt says that in Leeds quite young men have aortic valvular disease ; and Dr. Peacock men-
tions sevf.ral cases wliere it has occurred in young girls who have been placed at service before they were
fully developed. Corvisart and Virchow both admit the possibility of syphilis being a cause of aortic
valvular disease, but clinically this is not yet proven.
446 DISEASES OF THE HEART.
oftener non-rheumatic in origin than mitral lesions. It is slower in its
development, and is more frequently met with in advanced life.
Symptoms. — The subjective symptoms of aortic stenosis are rarely well
marked. Although extensive, it may cause no discomfort, for as the ob-
struction increases, compensatory hypertrophy relieves pulmonary pressure ;
but when this no longer compensates for the obstruction, the arteries are
inadequately filled, the left auricle cannot empty itself, and consequently
the pulmonary vessels and the venous system are abnormally full. The
scanty arterial supply causes pallor of the face, and syncope may occur
from cerebral ansemia, but these are late symptoms, not usually appearing
until after the mitral valve has become secondarily involved. The pulse is
normal in frequency, diminished in volume and fulness, and, as a rule,
regular in rhythm, though it may be intermittent, compressible, and
'' jerky " in character. Signs of arterial anasmia usually precede those of
venous engorgement. The sphygmograph gives a slanting or oblique up-
stroke, showing that the influence of percussion is lost, and the tracings
may show considerable sep-
aration between the "percus-
sion " and " tidal " waves.
The pulse is rarely slowed.
There may be slight palpita-
tion and paroxysmal pain in
the chest.
Aortic stenosis is more often
'^^^■^^- associated with cerebral em-
Sphygmographictracing in a case of Aortic Obstruction, with ^ j- ^^ ^j j_
marked separation of the percussion and tidal waves. J
vular lesion, and the splenic
and renal vessels are frequently the seat of emboli. The left middle
cerebral artery is the most common seat of cardiac emboli ; and the left
lower limb is more subject to embolism from aortic valvular disease than
the right. Embolism may be due to small auricular or ventricular clots
that form behind the obstruction ; such clots have occluded the aortic ori-
fice and caused sudden death.'
Physical Signs. — The physical signs of aortic stenosis are usually distinc-
tive and easily appreciated.
Inspection shows the area of cardiac impulse to be abnormally increased.
Very extensive increase of this area is often accompanied by lifting of the
chest over the precordial region.
Palpation. — The impulse is felt to be forcible, and may be accompanied
by a heaving or lifting sensation. The apex is displaced to the left and
slightly downward. An indistinct thrilling sensation is often imparted to
the hand during the systole. This systolic fremissement is nothing more
than an intensified endocardial thrill, and it generally radiates to the ensi-
form process, being most intense in the second right intercostal space.
Percussion. — The area of cardiac dulness increases in proportion to the
displacement of the apex beat to the left.
1 Path. Tran!^., vol. ix., p. 9.
AORTIC OBSTRUCTION", OR STENOSIS. 447
Auscultation. — Aortic obstructive murmurs are loudest and most distinct
at the second right intercostal space and at the sternal insertion of the third
left costal cartilage. They are systolic, and oftener accompany, than replace
the first sound ol the heart. The maximum intensity of this murmur is at
the second sterno-costal articulation of the right side, but it may be heard
with equal intensity over the whole upper part of the sternum, and may be
audible at the xiphoid cartilage. It is always a harsh murmur, heard most
distinctly at the commencement of the systole. In uncomplicated aortic
stenosis, the aortic second sound may be inaudible ; it is always feeble, but
the pulmonic second sound is always audible. The area of diffusion of this
murmur follows the law that a murmur is propagated in the direction of
the blood-current. It is conveyed along the aorta into the carotids, and
one of its characteristics is that it is heard in the great vessels of the neck.
It may be heard in the thoracic and abdominal aorta. When an aortic ob-
structive murmur is heard at the apex, its intensity is diminished, and
when heard behind it is most distinct at the left of the third and fourth
dorsal vertebrae, near their spines, and frequently extends downward along
the spine in the course of the aorta, but with diminished intensity. It is
to be noted that a systolic murmur, audible at the base and traceable along
the ascending arch toward the end of the right clavicle, is by no means
limited to cases of aortic stenosis, although this lesion always produces a
murmur with these characteristics. When the mitral or tricuspid valves
are thickened or incompetent, or when the myocardium undergoes fatty de-
generation, this murmur will entirely replace the first sound of the heart.
DiiFerential Diagnosis. — Aortic obstruction may be mistaken for mitral
and tricuspid regurgitation, an aticBinic h'uit, or the murmur of a tlioracic
aneurism. Both mitral and tricuspid regurgitation and aortic stenosis pro-
duce a systolic murmur. The murmur of aortic stenosis is heard with its
maximum intensity at the third left sterno-costal articulation, and dimin-
ishes in intensity toward the apex of the heart. The murmur of mitral
regurgitation is heard loudest at the apex-beat. The murmur of aortic
stenosis is conveyed into the vessels of the neck ; that of mitral regurgita-
tion to the left, in the direction of the apex-beat, and is heard behind, be-
tween the fifth and eighth dorsal vertebrse, at the left of the spine, with
very nearly the same intensity as at the apex. The pulse in aortic stenosis
is hard, firm, wiry, but regular ; while in mitral regurgitation it is irregu-
lar in rhythm and force, but never incompressible, and is easily increased
in frequency. Gastric, intestinal, renal, hepatic, and bronchial symptoms
are present in mitral regurgitation, while the subjective symptoms of aortic
obstruction are cerebral in character. The pulmonic second sound is feeble
in aortic stenosis, but in mitral regurgitation it is intensified. The mur-
mur of aortic stenosis is harsh, that of mitral regurgitation soft, and often
musical.
Tricuspid regurgitation is accompanied by a systolic murmur which is
rarely heard above the third rib ; while that of aortic stenosis has its point
of maximum intensity at the right second sterno-costal articulation. Tri-
cuspid regurgitation is accompanied by jugular pulsation ; while the mur-
448
DISEASES OF THE HEAET.
mur of aortic obstruction is heard in the arteries of the neck/ The area of
transmission of tricuspid regurgitant murmurs is not more than two inches
from the point of their maximum intensity, while aortic stenotic murmurs
are conveyed into the vessels of the neck. The pulse in tricuspid disease
is normal ; in aortic stenosis it is hard and wiry.
Anmmia produces a murmur heard loudest in the carotids and accom-
panied by a venous hum, which is continuous and best heard on the right
side of the neck. Thus, in anaemia there are three murmurs : cardiac,
venous, and arterial. In aortic disease the point of maximum intensity
and the absence of a ''venous hum" will aid in the diagnosis; besides,
there will be cardiac hypertrophy and an increase in the force of the apex-
beat, while the impulse is feeble in anaemia. The murmur is soft and
blowing in anaemia, and harsh in aortic obstruction. The pulse is charac-
teristic in aortic stenosis, in anaemia it may have a thrill, but is never
hard and wiry. The etiology and subjective symptoms of these two are
strikingly dissimilar.
In tlioracic aneurism the dilating impulse on palpation, the normal force
of the heart-beat, the single and double bruit, and the pain are all impor-
tant signs, which are absent in aortic stenosis.
The prognosis and treatment of '' valvular diseases of the heart" will be
considered at the end of their history.
AOETIC INSUFFICIENCY, OR REGUEGITATIOlSr.
This is an abnormal condition of the aortic valves, which prevents their
complete closure, and allows a backward current of blood to flow from the
aorta into the left ventricle during its diastole. It is usually associated
with more or less aortic stenosis.
Morbid Anatomy. — In aortic insufficiency, the flaps of the valves may
be thickened, puckered, or shortened, so that
they do not meet. If the centre of a valve is
indurated, it will curl up, either toward the ori-
fice or back against the aortic wall. In the
former case, there is insufficiency with great ob-
struction ; in the latter, insufficiency with only
slight obstruction. This valvular thickening
or shortening may be due to endocarditis. In
some cases, the flaps of the valves may become
adherent to the walls of the aorta, or a diseased
valve may be torn or ruptured, which will al-
low a free opening for the regurgitant blood.
View of Aortic Semiinnar Valves FoUowing stenosis, little tunucls may form by
torvtirs'trlhfcke^^^^^^^ the side of the vaWes and permit of a regurgi-
Z^^^to^^tXl^LKT^;.^^^'^^^^^^^'^' The aortic valves are more lia-
tic orifice. I^lg |-Q laceration than any other valves. In
aortic regurgitation, during a cardiac diastole,
1 To distinguish between intrinsic pulsation of the jugular vein and throbbing of the carotids, press
fightly on the vein above the clavicle ; this arrests pulsation when due to tricuspid disease, while if due
to aortic stenosis, the result is negative.
Fig. 97.
AORTIC INSUFFICIENCY, OR REGUEGITATION. 449
there is added to the blood, which normally flows from the auricle into
the ventricle, a regurgitant current from the aorta, and so over-distention
of the left ventricle results. Thus, after a time, the left ventricle becomes
permanently dilated. To overcome this distention compensatory hyper-
trophy takes place. The left heart is often greatly enlarged. As a result,
the arterial system is over-distended at each cardiac systole.
The extra ventricular power and the abnormal quantity of blood thrown
against the arterial walls lead to endarteritis and subsequent atheroma,
and the degeneration of the vessels predisposes to apoplexy and to aneu-
rism. Since, normally, aortic recoil fills the coronary vessels, aortic regur-
gitation must be followed by imperfect blood-supply to the heart, and dila-
tation again commences at the expense of the walls of the heart, the hyper-
trophy ceasing to compensate for the increased dilatation. Atrophy of the
papillary muscles may allow the mitral flaps to pass beyond their normal
line at the auricles, when there is an increase in blood pressure, and then
mitral regurgitation and impeded venous circulation will result. Passive
pulmonary hyperemia may be present wWiout mitral lesions, when the left
auricle cannot wholly empty itself.
Etiology. — This is similar to that of aortic stenosis. Eheumatic en-
docarditis is its chief source ; but it may follow sudden and violent
muscular effort, atheroma of the aorta or endarteritis. Congenital mal-
formation, according to Virchow, is a frequent cause in chlorotic females.
The atheroma which causes aortic insufficiency is often of gouty origin,
especially when gouty kidneys coexist or when alcoholismus is associ-
ated with a gouty diathesis. Dilatation of the aorta at its origin may in-
duce it. Fagge says only fifty per cent, of the cases of aortic insufficiency
give a rheumatic history. The violence with which the valves are closed
during prolonged and violent physical exertion may induce an interstitial
endocarditis which will lead to it-
Symptoms. — So long as hypertrophy compensates for the regurgitation,
there is little or no inconvenience experienced by the patient, even
though the regurgitation is extensive. When the regurgitant stream is
small, there is no disturbance of the general health, but in time the hyper-
trophy induces excessive heart-action during excitement or violent muscu-
lar effort. The heart-action then becomes labored and the patient is anx-
ious, nervous and fretful, and knows well that exercise will augment his
uncomfortable symptoms. The respirations are accelerated with the cardiac
palpitation ; as the disease advances attacks of headache and vertigo be-
come more and more prolonged and severe ; the patient complains of muscas-
volitantes, dyspnoea, and giddiness, and is compelled to sleep with his
head elevated. Palpitation and a visible carotid impulse are now con-
stantly present. A comparatively frequent symptom is a distinctly par-
oxysmal shooting or stabbing pain over the heart, in the left shoulder, or
extending down the left arm. This pain may be accompanied by numb-
ness and a peculiar whiteness of the skin along the line of pain. In other
cases, the pain passes from the middle of the sternum down the right arm..
This pain is increased by excitement, physical exercise, and over-distention,
29
450
DISEASES OF THE HEART.
of the stomach. Sometimes these patients complain of a sickening flutter-
ing of the heart when the nutrition of the heart walls becomes interfered
with ; and when mitral insufficiency exists, the systemic veins become over-
loaded and cyanosis and dropsy result ; the dropsy appears first as oedema
of the feet, and gradually extends upward until there is general anasarca.
The cyanosis is increased after slight exertion, and is accompanied by vio-
lent i^aroxysms of dyspnoea, carotid pulsation, and puffiness of the face.
Later in the disease, there is orthopnoea, sudden startings in sleep,
angina pectoris, and there may be albuminuria and enlargement and
tenderness of the liver. Attacks of syncope at first occur only after active
exercise ; later, they occur independently, and are very distressing. These
patients may die at any moment, either when perfectly quiet or when under
intense excitement ; the danger is greatest, however, during exertion.
The pulse is the most characteristic subjective symptom, and was first
accurately described by Sir D. Oorrigan,' and is therefore often called "Cor-
riga7i's2nilse." He said the disease was indicated by visible pulsation of the
vessels of the head, neck and upper extremities. On account of the elonga-
tion of the arteries during their pulsation, and their flexuosity, the pulse is
often called the "piston pulse f' it is large and ' distinct, and rapidly pro-
jected against the finger, and the arterial tension sinks just as quickly to
a minimum. It may be accompanied by a vibrating jar, on account of which
it is called the '^water-hammer," "jerking," "splashing," or *' col-
lapsing " pulse. Its characteristics are more apparent when the arm is raised
above the head ; although slightly infrequent, quick, and jerking, it is
always regular in rhytlim; — the radial impulse is felt a little after the apex-
beat. As soon as the systemic circulation is overloaded from insufficiency
of the heart or from secondary mitral insufficiency, the pulse becomes
feeble, irregular, and sometimes intermittent, but always " jerking." The
sphygmograph shows a high upstroke and an absence of the dicrotic wave.
The pulse-tracing of aortic
regurgitation resembles the
senile pulse, but a senile pulse
gives a rounded instead of a
pointed summit. The pecu-
liar crochet or beak is very
noticeable.^
Physical Signs. — Inspection
reveals an increase in the area
and force of the apex-beat,
which is visible over a wider
area than in aortic stenosis. The vessels of the neck and upj)er extremities
often pulsate ; when compensation ceases to balance the forces in the heart,
the apex-beat becomes feeble and diffused. Pulsation of the retinal vessels
has been observed. '
1 Edin. Med. Surg. Jonr., April, 1832.
2 Stokes has described a peculiar and characteristic pulsation (steel-hammer pulse) occurring in cases
of acute rheumatic arthritis, and supervening iipon aortic insutficienc.v. This pulse is abrupt and ener-
getic as the rebound of a smith's hammer from the anvil ; it is only exhibited, however, in the arteries
near the affected joints.
3 Lond. Ophth. Hosp. Rep , Feb., 1873.
Sphygmographic tracing in Aortic Regiirgitation, showin:
marked amplitude with absent dicrotic wave.
AORTIC INSUFFICIENCY, OK REGURGITATION. 451
Palpation. — A heaving, lifting imjDulse will be appreciated which is
transmitted over a large area. The apex-beat is displaced down and toward
the left, sometimes as far as the eighth rib, and two and one-half inches to
the left of the left nipple. A continuous diastolic thrill is sometimes felt
over the site of the aortic valves. There may be slight pulsation in the
scrobiculus cordis.
Percussion. — The superficial and deep areas of dulness correspond to the
extent of the cardiac enlargement. As soon as dilatation exceeds hyper-
trophy, the area of dulness will extend horizontally and slightly upward,
the apex beating in the axillary line. Dulness may extend six and a half
inches from right to left and from the third rib to the line of liver dulness.
Superficial dulness is increased horizontally and to the left.
AuscuUatio7i.—AovtiG regurgitation is attended by a diastolic murmur,
which may take the place of, or immediately follow, the second sound of
the heart. This murmur has its maximum intensity at the sternal end
of the second right intercostal space, or at the sternal junction of the third
rib on the left side. It is transmitted over the sternum and may be loud-
est at the xiphoid cartilage and is thence transmitted in the direction of
the apex. Its area of diffusion is greater than any other cardiac murmur :
it is not only conducted down the sternum to the apex, but it may be
heard at the sides of the chest, along the spinal column, faintly in the
ascending and transverse arch, in the carotids, and sometimes as far as the
radial arteries. The murmur is "substitutive" rather than "accompany-
ing," for the pulmonic second sound is audible at the right base. Incom-
petency of the posterior segment of the aortic valve induces a murmur
which is conducted to the apes, while inadequacy of the anterior flaps pro-
duces a murmur which is conveyed toward the ensiform cartilage ; the
former murmur would indicate a more favorable prognosis, owing to the
relationship of the anterior segments to the coronary arteries. When the
second sound of the heart is distinct, the murmur immediately follows it.
Some call this a " post-diastolic aortic murmur."
Although an aortic regurgitative murmur has the greatest area of dif-
fusion, it is not the loudest murmur ; it is soft, blowing, sometimes rough,
and frequently musical. It is loudest at the beginning of diastole, gradu-
ally decreasing in intensity, although it may be " rushing " or " blowing ; "
this murmur may temporarily disappear during the whole diastole. When
aortic stenosis coexists there will be a double murmur, audible over a very
large area, and having its maximum intensity at the right edge of the
sternum in the second interspace. Systolic and diastolic murmurs may run
into each other. If mitral occurs with aortic regurgitation, each murmur
retains its own place of maximum intensity. Earely, when two segments
of the valve are healthy, a clear aortic second is heard, preceded by a faint
"reflux " murmur, said to be pre-diastolic in rhythm.
Aortic murmurs are sometimes so indistinct as to be heard only when the
patient is in a recumbent posture. A diastolic murmur heard at or below
the level of the aortic valves, and chiefly audible in tlie line of the sternum,
indicates considerable regurgitation. When a diastolic murmur is inaudible
452 DISEASES OF THE HEART.
in the carotids, it is because preceded by a systolic murmur which has its
maximum intensity in the " aortic area." Such a murmur indicates much
more obstruction than regurgitation. When a diastolic murmur is heard
distinctly in the carotids, and is also preceded by a systolic murmur in
them, the combination indicates trifling obstruction with considerable in-
competence.
Differential Diagnosis. — The diagnosis of aortic regurgitation is generally
not difficult, as it rests almost exclusively upon the existence or non-existence
of a diastolic murniiir. It may be mistaken for aortic stenosis, mitral ob-
struction, pericarditis localized over the aorta, aneurism of that portion
of the aorta immediately above the valves, patency of the ductus arteriosus,
insufficiency of the pulmonic valves, and occasionally for a rough and in-
elastic condition of the ascending aorta.
Mitral obstruction gives a presystolic murmur, while aortic reflux pro-
duces a diastolic murmur. Mitral stenosis is accompanied by no hyper-
trophy or dilatation of the left ventricle; whereas these conditions are
always present in aortic reflux. The quality of a presystolic mitral murmur
is harsh and rough, and it has a churning, blubbering or grinding character ;
while aortic reflux has a murmur of low pitch, and a soft, blowing or musi-
cal character. Mitral stenosis is accompanied by a purring thrill, which is
absent in aortic regurgitation. The murmur of mitral stenosis is the
longest of all cardiac murmurs, and is never heard behind; whereas that
of aortic regurgitation is heard at the sides of the chest and along the
spinal column. Finally, mitral stenosis is attended by well-marked pul-
monary symptoms during active physical exertion, which are rarely pres-
ent in aortic insufficiency.
A pericardial friction sound over the aorta has its maximum intensity
over the seat of its production, and is usually audible during both the
cardiac systole and diastole. In aortic regurgitation, the character of the
pulse, the existence of hypertrophy and dilatation of the left ventricle, and
the carotid pulsation will establish the diagnosis.
An aneurism at the sinuses of Valsalva is diagnosticated by the history of
the case, the presence of the murmur over the pulmonary artery, the evi-
dence of arterial degeneration, the absence of left ventricular dilatation and
hypertrophy, and by the peculiar jerking pulse. An aneurismal murmur
is circumscribed, has a booming quality, is usually systolic in rhythm, and
is never transmitted to the apex of the heart.
Patency of the ductus arteriosus is a rare condition ; in a case where it
was diagnosticated ' the murmur was audible at the left of the sternum, was
not everywhere continuous with the second sound, was only transmitted
very feebly to the left, and had a wavy character sufficient of itself to distin-
guish it from aortic regurgitation.
Insufficiency of the pulmonic semilunar valves is the rarest of all valvu-
lar lesions ; the murmur should be diastolic, having its maximum intensity
in the second intercostal space of the left side, it would be transmitted
only downward and toward the right apex, and would not be attended
1 Guy's Hosp. Rep. Series 3, vol. xviii., 1873-3.
MITRAL STENOSIS.
453
by arterial pulsation, a jerking pulse, or left ventricular dilatation and hy-
pertrophy.
A diastolic murmur in the ascending arch due to roughening, rigidity,
and dilatation of the artery is also rare, while the condition, which some
say can produce it, is very common. Two cases are recorded in which the
diagnosis rested upon the character of the pulse, throbbing of the arteries
and the absence of left ventricular hypertrophy and dilatation.'
MITRAL STENOSIS.
Stenosis or obstruction of the auriculo-ventricular opening of the left
heart, is due partly to constriction at the base of the mitral valves, and
partly to adhesion of the valve tips or chordae tendinese. It usually occurs
as a consequence of rheumatic endocarditis, — rarely of atheromatous degen-
eration, — and is most likely to occur in endocarditis affecting young persons.
Usually, insufficiency and stenosis of the mitral orifice occur together, and
stenosis probably never occurs without some insufficiency.
Morbid Anatomy. — As a result of acute exudative or interstitial endo-
carditis, the valves are rendered shorter and narrower, as well as thicker
and more cartilaginous than normal. These rigid valvular projections not
only obstruct the flow of blood from the auricle into the ventricle, but
allow of its regurgitation from the ventricle into the auricle. In mitral
stenosis, there is not only thickening and contraction of the valves, but
the valve-tips or the chordae tendineae become adherent and sometimes each
papillary muscle is changed into a corrugated, cylindrical mass, pierced
with one or more slits, indicating the chordae of which it was originally
made up. The wall of the valve, especially toward its free edge, is greatly
thickened, and these thickened por-
tions are so dense that they have a dis-
tinct cartilaginous feel. On the val-
vular flaps that have undergone this
sclerotic change calcareous masses are
very frequently developed, and cal-
careous nodules are especially liable
to form when a gouty diathesis exists.
When the chordae tendinege and pap-
illary muscles have become adherent,
the edges of the valves are drawn down
toward the apex of the heart ; and since
the flaps are adherent at a greater or less
distance upward from their base, the
valve presents a funnel-shaped appear-
ance with its base looking toward the
auricle, and its apex toward the ven-
tricle, whose smaller opening, rarely
circular, usually resembles a slit whose axis runs with the line which unites
Pig. 99.
View of the Mitral Valve in a case of Mitral Ste-
nosis. The chordse tendineae are thickened and
shortened, and the edges of the valve are calci-
fied and drawn downward, giving the funnel-
shaped appearance.
' Bellingham, Dis.
cle by Prof. Law.
of Heart, 1875, p. 152. Also Trans. Path. Society, vol. iii., Mar.,
p. 3. Arti-
454
DISEASES OF THE HEART.
the original segments of the valve. This " button-hole " slit may scarcely
admit the tip of the little finger, while the normal mitral orifice permits the
-easy introduction of three fingers. Annular (ring-like) stenosis is far more
common at the mitral than at the aortic orifice. Sometimes the funnel-
shaped appearance is wanting, and the flaps are stretched horizontally
across, with a small opening in the centre, like a diaphragm ; looked at
from the auricle, this slit often appears crescentic.
In cases of long standing the vegetations may become calcified. If the
new tissue in the diseased valves undergoes
fatty change and softens, ulcerative processes
are set up and the chordae tendineae may
rupture. On the floor of such ulcers cal-
careous masses and debris are frequently
found. Dr Hayden thinks that '• all funnel-
shaped mitral stenosis is the result of primary
acute inflammation of the valve segments
with cohesions of their adjacent edges." Out
of sixty-two cases of mitral stenosis, fifty-
nine assumed the "button-hole" form and
three only the funnel shaped.' In rare in-
stances the tendons will adhere to the wall of
the heart. Adjacent to the valves, the endo-
cardium will usually be found slightly thick-
ened. The valves presenting the roughest
and most irregular surfaces do not give rise
to the harshest or loudest murmurs.
The following changes are developed in
the heart and vessels as a result of mitral
stenosis. The left ventricle becomes smaller,
sometimes its walls are thinner than normal.
The aorta is also small and thin-walled. An
almost necessary result of mitral stenosis is
dilatation with subsequent hypertrophy of the left auricle. Sometimes the
auricular cavity is enormously dilated, and its appendix is elongated and
curved. Not infrequently the left auricular walls are from one eighth to
one-seventh of an inch in thickness. As soon as the auricular hypertrophy
ceases to be compensatory, the pulmonary circulation becomes obstructed,
causing tension in, and distention of, the pulmonary vessels. The walls of
the pulmonary vessels, especially those of the main trunk, are thickened
and hypertrophied ; they have been found tivice the thichness of those of
the aorta. Although mitral stenosis is a disease of youth, and atheroma
one of old age, yet it not infrequently happens that, even before the age of
puberty, atheromatous degeneration occurs in the pulmonary vessels, espe-
cially in the small branches, as a result of the increased blood tension in
the pulmonary system.'^
The passive pulmonary hyper^emia which results from the obstructed
Fig. 100.
the
tlie
View of the Mitral orifice from
Auricle, with calciflcation of
valves and reduction of the opening.
In the above case the point of the
little finger was barely admitted
through the " button-hole " slit. Tlie
valves are stretched horizontally
across.
' Fagge and Hayden.
''Trans. Path. Society, xvii., p. 90.
MITRAL STENOSIS. 455
pulmonary circulation may lead to changes which collectively constitute
hrown induration of the lung. Another occasional occurrence directly due
to extensive mitral stenosis is nodular hemorrhagic infarctions. In some
instances an extensively dilated left auricle may, by pressing on a bronchus,
reduce its calibre one-half, and thus interfere with the functional activity of
the left lung. When the pulmonary hypergemia is extensive, violent physi-
cal exertion or violent coughing may cause a rujoture of one of the larger
pulmonary vessels, and true pulmonary apoplexy results. Bronchorrhoea is
a frequent result of the intense hypergemia of the mucous membrane of the
bronchial tubes which may be produced in mitral stenosis. The lungs are
always so liable to congestion and oedema that any sudden or violent exer-
cise may cause sudden death. Again, when the above conditions have
existed for some time, mitral stenosis may lead to dilatation and hyper-
trophy of the right heart. In some rare cases, the tricuspid orifice has
become slightly insufficient.
Etiology.— Mitral stenosis is most frequent in the young ; it rarely occurs
after fifty. Statistics show it to be twice as frequent in females as in males.
It is not infrequently of congenital origin. Acute rheumatic endocarditis
is its. most frequent cause. In some few instances stenosis results from ex-
tension of the inflammatory process from the aortic valves. It is a question if
endocarditis in scarlatina or diphtheria in children ever causes mitral stenosis.
Symptoms. — The subjective symptoms of mitral stenosis are few. Usually
after violent exercise there is more or less cai'diac palpitation, and this will
cease as soon as the auricle can empty itself, which is accomplished by the
patient assuming a recumbent position on the right side, with the head
slightly elevated. This class of patients are usually pale and anaemic,
and frequently experience a sharp pain in the region of the apex-beat. The
pulse is regular and normal in character, so long as the auricular hyper-
trophy compensates for the auricular dilatation. When the ventricle does
not receive and discharge its normal quantity of blood with normal regu-
larity, the pulse becomes small in volume, feeble in force, rapid and irregular
in rhythm. The sphygmograph exhibits a tracing, sometimes called the
*' mitral pulse," the nature of which is the same as when the ventricle
throws a greatly diminished blood current into the aorta, i The auricular
systole commences earlier than
normal on account of the hy-
pertrophy of the auricle. This
premature contraction of the
auricle stimulating ventricular
contraction, is indicated by a
second ventricular systole,
which is much less forcible
than the first. Fre. loi.
TTiP niQciira mil TYinnQT-^r >.t7 Sphyf^jmographic tracins: in a case of Mitral Stenosis. The line
xijc jJtis&ivt! puiiiiuiid,i_y xiy- of descent is broken by pulsations from premature con-
persemia which attends the ad- ^'^^"*^°° "^ '^" over-fliied auricle.
' Balfour differs from other authorities in the statement that among the most remarkable subsidiary
phenomena of mitral stenosis is irrefjularily of cardiac rhythm which is always present in a greater or less
degree.
4-56 DISEASES OF THE HEART.
vanced stages of this form of cardiac disease causes habitual dyspnoea,
which is exaggerated by physical exertion and by a dry, hacking, " teas-
ing" cough, which resembles the so-called ''nervous" cough. After
violent or prolonged exertion there may be bronchorrhcea, a pint of glairy,
watery mucus often being expectorated in a few moments. Severe exercise
sometimes induces attacks of profuse, watery, blood-stained expectoration,
indicative of pulmonary congestion and oedema. The exertion of walking
rapidly against a strong wind will often cause such intense congestion and
cedema of the lungs in one with extensive mitral stenosis as to induce sud-
den death. Haemoptysis is not infrequent, small. quantities of pure, florid
blood being expectorated. Orthopnoea is a rare symptom, for even in ex-
tensive and long-standing cases the pulmonary congestion is not constant,
for the auricle is ordinarily able to empty itself, and only becomes engorged
during active physical exertion or great excitement.
Physical Signs — Inspection. As the left ventricle does not receive its
normal quantity of blood, the cardiac impulse is feeble. Sometimes it has
a visible undulating movement.
Palpation. — On palpation, although the apex-beat is less forcible than
normal, a distinct purring thrill will be communicated to the hand ; this
thrill is a constant attendant of mitral stenosis. While mitral stenosis is
always accompanied by a purring thrill, it should be remembered that a
purring tlirill does not always indicate mitral stenosis. It is most distinct
at the apex-beat, although it may be diffused over the whole precordial
space. It either continues through the entire diastole, or is only present
just before the systole. It is sometimes called a " presystolic " thrill. It
ceases at the apex-beat.
Percussion. — The increased size of the left auricle may cause an increase
in the area of cardiac dulness, upward and to the left, at the inner part of
the second left intercostal space. This increased area of dulness will only
be recognized on careful percussion during expiration.
Auscultation. — Mitral stenosis is characterized by a loud "churning,"
"grinding," or "blubbering" presystolic muraiur ; this murmur is of
longer duration than any other cardiac murmur, on account of the time re-
quired for the blood to pass through the narrowed and obstructed orifice. It
ends with the commencement of the first sound and the apex-beat, being
synchronous with the purring thrill. The murmur is heard with its maxi-
mum intensity a little above the apex-beat. It is louder when the patient
is erect than when in a recumbent posture. When there is great debility
or just before death, the murmur becomes indistinct. A presystolic mur-
mur is never present unless there is narrowing of the auriculo- ventricular
orifice, and then it is seldom, if ever, absent. A prolonged murmur and a
sharp first sound indicate a "funnel-shaped" stenosis. The pulmonic
second sound is intensified. When mitral reflux and mitral obstruction co-
exist, the two murmurs run into each other, constituting a single murmur.
A mitral obstructive murmur is never soft or musical ; it is usually sepa-
rated from the first sound by a short interval. In about one-third of all
cases, the second sound is reduplicated. Pulmonary congestion sufficiently
MITEAL EEGURGITATIO]Sr. 457
accounts for the redaplication.' Some regard the length of the pause
between the murmur and the first sound as a measure of the stenosis : the
shorter the pause the greater the stenosis.
Differential Diagnosis. — The diagnosis of mitral stenosis is not difficult :
it depends upon the existence of two physical signs, the " purring thrill "
and a loud, long, blubbering jn-esystolic murmur. It may be mistaken for
pericardial friction, for a prolongated systolic murmur replacing the first
sound at the apex, and for a pre-diastolic basic murmur transmitted to the
apex.
To diagnosticate between local pericarditis and mitral stenosis the same
methods are employed and the same rules are to be observed as in the diag-
nosis between aortic murmurs and local pericarditis (g. v.).
A prolonged systolic apical murmur reaching to the second sound is dis-
tinguished from a presystolic murmur by its soft and blowing character,
and its synchronism with the systolic impulse and carotid pulsation.
K pre-diaxtolic murmur is distinguished from a mitral stenotic murmur
by its progressively diminishing intensity, from the base to the apex, by its
not being accompanied by hypertrophy of the left ventricle, and by a jerk-
ing, irregular pulse.
MITEAL EEGTJEGITATIO]^.
Eegurgitation at the mitral orifice is due to a condition of the mitral
valves which allows the blood to flow back from the left ventricle into the
left auricle.
Morbid Anatomy. — The most common lesions are thickening, induration
and shortening of the mitral valves. In rare instances, regurgitation may
occur independently of valvular disease, from displacement of one or more
of the segments of the valve, the result of changes in the papillary muscles,
chordge tendinese, or the ventricular walls. It may also occur in extensive
anaemia or from relaxation of the papillary muscles and dilatation of the
left ventricle without a corresponding elongation of the papillary muscles,
and from rupture of the chordae tendinese. In most instances, however,
the valves are shortened, thickened, and indurated. In some cases, lime
salts and large masses of chalky matter are found embedded in the in-
durated valves. In such cases the surface and edges of the valves are so
rough and jagged that more or less obstruction accompanies the regurgi-
tation. All these changes, except calcification, may also occur in the chordas
tendineae and columnse carnese. The valves may also become adherent to
the walls of the ventricles, or, as a result of the shrinking and shortening
of the chordae tendineae, the valve-flaps will not pass back to the plane of
the orifice. Again, the chordae tendinese may be ruptured so that the
valves are pressed back into the auricle during the cardiac systole. If the
chordae tendineae which are inserted nearest the centre of the valve become
> Geigel ascribes it to " non-coincidence in the closure of the valves." Guttman regards it as originat-
ing at the stenotic orifice itself. Balfour thinks that thrill and reduplication of the second sound are suf-
ficient to make a diagnosis in the absence of murmur.
458
DISEASES OF THE HEART.
Pig. 102.
View of the Left Heart in Mitral
Regursjitation.
lengthened, that part of the flap will be bent upon itself, having evidently
yielded to the blood pressure, and. this allows of regurgitation. Sometimes
when the valves appear perfectly healthy they will
be found by the application of the " luater test "
to be insufficient.
The first effect of mitral regurgitation is dilata-
tion of the left auricle, due to the pressure of the
two blood currents during its diastole, one from
the lungs, and tbe other from the left ventricle.
The dilatation leads to thickening and hypertrophy
of the left auricular walls ; as a result, the pul-
monary circulation is impeded. The pulmonary
vessels enlarge and may undergo degeneration, as a.
result of the continued regurgitant j)ressure. Passive
hypersemia of the lungs, with brown or pigment
induration, is an early pathological sequel of mitral
regurgitation. The constant interference with the
return circulation from the lungs, more or lesa
obstructs the outward current of blood to the lungs
from the right ventricle. As the obstruction is a
The avHcrdo-ventricuiar valves aradual oue, tlic riffht vcntriclc bccomcs sufficient-
are thickened with calcareous ^ ^ o
deposits, as shown at B, B. w hvpertrophied to overcome it, consequently the
The aortic valves A, A, were •^-'J- t -, . . , , • ■, Z j^ ±^
in this case the seat of like de- hypertrophicd right vcntricle Compensates lor the
mitral regurgitation.
So long as the hypertrophied right ventricle is able to fully overcome
the abnormal pressure of the blood in the lungs from the mitral regurgi-
tation, the patient is comfortable. Sooner or later, however, the compen-
satory hypertrophy of the right ventricle ceases, and a secondary dilata-
tion occurs which admits of no compensation. This final dilatation of
the right ventricle is favored by the myocardial degeneration which occurs
as a result of defective nutrition of the heart walls ; when this condition is
reached, the veins throughout the body are placed in a similar condition to
those in the lungs. This general venous congestion is indicated by passive
hypersemia of the abdominal viscera and by cyanosis of the surface during
active physical exercise. The liver is the organ first affected on account
of its great vascularity, and from the fact that the hepatic veins do not col-
lapse readily and possess no valves. Thus, the liver becomes enlarged and
has a stony hardness ; as a result of the obstruction to the emptying of the
hepatic vein the portal vein is obstructed, and this leads to passive hyper-
emia of the intestines and stomach, and enlargement of the spleen. The
impediment to the return of venous blood to the heart causes cerebral con-
gestion, renal congestion, and, in fact, general systemic venous congestion.
In addition to these changes, the dilated and hypertrophied left auricle
throws an abnormal quantity of blood with abnormal force into the left
ventricle during the diastole, which leads to dilatation of its cavity, and
necessitates a compensatory hypertrophy of the left ventricular walls; this
hypertrophy increases the force of the reflux current, so that during ex-
MITEAL EEGUEGITATION". 459
■sitement and active physical exertion, pulmonary congestion and cedema
are liable to occur.
Etiology, — Mitral regurgitation may occur at any age ; it is especially
liable in the young to follow rheumatic endocarditis, which causes exten-
sive valvular retractions and thickenings. It is not infrequently second-
ary to changes at the aortic orifice produced either by an extension of endo-
carditis from the aortic to the mitral valves and their appendages, or by
the secondary mitral valvulitis excited by the regurgitant blood current
from the aorta. Mitral insufficiency may also be the result of that enlarge-
ment of the left auriculo-ventricular orifice which accompanies excessive
dilatation of the left ventricle. Diseases of the columnae carneae and chor-
dse tendineae, when their structures are so weakened as to allow the flaps of
the valves to pass back of the plane of the orifice, will also cause miti-al
insufficiency. Ulcerative endocarditis may also cause it, either by perfora-
tion and rupture of the valves or by rupture of the chordge tendinese.
Symptoms. — During the early stage, when the hypertrophy of the right
ventricle compensates for the regurgitation, there are no rational symp-
toms which would lead one to suspect its existence ; but when the right
ventricle is unable to overcome the obstruction to the jDulmonary circu-
lation caused by the regurgitant blood current, there will be more or less
dyspnoea accompanied by a short, hacking cough with an abundant expec-
toration of frothy serum. Sometimes the watery expectoration is blood-
stained. Active physical exertion increases the dyspnoea and causes cardiac
palpitation.
In advanced cases, the extremities, face, and lips become blue, the result
of the interference with the capillary return circulation. The liver becomes
enlarged and hardened, a condition easily recognized by palpation and per-
cussion. The patient will complain of a sense of weight and fulness in the
right hypochondrium, and there will be anorexia, nausea, and a sense of
oppression in the epigastrium, and sometimes the hepatic circulation be-
comes so obstructed that the biliary secretion is interfered with and a jaun-
diced hue of the surface will be added to the cyanotic discoloration, which
■will give to the skin a greenish tint. Headache, dizziness, vertigo, stupor,
somnolence, and sometimes a peculiar form of delirium of short duration,
result from the passive cerebral hyperaemia induced by obstruction in the
superior vena cava. Following the hepatic derangement, are frequent
attacks of gastric and intestinal catarrh, and evidences of embarrassed renal
circulation. The urine is diminished in quantity, high colored, and loaded
with lithates. Sometimes albumen and blood casts are found in it. Fre-
quently the blood-stained expectoration is accompanied by free haemoptysis j
a cough and watery expectoration with occasional dark blood stains are
usually present as advanced symptoms of mitral regurgitation. Another
late symptom of mitral regurgitation is dropsy ; it first appears in the lower
extremities, and gradually extends over the whole body. With the general
anasarca there is more or less dyspnoea. Late in the disease, pulmonary
hemorrhagic infarctions may occur.
The pulse of mitral regurgitation is, at first, regular in force and rhythm;
460 DISEASES OF THE HEABT.
later it becomes diminished in volume, irregular m rhythm, and diminished
in force ; it is never jerking in character. Wlien the heart's action is
excited, it becomes feeble and com-
pressible and has a certain tremu-
lousness. The sphygmographic
tracing shows great depth and
amplitude of the diastolic notch.
Physical Signs. — Inspection.
The area of the visible cardiac
impulse is increased, and not in-
PiG. 103. frequently there is a slight pulsa-
Sphygmographic tracing in Mitral Regurgitation show- tiou. Corresponding in rhythm
ing great depth and amplitude of the diastolic notch. ■ ■, , -, i mi
With the heart beats. The epi-
gastric pulsation is due to right ventricular hypertrophy, which is a con-
dition always found with extensive mitral regurgitation. The jugular veins
appear swollen, especially when the patient is lying down.
Palpation. — The apex-beat is displaced to the left and is felt lower than
normal. When the dilatation exceeds the hypertrophy, the apex-beat is
carried outward and often slightly upward. The impulse is dilfused and
more or less forcible, according as right or left ventricular hypertrophy
predominates. Palpation sometimes reveals a systolic thrill, which is con-
fined to the region of the second left intercostal space near the sternum.
This sjstoWc fremissement is not noticeable when the base of the heart lies
close to the chest-wall because of retraction of the margin of the left lung.
A purring tremor, systolic in rhythm, felt most intensely at the apex, and
becoming feebler the farther the hand is removed from that part, either to
the right or upward, is invariably due to mitral regurgitation.''
Percussion. — Percussion reveals an increase in the area of cardiac dul-
ness, especially laterally ; it extends both to the left and right of the normal
line, as well as downward. The area of the superficial as well as of the
deep-seated dulness will be increased laterally and downward.
Auscultation. — Mitral insufficiency is attended by a systolic murmur,
which either completely or partially replaces the first sound of the heart.
The quality of the murmur is variable, and not in itself distinctive. It is
usually soft and blowing ; sometimes, toward its end, the murmur will
assume a distinctly musical character. The first sound of the heart may
be heard distinctly in the early stages, but later the murmur nearly always
takes the place of the heart sound. Hence many English writers rightly
call this murmur " post-systolic " rather than " systolic " in its nascent
stages. It is heard with its maximum intensity at the apex-beat. Its area
of diffusion is to the left, on a line corresponding to the apex-beat. It is
audible at, or near, the inferior angle of the left scapula. It can he heard
between the lower border of the fifth and the upper border of the eighth
1 Skoda, Bamberger and Leyden record instances in which inspection showed a double impulse, accom-
panying, with more or less regularity, each cardiac systole. This only occurs in aggravated cases, and
arises from non-coincidence of contraction of the ventricles.
^ Hayden states that " it is exceptional to have a puning thrill with simple mitral reflux." I have never
found it, except in those cases where left ventricular dilatation greatly exceeded the hypertrophy.
MITRAL EEGURGITATION". 461
vertebra, at the left of the spine, with nearly the same intensity as at the apex.
The second sound of the heart, over the pulmonary valves, is accentuated,
while at the junction of the third rib with the sternum on the left side,
both heart sounds are feeble. Skoda first drew attention to exaggeration
of the second pulmonary arterial sound as a "positive and unerring" indi-
cation of mitral regurgitation. It is not always present. Whatever
may be its character, the murmur is generally loudest at its commence-
ment.
A loud systolic murmur at the apex, and not heard at the back, is not
indicative of mitral reflux. If stenosis and regurgitation occur in the same
individual, they give rise to a combined presystolic and systolic murmur,
which begins shortly after the second sound of the heart, and continues
until the second sound commences. The two sounds, although mingling
to form one murmur, can, in the majority of cases, be readily distinguished
from each other, for the point of maximum intensity and the very limited
area of diffusion of a presystolic murmur readily distinguish it from a mi-
tral systolic, which is audible in the left scapular region. It is important
to recognize the existence of both these murmurs in estimating the progno-
sis in any case.
DiiFerential Diagnosis. — It is usually not diflBcult to recognize mitral re-
gurgitation. The seat and rhythm of the murmur and its area of diffusion
are sufficient to distinguish it from other cardiac murmurs. The character
of the pulse, the symptoms referable to the right heart, and the pulmonary
complications will also assist in its diagnosis. It may, however, be mis-
taken for aortic olstruction, since each gives rise to a systolic murmur, for
tricuspid regurgitation, and for roughening of the ventricular surface of
the mitral valve, or of the ventricular wall near the aortic orifice. The di-
agnosis between mitral regurgitation and aortic stenosis has already been
considered.
Mitral and tricuspid itisufficiencg both produce a systolic murmur ; a
mitral regurgitant murmur has its maximum intensity at the apex, and is
conveyed toward the left axillary and scapular regions, while the maximum
intensity of a tricuspid regurgitant murmur is to the left of the base of the
xiphoid cartilage, and it is transmitted upward and to the right, — the area
of transmission establishes the diagnosis. Pulmonary symptoms are prom-
inent in mitral reflux and absent in tricuspid regurgitation. The pulmo-
nary second sound is markedly enfeebled in tricuspid regurgitation, and
markedly intensified in mitral regurgitation.
Roughening of the ventricular wall gives rise to a murmur which has its
maximum intensity at the base of the heart, and is transmitted along the
aortic arch and into the vessels which spring from it in the thorax. The
vibration of an irregular chorda tendinea stretched across the aortic orifice,
its extremities being inserted into opposite walls of the ventricle, may pro-
duce a systolic musical murmur, but the line of its transmission will cor-
respond to that of an aortic obstruction. A systolic mitral murmur, due to a
sudden rupture of one or a number of the valve-flaps, of the papillary mus-
cles, or tendons, is a loud, blowing murmur, usually appearing suddenly,
462 DISEASES OF THE HEART.
which is immediately accompanied by all the urgent symptoms of acute
pulmonary congestion.
TKICUSPID STET^OSIS.
This lesion is so rare that there are no rules for its diagnosis. Its rnorlid
appearances and etiology are similar to those of pulmonic stenosis. Its
symptoms would be those due to obstruction to the entire systemic venous
circulation. The right auricle would be dilated, and there would be vis-
ceral enlargements in the abdomen, cyanosis of the face and extremities,
scanty and albuminous urine, hemorrhoidal tumors, headache, dizziness
and vertigo (due to passive cerebral hyperasmia), and general anasarca. The
few cases recorded are associated with mitral stenosis, with one exception, a
case of Bertin's.' In a case exhibited by Quain, the tricuspid flaps, thick
and opaque, were united for one-third of their extent. In the other cases,
the flaps of the valve formed a diaphragm whose central opening admitted
only the point of one finger. In every recorded case of tricuspid stenosis
the heart was enlarged. Tricuspid stenosis (as also pulmonic stenosis) may
be the result of the pressure of a tumor. In all well-authenticated cases,
the chief symptoms seem to have been extreme lividity, palpitation, and
dyspnoea.
Physical Signs. — Inspection reveals general cyanosis. The jugulars are
turgescent and exhibit presystolic ^w?sa^40?i. This pulsation is sometimes
the only inconvenience the patient suffers.
Palpation may discover a venous thrill at the base of the neck.
Percussion may show the right auricle to be greatly enlarged, and car-
diac dulness will be increased laterally and toward the right.
Auscultation. — Tricuspid stenosis should be attended by a presystolic
murmur whose maximum intensity would be at the lower portion of the
sternum just above the xiphoid cartilage. This murmur may be propa-
gated faintly toward the base, but never toward the apex of the heart. It
is sometimes accompanied by fremitus. Hayden offers the following
''diagnostic point:" — the murmur of mitral stenosis (without which
tricuspid stenosis never occurs) is limited to the apex region ; a murmur of
the same rJiytJim is produced at the sternum by tricuspid stenosis, "and
between these two localities there is a point where no murmur can deheard.'^
It is unnecessary to consider its differential diagnosis. The lesion
would be diagnosticated (if at all) by exclusion, and prognosis and treat-
ment would depend upon the gravity of the accompanying condition. As
tricuspid stenosis never occurs unless there is extensive mitral obstruction,
the latter condition is always the predominant one.
TRICUSPID REGUEGITATIOIST.
This lesion is usually secondary, yet it may be primary. Mitral disease
is, in nearly every instance, the antecedent condition.
Morbid Anatomy. — The lesions are similar to those occurring in mitral
1 Traite. des Mai. du Coeur, Oba. 17.
TEICUSPID REGUEGITATI02S". 4G3
insufficiency. The valves are thickened, shrunken and opaque ; the papil-
lary muscles are shortened and thickened, and the chordae tendineae under-
go like changes and are sometimes adherent. The valves, or the columns
or cords, may rupture; in either case acute and extensive insufficiency re-
sults. Acute endocarditis of the right heart is rare in adults, but when it
occurs the tricuspid valves are its principal and primary seat, on account
of their anatomical structure and the tension to which they are subject in
mitral disease. They are rarely the seat of rheumatic or calcareous de-
generation. Ulcerative endocarditis in the right heart is seldom met with.'
Any infection from emboli from the tricuspid flaps will produce their
secondary effects in the lungs. The first effect of tricuspid regurgitation
is dilatation of the right auricle ; following this, there will be hypertrophy
of its walls. The auricular hypertrophy soon ceases to compensate, and
then venous engorgement occurs.
As soon as the valves in the subclavian and jugular veins are no longer
able to resist the regurgitant current, jugular pulsation follows. But, be-
fore this occurs, the tributaries of the inferior cava and the organs to which
they are distributed will become greatly engorged, for they have no valves
to resist the regurgitant current. The inferior cava and the hepatic veins
sometimes become enormously distended under these circumstances, the
liver showing the peculiar appearance on section that has gained for it the
name of nutmeg liver. Following the hepatic changes, the skin as-
sumes a dingy yellow hue. When this is combined with cyanosis it has a
peculiar greenish tint, only met with in heart disease. The spleen enlarges
and hardens ; the mucous memhrane of the stomach is congested and
ecchymotic, and often presents numerous hemorrhagic erosions. Intestinal
catarrh is subsequently developed, and the general venous congestix)n with-
in the abdominal cavity is exhibited by hemorrhoids and ascites. The
kidneys become congested and stony, and thrombi may form in the femoral
vein and induce subsequent pulmonary infarctions.
The stasis in the veins below the diaphragm is accompanied by transu-
dation of serum, first in the ankles, and thence the dropsy progresses up-
ward until the patient may finally reach a condition of general anasarca.
The resulting obstruction to the general systemic circulation may cause
hypertrophy of the left ventricle, and then we have the rare occurrence of
disease of the left heart following that of right. Since tricuspid reflux
has mitral disease for its principal cause, the heart becomes greatly en-
larged, and a condition of extreme cardiac dilatation and hypertrophy is
reached.
Etiology. — The most frequent cause of tricuspid regurgitation is mitral
stenosis and regurgitation. Tricuspid reflux from primary endocarditis is
very rare. Any condition of the lungs which will produce hypertrophy
and dilatation of the right ventricle will lead to it ; it is met with in
extreme pulmonary emphysema and in cirrhosis of the lung with exten-
sive chronic bronchitis. Balfour regards chronic bronchitis as its most
' Charcot and Vnlpian record a case where one of the tricnapid valves was softened and perforated,
presenting numerous vegetations. Scattered abscesses in the lungs were found in this case.
464 DISEASES OF THE HEART.
frequent cause after mitral stenosis. Any valvular disease in the left heart
of long duration may lead to it. In all these causes the rationale is the
same : the abnormal amount of blood in the right ventricle presses with
undue force against a valve which physiologists regard as normally slightly
insufficient, and the stress upon the valve flaps and the valvular attach-
ments is such that endocardial inflammation is excited at the part subject
to the greatest strain, and valvular insufficiency results.
Symptoms. — As tricuspid reflux is usually secondary to some other form
of valvular disease, or to some chronic pulmonary affection, the symp-
toms during its early stages are vague and masked by those of the
primary disease. But directly the venous return is markedly impeded,
a train of symptoms is developed which has its origin in the visceral de-
rangements. In addition to these symptoms, there may be, in extensive tri-
cuspid reflux, cardiac palpitation, cardiac dyspnoea, and marked irregularity
in the force and rhythm of the heart. The liver is enlarged!, the skin becomes
dingy, and there is obstinate constipation and hemorrhoids. The liver is
rendered liable in such cases to interstitial hepatitis. The spleen is en-
larged. Venous stasis in the stomach is evinced by dyspepsia, nausea, vom-
iting, and hsematemesis. The secretion of the kidneys is scanty, dark
colored, of high specific gravity, often containing albumen and casts.
Passive cerebral hypersemia is marked by headache, dizziness, vertigo, and
muscffi volitantes ; there is a peculiar mental disturbance which is not
met with in any other form of heart disease. Placing the patient in
a horizontal position, after the disease has existed for some time, causes
the face to become turgid and blue, and if the position be retained, stupor
and coma may supervene. Jugular and epigastric pulsation are its char-
acteristic physical signs. A very late symptom is dropsy, which begins at
the ankles, extending upward until there is general anasarca. It is a no-
ticeable point, that in the dropsy from tricuspid reflux the genital organs
suffer slightly, if at all.
Physical Signs. — Inspection. In extensive tricuspid disease, the area of
cardiac impulse is increased more than in any other valvular lesion. This
area sometimes extends from the nipple to the xiphoid cartilage, and it
may reach as high as the second right intercostal space. There is a visi-
ble impulse in the Jugular veins, more apparent in the right than in the
left. Sometimes the veins in the face, arms, and hands are seen to pulsate,
and even the thyroid and mammary veins.
Palpation. — The apex-beat is indistinct, except in cases where there is
marked hypertrophy of the left ventricle. Pulsation occurs in the epi-
gastrium, which maybe due to reflux into the enlarged hepatic veins, or to
the fact that the dilated and hypertrophied right ventricle so presses on the
river, that the impulse is conveyed through the diaphragm with each car-
diac pulsation. Early in the disease, the impulse in the jugular is con-
fined to the lower part of the vessel. Beyond this point, the vein rarely
undulates. Later, a systolic pulsation is felt as high as the angle of the
jaw, and may be accompanied by distinct, though feeble, presystolic pul-
sation. The liver may simply undergo systolic depression, chiefly at the
PULMOliriC OBSTRUCTION". 465
left lobe ; or the whole liver may pulsate from an impulse coming from an
enormously dilated vena cava ; or the systolic pulsation of the veins within
the organ may give rise to a palpable expanso-pulsatory movement. The
hepatic pulsation is synchronous with the cardiac impulse. In rare
cases it precedes jugular pulsation. Sometimes pulsation is felt in the
femoral veins. ^ Sphygmographic tracings of the Jugular pulse show it to
be dicrotic.
Percussion shows an increase in the area of cardiac dulness to the right
and upward, sometimes as far as the second intercostal space.
Auscultation. — The murmur of tricuspid reflux is heard with, or takes
the place of, the first sound of the heart ; it is superficial, of low pitch,
blowing, soft, and faint, and is heard with greatest intensity over the lower
part of the sternum, at its left border between the fourth and sixth ribs.
It is rarely audible above the third rib, or to the left of the apex-beat. This
murmur is transmitted from the region at the base of the xiphoid cartilage,
upward and to the right, from one to two inches. Sometimes it is heard
over a very limited area, and then it may be overlooked.
Differential Diagnosis. — A tricuspid regurgitant murmur may be con-
founded with an aortic obstructive, pulmonic obstructive, aw(}i mitral regur-
gitant. A tricuspid regurgitant murmur is never audible above the third rib,
is accompanied by an accentuation of the second sound over the pulmonary
artery and by jugular and epigastric pulsation, and is heard with maximum
intensity near the base of the ensiform cartilage. These points are suffi-
cient to differentiate it from an aortic obstructive murmur.
The differential diagnosis between it and a mitral regurgitant murmur
has been given.
PULMONIC OBSTEUCTION".
Very little is known of diseases at the pulmonary orifice. Their diagnosis
is arrived at by exclusion, and they cannot be recognized, except by their
physical signs. Endocarditis in the right heart is rare, except in intra-
uterine life. Valvular diseases of the right heart are usually the sequelae
of valvular disease in the left. The pulmonary artery may become athe-
romatous, but, even then, disease of the pulmonary valves is rare. Balfour
believes that constriction of the pulmonary artery may occur at various
periods of intra-uterine life ; as a rule, the pulmonary valves are subject to
no lesions except congenital malformations.
Morbid Anatomy. — Bertin records an instance of pulmonary obstruction
where the distorted and adherent valves formed a horizontal sejotum across
the orifice, which was only one-fourth of an inch wide. A rigid tricuspid
valve has been found to be the cause of obstruction at the pulmonary ori-
fice, the pulmonary valves themselves being normal. A few auto^Dsies have
revealed obstructions at the pulmonary artery caused by aneurisms, tumors
of the pericardium or of the anterior mediastinum, enlarged bronchial
glands, or pressure of a solidified lung. The pulmonary artery may be oc-
1 Guttman thinks epigastric pulsation ib duewliolly to reflusinto the veins of the liver, and not to right
ventricular pulsation.
30
466 DISEASES OF THE HEART.
eluded just beyond the valves by a cancerous tumor, and there are exam-
ples where a phthisical process in the left lung has induced it. A murmur
indicative of pulmonary obstruction may be produced by a cardiac throm-
bosis.
The above statements I place under the head of morbid anatomy of the
lesion, as they cannot be appreciated nor their pathological significance
realized during life. Eeasoning from analogy, obstruction at the pulmo-
nary orifice ought to be followed by compensatory hypertrophy of the right
ventricle, and accompanied by tricuspid regurgitation and dilatation of the
right auricle. ' I have met with only two cases of pulmonic obstructive
murmurs in which autopsies were obtained. In both cases it was found
that the murmur had been produced by mediastinal tumors pressing upon
the pulmonary artery so as to diminish its calibre.
Etiology. — Pulmonary stenosis is rarely the result of endocarditis or of
degenerative changes in the pulmonary artery. Bertin states that when ab-
normal communication between the two sides of the heart has existed, the
arterial blood may excite endocarditis in the right heart. Syphilis has
been advanced as a possible cause of degenerations at the pulmonary orifice.
Symptoms. — The only rational symptoms that have been noted in the few
recorded cases of pulmonic disease admit of manifold explanations, and no
one is either constant or diagnostic. In some cases ansemia existed ; in
others there was cardiac palpitation, dyspnoea, cyanosis, and dropsy, but
none of these belong exclusively to a pulmonic lesion, nor do they necessa-
rily depend upon it.
Physical Signs. — Inspection, palpation, and percussion give negative re-
sults. Palpation may give a systolic thrill, confined to the second left in-
tercostal articulation. Such a fremissement results both from roughness
and contraction of the pulmonic orifice.
Auscultation. — A systolic murmur is heard with its maximum intensity
directly over the pulmonic valves ; it is very superficial and consequently
very distinct, and is limited in its diffusion. It is never heard at the xiphoid
■cartilage, nor along the course of the aorta. If it has an area of diffusion,
it is toward the left shoulder. The murmur is loud and soft in character,
sometimes " bellows ; " it is not audible in the vessels of the neck, nor is it
attended by arterial pulsation. When phthisical consolidation partially oc-
cludes the pulmonary artery, a loud but soft systolic murmur is heard,
which is sometimes high-pitched and musical, and which is often entirely
suspended during a full inspiration. In some few instances, there is a Iruit
de diahle in the jugular veins.
DiflFerential Diagnosis. — It is possible to confound a pulmonic obstructive
murmur with a mitral regurgitation which is propagated upward into the
left auricular appendix. But the area of a mitral regurgitant is also back-
1 Dr. Ormerod records three cases in which pulmonary obstruction was diagnosticated during life, and
■where the post-mortem proved the accuracy of the diagnosis. Two of these occurred in men under twenty-
eight, and the other in a woman twenty-one. In two of these cases all the cardiac valves were healthy,
except the pulmonic. The pulmonic orifice would barely admit a goose quill. Warbiirton Begbie men-
tions a case (man: aet. 18) in whom reflux and stenosis at the pulmonary orifice coexisted. There were
four valves, and these were incompetent. All the other valves were normal. Congenital stenosis of the
infundibulum of the right ventricle is the probable result of foetal myocarditis or syphilis.
PULMONIC REGURGITATION. 467
ward, and by this it could be distinguished from a pulmonic obstruction.
Beside, in mitral disease the pulse is very different from the pulse of pul-
monary stenosis.
Aortic stenosis can hardly be mistaken for pulmonary obstruction, for the
arterial pulsation, the peculiar pulse, aud the transmission of the murmur
into the arteries of the neck will suffice to discriminate between them. An
aneurism at the sitius of Valsalva may produce a murmur in the pulmonary
artery by the pressure which is exerted upon that vessel. It would be im-
possible to distinguish this murmur from that of a pulmonic stenosis.
The diagnosis of pulmonary obstruction is usually reached only by ex-
clusion.
PULMONIC EEGUEGITATIOJSr.
Many doubt the occurrence of this form of valvular lesion. There are
only a few well authenticated cases,' and in them the lesion has been the
result of injury or congenital defect. The statement' that the pulmonary
valves exhibit a cribriform condition nearly as often as the aortic, is not
sustained by post-mortem examinations. In one of the cases to which I
have referred as an example of pulmonary stenosis, the valves were also in-
sufficient. In Dr. Begbie's case, where there were four flaps to the valves
(producing obstruction), marked insufficiency coexisted. The morUd an-
atomy^ etiology, and rational symptoms do not require a separate considera-
tion. The anatomical conditions are the same as those found in similar
conditions of the aortic valves ; and the etiology and rational symptoms
are those of pulmonic stenosis.
Physical Signs. — Theoretically pulmonic regurgitation should be accompa-
nied by a diastolic murmur having its maximum intensity over the pulmonic
valves ; and its area of diffusion should be downward and toward the xiphoid
cartilage. It should be soft and blowing in character. This murmur is
rarely heard alone ; it is usually associated with obstruction at the same
orifice, or with some murmur whose origin is on the left side of the
heart. Niemeyer states that dyspnoea, hemorrhagic infarction, and con-
sumption of the lungs have followed insufficiency at the pulmonary orifice.
No other authority mentions such symptoms, while the assignment of val-
vular disease as a cause of phthisis is absurd. With a pulmonic regurgitant
murmur there should be, on palpation and percussion, physical evidences of
hypertrophy and dilatation of the right heart, the rationale of whose pro-
duction should be identical with that which was considered in aortic re-
gurgitation. I have never heard a regurgitant pulmonic murmur.
Differential Diagnosis. — The murmur of pulmonary regurgitation may be
mistaken for that of aortic regurgitation. The points in connection with
their differentiation have already been given. The prognosis and treat-
ment are the same as those of the former lesion.
Prognosis in Valvular Disease of the Heart. — The duration of life in valvu-
lar disease of the heart varies greatly.
1 Path. Trans., vol. xvi., p. 74. " Dis. of Heart. Bellingham.
468 DISEASES OF THE HEAET.
To establish, a basis of comparison, I shall give a resume of eighty-one
cases, in all of which the diagnosis of valvular disease was confirmed by a
post-mortem examination. ' In fourteen cases of different valvular diseases,
each of which was complicated by cardiac hypertrophy and dilatation, fifty
per cent, of deaths were directly due to the valvular lesion. In one of
these, where there was stenosis at both the mitral and tricuspid orifices,
death was sudden. In fifteen cases in which there was only cardiac hyper-
trophy, eleven deaths occurred from the heart-lesion, five of which were
sudden and directly due to the valvular lesion. In six cases in which dilata-
tion alone existed, four deaths directly resulted from the heart-lesion, and two
of these were sudden. In not one of fifteen cases of aortic disease did death
occur directly from the heart-lesion. Of these fifteen cases, sudden death
occurred in only two. In twelve cases of calcified mitral valve, no death oc-
curred directly from the heart-lesion ; there were but two sudden deaths,
both from cerebral apoplexy. The aortic and mitral valves were diseased in
fourteen cases ; two deaths were due to the heart-lesion, and there were but
three sudden deaths (uraemia, apoplexy, and croupous laryngitis). The aortic
and pulmonary valves were involved in three cases, all of which died suddenly,
and none directly from the heart-lesion. In two instances, the aortic, mi-
tral and tricuspid were involved, in neither of which sudden death occurred.
Thus, of eighty-one cases, twenty-four deaths only were directly due to the
heart-lesion, and of these only eight were sudden.
From the above cases it seems evident that the prognosis is not bad in
valvular disease, except when hypertrophy and dilatation coexist, and then
many complications are liable to occur. In 1870, I had a patient sixty
years old with extensive aortic reflux, who had had three attacks of pneu-
monia during the eight years he was under my observation. There was only
slight cardiac dilatation in this case.*
In aortic stenosis, life may be prolonged many years. So long as the
left ventricular hypertrophy compensates for the stenosis, the prognosis is
good ; but when it fails, and dilatation begins, cerebral anaemia soon re-
sults. If violent or prolonged efforts are followed by irregular heart-
action, sudden death may occur. Hypertrophy and dilatation, syncope,
cerebral anaemia, vertigo, muscular debility, a very pale face, and an irreg-
ular pulse render the prognosis unfavorable. Should vegetations be
suspected, there is danger of cerebral embolism. Complicating (secondary)
mitral disease renders the prognosis unfavorable. Death results from
complications, degenerations of the heart, and pulmonary cedema.
Aortic regurgitation is a graver form of disease than aortic stenosis. Its
duration is indefinite, as it may give rise to no symptoms until it is far ad-
vanced. Twenty-one days and five years are the extreme limits recorded.
In no other volvular disea!>e is sudden death so liahle to occur. Refer-
ence to the above cases shows that mitral stenosis ranks nearly equal to it
in this respect. The shorter and more gushing the murmur, the more ex-
1 Med. Rec, N. Y., Apr. 1, 1870, p. 66, etc.
* Dr. Walshe states that the oi-der of relative gravity of valvular lesion is : Tricuspid reflux, Mitral
reflux and stenosis, Aortic reflux, Pulmonarj' stenosis and Aortic stenosis.
PROGNOSIS IN CARDIAC YALVL'LAR DISEASE. 469
tensive the regurgitation, the effects of which must always be carefully esti-
mated before a prognosis can be given. Aortic regurgitation is, however,
more serious in the young than in adults, because in children the changes
are less atrophic and more inflammatory. In middle life and in those
who are subjected to great physical or mental strain, the prognosis is un-
favorable ; if the vessels in these patients show evidences of degeneration,
apoplexy and cerebral thrombosis are liable to occur. In the very old, I
have known extreme aortic regurgitation to exist a long time and cause
little inconvenience. Cyanosis and dropsy .and signs of heart failure, dila-
tation, or degeneration of the walls of the heart, render the prognosis un-
favorable ; if mitral regurgitation is developed, visceral derangements
occur and hasten the fatal issue. Sudden valvular incompetence is far
more dangerous than that which has developed slowly. The prognosis is
determined more by the condition of the heart walls and the general nutri-
tion of the patient than by any other elements. When aortic regurgitation
is complicated by aortic stenosis and mitral regurgitation with marked
derangement of the general circulation, the prognosis is bad. Death may
result from embolism, apoplexy, dropsy, pulmonary oedema, sudden cardiac
insufficiency, or from visceral complications. When the radial impulse is
felt a little after the apex-beat, it is always important to determine whether
the heart's action remains regular under mental excitement or violent
physical exertion ; if it does, the prognosis is good.
Mitral stenosis admits of no compensation. If extensive, it is always a
grave disease. The prognosis is estimated by the severity of the thoracic
symptoms ; if these are greatly increased by physical exertion, the prognosis
is bad, for pulmonary congestion and oedema, infarctions and diffused pul-
monary apoplexy with large extravasations are liable to occur. Statistics
show that sudden death occurs nearly as often in mitral stenosis as in aortic
regurgitation. Congenital mitral stenosis is not dangerous, nor does it occa-
sion inconvenience, for it is always associated with hyperplasia of the arterial
system. The later in life mitral stenosis occurs, the worse the prognosis.
Mitral regurgitation, when uncomplicated, gives rise to very little dis-
turbance of the circulation, because it is generally most fully compensated
for, and the changes which lead to it are of slow growth and their tendency
is to remain stationary. Patients with moderate regurgitation suffer little,
even on exercise. As long as right ventricular hypertrophy compensates,
there is no dyspnoea. As regards the duration of life, the pi'ognosis in
mitral reflux is good. When, however, stenosis and regurgitation coexist,
sudden pulmonary complications are very liable to occur, and the prognosis
is bad. When signs of right heart failure occur, the prognosis is bad.
CEdema of the extremities, fluid in serous cavities, cyanosis, dyspnoea, and
haemoptysis are indications of such failure. Death may result from gen-
eral anasarca, serous effusions into the pleurae, peritoneum, or pericardium,
pulmonary cedema and congestion, or from sudden cardiac insufficiency.
Extensive obstruction or regurgitation at the pulmonic orifice would lead
to serious results, but we have no statistics upon which to base a prog-
nosis.
470 DISEASES OF THE HEAET.
Tricuspid stenosis and obstruction, when associated with mitral dis-
ease, are very grave lesions, but not so bad as when resulting from chronic
bronchitis or pulmonary emphysema. When Jugular and epigastric pul-
sation are marked, the changes in the viscera already referred to quickly
ensue. Walshe says : " Tricuspid regurgitation is the worst of all valvular
lesions." Patients with tricuspid regurgitation are in constant danger
from intercurrent attacks of acute pulmonary hypersemia. Tricuspid dis-
ease leads more rapidly than any other valvular lesion to cyanosis and
dropsy.
Treatment of Valvular Diseases of the Heart. — The treatment of aortic
valvular disease can be summed up in, rest, diet and regimen. Rest must
be mental as well as physical. The appetite, emotions and passions must
be under perfect control, hence a sedentary country life is best. Strain-
ing, especially when the hands are above the head, is to be avoided. The
nutrition must be kept as perfect as possible to guard against cardiac de-
generative processes. Sugar, sweet vegetables, and animal fat must be
sparingly used. The food should consist of nitrogenized material taken
in quantities that do not interfere with the heart's action. In aortic re-
gurgitation, patients while sleeping should assume, as nearly as possible, a
horizontal position, as they thus lower the height of the distending column
of blood, and relieve both the cardiac circulation and the tendency to pul-
monary congestion. When, defective aortic pressure reacts injuriously on
the gastric and hepatic secretions, moderate alcoholic stimulation may be
cautiously employed. The bowels should be daily gently moved. That
the skin may be active, the body must be warmly clothed. Prolonged ex-
posure to cold is to be avoided. Warm baths, especially warm sea-baths,
are beneficial. Medicine is not to be given until the hypertrophy ceases
to compensate. In aortic reflux with feeble heart-power, tr. digitalis
and tr. ferri perchlor. are to be given in ten-drop doses, three times a day.
The iron is especially called for when anaemia is present. Digitalis is
given as a cardiac tonic, hence small doses only are required. As long as it
increases the urinary secretion it is safe to continue it. When vertigo and
syncope are prominent symptoms, quinine and strychnia may be given
with the digitalis. Should the heart act with violence and rapidity, or
if there is evidence of high arterial tension, aconite is serviceable.
In aortic incompetence small doses of arsenic have a stimulating effect,
when given with digitalis and iron. Iron may disturb the stomach ; arse-
nic seldom does. Quassia or calumba should always be given luith iron.
When the hepatic or gastric vessels are engorged, three or four leeches
over the epigastrium or liver, followed by warm anodyne poultices, will
often afford relief. Large quantities of fluid should never be taken into
the stomach at one time. Symptoms of angina pectoris with dyspnoea and
local pain are signs of aortitis, which demands leeches over the sternum
and small doses of mercury. The treatment of dyspnoea, dropsy, etc., etc.,
will be considered in the treatment of mitral disease. The pain of aortic
disease may be so severe as to demand an anodyne ; opium by the mouth
cannot be given, but the sulphate or hydrochlorate of morphia can be
TBEATMENT OF CAKDIAC VALVULAR DISEASE. 471
given hypodermatically. Nitrite of amyl often relieves the angina
promptly.'
The first thing in the treatment of mitral stenosis is to have the patient
fully understand his exact condition, that he may follow your advice im-
plicitly, for the treatment is for the most part in his own hands. As to
nutrition, the same rules hold as in aortic disease. There must be at least
one gentle daily evacuation of the bowels. Straining at stool is to be
avoided. The use of alcohol, strong tea or coffee or tobacco is to be pro-
hibited. If anaemia exists, give iron one-half hour after meals, gr. x — xx
of Vallette's mass, two or three times daily for a long period. The pro-
longed use of the voice is dangerous. Small doses of quinine and strych-
nia alternating with the iron are advantageous. If there is anorexia, the
vegetable bitters are to be given. The triple phoi^phates of iron, quinine
and strychnine, or small doses of dilute sulphuric acid will improve these
patients when they show signs of extreme debility. In every case of mitral
disease there comes a time when pulmonary hypergemia shows failure of
right cardiac compensation. An adjustment of the heart to the circula-
tion is now effected by administering digitalis, which should only be given
when heart failure is marked and is accompanied by pulmonary congestion.
Half an ounce of the infusion, every two hours for twenty-four or
forty-eight hours, is often required to overcome the cardiac failure. The
time will come when digitalis ceases to sustain the heart, hence it should
be used sparingly and carefully — never continuously. When the pulse is
rapid, feeble, and irregular, more time and greater force for the ejection of
blood from the ventricle are demanded. Digitalis meets both indications.
The pulse becomes regular, full, and forceful. The urine becomes abun-
dant and normal. Pulmonary engorgement diminishes and commencing
dropsy slowly disappears. Hayden advises ]0 drops of chloroform, 15 drops
of tincture of digitalis, and 15 drops of tincture ferri perchloridi, in one
ounce of water every three hours. When asystolism is present, or sup-
pression of urine is threatened, digitalis must be given in large doses. In
most cases of mitral stenosis digitalis is contraindicated. The dropsy of
advanced mitral reflux may be promptly relieved by pulvis jalapm co. com-
bined with calomel in sufficient quantity to produce prompt and free cathar-
sis. Squills, juniper, broom, and cream of tartar act as diuretics in such
cases.
In mitral regurgitation a compound of digitalis and nitrous ether acts
well as a diuretic. Whenever a diuretic is given in heart disease, the loins
should be cupped or warm poultices applied and the bowels freely purged.
In copious hasmoptysis in cardiac disease, ergotin in full doses hypoder-
mically may be given. The haemoptysis that accompanies pulmonary apo-
plexy of heart disease may relieve the dyspnoea ; hence Drs. Dickenson,
Fagge and other English authorities recommend venesection for relief of
pulmonary engorgement. Precordial pain accompanying valvular disease
may be relieved by the application of leeches over the precordial space.
I Barlowe and Fagge advise senega and caibunate of ammonia for the less severe effects of aortic regu^
gitation, which they regard as least amenable to treatment of all cardiac diseases.
472 DISEASES OF THE HEAET.
Hyoscyamus, hydrochlorate of morphia, nitrite of amyl, chloroform, and a
belladonna plaster over the precordiam may be employed for the same pur-
pose. Such pain is the cry of a heart-muscle for higher nutrition. Bleed-
ing favors dropsy by thinning the blood and by diminishing the heart-
power ; it should never be practised except in emergencies,^ When digi-
talis fails to regulate the circulatory disturbances, its use does harm ; but
in all cases of mitral disease where this drug has not been used, it is safe to
say that its administration will give prompt relief. Morphia is the best
anodyne and hypnotic to be used in mitral disease.
Hygiene, diet, and exercise are to be the same in pulmonary, as in
mitral disease, further treatment is solely symptomatic.
The treatment of tricuspid ohstruction depends on the gravity and
sequelae of the accompanying mitral disease. For tricuspid stenosis never
occurs till mitral stenosis is excessive, and the latter condition is the pre-
dominant one. The general treatment is the same as in aortic and mitral
diseases. The patient should lead a perfectly quiet life in a warm, equa-
ble climate. When this lesion occurs with mitral disease, digitalis should
not be omitted, for the drug promotes ventricular contraction, and thus
relieves the tricuspid pressure. In tricuspid regurgitation with emphysema,
this drug should be very cautiously given, and its use or omission must
depend upon the effects produced in each case. If cerebral symptoms are
exaggerated it must be stopped. Tonics should be given on the same prin-
ciples as in mitral disease and the same drugs used. A drastic purge or
talking a few ounces of blood from the arm temporarily relieves the venous
engorgement. Dropsy and local oedema are treated as in mitral disease.
For the relief of the gastric, hepatic and intestinal symptoms, which are
often the most troublesome occurrences in tricuspid regurgitation, I have
found one or two purgative doses of calomel to act promptly and satisfac-
torily — in fact, in all cases of heart disease in which there is evidence of
hepatic hypersemia, an occasional calomel purge will be followed by marked
relief and improvement.
CAEDIAC HYPERTEOPHT.
By the term cardiac hypertrophy is meant thickening of the walls of the
heart by an increase in their muscular tissue. This muscular increase may
be confined to one portion of the heart, or it may involve the walls of both
auricles and ventricles. There are three recognized forms of cardiac
hypertrophy : —
I. Simple Hypertrophy. — In this form there is an increase in the thick-
ness of the cardiac walls, the capacity of the cavities remaining normal.
Simple hypertrophy is usually confined to the left ventricle, and is most
frequently met with in connection with chronic Bright's disease and chronic
alcoholismus.
II. Eccentric Hypertrophy. — In this form there is thickening of the walls
■of the heart, with increase in the capacity of its cavities. It is most com-
1 Niemeyer advises arsenic and antimony in mitral valvular disease ; when and why be does not say.
CAEDIAC HYPERTROPHY. 473
monly met in connection with, or occurs as the result of, some valvular
lesion.
III. Concentric Hiipertro])liy. — In this form there is thickening of the
walls of the heart, with diminution in the size of the cavities. Some ob-
servers deny the occurrence of this form of hypertrophy, and claim that the
diminution in the capacity of the cavities is only apparent — that it is the
result of violent ventricular contraction just prior to death. I have never
seen any example of this form of hypertrophy.
Morbid Anatomy. — The anatomical changes in cardiac hypertrophy
vary according to its seat, and sometimes according to the character
of the hypertrophy. In eccentric hypertrophy, there will always be an
increase in the size of the papillary muscles, and the septum will be
thickened, which does not necessarily occur in connection with simple
hypertrophy. The ventricular septum is far less liable to hypertrophy
than the rest of the ventricular parieties. It is often difficult, even after
death, to determine the existence of a moderate degree of cardiac hyper-
trophy, while extensive hypertrophy is very readily recognized.
When cardiac hypertrophy exists, the first thing noticed is a change
in the shape of the organ, and this change will correspond to the seat of
the hypertrophy. If the hypertrophy js confined to the left ventricle, either
simple or eccentric, the heart will assume a more than usual pyriform
shape, and will become elongated — the right ventricle seems to be a mere
appendage to the left. On the other hand, hypertrophy of the right ven-
tricle increases the horizontal measurement of the organ and gives it a more
oval shape, the apex not being as pointed as in health, since the extremities
of both ventricles are on the same level. If all the cavities of the heart
are increased in capacity, and their walls hypertrophied, the whole heart
will be increased in size, but the change will be most marked in its hor-
izontal direction, and the organ will assume a globular shape. Sometimes
the shape of the organ is not notably changed in general hypertrophy.
Left ventricular hypertrophy occurs oftener than right, and hypertrophy
of the riglit auricle much oftener than that of the left. The ventricles are
hypertrophied oftener than the auricles. In all varieties of hypertrophy
the cardiac walls are stiff, so that when the cavities are opened and the
blood has been removed from them, they do not collapse. The substance
of an hypertrophied left ventricle can generally be torn with ease, while an
hypertrophied right ventricle is tough and leathery. The color of the
muscular tissue is redder than normal ; there is an increase in the
number of the muscular fibres, which differ in no way in their anatom-
ical structure from those of normal heart muscle. Occasionally there
is an increase in the size of the cardiac muscular fibres.^ There may be
more or less increase of connective-tissue between the muscular bundles ;
and Dr. Quain stated that this may be so excessive as to be a ''false hyper-
trophy." Sometimes there are accumulations of fusiform involuntary
• Cornil and Ranvier state that "it is not yet known whether hypertrophy is entirely due to increase in
size of the muscle-fibres, or to a new formation of these fihres. The phenomena of development of new
tuuscle-fibres have never been observed, so that the former hypothesis seems the more probable."
474 DISEASES OF THE HEAET.
fibres which have not as yet developed into the higher state of striked
fibres.
There is no limit to cardiac hypertrophy. The heart may reach such a
degree of enlargement as to weigh forty ounces more than in its normal
state ("cor hovinum'-). After the hypertrophy reaches a certain point
there is dilatation, preceding and accompanying which is fatty degen-.
eration, which first occurs in the more recently formed muscular fibres.
An increase in the number or size of the muscular fibres of the heart walls,
causes a corresponding increase in the heart power. The walls of the
hypertrophied heart vary in thickness according to the cause of the liyper-
trophy. The walls of the left ventricle may become an inch and a half, or
even two inches thick, while those of the right ventricle rarely reach
an inch in thickness. The auricles are seldom more than double their
normal thickness. The columnas carnese of the right ventricle are more
liable to hypertrophy than the walls. Sometimes the walls of a cavity are
thinned at one point while they are hypertrophied at another. The heavier
a heart becomes the deeper does it lie in the thoracic cavity ; the diaphragm
is pushed down and the heart inclines more to the left of the thorax.
Etiology. — In general terms cardiac hypertrophy is caused by over- work ;
for some reason the cardiac walls are called upon to perform more than
their normal amount of labor, and an increase in the number of their muscu-
lar fibres necessarily follows. Whenever the function of the heart is per-
manently or repeatedly overtaxed, or when the resistance which it should
normally encounter is increased, hypertrophy of its walls is the result. The
modes by which it is directly induced are as follows : —
(1) Dilatation of the Cavities of the Heart. — Under certain circumstances
dilatation of one or all of the cavities of the heart takes place during its
diastole ; the capacity of the cavities is consequently increased, and they re-
ceive more than their normal quantity of blood. A certain degree of force
is required to discharge the normal quantity of blood ; if there is more
than the usual amount, an abnormal degree of force is required to expel
it. This demand for increased heart power is supplied by an increase of mus-
cular fibres in the heart walls, — the hypertrophy is developed in proportion
to the increase of force required. This is the cause of those forms of car-
diac hypertrophy which occur in connection with valvular insufficiency.
Under these circumstances the hypertrophy is always eccentric, and is not
due so much to the valvular lesions as to the dilatation of the heart cavities
which occurs as a result of these lesions. The order is, first, dilatation,
then hypertrophy to compensate for the dilatation. Dilatation is devel-
oped during cardiac diastole ; hypertrophy during cardiac systole.
(2) Mechanical Obstruction. — Of those causes which originate in the
heart, aortic stenosis gives rise to hypertrophy of the left ventricle ; mitral
stenosis to hypertrophy of the left auricle ; pulmonic disease to hypertro-
phy of the right ventricle ; and tricuspid stenosis to hypertrophy of the
right auricle. In the list of mechanical causes are included all those dis-
eases of the arteries which diminish their elasticity. The walls of the large
arteries may lose their elasticity from atheromatous degeneration, or tney
CARDIAC HYPERTROPHY. 475
may be constricted or dilated, and thus offer obstruction to the blood cur-
rent. An aneurismal tumor may have developed sufficiently to obstruct
the current of blood/ or some tumor may press upon and diminish the
calibre of the aorta ; under such circumstances a more than normal amount
of work wiil be imposed upon the left ventricle, and simple cardiac hyper-
trophy will be developed as the result. Twisting of the thorax and de-
formities of the spine, thorax, etc., may act in the same way. Again, ob-
struction to the pulmonary circulation will give rise to hypertrophy of the
walls of the right ventricle ; in many instances dilatation will occur prior
to the hypertrophy, but in quite a large number of cases direct hypertrophy
of the right ventricular walls will occur as the result of obstruction to the
pulmonary circulation. Such obstruction may be developed in connection
with pulmonary emphysema, fibroid and compressed lung, chronic pleurisy,
asthma, hydrothorax, and other chronic diseases which interfere with the
circulation of blood through the lungs. It does not occur in the early stage
of pulmonary phthisis, for the pulmonary circulation is not obstructed un-
til the advanced stage of the disease. Hypertrophy of the left ventricle may
also result from interference with the general capillary circulation. Exam-
ples of this are met with in chronic Bright's disease.
Simple hypertrophy of the cardiac walls is one of the most constant
attendants of the cirrhotic form of ividney disease. Gull and Sutton regard
this as secondary to arterio-capillary fibrosis.'^ In chronic alcoholismus,
rheumatic hyperinosis, or any other condition which interferes with the
systemic capillary circulation, more or less extensive, simple cardiac hyper-
trophy of the left ventricle is developed.
Anything which increases for any length of time the rapidity and force
of the heart's contraction may produce cardiac hypertrophy. Among this
class of causes may be included excessive and prolonged muscular exercise,
especially in young suljeds, and in soldiers who are on the march. Emo-
tional conditions that produce cardiac palpitation, prolonged mental excite-
ment, the immoderate use of strong coffee or alcohol are causes of cardiac
hypertrophy. These are styled ''nervous" causes (Quain) ; and to this
class probably belong those cases occurring in Grraves's or Basedow's dis-
eases. Pericarditis is not infrequently a cause of cardiac hypertrophy,
either by inducing softening and dilatation of the ventricles, or by the ob-
struction which is offered to the heart's action by the adhesions between its
two surfaces. The heart becomes hypertrophied in pregnancy, but returns
again to normal after delivery. Sometimes no cause can be found for car-
diac hypertrophy.
Symptoms. — The valvular lesions, arterial changes, or capillary obstruc-
tions which are associated with cardiac hypertrophy modify, or to a greater
or less extent obscure the phenomena which attend the hypertrophy. Total
eccentric hypertrophy usually cannot be detected except by a physical ex-
ploration of the chest. There are, however, certain subjective symptoms
' But this is rare ; Axel Key has shown that aneurism of the Morta a!one. 1? not prodactive of left ven-
tricular hypertrophy, since it does not lead to increase in the arterial tension.
2 The connection between chlorosis and cardiac hypertrophy has recently been widely discussed. Lew-
insky concludes that from " lessening of the hiemoglobin in chlorosis cardiac hypertrophy results."
476 DISEASES OF THE HEAET.
which are important and which will aid in its diagnosis. The direct effect
of general hypertrophy of the heart is to cause an abnormal fulness of the
arteries and a lack of blood in the veins. The pulse is full and strong, and
is bounding in character ; the face is easily flushed, the eyes somewhat
prominent and brilliant, and there is carotid pulsation. The respiration is
not usually disturbed until the heart becomes so increased in size as to give
rise to pressure upon the adjacent lung-tissue and upon the diaphragm ;
then the patient will have a sense of fulness about the chest, and with that
sense of fulness there will be more or less uneasiness in the epigastrium,
and the stomach digestion may be more or less interfered with. If dyspnoea
is present it is due to the pressure of the enlarged heart rather than to any
change in the lung-tissae. In eccentric hypertrophy with dilatation, more
especially when the right cavities are affected, pulmonary oedema and con-
gestion are usually present, and then there is marked dyspnoea.
In simple hypertrophy there is often a dry irritating cough ; and in young
fleshy females it has a wheezing character. In right heart enlargements the
cough is often distressing. This class of patients when excited are very apt
to complain of cardiac palpitation. The heart's action is often irregular
and intermittent. In almost all cases there is some cerebral hyperaemia,
consequently it will be found that in those who are the subjects of eccen-
tric cardiac hypertrophy alcoholic stimulants, nervous excitement, and
active physical exercise will cause headache, vertigo, ringing in the ears and
bright spots or flashes before the eyes. In left hypertrophy, haemoptysis is
common and comes on suddenly. Eupture of the bronchial arteries may
occur, ^ Cerebral apoplexy may at any time occur, when the arteries are
predisposed to, or have already developed small aneurisms. In fact, the
majority of ce,rebral apoplexies which occur in young subjects are as-
sociated with cardiac hypertrophy. It is now well established that there
is a close connection between atheroma of the arteries and cardiac hyper-
trophy. Some observers claim that the cardiac hypertrophy is secondary
to the arterial changes ; but it is a fact of every-day observation that hyper-
trophy from valvular changes will give rise to atheromatous changes in the
arteries for reasons which have already been fully considered in connection
with the history of valvular diseases. The steps of the change are, first,
cardiac hypertrophy ; second, endarteritis ; and, lastly, atheroma. The
general syniptoms considered in connection with its physical signs render
its diagnosis easy.
Physical Signs. — The physical signs of cardiac hypertrophy will vary with
the seat and extent of the hypertrophy. When it is general, upon inspec-
tion it will be noticed that although the heart's action is regular there is an
increased area of impulse, and that there is a motion with each cardiac
pulsation over and even beyond the precordial space. In children there
is often bulging of the precordial space.
In right ventricular hypertrophy, inspection may reveal a rounded
smoothness of the epigastrium, with, perhaps, some bulging of the ensi-
1 Niemeyer states that epistaxis is not infrequent. When the right heart is hypertrophied melsena or
haematemesis may be produced from obstructed liepatic circulation.
CARDIAC HYPERTROPHY.
477
Fig. 104.
Diagram illustrating the Physical Signs ia Hypertrophy
of the Left Ventricle.
A. Bight ventricle ; B. Left ventncle ; C. Bight au-
ricle ; B. Left auricle ; E. Aorta ; F. Pulmonary
artery ; ff, H. Dotted lines showing limit of hyper-
trophy of the venti'icle.
form and lower left costal carti-
lages. The apex-beat may be dif-
fused, extending toward the ensi-
form cartilage.
On palpation the cardiac area is
abnormally increased, and the im-
pulse has a heaving, lifting char-
acter. The shock of an hyper-
trophied heart may be perceptible
over the whole precordial space,
and in cases of extensive hyper-
trophy the head of the listener is
often lifted by the shock. When
the right ventricle is the seat of
the hypertrophy, it may cause a
strong epigastric impulse. When
the left ventricle is the seat of the
hypertrophy the apex-beat is felt
farther to the left than normal,
sometimes three inches below, and
three or four inches to the left of
the normal position.
On percussion, in general cardiac hypertrophy, the normal area of
cardiac dulness, both deep-seated
and superficial, will be increased
to the right, left and downward.
The dulness is increased upward
only when the auricles are not only
hypertrophied but also dilated. If
the hypertrophy is confined to the
right ventricle the area of dulness
may extend considerably to the
right of the sternum, sometimes
reaching an inch or more beyond
the right sternal edge, and extends
lower down than normal. While if
the hypertrophy is confined to the
left side of the heart, the area of
dulness may extend considerably
beyond the left nipple. The area
of superficial dulness will also be
increased. In eccentric hypertrophy
of the left ventricle, the superficial
area of dulness will be increased to the left ; when the same condi-
tion of hypertrophy is present in the right ventricle, the superficial area
of dulness will be increased to the right and downward.
On auscultation, the first sound of the heart, if not accompanied by a
Fig. 105.
Diagram Illustrating the Physical Signs in Hyper-
trophy of the Right Venticle.
A, A. Limit of hypertrophy.
478 DISEASES OF THE HEART.
murmur, is dull, muffled, and prolonged, and in some cases greatly in-
creased in intensity. The post-systolic silence is shortened. If the hyper-
trophy is confined to the left ventricle, the second sound heard over the
aortic orifice is increased in intensity ; if the right ventricle is hyper-
trophied the second sound over the pulmonic orifice will be increased in
intensity. In hypertrophy of the right ventricle the first sound is more
distinct and more superficial than normal, and the second sound is not
infrequently reduplicated. In extensive hypertrophy both sounds of the
heart often have a metallic ring. There is a diminution or an entire ab-
sence of the respiratory murmur over the normal precordial region. When
extensive pulmonary emphysema exists, although the heart may be very
much increased in size, the increase in the volume of the lungs will prevent
appreciation of the increased force in the apex-beat, and the heart-sounds
will be diminished rather than increased in intensity. It may, however,
be assumed that when extensive pulmonary emphysema is present and is
attended by venous pulsation in the neck, there is hypertrophy and dilata-
tion of the right ventricle.
Differential Diagnosis. — Cardiac hypertrophy may be confounded with
cardiac dilatation, thoracic aneurism, mediastinal tumors, consolidation
of lung-tissue surrounding the heart, and displacement of the heart. Under
certain circumstances pleuritic effusion may be confounded with cardiac
hypertrophy. The differential diagnosis of the first four conditions can
be better considered in connection with cardiac dilatation.
Displacement of the (normal) heart may be distinguished from hyper-
trophy by there being no increase in the area of dulness, no change in
character or intensity of heart-sounds, and no '* heaving " impulse. Be-
sides, certain subjective symptoms, especially those of cerebral hypergemia,
are marked in cardiac hypertrophy and absent in displacement.
Prognosis. — Cardiac hypertrophy admits of a more favorable prognosis
than any other cardiac affection. In almost all instances it is compensa-
tory ; the urgent symptoms of some other cardiac affection are relieved by
it and life is prolonged. Simple cardiac hypertrophy, unless the result of
aortic stenosis, may exist for years without the occurrence of any danger-
ous or very troublesome symptoms. Slight hypertrophy of the left ventri-
cle is very common in those who have led an active life, and have been
compelled to perform active and prolonged physical labor ; the hyper-
trophy is no more than is required to maintain an equilibrium in the cir-
culation, and in no way interferes with duration of life. In the young and
in athletes, if the cause be removed, the prognosis is very favorable. The
patient should not be made aware of the presence of such hypertrophy, for
although there is no danger attending it, a knowledge of the fact may
greatly alarm him. When there is not only hypertrophy but also degen-
eration of the hypertrophied walls, the result of imperfect nutrition, the
prognosis is very unfavorable.
The prognosis in hypertrophy of the right ventricle is not as favorable as
in hypertrophy of the left, because it must inevitably be accompanied by
considerable pulmonary obstruction, and consequently is rapidly progres-
CARDIAC HYPEETROPHY. 479
sive. In Bright's disease, or when there is disease of the arterial coats, the
prognosis is unfavorable. The prognosis in any case of cardiac hyper-
trophy depends upon the cause of the hypertrophy, and upon the kind of
valvular or other cardiac lesion coexisting.
Treatment. — Althougii cardiac hypertrophy cannot be removed, still,
much can be done to arrest its development by removing the causes which
produce it, or by rendering them inoperative. Patients with cardiac hy-
pertrophy must especially avoid alcoholic stimulants, immoderate eating,
active and prolonged physical exercise and mental excitement. All those
conditions which interfere with the general circulation must, if possible,
be removed. This embraces interference with the abdominal circulation,
as well as with the pulmonary and systemic. Straining at stool and con-
stipation should be avoided by daily keeping the bowels freely moved. This
condition of the bowels should be maintained chiefly by habits of life and
regulation of diet, cathartics being resorted to only in exceptional cases.
As little liquid as possible should be taken into the stomach. Any symp-
toms of cerebral hyperaemia must be immediately relieved by those means
which diminish the force of the heart's action. When the pulse is full and
strong and there are evidences of cerebral hyperaemia, it has been the prac-
tice of some to bleed, but this treatment is contraindicated, for the pres-
ence of anaemia greatly aggravates the dangers arising from cardiac hyper-
trophy, since it increases irritability and excitability of the heart. The
symptoms must be very urgent to warrant venesection.
Of all the remedial agents which diminish the force of the heart's action,
I have found aconite the best. When given in full doses it is more reliable
than any other means. From two to three drops of Fleming's tincture of
the root may be administered every three or four hours. No drug that I
have used so fully and promptly relieves the vertigo and other painful sen-
sations that attend cardiac hypertrophy. Hydrocyanic acid, belladonna,
and conium are used, but are inferior to aconite. Whenever the dilatation
of the cavities exceeds the hypertrophy of the cardiac walls, aconite does
harm.
Digitalis is contraindicated, unless there is evidence of heart insuffi-
ciency. When digitalis is administered in chronic Bright's disease, although
hypertrophy of the left ventricle is one of its constant attendants, its ad-
ministration is for the relief of the kidneys, which, when relieved, give
secondary relief to the hypertrophied heart. Besides, in many cases of
Bright's disease, the heart, although hypertrophied, is not able to overcome
the obstruction to the circulation in the small arteries and capillaries, and
the tonic effect of the digitalis raises the heart-power to the point where the
obstruction is overcome and the equilibrium of the circulation established.
Acetate of lead and veratrum viride axe much thought of by many Ameri-
can authorities. For painful palpitation, wild cherry bark is the best drug.
Morphine is seldom of service.
480 DISEASES OF THE HEAET.
CAEDIAC DILATATIOlSr.
By the term cardiac dilatation is understood a condition of the heart in
which there is an increase in the capacity of its cavities, with diminution
of its contractile power. There are three forms : —
I. Simple Cardiac Dilatation, in which the capacity of the heart-cavities
is increased without any marked change in the cardiac walls. Such a con-
dition is apt to occur during convalescence from any disease in which there
has been great impairment of nutrition, such as typhoid fever.
II. Hypertrophic Cardiac Dilatation. — In this form there is increase in
the capacity of the heart-cavities and increase in the thickness of the heart-
walls ; but the contractile power of the heart may be diminished as the re-
sult of a degeneration following eccentric hypertrophy, or independent of
any hypertrophy of the cardiac walls.
III. Atrophic Cardiac Dilatation. — In this form the capacity of the heart-
cavities is markedly increased, and the cardiac walls are thinner than nor-
mal. Sometimes the ventricular walls are not more than two or
three lines thick, and the auricular walls may become so thinned that
they will present the appearance of a simple membrane. Under these
circumstances the contractile power of the heart is. almost lost. Anatom-
ically, as well as clinically, the significance of cardiac dilatation is in pro-
portion to the excess of the capacity of the cavities over the thickness of
the cardiac walls. A cardiac cavity may be very much increased in capac-
ity, but so long as there is an increase in the muscular power of its walls
sufficient to meet the demand for the increased work they are called upon
to perform, there will be little or no disturbance of the general circulation.
Eccentric hypertrophy and hypertrophic dilatation approach each other
very closely, and it is often very difficult to draw the line between them.
Morbid Anatomy. — One or all of the heart cavities may be the seat of
dilatation. The shape of the heart is changed according to the cavity
which is the seat of the dilatation. If the dilatation is confined to the
right ventricle, the heart will be increased in breadth and the apex may
appear bifid ; while if the dilatation afPects mainly, or only, the left ven-
tricle the heart will be elongated. Dilatation occurs most frequently in
the auricles, and thinning of the cardiac walls is most commonly met
with here ; next the right ventricle and last of all the left ventricle is the
seat of dilatation. When all the ■ cavities are dilated the entire organ is
increased in size and assumes a globular shape. "When the ventricles are
excessively dilated, the trabeculge are sometimes reduced to the condition
of fleshy tendinous cords. When the walls of the left ventricle are very
much thinned they collapse when the ventricle is cut into. It is a question
whether dilatation ever exists without some hypertrophy.. The hypertro-
phy is apt to be overlooked, for the walls of the dilated cavities seem to
be of normal thickness.
The structural changes which take place in the muscular tissue of the
walls of the dilated cavities vary with the morbid process which precedes
CAEDIAC DILATATION". 481
and attends the dilatation. When it results from pericarditis or myocar-
ditis there are serous infiltration and granular degeneration of the muscu-
lar fibres ; when it is the result of fatty metamorphosis the muscular fibres
undergo fatty degeneration. In hypertrophic dilatation it is often impossi-
ble even by a microscoj)ic examination to determine the exact changes
which the muscular fibres undergo ; the abnormal state of the muscular
fibres can only be determined by the other evidences of feeble heart power.
A heart distended with blood and relaxed by putrefaction may, on first
view, be mistaken for a dilated heart. The distinctive marks of a heart
softened by the putrefaction processes are its extreme softness, its satura-
tion with the coloring matter of the blood, and the evidences of decom-
position in other parts of the hody.
Etiology. — The causes of cardiac dilatation are numerous. One class of
causes may be included under the head of changes in the muscular tissue
of the cardiac walls.
I. Changes in the muscular tissue which accompany pericarditis and
endocarditis.
II. Fatty degeneration of the muscular fibres.
III. Cardiac dilatation which occurs with certain forms of protracted dis-
ease, such as typhoid fever, when the most careful microscopical examina-
tion will fail to detect any uniform change in the muscular fibre, except,
perhaps, a general atrophy of all the tissues.
All the causes of cardiac hypertrophy may become the causes of dilata-
tion in a heart which has a feeble resistant power, either inherent or ac-
quired. This group of causes may be classed under three heads.
I. Internal pressure during a cardiac diastole. — The wall of a heart
may become weakened hy the changes which occur in certain prolonged
diseases, or it may become the seat of serous infiltration or some form of
degeneration ; then, an abnormal pressure within its cavities during its
diastole will cause the cai'diac walls to yield beyond their normal limits.
Such distention is certain to be followed by permanent dilatation of its
cavities. Most of the valvular lesions may be the direct cause of such
internal pressure during the cardiac diastole, after the manner already de-
scribed in connection with the etiology of cardiac hypertrophy. Gener-
ally, when the cardiac cavities become distended beyond their normal lim-
its, and thus temporarily lose their contractile power, rapid hypertrophy of
the cardiac walls is developed which compensates for, and to a certain ex-
tent overcomes, the dilatation. But, if the cardiac walls are enfeebled
by any degenerative changes, such compensatory hypertrophy does not take
place. Any valvular lesion which will permit a double current of blood
to flow into a cardiac cavity during its diastole, the heart walls having be-
come enfeebled by degenerative changes, will give rise to dilatation.
II. Wien the muscular tissue of a heart is the seat of primary fatty de-
generation, after a time dilatation of the cavities takes place, the normal
blood pressure being sufficient to produce the dilatation. In the same man-
ner a heart will become dilated when its walls are the seat of myocarditis.
That form of cardiac dilatation which follows rheumatic fever, pyaemia,
•J I
482 DISEASES OF THE HEART.
erysipelas, typhus and typhoid fevers, or chlorosis, usually disappears
when the attenuated muscular fibres of the heart, with the general muscu-
lar system, regain their normal condition ; but the dilatation which results
from fatty or fibroid degeneration of the muscular walls of the heart or from
new growths steadily increases.' These fibroid changes usually accom-
pany chronic alcoholismus.
III. Another cause of cardiac dilatation, which has already been referred
to in connection with the history of valvular diseases, is degeneration of the
muscular substance of the heart, which is the seat of eccentric hypertrophy j
the manner of its development has been already described. The dilatation
does not occur in this class of cases until long after the development of the
valvular diseases which give rise to hypertrophy. Usually the hypertrophy
becomes very extensive before the degenerative dilatation commences, but
when it once begins it progresses very rapidly, and the failure of heart
power is attended by very distressing symptoms. The power which ob-
struction to the pulmonary circulation has to produce dilatation of the
right ventricle, has been considered in connection with valvular diseases of
the heart. When these obstructions exist, eccentric hypertrophy, rather
than dilatation, is generally developed.
Symptoms. — The symptoms that attend the development of cardiac dila-
tation will depend upon the character and seat of the dilatation. In simple
cardiac dilatation the heart walls are of normal power, but the capacity of
the cavities is increased, and the amount of blood to be expelled with each
cardiac pulsation is greater than normal ; consequently there is labored
action of the heart (often so great as to be mistaken for the action of an
hypertrophied heart), yet the force of the heart's action does not increase,
and therefore we have a feebleness of the radial pulse. The rhythm of
the heart's action will not be disturbed. In that form termed atrophic
dilatation there is a very different state of affairs. The heart cavities are
not only dilated, but the walls of the cavities are thinner than normal ; the
heart power is insufficient for the expulsion of the blood from its cavities, and
as a result there is a labored action, and the heart, on account of the increased
amount of labor, staggers in its action, the arteries are imperfectly filled
with blood, the veins become over-distended, the rhythm of the heart's
action is disturbed, and the radial pulse becomes markedly feeble and inter-
mitting. These latter points are of special importance as affecting the
question of prognosis, for if a patient has all the symptoms of cardiac
dilatation without an irregular and intermitting pulse, the prognosis is com-
paratively good. The same disturbance of the circulation occurs in that
form of dilatation which is developed from the degeneration of eccentric
hjrpertrophy.
The first and perhaps the most constant symptom which is common to
all varieties of cardiac dilatation, is cardiac palpitation. At times this
palpitation is very distressing. There is almost constantly a sense of pain-
i Eecently not a f ew cases of idiopathic cardiac dilatation have been recorded. Extreme but passing
debility, the occurrence of the menopause, and too hard physical work for the years of strength — these
have induced marked dilatation, which in most cases was recovered from. (Med. Times and Gaz., AprU
^7, 1880.)
CAEDIAC DILATATION. 483
ful pulsation in the region of tne heart. The patient complains of weight,
oppression, or uneasiness in the cardiac region, with a sense of fluttering
and a tendency to sighing respiration. Very soon after the palpitation has
manifested itself, the patient will begin to suffer from dyspnoea on slight
exertion; when he is perfectly quiet he suffers very little. As the irreg-
ularity of the heart's action and the palpitation increase, the patient's
countenance assumes a pale, languid, anxious expression, with more or less
lividity of the lips. The extremities are habitually cold. On excitement,
or active physical exertion, the entire face and neck become livid ; the
pulse, which is usually regular, for a time becomes irregular and inter-
mittent. In this condition patients often live some time in comparative
comfort; but they are conscious not only of a loss of physical, but also of
mental power, and they are troubled with dyspeptic symptoms and a sense
of fulness about the epigastrium. Vomiting is not infrequently a trouble-
some symptom.
As the cardiac dilatation reaches a point at which there is constant car-
diac insufficiency, the patient suffers constant dyspnoea, which becomes
severe on slight exertion ; the cardiac palpitation is always present, and
often accompanied by attacks of syncope. The countenance assumes a still
more anxious expression, and the lips are always livid ; the pulse is
constantly irregular and intermitting. With these symptoms there will
be scantiness of urine, which will contain albumen and perhaps blood ; the
feet and ankles become oedematous, the oedema generally extending up-
ward until the patient is in a state of general anasarca. The breathing
becomes very difficult, so much so that the patient is unable to lie down,
but is obliged to sit with his head inclined forward and resting on some
firm support ; he is unable to utter more than a single word at a time. The
respirations may be thirty or forty per minute, and panting and noisy in
character. Cough and expectoration are not uncommon; hsemoptysis may
occur, and in some cases pulmonary infarctions form. Petechial extravasa-
tions not infrequently occur, especially in dilatation of the right heart.
The extremities become cold and blue ; the mind wanders, the skin as-
sumes a yellow tinge, and the patient dies from general anasarca with pul-
monary oedema or from urinary suppression. During the advanced stage
of this affection violent paroxysms of dyspnoea sometimes occur, in some
cases of which it seems as though the patient must die, yet they are rarely
immediately fatal, but the patient passes from them into a state of coma
and, later, dies unconscious. There is always danger from sudden syncope,
which may prove immediately fatal.
Although the general symptoms vary greatly in different cases, the
physical signs are very distinctive.
Physical Signs. — Upon inspection it will be noticed that the area of the
cardiac impulse is increased ; but it is so indistinct that it will be difficult to
determine (by inspection) the exact point where the apex of the heart strikes
the walls of the chest. This is especially the case if the chest walls are cov-
ered with adipose tissue, or are at all oedematous. Epigastric pulsation oc-
curs in dilatation of the right ventricle. In persons with thin chest- walls.
484 DISEASES OF THE HEAET.
there will sometimes be noticed an undulating motion over the whole of the
precordial space. Successive beats strike the chest-wall at different points,
and cause the undulatory motion.
Upon palpation, dilatation can readily be distinguished from hypertro-
phy by the feebleness of the cardiac impulse. Although it can sometimes
be felt as far to the left as the axillary line, yet there is an absence of the
lifting, forcible impulse which attends cardiac hypertrophy. It is often
difficult to determine the exact point of its maximum intensity, but it will
be accompanied by an undulating motion, wanting in power. Sometimes
a purring thrill may be obtained.
Percussion shows a greatly increased area of lateral dulness. The area
will be increased to the right if the right side of the heart is dilated, and
it may extend to the right nipple. If the left side of the heart is the seat
of the dilatation, the area of dulness will be increased to the left, and it
may extend well into the axillary space. In general dilatation the shape
of the increased precordial area will be oval. This point is of importance
in the differential diagnosis between cardiac dilatation and pericardial effu-
sion. The area of the superficial cardiac dulness is not increased in the same
proportion as the deep-seated, as is the case in cardiac hypertrophy. Di-
lated auricles are recognized by an upward increase in the area of dulness,
even to the first rib. When the Jugular veins are permanently dilated and
knotted, the existence of dilatation of the right auricle will not be difficult
to determine.
Auscultation. — The sounds of a dilated heart are short, abrupt, and fee-,
ble ; the second sound is often inaudible at the apex, and the two sounds are
of very nearly equal duration and character, so that it is very often difficult
to distinguish them. Eeduplication of the first sound sometimes occurs.
A systolic murmur generally accompanies dilatation ; many authorities re-
gard its production as possible without attendant valvular lesion, from
tardy and incomplete contraction of the ventricle. Whenever a cardiac
murmur has existed prior to the development of the dilatation, the rhythm
of the murmur is lost as the dilatation develops, and it becomes simply a
confused murmuring sound. This condition has been denominated asys-
tolism. It is a condition in which it is impossible to determine whether
the murmur is synchronous with the first or second heart-sound ; pauses or
intermissions occur at irregular intervals, which are of more frequent oc-
currence during exercise than when the patient is quiet. When the asys-
tolic condition is present, the prognosis is very unfavorable, independent of
the general condition of the patient ; under such conditions the patient is
liable to die suddenly. Asystolism is generally accompanied by a diffused
cardiac impulse, which is peculiar, and readily appreciated by the ear as
it rests over the precordial space. The respiratory murmur is diminished
in intensity over the whole of the upper portion of the left lung.
Differential Diagnosis. — The diagnosis of dilatation of the heart rests
mainly on the following conditions : — feeble heart action, undulating im-
pulse, indistinctness of apex-beat, lateral increase in the area of percussion
dulness, very nearly square in its outline ; short, abrupt and feeble heart
CARDIAC DILATATION". 485
sounds that strikingly resemble each other, and a feeble, irregular and in-
termitting pulse, accompanied by the general symptoms of systemic and
pulmonary obstruction and congestion.
The differential diagnosis between cardiac hypertrophy and cardiac dila-
tation is never difficult. The heart sounds are intensified in hypertrophy
and feeble in dilatation. In both cases there is an increased area of apex-
beat, but in hypertrophy it is distinct and forcible, in dilatation it is feeble,
diffused and indistinct. The fact that an individual has had cardiac hyper-
trophy with all its attendant symptoms, but now has a tired expression of
countenance, livid lips, and loss of physical vigor, daily becoming more and
more marked, and accompanied, it may be, by oedema of the feet, shows that
cardiac hypertrophy is giving place to cardiac dilatation. The pulse is full,
strong and bounding in hypertrophy, and weak and feeble in dilatation.
The first sound is dull, muffled, prolonged, and intensified in hypertrophy ;
while it is indistinct and resembles the second sound in dilatation. The
face is flushed in hypertrophy ; pale, livid and anxious in dilatation. The
presence of distended, irregular, turgid jugular veins tells very positively of
dilatation of the right auricle ; and pulsation in the jugulars, with feeble
heart action and increase in the area of cardiac dulness to the right, indi-
cates dilatation of the right ventricle associated with tricuspid regurgitation.
At the same time there will be hepatic, renal, and cerebral disturbance.
The differential diagnosis between enlargement of the heart (whether from
dilatation of its cavities or hypertrophy of its walls) and thoracic tumors is
sometimes difficult. One very reliable differential sign is the direction of
the increased area of percussion dulness ; thoracic aneurisms and medias-
tinal tumors always enlarge upward and to the right or left, while in car-
diac enlargement the area of dulness is increased laterally and downward.
In aneurism there is a dilating impulse, vibratory thrill, dysphagia, pain
in the dorsal spine and the peculiar aneurismal " bruit."
Consolidation of lung-tissue in the region of the heart may give rise to
some of the signs of cardiac enlargement, but the other attending physical
signs of pulmonary consolidation will distinguish between the dulness on
percussion thus produced and the increased area of dulness due to cardiac
enlargements. The character of the first sound of the heart, the pulse, the
shape of the dulness and the presence or absence of pulmonary or bronchial
symptoms will aid in the diagnosis.
Prognosis. — The prognosis in cardiac dilatation is always bad, and the
danger to life is increased in proportion to the excess of the capacity of the
cavities over the thickness of their walls. The greater the increase in
the capacity of the cavities, and the greater the diminution in thickness of
the cardiac walls, the greater will be the danger to life. Feebleness of
the general muscular system and impoverishment of the blood increase
the danger. The presence of disease of the kidney, or other disease of the
heart renders the prognosis in dilatation very grave. If patients have been
subject to paroxysms of dyspnoea and attacks of syncope, the prognosis is
especially bad, for then there is danger of sudden death. Whenever dropsy
exists, the prognosis is immediately unfavorable ; under such conditions few
486 DISEASES OF THE HEAUT.
patients, even with the best of care, live more than eighteen months; the
majority die within a year. In those cases in which the pulse is regular
or only becomes irregular after violent physical exertion, the prognosis is
comparatively good ; much can be done to relieve symptoms and prolong life.
When general anasarca exists and the patient is no longer able to assume the
recumbent posture, relief may be given, but it will only be temporary.
Treatment. — Cardicic dilatation is incurable. Even the good effects of
palliative measures are temporary. There are, however, two important
things to be accomplished. First, the nutrition of the body must be main-
tained at its highest point. Second, all irregular or violent action of the
heart must be prevented.
To accomplish the first result, the diet must be most nutritious and taken
in small quantities and at short inteiYals. An exclusive milk diet will often
be found most advantageous ; stimulants must only be taken in small quan-
tities and with the food. When symptoms of angemia are present, iron may
be administered with the food ; as a rule it is always safe to daily administer
iron to a patient with dilated heart. Strychnia and arsenic are recom-
mended with iron. The greatest amount of fresh air and the best hygienic
surroundings should be secured.
To accomplish the second result, this class of patients must be placed
under strict rules in regard to exercise. They should never allow them-
selves to be placed in such circumstances as to render sudden and violent
exertion necessary, for a single violent physical strain may jeopardize life.
Flannel should be worn next the skin. A dry, bracing air generally best
agrees with this class of patients. As regards the medicinal agents to be
employed, each case must be studied by itself. All discharges that are ex-
hausting must be arrested. If hypergemia of the liver and of other abdom-
inal viscera exists, it must be relieved by the occasional administration of
an aloetic or mercurial purge ; excessive purgation is not admissible, but a
daily movement of the bowels without exhausting is important. When
there is loss of appetite and impaired digestion, vegetable tonics and mineral
acids are indicated.
Those remedial agents which have a direct effect upon the heart itself are
important. The most serviceable of this class of remedies is digitalis. It
can always be administered in full doses, or at least in sufficiently large
doses to regulate the heart's action. Often when the feet become cedema-
tous and the patient cyanotic it has a wonderful effect, entirely removing
for a time all unpleasant symptoms. When the heart's action becomes
regular, the digitalis may be given in smaller doses, but the small doses
must be continued for a long time. If, after a time, the heart's action
cannot be controlled by the digitalis, belladonna or opium may be combined
with it ; the effect of the combination is to tranquillize the excited heart,
but they should only be resorted to when the digitalis has been thoroughly
tested and has failed. In the use of digitalis the same restriction is to be
observed which was described in connection with the treatment of other
cardiac diseases — that is, it should never be used indiscriminately. It is
always desirable to postpone its use as long as possible Should the heart
MYOCARDITIS.
487
become nervously excited during the administration of the digitalis, as it
often does, the various antispasmodic remedies may be employed. Should
cough be j)ersistent morphine may be given. Paroxysms of dyspnoea may
be temporarily relieved by lobelia, hydrocyanic acid, cannabis indica, ether,
and dry cujoping along the spine.
During the slow progress of a chronic case of cardiac dilatation, a great
variety of measures may be indicated and afford temporary relief; still, our
chief reliance will always be upon digitalis and iron, combined with the
most nutritious diet and absolute rest. Ammonia and the diffusible stim-
ulants are rarely of service.
JVIYOCARDITIS.
{Carditis.)
Myocarditis, or carditis, is an inflammation of the muscular structure of
the heart ; it may be acute or chronic. The chronic form is attended by
fibroid changes, general or local. It is met with most frequently in con-
nection with peri- or endocarditis.
Morbid Anatomy. — The diseased process consists in changes which take
place either in the primitive bundles of muscular fibre or in the connective-
tissue. Both are usually involved, but when the muscular structure alone
is attacked, it is called parencliymatous myocarditis. When the change
primarily affects the connective-tissue it is called interstitial myocarditis.^
Although these two varieties may not be determined during life, they are
very readily recognized after death.
As a rule, the layers of myocardium
just beneath the peri- and endocardium
are primarily and chiefly affected. The
change may have its seat in any portion
of the muscular tissue of the heart ;
the portion most frequently affected is
the left ventricle. The first, change
noticed is one in color ; at first, the
muscle is a dark red, later it assumes
a grayish, mottled, opaque, buff color,
and finally it changes to a dark green.
The microscopical appearances will
vary with the stage of the inflamma-
tion. At first the primitive bundles
are large, opaque, and swollen from
infiltration of serum ; their stride be-
come indistinct, and there is nuclear
proliferation. Later the fibrillae rupt-
ure and break down into a finely
granular detritus ; then the muscular
fibre is replaced by connective-tissue, or the degenerative process goes on
Fig. 106.
Section of Acute Mj'ocarditis.
A. Longitudinal section showing granular muscle-
fibres, obliteration of strice, and prominence of
nvcki.
At B the section includes some fasicidl cut ob-
liquely and transversely. The connective-tissve
inJUtration may be noted at C, C. x 500.
' Cornil and. Ranvier deny the existence of Virchow'B parenchymatous myocarditis, p. 200.
488 DISEASES OF THE HEART.
until there is a breaking down of tissue and the formation of abscesses.
When a large amount of the muscular tissue of the ventricular wall is
replaced by new connective-tissue formations, the power of resistance of
the ventricular wall is diminished, so that during the ventricular diastole
the new connective-tissue is liable to become gradually and slowly stretched,
and finally it gives rise to aneurism of the heart. This is the manner in
which aneurisms of the heart are most commonly formed. Calcareous
matter may also be deposited in the newly formed connective-tissue, and
then calcareous developments will take place in the walls of the aneurism.
When the inflammatory process terminates in the formation of an. abscess
the molecular degeneration replaces more and more the muscular fibres,
until finally there are formed swollen yellow-white masses (abscesses) sur-
rounded by red ecchymotic and boggy embryonic tissue, which gives, on
section, a small quantity of various colored puriform material consisting of
pus and muscular debris. Sometimes the whole cardiac tissue is infiltrated
with pus. This form is not met with except in pyaemia and low forms of
fever. Abscesses from acute local myocarditis are small ; they may burst ex-
ternally into the pericardium or one of the heart cavities. As a result of
this gradual destruction of muscular tissue, rupture of the heart may take
place with or without abscesses, and at the post-mortem the pericardium
will be distended with blood. Pycemic abscesses are very small and multi-
ple, they may project from either surface of the heart, and the surround-
ing muscular tissue may be either fatty or granular ; bacteria are often
present. There may be emboli in the coronary arteries that serve as foci
for the pygemic abscesses.
Etiology. — The causes of myocarditis, endocarditis, and pericarditis are
almost identical. Rheumatism, the most frequent cause of pericardial and •
endocardial inflammation, is a frequent cause of myocarditis. It is main-
tained by some that endocarditis and pericarditis never occur unless they
are associated with some myocarditis ; but in most cases, the myocarditis is
so slight that it little affects the diagnosis or prognosis. Myocarditis may
be the result of embolism or degeneration of the coronary arteries. It oc-
curs in connection with all septic dieases, such as pyaemia, septicaemia,
typhus, typhoid fevers, and acute ulcerative endocarditis. When it occurs
with pygemia it generally terminates in abscess ; when it occurs with
rheumatism, it usually terminates in connective-tissue formation, especially
at the apex of the left ventricle.
Eheumatic myocarditis may be independent of either peri- or endo-car-
ditis. It most frequently occurs in males before the twenty-fifth year.
Sometimes no cause can be discovered. Occasionally it has its starting-
point in syphilitic connective-tissue changes. Prolonged high temperature
and exposure to cold are mentioned as possible exciting causes.
Symptoms. — There are no distinctive symptoms of myocarditis. In a
large majority of instances it is impossible to positively determine its ex-
istence during life. A rapid, feeble, compressible, and irregular pulse,
•coming on suddenly in the course of an acute endocarditis or pericarditis,
is its most reliable symptom. Eestlessness and urgent dyspnoea are com-
MYOCAEDITIS. 489
mon. The face is anxious and cyanotic, there is great restlessness, anxi-
ety, and sometimes delirium. Tlie principal symptoms which should lead
one to suspect its existence, are attacks of cardiac palpitation, a feeble, ir-
regular, intermitting pulse, syncope on slight exertion, and all the phe-
nomena of heart failure ; if these come on suddenly in one who is suffer-
ing from some severe septic disease there is reason to suspect myocarditis.
There are no physical signs except those common to all conditions of
heart failure, though at first the heart action is violent. The heart sounds
are at first short and sharp, and then feeble. If, however, the myocarditis
has terminated in connective-tissue formations, and aneurism of the ven-
tricular wall has occurred it may be recognized by a change in the shape
of the heart.
The area of precordial dulness will be increased upward and toward the
left shoulder, rather more than when there is cardiac hypertrophy or dila-
tation. The diagnosis of myocarditis can only be conjectural. When ab-
scess of the heart occurs as a termination of myocarditis, it will probably
go unrecognized until the post-mortem. But the sudden occurrence of a
murmur indicative of rupture of a portion of the wall or of a valve, along
with restlessness, delirium, and rigors, may cause one to suspect it.
Differential Diagnosis. — The existence or non-existence of a murmur
alone enables us to distinguish endo- and peri- from myo-carditis. In chil-
dren it may be mistaken for acute meningitis.
Prognosis. — General myocarditis must of necessity prove fatal ; circum-
scribed myocarditis may be recovered from. The present state of our clin-
ical knowledge of the disease admits only of a speculative prognosis, based
rather on our knowledge of its pathological lesions than on any symptoms
to which these changes may give rise. Extensive connective-tissue for-
mations, frequently found in the cardiac walls, give evidence that circum-
scribed myocarditis is frequently recovered from. But the extent and stage
at which recovery is possible and the symptoms which indicate fatal termi-
nation are still undetermined. It lasts from a few hours to a few days,
death occurring from asthenia, heart failure, rupture, aneurism, hasmo-
pericardium, embolism, and secondary septicaemia.
Treatment. — If myocarditis is suspected in the course of an endocarditis
or pericarditis, the plan of treatment will not be materially changed. It is
essentially the same as that already indicated for the management of those
affections. Great care should be exercised not to overtax the heart. This
class of patients should never be allowed to go up-stairs or take active ex-
ercise until some time after convalescence. "Warmth to the extremities is
of service, as it tends to equalize the circulation, and thus relieve and pre-
vent cardiac strain. It is probable that many cases of fatty heart are the
sequelae of myocarditis.
Palpitation is an indication for the moderate use of alcoholic stimulants.
Digitalis and ammonia should be very cautiously given. Not infrequently
septic and fever patients, after violent physical exertion during convales-
cence, die suddenly ; death under such circumstances may be the result of
overtaxing a heart weakened by myocarditis. Besides absolute rest and
490 DISEASES OF THE HEAKT.
sustaining measures, all tliat can be done for these patients is to relieve
unpleasant symptoms.
FIBEOID DISEASE OF THE HEART.
{Chronic Myocarditis. )
As has been stated, acute inflammation of the myocardium ends in ab-
scess or in connective- tissue formation. When fibroid tissue replaces part
of the muscular structure of the heart, we have a fibroid heart, or what
some call '" connective-tissue hypertrophy," a condition analogous to what
Gull and Sutton call arterio-capillary fibrosis.
Morbid Anatomy, — The walls of the ventricle are oftenest involved ;
there may be distinct patches of fibroid tissue or there may be patches just
under the endo- or peri-cardium, radiating from which are bands of fibrous.
tissue which insinuate themselves into the deeper muscular structure.
A '' fibroid patch " is most frequently found near the apex of the left ven-
tricle. When it is a continuation of endo- or pericarditis the new tissue
blends imperceptibly from the lining or covering membranes into the mus-
cular structure of the heart. The tissue is dense, firm, inelastic, and
gray-white in color. Sometimes it has a glistening blue or even green ap-
pearance ; the form of the masses is variable : sometimes they are little
spherical projections into some one of the cardiac cavities, and, again, they
bulge out into the pericardial sac. They may be dots, streaks, bundles,
or islands. The hard tissue interferes materially with the movements of
the heart. Aneurism, dilatation, and annular constriction within one of
tlie cavities not infrequently result from interstitial myocarditis. The
aneurismal dilatations sometimes contain thrombi.
In " connective-tissue " hypertrophy the heart is enlarged, the weight in-
creased, and the walls are firm, tough, and leathery. The color varies from
a pale pink to a deep purple. Gummy tumors are not infrequently found
along with fibroid (syphilitic) patches. Under the microscope the muscu-
lar tissue is seen atrophied, granular, or fatty ; in some places it has entirely
disappeared. The apices of the papillary muscles are not infrequently in-
volved in the same process.
Etiology. — All the causes of acute myocarditis are causes of chronic myo-
carditis. Rheumatism and syphilis are its most frequent causes. In the
latter case the fibroid mass is called a *' syphilitic patch," but histologically
it is identical with non-specific developments. Arterial fibrosis and cir-
rhotic kidney seem to be associated with its development. It occurs oftenest
in males who are past middle life. In many instances no cause can be made
out. It has been regarded by some as part of a " senile " change. '
Symptoms. — In limited or in slight general fibrosis there are no symptoms.
Slight precordial pain, palpitation on exertion or excitement, dyspnoea on
active exercise, small and sometimes irregular pulse, and later dropsy and
visceral complications are frequent accompaniments of fibroid disease of the
1 Long continued congestion of the heart, Jenner states, may lead to its induration.
FATTY DEGENERATION OF THE HEART. 491
heart.' Should fibrosis of the columnse carnese induce insufficiency on ac-
count of shortening of the papillary muscles, then there will be a systolic
murmur. But a murmur is usually evidence of the non-existence of fibro-
sis. The heart sounds may be sharp and short, resembling the sounds
''tick tack." The patients emaciate and are very feeble. In connective-
tissue hypertrophy, the phj^sical signs are in nowise different from those
of ordinary hypertrophy."
Differential Diagnosis. — The subjective symptoms of chronic endocardi-
tis simulate /a^^2/ degeneration of the heart. The etiology will aid in estab-
lishing a diagnosis, which can never be positive.
Prognosis.— The disease is not immediately fatal, though it is incurable
and sooner or later causes death. Its course is chronic, but sudden death
is possible at any moment, and a very common ending. Dropsy and con-
gestion and oedema of the lungs are common complications.
Treatment. — To relieve symptoms and aid nutrition, is all that can be
done unless syphilis be a cause, and then anti-syphilitics often cause marked
improvement. They should be administered tentatively in all cases and
the results carefully watched. Digitalis is of doubtful efficacy ; a restricted
diet is an imj)ortant part of the treatment.
FATTY DEGENEEATION OF THE HEART.
This is a common form of cardiac degeneration. It may he circum-
scribed or diffused. When circumscribed it has a local cause. There are
two distinct morbid processes connected with fatty degeneration of the
heart.
I. Fatty degeneration of the primitive muscular fihre, termed " Quain's
fatty degeneration."
II. Fatty accumulation on the surface
and in the substance of the heart so as
to interfere with its functions.
Morbid Anatomy. — In true fatty de-
generation the first change noticed is
that the primitive muscular fibres lose
their nuclei, their stri^ disappear, and
they become completely granular. This
granular material at first presents the
appearance of albuminous matter ; soon,
however, the sarcous substance gives
place to fat granules and to oil globules,
which are arranged in rows, and event- Teased Fibres from the Heart in Fatty De-
nally entirely obliterate the muscle ^^ ^ ^, ^ generation.
•J •' The fatty change is seen, m varying degrees
fibres. The dearenerated fibres are of from the granular condition A, to the com-
° T /^i All plete obliteration of the muscle fihres l)y fat
the same size as the normal fibres. All globules, b. x 4oo.
I Ruble, who has made a careful Btudj' of this disease (and considers it as fur more frequent nnd less
often diagnostieated than acute myocarditis) regards the irregularity and variability of the pulse, occurring
at any moment during the day, as being most characteristic.
* Hyde Salter's case was marked by epistaxis and haamoptysis.
492 DISEASES OF THE HEAET.
the fibres are not inyolved. The muscular tissue assumes a yellow, buff, oi
dirty brown color, and loses its power of resistance, sometimes tearing like
paper and readily breaking down under pressure. The heart in most
instances is dilated ; it may be hypertrophied. When a fatty heart is
hyjoertrophied it is friable, not flabby. The coronary arteries may be
atheromatous, calcified, obliterated, or normal; when the degeneration
occurs secondarily to muscular hypertrophy, the coronary circulation is
more or less obstructed and the fatty changes are local. Its most frequent
seat is in the left ventricle, and is most marked in the columnse carnese and
in the inner wall of the heart.
In fatty infiltration there is simply an increase of fat in the areolar
tissue of the heart ; this fat does not interfere with the function of the mus-
cular fibres except by its pressure.' If the fatty accumulation is extensive,
it may cause atrophy of the muscular fibres. Fatty degeneration may
cause death by so weakening the walls of the heart that rupture will take
place, or by so weakening the contractile power of the heart as to render
it incapable of performing its function.^ Fatty infiltration may diminish
the heart-power, but it rarely, if ever, either directly
or indirectly causes death.
Etiology. — All the causes of fatty degeneration of the
muscular fibres of the heart are as yet undetermined.
It is evident, however, that anything which interferes
with the nutrition of the heart tends to fatty degenera-
tion of its walls ; it is essentially a disease of middle and
advanced life ; it comes on with senile decay.^ It is
often a prominent sign of the marasmus which comes
FigHos ^^ ^^ Bright's disease, chronic alcoholismus (especially
Fatty Infiltration. when Combined with syphilis), gout, phthisis, cancer,
■^^roOT*%/r^ie«VTftrf ^^^-j when developed in this connection it never reaches
teamed and showing tj^e g, point where it seriously interferes with the action of
infiltration of fat, B, ^ . -^
in the areolar tissue the heart. In Quitc a large proportion of cases, fatty
With, CttvOwlV of 1/16 o X L 7 ,1
heart fibres, A. 'x 400. degeneration of the heart is the result of mal-nutri-
tion from some interference with the supply of blood through the coronary
arteries. Such interference may arise from atheroma or calcification of the
coronary vessels, embolic obstruction, external compression from pericar-
dial thickenings, or impairment of the aortic recoil ; it is met with in con-
nection with phosphorus poisoning, changes in the heart in specific
fevers, acute yellow atrophy, etc. The same degenerative tendency which
manifests itself in other tissues of the body, due to constitutional condi-
tions, either hereditary or acquired, predisposes to it.
Fatty infiltration of the heart occurs as a part of general obesity, which
so frequently develops after persons have passed middle life. It is quite
frequently met with in connection with chronic alcoholismus. Sedentary
habits increase the liability to its development.
1 Normally there is more or less fat in the auriculo-ventricular grooves.
^ One-half the cases of true fatty degeneration end in rupture of the heart. Partial rupture called
"cardiac apoplexy " is common; aneurism is not uncommon, and the weakened columnse carnese per-
mit of valvular insufficiency.
' Hence the French call it " senile cardiac softening."
FATTY DEGEKERATION OF THE HEAET. 493
Symptoms. — Moderate fatty degeneration of the heart will go unrecog-
nized. ; sudden death has occurred from this cause when there was no sus-
picion of its existence. As a rule, the progress of the disease is very gradual
and insidious, and most of the symptoms which attend its dfvelopment are
due to heart-insufficiency. Persons who are subjects of fatty heart cannot
under goactive physical exertion for any length of time, without complete
exhaustion ; their skin is of a pale, " pasty" yellow color, at times more or
less livid. Their extremities are cold and oedema is not uncommon, espe-
cially in old age ; digestion is feeble ; they persj^ire profusely on slight ex-
ertion ; they suffer from paroxysms of dyspnoea after physical exercise.
" Uneasy " feelings and pain about the heart, and sudden suffocating palpita-
tion of the heart are not infrequent. During these paroxysms the liver
enlarges, the respiration is feeble and irregular, often sighing in its charac-
ter ; " Cheyne-Stokes' breathing " is present in some cases, and is regarded
as an important symptom. The cardiac insufficiency is progressive. The
tissues become flabby ; there are evidences of arterial degeneration ; the
arcus senilis is often present. The temper is irritable ; there is habit-
ual depression of spirits, disturbance of vision, failure of memory, giddi-
ness and vertigo ; sudden cerebral ansemia may occur during excitement,
inducing syncope or epileptiform attacks. Frequent attacks of fainting in
one who has the symptoms of fatty heart are always alarming. The pulse
is peculiar : it is always feeble, although it apparently varies in force ; it
may be perfectly regular in rhythm while the patient is quiet, yet on slight
exertion it becomes greatly accelerated and irregular both in force and
rhythm. It may be very rapid for some minutes, then suddenly it becomes
irregular, not beating more than thirty or forty times in a minute ; — this
is very characteristic.
In an advanced stage of the disease, in addition to cerebral symptoms al-
ready referred to, patients sometimes get into a condition which bears a
stiking resemblance to a state of anaesthesia. Attacks of angina pectoris
sometimes occur in connection with fatty heart. Fatty infiltration of the
heart gives rise to no functional disturbance of the organ, and is not at-
tended by any unpleasant or dangerous phenomena. Should atrophy of
the muscular substance of the heart, from pressure of the fatty accumula-
tion, occur (which seldom happens), the attending symptoms and results
differ in no respect from those already detailed as attendants of fatty de-
generation of its muscular fibres.
Physical Signs. — The physical signs of fatty heart are few and not diag-
nostic.
On inspection, the apex-beat will be indistinct.
On palpation, no impulse will be detected over the precordial space, or it
will only be perceptible when the body is bent forward. If the fatty meta-
morphosis has occurred in an hypertrophied heart, there will be an undu-
lating motion similar to that which accompanies excessive cardiac dilata-
tion.
On perc ^ssion, the area of precordial dulness, both superficial and deep,
is normal.
494 DISEASES OF THE HEAET.
Upon auscultation, the muscular element of the first sound will be indis-
tinct or absent. The valvular element is " toneless/' and is followed by an
unusually long period of silence.
Differential Diagnosis. — Fatty heart may be confounded with other cardiac
degenerations. The differential diagnosis between cardiac dilatation and
fatty heart is always difficult. In both there may be a feeble, irregular pulse,
vertigo, ringing in the ears, and attacks of syncope. A dilated heart occu-
pies an abnormal space in the thoracic cavity, and consequently gives rise to
an abnormal area of cardiac dulness ; the area of a fatty heart does not ex-
ceed the normal area. The muscular element of the first sound may be
feeble in dilatation, but it is never absent, as in fatty heart. ' Cerebral symp-
toms, and Cheyne-Stokes' breathing are marked symptoms in fatty heart and
absent in dilatation. If fatty degeneration accompanies cardiac dilatation,
there will be a greater disturbance of the heart's action than in fatty degen-
eration ivitliout dilatation.
Prognosis. — The prognosis is always unfavorable ; its tendency is steadily
to advance.' Individuals with fatty heart may live for years, but when the
disease reaches an advanced stage, life is very uncertain ; a fatal termina-
tion may occur suddenly from syncope/ from rupture of the heart, coma,
or as the result of cerebral anaemia ; it may also terminate slowly by asthenia,
which is usually attended by dropsy.
Treatment. — There is no plan of treatment that can restore the degener-
ated muscular fibres. The principal thing is, to improve or rather increase
the tissue-making power of the blood ; to this end, iron, cod-liver oil,
and strychnine may be given in connection with a good nutritious diet, fresh
air, and light physical exercise. If alcoholic stimulants have been used
habitually, or to excess, they must be stopped. All active or violent physi-
cal exercise and excitement must be avoided ; the life of the patient must be
that of an invalid. By avoiding everything that may stimulate the heart's
action, and by strict observance of all the laws of hygiene, life may be pro-
longed. Digitalis does harm.
In fatty infiltration the only treatment which seems to be of any service
is to restrict the diet to animal food and place the patient under a system-
atic physical training so as to diminish or remove fatty accumulations in
other parts of the body. All the exci^eting organs must be kept active so as
to relieve the heart as much as possible. Quain says that galvanism applied
from the back of the neck to the precordium, by the interrupted current,
has been found useful.
AMYLOID DEGEKEEATION.
Amyloid or waxy degeneration of the heart is rare.
Morbid Anatomy. — This form of cardiac degeneration is never met with
except in connection with similar changes in other organs of the body, and is
due to a constitutional cause ; it consists in the formation of a shining
1 Rindfleisch states that " new fibrillse can be formed from cell-elements remaining within the ?arco
Jemma."
2 Quain says death is sudden in fatty heart in the proportion of five to one to any other mode of death.
PIGMKNTAIIY DBGENERATIOlSr OF THE HEART. 495
homogeneous substance in the primitive muscular fibres, which gives the
reaction of amyloid material. It is most frequently found in the walls of
the right ventricle, causing its cut surface to present the characteristic
appearance of waxy metamorphosis. The primary changes take place in
the connective-tissue surrounding the muscle-bundles ; it is often associated
with syphilitic gummata.
Etiology.— Waxy degeneration of the walls of the heart is due to those
causes which produce similar degeneration in the other organs and tissues
of the body ; among these causes syphilis stands first.
Symptoms. — There are no special symptoms attending it, except those
which are indicative of cardiac failure. Its existence can only be suspected,
never positively determined. If the signs of cardiac failure, with waxy de-
generation of other organs, as the spleen and liver, are present in an indi-
vidual who has never been the subject of rheumatism or any valvular dis-
ease, but who has a syphilitic history, there is good reason to suspect waxy
degeneration of the heart.
Treatment. — There are no special indications different from the treatment
of waxy degenerations in other organs.
PAEENCHYMATOUS DEGENERATIOlSr OF THE HEAET.
Parenchymatous or granular degeneration, or "cloudy swelling," is that
variety usually met with in acute (specific) diseases attended by high tem-
perature.
Morbid Anatomy. — The whole heart is soft, flabby, friable, and of a dirty
red-yellow, clouded appearance. It may be slightly enlarged. The peri-
cardium is dull, clouded, ecchymotic and somewhat oedematous. Under
the microscope the muscle-fibres are swollen, some of them rupture, and
they all have a granular appearance, which disappears on the addition of
acetic acid. The striations are very indistinct.
Etiology. — Parenchymatous degeneration of the heart is caused by ex-
tensive blood poisoning and high temperature combined.
Symptoms. — Its symptoms are obscured by those that attend the causa-
tive disease. The heart impulse is feeble, the apex-beat is indistinct. The
first sound gradually disappears and the second sound becomes indistinct.
Violent palpitations are often present.
The Diagnosis is made by the character of the pulse and the indistinct
apex-beat, common in the course of any acute febrile disease.
The Prognosis depends on the conditions under which it occurs. If in
the course of any acute specific fever, signs of heart-failure come on, the
prognosis is very bad .
Its Treatment consists in the prompt and judicious administration of
stimulants.
PIGMENTARY DEGElSTERATIOlSr OF THE HEAET.
Pigment granules are found in the cardiac muscle-fibres in nearly every
case of chronic valvular disease. In atrophy of the heart pigmentation is
496 DISEASES OF THE HEART.
especially marked, and the particles lie near the axis of the fibres. Pig'-
mentation also occui's in cases of long-standing jaundice. In melanosis we
find a pigmentary infiltration of the heart differing from the above by the
black color of the granules, 'by their seat being in the connective-tissue
and in the muscular-tissue at the same time, and by their localization in
points and circumscribed spots.
This condition has no clinical importance.
ATEOPHT OF THE HEAET.
Atrophy is a diminution in the size and weight of the heart. When
the term eccentric atrophy is used a condition of simple dilatation is indi-
cated. Atrophy may be confined to the walls of one cavity, or it may in-
volve the walls of all the cavities of the heart.
Morbid Anatomy. — Some writers describe atrophy of the heart under the
head of simple, concentric, and eccentric ; but these terms are hardly nec-
essary, as all cases of true cardiac atrophy are concentric ; that is, are ac-
companied by diminution in the capacity of its cavities. In some cases,
wasting of the cardiac muscles is attended by inter-muscular connective-
tissue increase ; in such cases there will be no decrease in the size of the
heart, but a marked diminution in its contractile power. There may be a
decrease in size and number of the muscular fibres. The pericardium is
puckered and opaque. The coronary vessels are tortuous and prominent.
When fatty or fibroid changes have induced by (pressure) atrophy of the
heart-muscles, the term "yellow atrophy "has been given to it. Senile
("brown") atrophy is due to extensive pigmentation. There may be no
histological change in the muscular fibres, or they may undergo fatty de-
generation.
Etiology. — Any chronic exhausting disease, as phthisis, syphilis, can-
cer, or any disease that is accompanied by wasting of the general muscular
system, may produce atrophy of the heart. It is frequently met with in the
very aged. Atrophy of the heart may result from the pressure of extensive
chronic pericardial effusion. Mediastinal growths may also cause it, by
their pressure. Fibrous thickening of the pericardium, causing constric-
tion of the coronary arteries, as well as atheroma and thrombosis of these
vessels, may cause partial or complete cardiac atrophy. Abnormally small
hearts are not infrequently congenital, and are associated with imperfect
vascular and sexual development.
Symptoms. — Cardiac atrophy is usually attended by no special symptoms,
as it is rarely met with except in connection with wasting of the muscles of
the general system. It is difficult to decide whether the symptoms indi-
cating enfeebled circulation depend upon loss of heart-power or upon gen-
eral muscular feebleness. The existence of that form of cardiac atrophy
which is met with in the aged cannot be positively determined during
life. That form which results from local interference with the nutrition
of the heart is attended by symptoms similar to those of fatty heart. In
CARDIAC THROMBOSIS. 497
both forms, the heart's impulse is feeble and its sounds indistinct, and the
apex-beat is to the right of and above its normal position.
Prognosis. — The prognosis depends upon the cause and extent of the
atrophy. In extensive atrophy attended by fatty degeneration, and in
atrophy depending upon the pressure of a pericardial effusion, the progno-
sis is unfavorable ; the atrophy of old age is not attended by any special
danger to life.
Treatment. — All that can be done in this disease is to avoid excessive
physical exertion and mental excitement. The food must be nutritious
and wine may be indulged in rather freely. Iron, which is so serviceable
in other cardiac affections attended by enfeebled nutrition and failure of
heart-power, will be found of service in this condition.
EUPTUEE OF THE HEAET.
Eupture of the heart rarely if ever occurs, unless preceded by degenerative
changes in the heart walls. The seat of the rupture is usually in the left
ventricle, and it may be single or multiple. The fissure generally runs par-
allel to the fasciculi of the heart fibres — it may be partial at first, and
complete some time after. Complete rupture may vary in size from two
inches to an opening only large enough to admit a probe ; ecchymoses are
usually found around the rent ; fluid blood and large coagula distend the
pericardium ; the rupture usually takes place from within outward, and
occurs or commences during the cardiac systole.
Etiology. — Rupture of the heart may follow atrophy, cardiac aneurism,
abscess, hemorrhagic softening, fatty and other degenerations of the cardiac
walls ; its immediate cause is usually some violent physical effort or mental
excitement. If it occurs during sleep, or when the individual is quiet,
there is reason to believe that it commenced some' time before it became
complete, and that this apparently sudden rupture is only its com-
pletion. It is rare before forty and occurs usually after the sixtieth
year.
Symptoms. — If the rupture is complete the patient's hand is suddenly car-
ried to the chest, a few convulsive twitches occur, and unconsciousness and
death immediately follow. If the rupture is partial, the symptoms are
those of collapse : — rapid, feeble pulse, restlessness, faintness, pallor, cold
skin, vomiting, dyspnoea, and perhaps convulsions ; death may not occur
for several hours. Eupture of the heart sometimes occurs in connection,
with a paroxysm of precordial pain resembling angina pectoris.
Prognosis. — Death is certain ; nothing can avert it. In seventy-five per
cent, it is sudden.
Treatment. — Necessarily this can only be palliative. Stimulants and nar-
cotics may be given to afford temporary relief,
CAEDIAC THROMBOSIS
At nearly every autopsy there will be found a dark red clot of blood in
the right heart, or in the auricles. This clot will be most firm in those
33
498 DISEASES OF THE HEART.
wlio die of chronic disease ; it will be more or less adherent to the cardiac
walls and the trabeculae and may extend like a cord into the vessels. In
phthisis they are usually very firm ; in anaemia they are jelly-like and pale ;
in leukgemia they are soft, creamy and puriform. In the exanthemata they
ar9 yery soft, and when an acute disease runs a very short sharp course
there is often no clot. At one time these clots are entirely composed ot
fibrin, and are of a pale straw-color ; at another time they contain red
globules, and are of a dark red color. The coagulum is not infrequently
whitish at its upper portion, and deep red at its lower, according to the
position of the body. These clots are formed during the last hours of life,
and immediately after death. They have no pathological significance.
They are often called passive coagula.
Morbid Anatomy. — In true cardiac thrombosis coagula are formed in the
heart-cavities, either a short time before death, or they may have existed
for years. They vary in size from a pin's head to a walnut, and may fill
the greater part of one of the heart-cavities. If they are of small size and
firmly adherent to the valves or chordae tendinese, they are called vegetations.
If they are of large size, they are called thrombi, and form in any of the
heart-cavities ; they are more or less firmly adherent to the endocardium.
Their projecting portion is smooth and globular. In those diseased con-
ditions which interfere with the free circulation of the blood through the
heart, thrombi usually form in such portions of the heart-cavities as
are farthest removed from the active blood-currents. The constitution of
these thrombi varies; sometimes they are firm, dry and of a whitish color,
composed of exsanguinated fibrin ; at other times they have a globular
outline, are firmly attached to the endocardium, and have the constitution
of cysts.
Cardiac thrombi may remain permanently attached to the endocardium,
or they mav become separated from it in masses of considerable size, or in
minute particles, giving rise either to embolism or septic infection ; they
may be detached, and, as '^ fibrinous balls," lie free in the auricular
.cavities. ^
Etiology. — All cardiac thrombi originate in coagulation of the blood. In
;some instances the coagulation is rapid and the coagula are of large size ;
in others, the coagulation is slow, and the coagula are of small size. The
conditions which favor these coagulations are, first, obstruction to the pas-
sage of blood through the heart ; second, abnormal changes in the compo-
sition of the blood ; and third, inflammatory changes in the interior of the
heart. Obstruction to the passage of blood through the heart may be due
to valvular lesions, cardiac dilatation, or feebleness of the contractile power
of the heart, inherent, or from degenerations. The thrombi in the latter
case are called marantic tJirombi. The condition of the blood which
favors its coagulation, is that which we find in acute inflammation,
rheumatism, Bright's disease, and certain acute infectious diseases, as
1 According to the theory of Schmidt, the formation of true or cardiac thrombi is due to condensation
of the fibrogenic substance of the blood in contact with an inflamed wall. Hence results a slow coagula-
tion and one that does not include the red corpuscles.
CAEDIAC THKOMBOSIS. 4-99
hemorrhagic variola and puerperal fever. Phosphorus poisoning causes it.
Coagulation in endocarditis is due to the roughening of the endocardial
surface produced by the inflammation.
Symptoms.— The symptoms of cardiac thrombosis in its gravest form are
urgent. At the moment of coagulation, the heart's action becomes fre-
quent and irregular, the pulse is small, weak, and irregular in force and
rhythm. Partial syncope, with restlessness and jactitation are combined
with symptoms of more or less complete pulmonary obstruction. Dyspncea
is intense, there is active delirium, convulsions, and finally a fatal coma.
Pulmonary congestion, infarction and cedema occur. Life is rarely pro-
longed beyond the third day.
In less grave forms, the symptoms are not so urgent. The dyspniea is
slight, the cyanosis is not extreme, the jugular veins are but slightly dis-
tended, the respiration is somewhat hurried, and the pulse is increased in
frequency, is intermittent and irregular ; the symptoms are those of ad-
vanced heart disease. Where the coagula are of small size, and the coagu-
lation takes place slowly, there will be few, if any, subjective symptoms to
indicate their presence, and life may not be seriously endangered ; these
latter cases, however, are rather cases of vegetations forming on the valves
and chordae tendinese, than true cardiac thrombosis. The dislodgment of
a large piece of a thrombus en masse may block up a valvular orifice com-
pletely, and thus cause sudden death. Arterial embolism results from
breaking off of small pieces, and there may be subsequent well-marked
pygemic symptoms.
Physical Signs. — Inspection and palpation show irregularity in the cardiac
impulse. The area of cardiac percussioti dulness is increased to the right
of the sterniTm.
On auscultation, there is marked irregularity in the heart-sounds.
New murmurs are developed, or, if murmurs existed prior to the occurrence
of the thrombosis, they are increased in intensity. The most common
murmur is that indicative of obstruction at the right auriculo-ventricular
or at the pulmonic orifice, having its maximum intensity at the xiphoid
cartilage and being conveyed to the left of the sternum. Occasionally
there will be a murmur indicating obstruction in the left ventricle. If the
coagula are of small size, the murmurs are similar to those which accom-
pany endocarditis.
Differential Diagnosis. — The symptoms of sudden shock to the heart, and
the systemic effects of sudden intra-cardiac obstruction, taken in connection
with the sudden development of a loud cardiac murmur evidently origi-
nating on the right side of the heart are sufficient to lead one to suspect
the existence of cardiac thrombosis. The only condition which is liable to
be mistaken for it is the rupturing of a valve, or of one of the cTiordoR
tendinecB from ulcerative endocarditis. I know of no means by which a
differential diagnosis can be made between them until some time after the
occurrence.
Prognosis. — It is unfavorable in all cases of extensive cardiac throm-
bosis. If the coagula are small, it is possible for them to disappear after a
500 DISEASES OF THE HEAET.
time, or to become changed into vegetations ; but large cardiac thrombi
destroy life, sometimes in twelve hours, and at other times life may be pro-
longed for two or three days.
Treatment. — Theoretically, the alkaline carbonates have the power of ar-
resting or preventing the formation of cardiac thrombi, hence some give ses-
quicarbonate of ammonia in endocarditis and pneumonia, to prevent the
formation of heart-clots, which they believe to be very frequently the cause
of sudden death in these diseases. There is no positive evidence in favor
of, or against this theory. Bleeding, and every agent which has a tendency
to enfeeble the heart-power must be avoided. Absolute quiet must be in-
sisted upon and digitalis and opium may be administered in small doses.
Alcoholic stimulants must be given with great care, and only to prevent
collapse. Formerly many described cardiac thrombosis as ''polypi" and
polypoid growths in the heart.
ANEUBISM OF THE HEAET.
Aneurisms of the heart may be fusiform, sacculated, or globular, and
they are usually situated in the wall of the left ventricle near its apex.*
They may be single or multiple, and if multiple, open separately or in com-
mon. Sometimes cardiac aneurism looks like an elongated sac winding
around the aorta.
Morbid Anatomy. — In most instances, cardiac aneurisms form slowly,
and are the result of inflammatory processes in the endocardium and myo-
cardium. These processes (as I have already stated) may convert a small
or large portion of the muscular wall of the ventricle into fibrous tissue.
The portion so charged yields to the internal blood pressure, and a cir-
cumscribed pouch or sac is formed which communicates with the heart-
cavity by an opening which may be very narrow, or may be the largest
part of the sac. The neck is hard, often cartilaginous, and may be smooth
or jagged. As these pouches increase in size, their walls become thinner
and sometimes rupture ; they may undergo calcification. The wall consists
mainly of fibrous tissue with endocardium internally and pericardium ex-
ternally.^ Adherent pericardium usually strengthens the sac, which varies
in thickness from that of a sheet of paper to a quarter of an inch. These
sacs may be partially or completely filled with fibrin, fluid blood, or blood-
clots. Aneurisms of the inter- ventricular septum, and at the base, usually
result from the extension of a " valvular aneurism." The heart is usually
enlarged.
Etiology. — Among the causes of aneurism of the heart may be included
endocardial, pericardial, and myocardial inflammations, the different forms
of degeneration, fibroid changes, and tuberculous and syphilitic new
growths. Eare before twenty, it seems to become more frequent as age
advances. Males suffer twice as frequently as females.
Symptoms. — The symptoms of this affection are obscure. There is noth-
1 In Quain's 56 cases, 52 were in the left ventricle.
a The cells are flat and arranged parallel to the surface of the aneurism on account of pressure.
NEW FOEMATIONS IN THE HEAET. 501
ing in its clinical history which distinguishes it from other diseases of the
ventricular walls. In some instances every known symptom of cardiac dis-
ease is present.
The pliysical signs are equally unsatisfactory and unintelligible.' The
physical signs of chronic pericarditis, endocarditis, hypertrophy, and dila-
tation are sometimes all present. In twenty per cent, of cases murmurs
exist that replace the heart sounds.
Prognosis. — Sudden death may occur from rupture of the heart into the
pericardium, or the patient may be worn out by the attendants of cardiac
dilatation.
Treatment. ^It has no special treatment. Those means advised for the
relief of cardiac dilatation will be found most serviceable.
NEW EOKMATIONS UST THE HEART.
Morbid growths, or new formations in the walls of the heart have no
clinical importance, and I shall only enumerate them.
Cancer of the heart, as a primary affection, is exceedingly rare ; while
cancerous nodules in the walls or on the surface of the heart, in connec-
tion with general cancerous infection, occasionally occur. It is apt to be
associated with cancer of the lungs, or mediastinum. Under these circum-
stances, the disease usually manifests itself in the form of small circum-
scribed medullary or melanotic tumors, which are developed either in the
heart walls or under the pericardium or endocardium. The surfaces of the
heart rather than the substance of the myocardium are affected, and the
right heart suffers oftener than the left, although the cancer nodules are
nearly always multiple. Encephaloid is the form most frequently met with,
and epithelioma is the rarest. When cancer of the heart is the result of
extension of cancer from the neighboring parts, large portions of the heart
may become transformed into cancerous tissue. Its existence cannot be
recognized during life ; it is of interest only pathologically. In a few cases
local pain, anginal symptoms, murmurs and symptoms generally indica-
tive of heart disease have led to suspicion of cancer of the heart when evi-
dences of cancer existed elsewhere.
Tubercle is found in the heart only in connection with acute general tu-
berculosis ; then it develops in the connective-tissue. Its existence cannot
be recognized during life. Both gray miliary and yellow cheesy masses are
found at the post-mortem. They are usually situated near the pericardium.
Fibroma, lymphoma, lipoma, sarcoma, and myoma are rare forms of cir-
cumscribed tumors found in the cardiac walls, or under the endocardium
or pericardium. Their existence cannot be determined during life.
Parasites. — The heart may be the seat of parasites. The echinococcus,
the cysticercus, and entozoa have all been found in the heart-walls, and
have been known to lead to their rupture, causing death. Three and one-
half per cent, of the cases of hydatid disease occur in the heart. ^ They
' Extensive dulness down and to the left nccompanied by a feeble impulse may cause one to suspect it
2 C'obbold states that hydatid cysts in the heart are commonly multiple.
502 DISEASES OF THE HEART.
project into the pericardium or into the heart-cavities as cystic tumors. The
sac may rupture in either direction, giving rise to embolism or to pericar-
ditis, usually with haemopericardium.
True cysts, containing serum or grumous fluid, are very rarely found
in the heart-walls. All of these developments have the effect of depress-
ing or interfering with the heart's action, hut their diagnosis in most cases
cannot be made.
TUBERCULOSIS OF THE PEEICARDIUM.
Tuberculosis of the pericardium is only met with in connection with
acute general miliary tuberculosis. Unless the tubercular development
takes place only a short time previous to death, it will give rise to pericar-
ditis. Its presence may be suspected from the existence of the pericarditis
in connection with the symptoms of general tuberculosis. In these cases
tubercles may develop in the layer of fibrinous exudation or be in the vis-
ceral membrane itself. Hemorrhage is common when the neoplasm is ac-
companied by pericarditis.
CANCEK OF THE PEEICARDIUM.
The pericardium may be the seat of cancer, but the cancerous develop-
ment is nearly always secondary to cancerous developments in other parts
of the body. It may comport itself (as to pseudo-membrane and exuda-
tion) precisely like tubercle in the pericardium. More frequent than either
is the formation of tuberculous or cancerous masses in the lung or medi-
astinum, which by pressure and nearness to the pericardium excite fatal
pericarditis, by some called cancerous or tuberculous pericarditis.
CARDIAC NEUROSES.
The two prominent neuroses of the heart are nervous palpitation and.
angina pectoris. Both are functional disorders.
Nervous Cardiac Palpitation. — As has already been stated, cardiac pal-
pitation is a very common symptom of organic disease of the heart. A
purely nervous cardiac palpitation may occur independently of organic
heart disease. It comes on suddenly, and is generally intermittent. Indeed,
all cardiac neuroses have a paroxysmal character.
Morbid Anatomy. — There are no known anatomical changes either in the
heart, or in its nerve-supply, which can be regarded as the constant causes
or concomitants of cardiac palpitation.
Etiology. — The direct cause of this affection is over-stimulation of the
cardiac muscle, or the excitability from functional derangement of the vagus
or cardiac ganglia, which is either induced by director reflex causes. Violent
physical exercise, or indulgence in intoxicating liquors will accelerate the
circulation and give rise to a form of cardiac palpitation, which ceases as
soon as the cause is removed. Blows on the epigastrium cause it. Adults
with contracted chests, and young persons about the time of puberty, whose
CARDIAC NEUROSES. 503
growth has been raj)id, often complain of palpitation. In these cases it
seems to be caused by the narrowness of the chest, which interferes with the
free play of the heart. Palpitation is a very frequent symptom in states of
debility or anaemia. Under this head are included sexual excesses, chlo-
rosis, enervating habits, diabetes, and all acute infectious diseases that are
attended by extensive nutritive disturbances, as typhoid fever, scurvy,
etc.
Cardiac palpitation is of frequent occurrence in persons with what is
called a nervous temperament, induced by late hours, the habitual use of
strong tea and coffee, the inordinate use of tobacco, derangements of the
digestive organs, sudden shock or fright, chorea, etc. The excessive habit-
ual use of aconite and digitalis is known to have caused it. Cardiac palpi-
tation is frequently met with in those with a gouty diathesis and chronic
diease of the liver, accompanied by dyspeptic symptoms which are attended
by flatulence. It is more common in women than in men, and often seems
distinctly allied to hysteria.
Symptoms. — In a perfectly healthy subject with a well-formed chest, the
cardiac impulse is so slight that the motion is not perceptible, unless the
hand be applied to the precordial space. Whenever a person becomes
sensible of the beating of his own heart, he may be said to have cardiac
palpitation ; by the term is understood an unnaturally strong cardiac im-
pulse accompanied by an unnaturally rapid action of the heart, which may
be irregular or intermitting. Sometimes there is a loss of three or four
beats which causes a sense of oppression or even of impending death. It
may be accompanied by a choking, paroxysmal, " fluttering " sensation.
In some cases the impulse communicates a quick shock to the chest walls ;
in other cases the impulse is prolonged and heaving in character, and in
others is weaker and almost imperceptible. The heart-sounds may be so
increased in intensity as to be audible to the patient when he lies on his
left side. There may be precordial pain, but usually it only amounts to
precordial "anxiety." The carotids throb ; the heart may beat from thirty
to one hundred beats in a minute ; the impulse and sounds increase and
diminish at the same time ; the fits of palj)itation may come on suddenly,
and be of short duration, or they may come on gradually, and be protracted
and severe. Murmurs are usually due to the accompanying ansemia. Re-
duplication of the second sound is quite characteristic. Sometimes there
is extreme dyspnoea and headache, vertigo and ringing in the ears, and
photophobia. The mind may be bewildered and the jjatient may stagger,
yet no paralysis or vertigo exists. The respirations are irregular or op-
pressed, with dyspnoea and a short, dry cough.
DifiFerentialDiagnosis. — To distinguish between cardiac palpitation inde-
pendent of organic disease of the heart, and cardiac palpitation depending
upon organic cardiac disease, is of the greatest importance. Cardiac pal-
pitation independent of cardiac disease comes on suddenly, and is not con-
stant, whereas organic cardiac palpitation comes on slowly and is constant.
In functional palpitation, all the physical signs of organic cardiac disease
are absent. Persons free from organic heart disease complain more fre-
504 DISEASES OF THE HEAET.
quently of palpitation than those who are the subjects of organic disease ;
palpitation of organic heart disease is increased by exercise.
Prognosis. — In cardiac palpitation independent of organic heart disease,
the prognosis is always good ; although it may cause the patient great un-
easiness, it neyer destroys life.
Treatment. — In each case of cardiac palpitation it is important to find out
and, if possible, remove its cause. Ansemic subjects should take iron in
large doses for a long period. In hysterical palpitation all uterine derange-
ments must be relieved. If the excessive use of alcoholic stimulants, to-
bacco, strong tea or coffee, causes it, they must be stopped. Occurring in a
gouty subject, those means which have been found to relieve gouty mani-
festations must be employed. Those in whom no special cause can be
found, should be directed to sponge the surface of the body night and
morning in cold water, exercise moderately in the open air, and live on a
nutritious diet.
During the attacks, relief will usually be obtained by the administration
of some of the more reliable nervines and diffusible stimulants. Narcotics
generally do harm. Digitalis should never be given in purely nervous car-
diac palpitation. Ether, ammonia, chloral hydrate, and tlie bromides are
occasionally useful ; sometimes camphor, assafcBtida, musk and valerian are
serviceable as anti-spasmodics. A very important element in the successful
management of an attack of nervous cardiac palpitation, is the positive
assurance of the medical attendant that there is ho danger attending the
paroxysm, and that there is no disease of the heart.
ANGINA PECTOEIS.
Angina pectoris is a neurosis of the heart due to organic changes in its
structure or to diseases involving its nerve supply ; strictly speaking, it is a
symptom or a collection of symptoms of organic cardiac disease. It has no
special morbid anatomy.
Etiology. — There is no form of cardiac or aortic disease with which angina
pectoris has not been found associated, and there is no form with which it
is invariably or even generally present. Inherited, nervous or ^^ neuralgic "
tendencies predispose to it ; eighty per cent, of cases occur after the fortieth
year. Gout, albuminuria, diabetes, and certain hepatic diseases are often
associated with it. Trousseau dwells on the relationship between angina
pectoris and epilepsy. There are, however, two forms of heart disease with
which it is especially liable to occur : — obstruction to the coronary circula-
tion, and fatty degeneration of the heart.
The other diseased states with which it is liable to occur are, insufficiency
of the aortic valves, with a rigid dilated state of the ascending portion of
the arch of the aorta, combined with dilatation of the left ventricle. When
these conditions exist, angina pectoris will not occur unless the heart's
action is suddenly disturbed, or its movements impeded by some mechanical
cause.
Symptoms. — The symptoms which attend an attack of angina pectoris are
AISTGIKA PECTORIS. 505
quite characteristic. The ])atient is suddenly seized with an intense ago-
nizing pain in the precordial region (usually commencing on a level with the
xiphoid cartilage) extending tlirough the back and along the left arm
This pain is of a stabbing or lancinating character and produces a sensa-
tion of impending suffocation — a feeling as though death was near at
hand. There may be true laryngeal pain. At the commencement of
this pain the countenance becomes deadly pale and is expressive of ex-
treme anxiety and suffering ; the surface is covered with a cold perspira-
tion, the pulse falters, and may be almost imperceptible, the respiration is
short and hurried, the face livid, and the patient is unable to lie down or
even to move, for the least motion aggravates his sufferings. His conscious-
ness is undisturbed, and his spinal as well as his cerebral functions are un-
affected, but there may be slight wandering as the attack passes off. Not
infrequently the rhythm of the heart's action is undisturbed and the patient
does not even experience palpitation. Sometimes the action of the heart is
so much deranged that syncope or even sudden death occurs. The pulse
may be slow and feeble or markedly irregular. Usually after the paroxysm
has continued for a few moments, or at the longest an hour, it gradually
subsides. The attack may come on during sleep.
At first, there are long intervals between these attacks, but after a time
they become frequent. Between the attacks the general health may be un-
impaired.
DifFerential Diagnosis. — Angina pectoris may be confounded with spas-
modic asthma, hysteria, intercostal neuralgia, myalgia, and the first stage
of acute pleurisy.
Although the phenomena attending a paroxysm of angina pectoris may
bear a striking resemblance to those of spasmodic asthma, a physical ex-
amination of the chest will detect the presence or absence of the
characteristic physical signs of the asthma, and thus lead to a correct
diagnosis.
The intermitting and irregular character of the pulse in angina pectoris
will distinguish it from an hysterical paroxysm.
In intercostal neuralgia, the duration of the attack, the points of tender-
ness, the direction of the pain, and the absence of cardiac disturbance, will
distinguish it from angina pectoris.
Myalgia and acute pleurisy may simulate angina pectoris. In each,
acute pain and catching breath are present ; but the condition of the circu-
lation, taken in connection with the locality of the pain and the physical
signs of pleurisy, will generally decide the question.
Prognosis. — The prognosis in angina pectoris is necessarily unfavorable.
Sometimes the first attack proves fatal ; in more instances the second or
third, while in many more, perhaps in the majority of instances, the
patient at irregular intervals experiences a succession of attacks, each
paroxysm being more severe than the previous one, until finally, after a
period extending from one to six or eight years, an attack occurs in which
the heart's action is arrested and death ensues. The later attacks are excited
by trivial causes, or apparently come on spontaneously. The tendency of
506 DISEASES OF THE HEART.
angina pectoris associated with organic disease of the heart is to grow
steadily worse, and terminate in death within a year.
Treatment. — During an attack, means should be employed to alleyiate or
arrest the paroxysm ; during the interval the exciting cause should be re-
moved or its predisposing power diminished. It is doubtful whether there
are any remedial agents that have the power to arrest or very greatly relieve
a paroxysm. Diffusible stimulants,. sedatives, and anti-spasmodics have all
been employed, but so far as my experience goes they have no power to
alleviate or arrest the paroxysm. Kest, and the free administration of
digitalis, are of the greatest service. Chloroform should not be used. An
emetic for an overloaded stomach, or hot foot baths, etc., when cold causes
a paroxysm, are often advantageous. Quain and many others advocate the
nitrite of amyl, tti, v — vi, inhaled from the handkerchief ; nitro-glycerine
(1-1 00 TTl a dose) is very useful, and hypodermatics of morphine may be
given in conjunction with it.
During the interval all violent emotions and all active physical exercise
must be avoided. Indigestion, or flatulence, when present, should be
relieved by careful attention to the diet. The only medicinal remedies
whicl^ I have found of service in delaying and I'endering less severe
the paroxysm of angina pectoris are iron, strychnine, and arsenic ; these
should be administered daily in small doses. Phosphorus and zinc are
useful in "nervous temperaments." When angina pectoris is associated
with fatty heart, the rules given for the management of the latter disease
should be observed. Quain states that a continuous current, the + pole
on the sternum and the — pole on the lower vertebrae, has often produced
marked amelioration of anginal paroxysms. Trousseau strongly advises
belladonna given continuously in small doses, on the ground of the analogy
of the affection to epilepsy.
HYDEOPERICAEDIFM.
{Dropsy of the Pericardium.')
Hydropericardium is a sero-albuminous effusion into the pericardial
sac, non-inflammatory in character, and when absorbed leaves no trace
behind it. It is often very abundant and a source of great discomfort to
the patient, but rarely directly causes death. The effect of such fluid
effusions is to embarrass the action of the heart, while the heart-fibre be-
comes pale and is easily torn, the result of the serous infiltration. Six,
seven, or more ounces of fluid are usually found, of a yellow, green, red,
or red-brown color. Thirty-three per cent, of albumen is usually present,
and a small amount of fibrinous matter that coagulates on exposure to the
air.
Etiology. — l^on-inflammatory effusions into the pericardium occur most
frequently in connection with renal and cardiac diseases. In that form of
renal disease which complicates scarlatina, it is especially liable to occur,
and under such circumstances it is passive in character and is soon reab-
sorbed on the restoration of the renal function. When it occurs in chronic
PNEUMOPERICARDIUM. 507
forms of Bright's disease, it is more serious and obstinate. When it ac-
companies chronic cardiac disease it is the result of tha general venous
congestion, and its pressure greatly embarrasses the already enfeebled
heart. It may result from any disease where there is, from physical causes,
a tendency to serous transudation into the cavities of the body.
Symptoms. — The symptoms and the physical signs "N^mh attend such
effusions do not materially differ from those already detailed as marking
the stage of fluid effusion in pericarditis, except that there is entire ab-
sence of any febrile disturbance. There is no friction sound present at
any time during the progress of the effusion. It is an early symptom
when due to heart or lung disease ; and occurs late when due to splenic,
hepatic, or renal disease. It occurs very late in the tuberculous and can-
cerous cachexiae.
Prognosis. — In chronic Bright's disease and in advanced cardiac disease,
it is usually the precursor, although it can scarcely be called the cause of
death. In other conditions the prognosis will depend upon the circum-
stances which attend its development.
Treatment. — In the treatment we must be guided by the peculiarities of
each case. All the measures recommended for the treatment of hydro-
thorax may be employed in the treatment of hydropericardium. To find
out and remove its cause is of the greatest importance ; in other words,
treat the diseased condition which gives rise to, or permits the effusion.
Only in scarlatinal albuminuria is the accumulation so sudden that para-
centesis may be demanded.
PNEUMOPERICAEDroM.
Pneumopericardium, or air in the pericardial sac, is the result either of
a perforating wound of the thorax, or the perforation of the pericardial
sac by an ulcerative process and the admission of air from some organ
naturally containing it — stomach, intestine, lung, or oesophagus ; or to the
putrefaction of an exudation.
The diagnosis of this accident rests on the tympanitic percussion sound
over the pericardial space, and the tinkling, splashing, or metallic sound
heard directly over the heart. With the exception of those cases which
are of traumatic origin, this accident rapidly proves fatal ; 80 per cent,
die in non-traumatic and 50 per cent, in traumatic cases. Its treatment is
altogether symptomatic.
H iEMOPERIC ARDroM.
Hsemopericardium,' or blood in the pericardial sac, may be of trau-
matic origin, or may result from rupture of the heart, or, far more fre-
quently, the pericardium becomes distended with blood from the rupture
of one of those small aortic aneurisms which develop on that portion of
the aorta included within the pericardial sac. Unless of traumatic origin,
1 nifimoperioardium is non-inflammatory. Blood may fill tlie sac when inflammation exists ; then the
name hemorrlia;^ic pericarditis is api)lied,
508 DISEASES OF THE HEART.
it rapidly proves fatal, and will be found at the autopsy of many cases of
sudden death. When of traumatic origin, the effused blood is not often
absorbed.
SYPHILITIC DISEASE OF THE HEART.
There may be two manifestations of syphilis in the heart,— the fibroid
vatch and the gummy tumor or gumma.
Morbid Anatomy. — Pale, yellow, gummy masses are found, usually inti-
mately blended with the cardiac substance, but often projecting as nodules
from its surface. At first they are elastic, firm, homogeneous, often very
hard ; later they soften and become cheesy. They may become fluid and
open inward and give rise to cardiac aneurism. As a rule the cheesy prod-
ucts are absorbed and a puckered, fibrous scar remains at their site. Some-
times the gummata — which are nearly always multiple — appear as " infil-
trations " or "deposits." They may occur in miy portion of the heart.
When the outer zone of a gumma undergoes development into fibroid tissue,
the caseous portion remains as a compact mass. Bruce regards this as an
intermediate form between the fibroid patch and the true gumma or
••syphiloma." The myocardial vessels are not infrequently the seat of
(syphilitic) endarteritis obliterans, giving rise to infarctions in the wall of
the heart ; and the pericardium is commonly found adherent.
Etiology. — Fibroid patches and gummata arise both from congenital and
acquired syphilis.
Symptoms. — Symptoms of cerebral or visceral syphilis may and often do
mask those of the cardiac affection. Should the puckered fibroid tissue nar-
row or distort any part of the heart, or involve the valves to such an extent
as to cause obstruction or allow of regurgitation, then a murmur — differing
in no respect from other murmurs — will be the chief symptom. Syncope,
infrequent pulse, palpitation, dyspncea, choking, and many other symptoms
of heart disease have occurred in the few recorded cases of syphilis of the
heart.
The diagnosis rests mainly on the exclusion of all other forms of heart
disease, and the evidences of syphilis, hereditary or acquired, in the indi-
vidaal
The prognosis would be more favorable than, probably, with any other
similar condition, on account of its amenability to treatment, which, of
course, is purely anti-syphilitic.
Basedow's disease.
{Exophthalmic Goitre,)
Basedow's or Graves' disease is an affection in which there is enlargement
and hyperemia of the thyroid body, protrusion of the eyeballs, cardiac pal-
pitation and anaemia. It is closely allied to functional cardiac diseases.
Morbid Anatomy.— It is attended by no constant morbid lesions. The
enlargement of the thyroid body is due to a dilatation of its vessels. The
protrusion of the eyeball is caused by dilatation of the vessels behind the
BASEDOW'S DISEASE. 509
globe ; both of these changes appear simultaneously with derangement of
the circulation, and cardiac palpitation. There are many circumstances
which render it probable that the enlargement of the vessels is due to some
vasa-motor disturbance which allows of their passive dilatation in the neck,
the thyroid body, and the orbit ; at the same time it causes an excited
action of the heart. The thyroid body may be filled with cysts or be the
seat of hyperplasia. Atheroma of the ophthalmic arteries has been
found.
Etiology. — It rarely occurs in males. It is met with in women between
twenty and thirty years of age. A " neuropathic tendency " is usually
strongly marked. Menstrual derangements attended by violent mental
emotions of various kinds often precede its development.
Symptoms. — This disease may come on suddenly or slowly ; if it develops
slowly, the patient will at times for a long period complain of severe attacks
of cardiac palpitation, and pulsation in the arteries, gradually these attacks
of palpitation will become more frequent and severe, the eyes will become
slightly prominent and staring, and after a time they may become so promi-
nent that the lids will not cover them. Occasionally the insertion of the
recti muscles can be seen. The protrusion is often greatly increased under
excitement. The attacks of cardiac palpitation grow more severe, the thyroid
gland visibly enlarges, and the eyes become lustrous and projecting.' On
casting the eye down, the eyelids follow but slowly; — this gives a peculiar
look to the patient. Vision is not usually disturbed, but there may be
slight loss of co-ordination. In proportion as the eyes bulge the eye-
lashes and eyebrows fall out. Diplopia, traceable to paresis of the right
trochlearis has been noted. Profuse lachrymation is not uncommon.
Exophthalmus is often more marked on one side than the other, and is
then apt to be attended by enlargement of the thyroid body on the opposite
side.
The thyroid gland usually enlarges slowly ; the patient's attention is first
attracted to it on account of a continued pulsation of the lower part of the
neck. It is usually unequally enlarged, is soft, elastic, and at first pul-
sates, due to the dilatation of the vessels in the gland ; after a time there
is increase of tissue, and blowing sounds are audible over the enlargement.
There may be a change in the pitch of the voice, perhaps from pressure of
the enlarged gland on the recurrent laryngeal nerve. Sometimes the voice
is hoarse or entirely lost. There is always danger from pressure of the en-
larged thyroid gland upon the trachea. The cardiac palpitations are rapid
and irregular, the pulse-rate varying from one hundred to one hundred and
forty per minute. The heart-sounds are loud, and a soft, systolic bellows-
murmur may be heard at the base and in the large arteries. There may
be a distinct thrill. The carotids may be dilated. The circulation is rapid,
the veins filling rapidly, and the pulsation of the small arteries is felt by
the patient. Mental emotion and violent physical exertion bring on attacks
of palpitation, which may be so violent as to produce a visible enlarge-
J Eulenberg regards increased development of fat in' the cellular tissue of the orbit, as, in part, the
c^use of the bulging cf the eyeballs.
510 DISEASES OF THE HEART.
ment of the precordia with every heat. Stimulation of the accelerator
nerves of the heart probably causes the palpitation.'
Debility, anaemia, indigestion, anorexia, and diarrhoea may be present
during the whole course of the disease. Insomnia, amenorrhoea, and hys-
terical symptoms are very frequently observed in nervous females. In a
few instances the temperature is often elevated to 103° F., and followed by
profuse sweats.
LifFerential Diagnosis. — When the three classical symptoms are present in
a female, viz., bulging of the eyeballs, cardiac palpitation, and enlargement
of the thyroid, a mistake in the diagnosis will scarcely occur. Von Graefe
makes a diagnosis on the " want of harmony between the movement of the
eye and its lid."
Cystic goitre is not accompanied by exophthalmus, nor by paroxysmal
enlargements. The thyroid in Basedow's is far more elastic than in cystic
goitre.
The lustrous appearance of the eye suffices to diagnosticate it from prom-
inence due to heart disease {e. g., hypertrophy), which latter would give evi-
dence of organic changes.
Local orbital or cranial causes of exophthalmus are excluded by the
absence of squint and other cerebral symptoms.
Prognosis. — This must always be guarded. It may increase for months,
remain stationary for a year or two, and then gradually decline but not
wholly disappear. In some instances its course has been acute and rapid.
Recovery occurs in from four to five per cent, of cases. G-reat im-
provement has occurred in from thirty to forty-five per cent, of cases.
It does not directly cause death, but intercurrent affections are gen-
erally ill-borne and fatal. Any heart-disease (organic), great anaemia, or
evidence of the ' ' neuropathic disposition, " renders the prognosis unfavora-
ble. Pregnancy is said to have a favorable influence.^ Death may occur
from valvular disease of the heart, pulmonary tuberculosis, gangrene of the
extremities, pulmonary apoplexy, or oedema.
Treatment. — The first remedies proposed in the treatment of this affection
were quinine and iron, and their use is still followed by the best results.
Traube gives them alternately, five grains of quinine one day, and ten grains
of iron, in the form of Vallett's mass, the following day. Arsenic does
harm. Iodine is condemned by some and recommended by others. It has
been claimed that belladonna, hydrocyanic acid, and ergot tranquillize the
heart. Galvanization of the cervical sympathetic diminishes the exoph-
thalmus and lowers the pulse-rate : — it is to-day the favorite plan of treat-
ment with many. Hydropathic treatment is highly praised by some French
authorities. My own experience has shown that a prolonged residence in
a high elevation (Colorado) seems to arrest its progress, and in one instance
led to apparent recovery.
1 Friedrich'g ingenious theory is that, the vaso-motor nerves being paralyzed, dilatation of the coronary
artery follows, and hence there is increased excitement in the ganglia of the heart.
2 Trousseau and Corlies.
CHRONIC ENDARTERITIS, 511
DISEASES OF THE BLOOD-VESSELS.
Under this head will be considered the following diseases of the arteries
and veins.
DISEASES OF THE ARTERIES.
I. Acute Endarteritis. V. Syphilis of Arteries.
IL Chronic Endarteritis, or "Ather- VL Atrophy, Hypertropay
oma.'" Dilatation, Narrowing.
III. Periarteritis.
IV. Degenerations : Fatty, Waxy, and Calcareous.
DISEASES OF THE VEINS.
I. Acute and Chronic Phlebitis. II. Dilatation of the Veins.
Emtolism and Thrombosis.
ACUTE EISTDAETERITIS.
Acute endarteritis is an inflammation of the tunica intima, which is
formed of endothelium lying on longitudinally arranged elastic tissue. As
an isolated lesion it is rare.
Morbid Anatomy. — Along some vessel, chiefly the aorta, numerous ele-
vated round patches are seen projecting from the internal layer. They are
red, opalescent, soft, and elastic {" gelatinous patches of the aorta "). The
elevated patches are made up of embryonic cells arranged in parallel lines.
These patches may undergo ulceration. Fibrin may form on their surface
and inclose either the white blood corpuscles or the proliferated and free
elements of the diseased surface. Pus formations and gangrene may result.
The middle coat is not extensively involved, but a periarteritis nearly al-
ways occurs. The whole vessel becomes friable. Emboli form, and coagu-
lation may result in arterial thrombosis.
Etiology. — Wounds, emboli, extension of inflammation from without, and
irritation from a hard vegetation may cause it. Acute aortitis is usually of
rheumatic origin. A purulent aortitis is described by some as occurring in
septic conditions.
Symptoms. — There are no special symptoms by which it can be distin-
guished. When coagula are formed thrombi result, and then the symptoms
will be those of thrombosis complicated by pyaemia.
CHEOlSriC ENDAETEEITIS.
A theroma, or endarteritis deformans, is a common disease.
Morbid Anatomy.— It is an inflammation of the internal coat, with thick-
ening in patches, the thickening being due to multiplication of the cellu-
lar elements ;— granular fatty degeneration of these elements and of the
middle coat follows, and a yellow atheromatous focus is produced, separated
512
DISEASES OF THE BLOOD-VESSELS.
from the blood current by a thin tense pellicle. As the atheromatous
changes take place, the centre of the patch contains a putty-like mass
of cholesterin crystals, fat granules, and crystals of fatty acid. When
there is little or no fatty
change in the patches, the
process is called "sclero-
sis," and they are then
stained dark brown. When
these processes progress
slowly, calcareous granules
infiltrate the tunica intima,
and, later, form thin, fria-
ble calcareous plates just
underneath an internal pel-
licle. The vessels above
the heart in the thorax are
most frequently affected ;
they become enlarged, ir-
regular, and friable. When
the stiffened internal coat
breaks, chinks are formed
^'«- ^0^- which fill with blood and
M .^ ^Chronic Endarteritis :Atherom^^^ later bccome melanotic. In
Magnified View of a Small Artery, partly diagrammatic. • t ti
A. Endotheliu7nofariery,ceUsturnedinward.—B. Intima thrmvn ^"^^ aorta the middle COat
into folds by C, the elastic lamina. — D. Muscular coat {tunica often disannears COnnCCt-
ive-tissue taking its place ;
destruction of the middle
coat is the only cause of
spontaneous aneurism of
the aorta. The external coat finally assumes the histological characters of
the altered internal coat. After the aorta, the cerebral, coronary, and
splenic vessels and those of the lower extremity may become involved. In
the small vessels, narrowing and stenosis are the results of chronic arteritis.
Cardiac hypertrophy is a common result of the rigidity and inelasticity of
the aorta and its branches.
Etiology. — Atheroma or arterial sclerosis is a disease of advanced life.
Men are far oftener affected than women. It is predisposed to by gout,
rheumatism, syphilis, Bright's disease, lead poisoning, and especially by
alcoholismus. Over-strain of the vessel is often its immediate cause. It
is said sometimes to be an extension from the endocardium into the
aorta.
Symptoms. — Nearly all its symptoms are the mechanical results of rigidity
of the artery. The left ventricle is hypertrophied. The peripheral arteries
are enlarged, lengthened, and tortuous, and an irregular outline is readily
felt along their course. The pulse is feeble, sometimes imperceptible ;
the sphygmograph shows a short up-stroke and a flat summit (pulsus tar-
dus). The extremities are cold and parts may become gangrenous (senile
media).— E. Adventitia.
F. Swollen and proliferating intima.
G. Irregular spaces containing calcareous, granular, and fatty mat
ter.
H. Elastic lamina, limiting the degenerative process.
I. Lumen of tlie vessel encroached upon one side only.
PEEIARTERITIS. 513
gangrene). Apoplexy may occur, and some ascribe epilepsy and senile de-
mentia to atheromatous arteries. The different organs atrophy, the skin
becomes dry, and the lungs are frequently emphysematous. Dissecting
aneurisms may be induced after a rupture of an atheromatous abscess ;
persistent anasarca of the legs in old men is often due to calcified
arteries.
Diiferential Diagnosis. — Aortitis sometimes gives rise to symptoms that
can establish a diagnosis. These are acute substernal pain with oppres-
sion, palpitation, quick and feeble pulse. "With these symptoms may be
associated a hard systolic murmur, originating at the seat of inflam-
mation, and transmitted to a distant point of the aorta. Paroxysms of
pain like angina pectoris are sometimes marked.
Prognosis. — It is a condition which cannot be cured.
Its treatment is altogether hygienic.
PERIAETEKITIS.
In periarteritis the adrentitia and very soon the surrounding cellular tis-
sue are hypersemic, swollen and infiltrated with cells. The external coat
becomes homogeneous and gelatinous. The process terminates either in
connective-tissue or pus formation. In purulent infiltration of the exter-
nal coat the intima is not affected ; but should the middle coat become
involved pus may open into the blood current and an aneurism is liable to
be formed.
Etiology. — Periarteritis occurs from wounds, extension of inflammation
from adjacent parts, or during the course of pyaemia.' Periarteritis is the
first step in the formation of those miliary aneurisms occurring in the
cerebral vessels, and which are always found preceding cerebral hemor-
rhages.
Fatty degeneration, apart from atheroma, is rare. It occurs chiefly in
the aorta. In the internal coat the fat granules occur in flat layers, and
in the middle coat they are found between the flbres, and when very
abundant the muscular elements cannot be distinguished. Sometimes the
endothelium alone is involved, and it may desquamate, laying bare the
tunica intima. This is said to accompany erysipelas and relapsing fever.
Calcification of the arteries, independent of atheroma, is even rarer than
fatty degeneration.
Amyloid degeneration occurs in the small arteries, especially in the renal
glomeruli, but also in those of the spleen, liver, intestines and lymph glands.
Its causes, gross and microscopical appearances, tests, etc., are fully dis-
cussed under chronic Bright's disease.
Cancer only attacks the adventitia.
Tuberculous granules often stud the external coat of the small arteries.
Syphilitic Ai^ea^Q of the arteries chiefly attacks the cerebral vessels. G-reat.
thickening and nodose swellings are due to gummatous material infiltrating
' Kusfmaul and Maier describe a periarteritis nodosa wliich is usually fatal, and Gull and Sutton have:
called the hyaline fibroid appearance of the external coat of the arterioles arterio-ccqnllary fibrosis.
33
514 DISEASES OF THE BLOOD-VESSELS.
the outer coats. The walls are opaque and the lumen is considerably
diminished. Later, cellular growths occur in the internal coat. Throm-
bosis and cerebral softening are often the result. This neoplastic formation
has been called arterioma. When such a condition is suspected, mercury
and iodide of potash are to be given.
General dilatation of arteries may be due to atony or paralysis of their
muscular coat, or to atheroma or degeneration of their walls. The aorta
and the pulmonary arteries are those most frequently involved. Sometimes
the aorta and its branches are the seat of congenital uniform stenosis. This
occurs in females chiefly, and is associated with other malformations. The
■ symptoms are a small pulse, frequent palpitation, cold extremities, tendency
to syncope, and menorrhagia. Gastric ulcers are common. The aorta may
be contracted and nearly obliterated at its junction with the ductus
arteriosus.
PHLEBITIS.
Phlebitis may be acute or chronic.
Morbid Anatomy. — In acute phlebitis the adventitia maybe first involved
and the inflammation extend inward, a clot forming in the calibre of the vein;
or the inflammation may commence within, in connection with surrounding
inflammation and extend outward. If there is extensive connective-tissue
infiltration around the vein, adhesive obliteration of the vein I'esults ;
should the clot soften and disintegrate, pus formations result. The
presence of a clot may be regarded as an essential accompaniment of all
forms of phlebitis, except the adhesive or chronic.
In cJironic plilehitis the external coats of the veins are very much thick-
ened, while the intima may be normal. The connective-tissue around the
vein is greatly increased, there is hypertrophy of its muscular tissue, and the
vasa vasorum are very much dilated. In rare cases thickening, fatty
Of 703 cases of Sibson's (Medical Anatomy), 87 were within the pericardium, i. e., about 12 per cent.
2 Anatomically, aneurisms are divided into irve and false. True aneurisms are those in which all the
coats of tlic; artery are found in the walls of the aneurismal sac. False aneurisms are those in which a rup-
ture of one or more coats of the artery has occurred.
520 DISEASES OF THE BLOOD-VESSELS.
quently pedunculated, communicating with the aorta by a small orifice.
The J further exhibit a remarkable tendency to descend in the progress of
growth, involving in their course the heart or the root of the pulmonary
artery. By their position they are sheltered from direct influx from the
ventricle, whilst they are exposed to the maximum force of reflux from the
aorta. When, however, the orifice is partially or entirely above the level
of the valves, the main pressure sustained by the sac is that during influx
from the ventricle ; hence the direction of growth is upward.
Aneurisms near the sinus magnum produce erosion of the ribs and their
cartilages, the sternum and the right clavicle : — sections of the bones show
the lesions of osteitis. The adjacent muscular and connective-tissue is ex-
tensively infiltrated. The descending cava and the left innominate vein
may be so compressed as to have their channel completely closed. The left
recuiTcnt laryngeal, the left sympathetic, or the trunk of the vagus may
be compressed, atrophied, or entirely destroyed. The thoracic duct may
be compressed and ruptured into. Should aneurisms about the arch enlarge
backward, the trachea, oesophagus, and right lung will suffer from the
pressure.
In aneurism of the descending arch, or thoracic aorta, the spinal extrem-
ity of the ribs and the bodies of the vertebrae in the dorsal region may be
destroyed, and the left bronchus may be obliterated, causing consolidation
of the entire lung. The dorsal spinal nerves and sympathetic trunk may
be destroyed by pressure. All the secondary changes in thoracic aneurism
are "pressure effects," and they are never alike in any two cases.
The aneurismal sac also varies greatly in the appearance it presents at
the autopsy. All the tunics of the artery may be preserved ; but in large
aneurisms while the external and internal coats can be traced all over the
tumor, the middle coat ceases abruptly where the sac opens into the artery.
When an aneurism begins with rupture or dis-
ease of the inner coat of the artery, a lining
membrane of new formation meets and coalesces
with the intima, so that the appearance is the
same as if no rupture or change had occurred.
The aneurismal walls may undergo fatty or cal-
careous degeneration. The contents vary with
the size and shape of the sac and with the rapid-
ity with which it has formed. The sac may be
nearly filled with concentric layers of firm lami-
^^'^- ■'^^- nated fibrin containing small calcareous plates ;
Diagram illustrating the anatomy ., , ,. ,, „,, -, ^,^ ^ i
of spontaneous Arterial Aneurism. Or it may DC partially filled With lOOSCr layCrS
A. Internal coat of Artery; of fibrin inclosing recent coaarula. Sometimes
B. Middle coat of same ; C. Ex- °_.^^,P
ternaicoat. ircsh coagula and fluid blood are alone round.
D and E. External and internal rm i- j^ n-i • in • i
coats of the aneurismal tianoj- ihose lammse 01 nbrm nearest the aneurismal
showing the absence of the middle ■,-, i.i ji j.
arterial coat. Wall are the firmest.
Etiology. — The chief predisposing cause of
aneurism is disease of the arterial walls, the most common of which are
chronic endarteritis and atheroma. Age and occupation may also be re-
THORACIC ANEURISM. 521
garded as predisposing causes, the period between forty and fifty being
the favorite period of its development. It is a question whether aneurisms
occurring in middle life are the result of senile changes or violent physical
exertion. Atheroma and calcareous degenerations are commonest after
sixty; hence muscular effort probably has much to do in developing the
more frequent aneurisms in those who are younger, although it is doubtless
aided by commencing degeneration of the arterial wall. Mechanics, por-
ters, soldiers, and those liable to sudden and violent physical exertion are fre-
quent subjects of aneurism ; the irregularity and violence of the action is to
be considered, rather than its severity. Habits of life, intemperance m eating
and drinking, chronic alcoholismus and tight fitting garments (uniforms)
predispose to aneurismal developments. The majority of these who de-
velop aneurism before forty-five will give a syphilitic history ; hence syjah-
ilis must be ranked as a predisposing cause. Chronic Bright's, rheuma-
tism, gout, lead and mercurial poisoning are included in the predisposing
causes to arterial diseases, and consequently to aneurism. In aortic insuf-
ficiency the hypertrophied left ventricle throws a larger column of blood
with abnormal force against aortic walls ; chronic aortitis results and an
aneurism may follow.
The exciting causes are blows, falls from heights, wounds, excess or pro-
longed venereal excitement, and sudden violent strains, exerted on a de-
generated artery.
Symptoms. — The early rational symptoms of thoracic aneurism vary with
the site of the tumor. If the aneurism is near the sinuses of Valsalva, it
will give rise to no symptoms until rupture discloses its existence. If a
second murmur is heard over the pulmonary artery it may be caused by dis-
placement of the valve, or diminution in the calibre of the pulmonary
artery from pressure of an aneurismal tumor, and if it is accompanied by
venous stasis and congestion of the upper half of the body, an aneurism
may be suspected. "With all aneurisms within the pericardium there will be
some hypertrophy of the left ventricle. The development of an aneurism
near the sinus magnum is usually accompanied by very positive symptoms.
The patient often states that after some violent effort, some blow, or during
an excess of some kind, " he felt something suddenly give way," and then
followed a '^boring " pain near the sternum with dyspnoea, palpitation, and
perhaps haemoptysis.
As a rule there are no subjective signs of thoracic aneurism until the
tumor presses on the adjacent parts. By the direction of the pressure the
seat of the tumor may be determined. Aneurism of the ascending arch
usually presses forward, upward, and to the right ; — of the transverse
arch, backward and upward ; and of the descending portion of the arch,
backward and to the left. In whatever direction an aneurism presses, pain
is its first symptom. The pressure may be exerted upon (1) the nerves ;
(2) the bloodvessels ; (3) the trachea, oesophagus, the large bronchi, the lung-
tissue, the thoracic duct, and, indirectly on the heart.
The pain when present is constant. It is increased by acceleration of the
circulation, and is localized in the region of the tumor ; usually it is asso-
522 DISEASES OF THE BLOOD-VESSELS.
ciated with a sense of constriction. The pressure pain may be neuralgic,
paroxysmal and wandering. It radiates to the neck and shoulder and
may shoot down either arm. If the intercostal nerves are pressed on, there
will be attacks of excruciating intercostal neuralgia. If erosion of verte-
brae, sternum, or ribs occurs, there is a peculiar, constant " boring " pain.
When one or both vagi or recurrent laryngeal nerves are pressed on, spasms
and partial or complete paralysis of the laryngeal muscles cause dyspnoea
and voice-changes ; the voice becoming husky. Sometimes there is com-
plete aphonia. Violent paroxysms of dyspnoea are liable to occur, attended
by a congested, anxious countenance, and violent respiration followed by ex-
haustion. Cases are recorded where vomiting and pjrrosis resulted from
pressure on the pneumogastric. Pressure on the pulmonary plexus gives
rise to a harsh metallic '^ brassy" cougli. Pressure on the vagus may be
followed by congestion of the lungs, oedema and gangrene. An inequality
of the pupils may come from irritation or pressure on the cervical sympa-
thetic : irritation causes dilatation of the pupil ; and pressure (when annul-
ling the function) causes its contraction on the affected side. Disordered
vision may thus become a symptom of thoracic aneurism.
When Mood-vessels are compressed only the main trunks of one side are
involved, hence a delayed, even a suppressed radial pulse will be found
only on that side. In a few cases I have found no pulsation in either carotid
or subclavian on the affected side. Then cerebral anaemia and signs of im-
paired nutrition in the limb on that side were present. The effect of im-
peded venous return may lead to a diagnosis of the seat of an aneurism.
When an aneurism near the sinus magnum enlarges forward, the upper
half of the body shows congestion and oedema ; there is headache, drowsi-
ness and other cerebral symptoms, and the eyeballs protrude. Aneurism
of the innominata or of the right common carotid in the thorax, presses
on the external jugular, and hence the right side of the head and neck is
turgid. Such a condition on the left means aneurism of the left common
carotid.
When tracheal symptoms are urgent, they point to aneurism of the
transverse portion of the arch enlarging backward. The flattening of the
trachea induces difficult breathing, then follows a stridulous cough (with
no expectoration), having a metallic ring, like a ^'nervous cough." Such
compression may result from an accumulation of mucus which cannot be
expectorated ; hence, dyspnoea arises. The pressure may even produce
gangrenous patches, which lead to rupture and fatal hemorrhage. It is
readily seen why congestion of the lungs and pneumonia sometimes fol-
low compression of the trachea. The signs of pressure on a large tronclius
are, principally, a metallic cough, with tenacious mucous sputa, at times
blood-streaked, and, possibly, evidences of pneumonia and gangrene.
Pleurisy may be excited by a tumor's pressure, and it is always an important
sign taken in connection with signs of pressure upon the trachea and bron-
chus.
Dysphagia may be induced, but the oesophagus is rarely ruptured into
by an aneurism. Dyspepsia, reflex in origin, may be a symptom of thoracic
THORACIC ANEURISM. 533
aneurism. The lower third of the oesophagus is said to be widely dilated in
some cases of this kind. Enlargement of the lymphatics below the sac
results from pressure of an aneurism on the thoracic duct. Symptoms of
mal-assimilation, wasting and. inanition would also be present in such cases.
All these symptoms are never present together in any one case, but when
three or four of the prominent ones exist, they are strong evidence of
thoracic aneurism.
Physical Signs. — Inspection. — If the aneurism press on the cava descen-
dens, the face, neck and upper extremity will be swollen, livid, or oedem-
atous, the veins being turgid and varicose. Sometimes there is a thick,
fleshy collar around the lower part of the neck, due to capillary turges-
cence. Bulging is seen at some spot on the chest, probably along the
course of the aorta, and this may be as large as a cocoanut, or, again, may
be perceptible only after careful inspection. Non-existence of a tumor
does not, however, disprove the existence of an aneurism ; aneurismal tu-
mors deeply seated will not produce bulging. AVhen the visible tumor is
large it is generally conical. The skin over it is smooth, tense and shining.
Inspection may reveal pulsation in it, which is synchronous with the car-
diac systole, and when this bulging occurs on the anterior surface of the
chest there seem to be two beats within the thorax at the same time.
Pulsations are, at times, only detected by bringing the eye to a level with,
and looking across the chest. Aneurisms of the ascending arch usually
enlarge first to the right of the sternum near the second costal cartilage,
but if it is very large it may extend into hoth the mammary and infra-
clavicular region. Aneurisms of the transverse arch protrude above the
sternum, those of the descending arch to its left. In the latter case a
visible tumor is uncommon. Aneurisms of the descending aorta enlarge
to the left, rarely to the right, of the spine. They may sometimes give
rise to violent pulsations near the heart and simulate extensive cardiac hy-
pertrophy.
Palpation discovers more accurately the size and the condition of the
walls of the aneurism. The pulsation imparted to the hand is like that
of a blow from the centre outward in all directions, dilating or expansile ;
there may be a diastolic pulsation as well as systolic. The impulse is some-
times perceptible only when one hand is pressed over the sternum and the
other over the interscapular space. When the transverse arch is involved
the aneurismal thrill may be communicated to the hand by pressing the
fingers down behind the sternum. Palliation should be employed to de-
tect lung changes, fremitus, expansion, etc., etc.; it is noteworthy that con-
solidation of lung substance induced by thoracic aneurism is characterized
by absence of vocal fremitus.
Percussion elicits circumscribed dulness at some point along the line of
the aorta, corresponding to the seat and size of the aneurism. A resistance,
peculiar to aneurism, and increased by the force of the percussion -blow,
will be noticed over all large aneurisms. Consolidation of adjacent lung-
tissue may increase the area of dulness.
Auscultation. — The heart sounds accompanied by " murmurs" peculiar
524 DISEASES OF THE BLOOD-VESSELS.
to aneurism may at times be audible over the seat of the tumor, or both heart
sounds may be replaced by murmurs, the character of which varies. They
may be sawing, rasping, or grating. A diastolic murmur is rarer than a
systolic, and is' usually softer. With aneurisms near the sinus, the murmur
is booming or splashing, and is accompanied by a thrill not transmitted in
any direction. When a large bronchus is compressed, the respiratory mur-
mur is weak or suppressed on one side and exaggerated on the other.
There is loss of vocal resonance over the aneurism and over the side on
which the bronchus is compressed.
Differential Diagnosis. — It is always of the first importance to determine
at what point in the course of the aorta an aneurism is developed.
An aneurism near the sinuses of Valsalva may be mistaken for aortic in-
sufficiency. The latter is distinguished by the previous history, absence of
arterial degeneration, transmission of the murmur to the xiphoid cartilage,
absence of a murmur over the pulmonary artery, and the existence of left
ventricular hypertrophy and dilatation. Should the sinus of the right
auricle be pressed on, loth cavae will be obstructed and the liver will show
evidences of congestion.
The diagnosis between aneurism of the arch of the aorta and of the in-
nominate artery is difficult. In the latter the tumor appears earlier in the
neck, and on the right side at the sternal end of the clavicle ; while aneu-
risms of the arch are usually limited to the second right intercostal space, or
appear at the manubrium sterni or in the episternal notch, frequently ex-
tending to the left of the median line. Pressure on the right subclavian
or common carotid does not lessen the pulsation in aneurism of the arch ;
while if the innominate alone is involved, the impulse will be markedly
diminished. Impaired venous return and neuralgic pains are confined to
the right side in innominate aneurism, while the venous congestion is
bilateral and pain is on both sides in aneurisms of the arch. The hruit of an
innominate aneurism is less intense than that of an aortic. The radial
pulse is seldom altered in aortic aneurism, while a suppressed radial pulse
on the right side is a common and important sign of aneurism of the in-
nominate. The larynx and trachea are often pushed to the left by an in-
nominate aneurism ; rarely by an aortic.
Cancer of the pleura, mediastinal tumors, iony exostoses, pulsating em-
pyema, abscesses between oesophagus and trachea, laryngeal disease, in-
tercostal neuralgia, angina pectoris, consolidation of the lung near the apex,
and hydropericardium, — all may be mistaken for a thoracic aneurism.
In cancer of the pleura the personal and hereditary history is impor-
tant. The pain in cancer is constant ; in aneurism it is wandering, and
shifts with change in direction of the tumor. Anything increasing
heart action increases the pain of an aneurism ; this is not so in cancer.
The pulsation is dilating in aneurism ; heaving and lifting in cancer.
A harsh double Iruit is present in aneurism ; while if one is present in
cancer it is soft and blowing. In aneurism the centre of dulness and the
point of maximum dulness coincide ; this is not the case in cancer.
Enlarged veins and glands (axilla, neck, etc.) accompany cancer ; they are
THORACIC ANEUEISM. 525
not present in aneurism. In aneurism there is a subjective sense of
throbbing, never present in cancer. Infiltrated cancer of the lung induces
retraction of the chest-walls, and is not likely to be confounded with tho-
racic aneurism.
Localized empyema which pulsates must occupy the cardiac area and push
the heart to the right, and it has no murmur. Besides, the peculiar
wandering pain of aneurism is absent in empyema, and in this condition
the pulse is not altered. Irregular diurnal fever, chills, and sweatings
occur in empyema, never in aneurism. The exploring needle will settle
the question.
An abscess between the trachea and oesophagus is attended by no hruit,
no pulsation of an expansile character, no shifting pain, no pulse-difference.
Deep-seated fluctuation, chills, fever, and sweats accompany it, however.
An exostosis below the sterno-clavicular articulation may pulsate, but
the pulsation is lifting, not expansile, and there is no bruit.
Laryngeal disease may be recognized by the vocal changes. A physical
examination of the chest, and the laryngoscope will enable one to make a
correct diagnosis.
Tn intercostal neuralgia, the three diagnostic points of tenderness, i. e.,
at the exit of the nerve from the spme, midway between this and the
sternum, and at the edge of the sternum where the terminal branches be-
come superficial, will decide between it and aneurism.
Angina pectoris may occur with thoracic aneurism. But in all such cases
valvular disease or degeneration of the heart- walls will be found to co-exist.
Hence the diagnosis rests on the signs of a tumor in the one case, and the
symptoms of structural heart-disease in the other.
Pulmonary consolidation at one apex, with a murmur in the subclavian
or pulmonary artery, will be attended by the signs of phthisis and not by
those of a tumor. Fluid in the pericardium gives a triangular outline of
dulness never met with in aneurism.
Prognosis. — Although cases of thoracic aneurism have apparently recov-
ered, the rule is that they terminate fatally. The average duration is about
two and one-half years : — some terminate in a few months, others live five
or six years. There is always a liability to sudden death. The better the
general health and the smaller the swelling, the better the prognosis. The
prognosis in aneurism of the ascending arch is better than in any other
form of thoracic aneurism. Death may occur from jaressure on important
organs, or from rupture of the sac.
The sac may open into one of the serous cavities from sloughing, erosion
or laceration of its wall ; or it may open externally, or into a mucous canal. '
When the sac bursts into the pericardium or j)leura, it ruptures at the
thinnest part ; if into the oesophagus, trachea, or a bronchus, it breaks at
some point of adhesion between the two, which has subsequently become
thinned. External openings are produced by gradual atrophy from press-
ure, or by sloughing of the skin over the tumor. Pneumonia, pleurisy,
' In twenty-six ruptures, ten were into the pericardium, Ave into the left lung or pleura, four into the tra-
chea, three into the right lung or pleura, three into the left bronchus or oesophagus, one extei-nally.
526 DISEASES OF THE BLOOD-VESSELS.
bronchitis and gangrene may occur as complications to cause death. Press-
ure on nerves, lymphatics or ducts may induce death from exhaustion.
Emboli may arise and become a cause of death.
Treatment. — The treatment of thoracic aneurism is divided into those
measures which come strictly within the province of the physician, and the
more recent Gurgical procedures. In both, absolute rest is one of the essen-
tials. Anything that accelerates or increases the force of the heart's action
will do harm, in accordance with the simple physical law that every abnor-
mal dilating force applied to the walls of an aneurismal sac must favor its
growth and hasten the fatal issue. Blood rich in nutritive elements more
readily deposits its fibrin, thus favoring that formation of laminated layers
of fibrin within the aneurismal sac which is the first step in the curative
process. Fluids must be taken in minimum quantities. Mr. Tuf nell re-
stricts the food taken to two ounces of bread and butter, and two ounces of
milk for breakfast ; two or three ounces of bread with two or three ounces
of meat for dinner, with two to four ounces of milk or claret wine ; and
two ounces of bread and butter and milk for supper. Mr. Tufnell says
that this dietetic treatment, combined with absolute rest in a recumbent
position for two or three months, resulted in cure in a large percentage of
cases. These statements have not been sustained by the experience of
American observers. While this treatment has arrested the progress of an
aneurism in quite a number of cases, I have never yet seen a cure effected ;
and in almost every instance, just as soon as the patient began to show evi-
dences of anaemia, which are certain to appear after six or eight weeks, the
aneurismal tumor rapidly increased in size, and the cases advanced quickly
to a fatal issue. I very much question if the absolute restriction of diet
and movement prescribed by this plan is necessary or serviceable.
Various internal remedies have been used to favor the formation of a
coagulum within the aneurismal sac, either by increasing the coagulating
power of the blood, or by acting in some specific manner upon the walls of
the aneurism itself or upon the adjacent arterial walls. The principal
drugs used for this purpose are ergot, iodide of potassium, acetate of lead,
and the vegetable astringents. Iodide of potassium and ergot are the only
ones that have stood the test of experience. Both are used at the present
time, and seem to have power in staying the growth of aneurisms and re-
lieving painful phenomena.
The only remedy to be relied on for relief of the excruciating pain attend-
ing aneurismal development is the hypodermic use of morphine. It not
only relieves pain, but by its quieting and regulating influence on the heart
it delays the growth of the aneurism. It also diminishes restlessness and
impatience, and enables persons who are naturally irritable to obtain the
necessary rest which is so important a factor in any plan of treatment. The
external application of belladonna to the aneurismal tumor will often aft'ord
temporary relief to the local pain. The continued application of an ice-
bag to an external aneurismal tumor will often afford temporary relief of
the pain and reduce the tegumentary inflammation ; its use should not be
continued too long. When a patient with aneurism has an undue fulness
ABDOMINAL ANEURISM. 527
of the vessels, free purgation with salines will be attended by marked relief
for a time.
Surgical Treatment of Thoracic Aneurism. — Thoracic aneurism seldom
presents features which justify surgical measures. The methods employed
are ligation of one or more of the great vessels in the neck, galvano-
puncture, the injection of coagulating substances into the sac, and the in-
troduction of solid bodies with the object of starting consolidation. The
two latter methods have only been employed in a few desperate cases, and
death has always followed so rapidly that no deductions can be made. On
theoretical grounds it is improbable that either method could do good,
except in cases of pouched aneurism. Experience shows injection of coag-
ulating fluids to be very dangerous, usually inducing suppuration of the
sac. The permanent introduction of wire, horse-hair, and catgut has never
been followed by good results ; but in at least one case of (ileo-femoral)
aneurism no harm resulted. The temporary introduction of several acu-
puncture needles and their retention from one to two days has been tried
with good results in a few cases ; it is less dangerous than the other methods
mentioned. Gralvano-puncture has been employed by Ciniselli in twenty-
three cases, with five cures. The same method has been tried by other
surgeons, but the clot is liable to break down and cause inflammation of the
sac. This plan has been adopted when rupture of the sac was impending,
to delay for a time the fatal result. In some cases of supposed innominate
aneurism, which proved to be aortic, ligation of the carotid, or of the
subclavian, has been followed by marked relief. In two cases of aneurism
involving the transverse arch, the left carotid has been tied and the disease
cured or arrested for a v&ry long time. It would seem best to perform this
when the sac involves only the arch. Tracheotomy may be performed only
to insure a quiet death.
abdomi:n^al aisteueism.
An aneurism of the abdominal aorta, or of any of its branches situated
within the abdominal cavity, is called an abdominal aneurism. The coeliac
axis, the mesenteries, the renal, and the common iliacs are the branches
usually involved. The morbid changes are similar to those of thoracic
aneurisms, except that the pressure effects are different. The splanchnic
nerves, semilunar ganglia, and. the solar plexus may be involved. The bile-
duct or the renal vessels, the stomach and the duodenum may be pressed
on and narrowed. The bodies of the vertebrae may be eroded. Abdominal
aneurisms are not so often caused by " atheromatous " changes in the walls
of the artery as are thoracic aneurisms.
Etiology. — Its development is always preceded by some form of arterial
degeneration. It is rare before thirty-five, and is met with in men oftener
than in women.
Symptoms. — Intermittent, paroxysmal pain is its prominent symptom.
Agonizing ^am in the bach darts along the branches of the lumbar plexus.
This pain is apt to be continuous, and indicates erosion of the spinal column.
528 DISEASES OF THE BLOOD-VESSELS.
l^ausea and vomiting may result from pressure on the stomach ; dyspha-
gia from pressure on the oesophagus ; jaundice from pressure on the bile-
duct ; changes in the urine from pressure on the renal vessels ; and anasarca
of the lower limbs from pressure on the inferior cava, or in one limb from
pressure on one of the iliac veins. Aneurisms here may burst into the
peritoneal cavity, the retroperitoneal tissue, the spinal canal, or into the
substance of the mesentery, meso-colon, or great omentum, and in the
last-named instances there will be more or less obstruction about the region
of the pylorus. They may also open into the intestinal canal, the lung,
the pleura, the inferior cava, the pelvis of the kidney, the ureter, bile-
passages, or the oesophagus. Earely are the liver and heart displaced.
Physical Signs. — Palpation discovers in some instances a smooth, elastic
tumor to the left of the median line. It has an expansive, dilating impulse
(rarely double), and synchronous with the radial pulse.
There is dulness over the tumor.
On auscultation a single prolonged post-systolic murmur may be heard. '
A double murmur over the aneurism in front is rare. Seldom can any
murmur be heard when the patient is in any other than a recumbent pos-
ture,
DiiFerential Diagnosis. — If an abdominal aneurism is of considerable size,
the constant pain in the back and the presence of a dilating tumor will
establish a diagnosis ; forcible pulsation of the aorta may simulate an
aneurism, but the throbbing is felt along the entire course of the aorta
and its branches, and is not localized as in aneurism ; then the absence of
pain and of the " expansive " impulse and murmur will establish the diag-
nosis. A cancerous or other solid tumor may have a pulsation communi-
cated to it by the underlying aorta ; but the knee-chest position will re-
move doubts. In thin subjects especially, by grasping the solid, uneven
mass, it is easy to decide for or against an aneurism.
Prognosis. — Hayden gives fifteen days to eleven years as the extremes ; a
year or eighteen months is the average duration. After rupture the pa-
tients have lived for some time ; but death is certain sooner or later.
Treatment. — Posture, rest, a restricted diet, and mild laxatives are advo-
cated in the treatment of abdominal aneurism by Bellingham. Tufnell's
plan may also be followed. Iodide of potassium and ergot reduce vascu-
lar tension and are highly recommended. Aconite is highly recommended
by English surgeons. Pressure, ligation, tourniquets, etc., etc., are meas-
ures resorted to by surgeons.
MEDIASTIlSrAL TUMORS.
Cancer and sarcoma are, independent of aneurism, the most frequent
mediastinal tumors. In rare instances lymphadenomata, lipomata, cysts,
enlarged lymphatics, fibromata and osteomata may develop in the medias-
tinum. The lymphatic glands in the anterior mediastinum are most fre-
1 If the patient be placed in the knee-elbow position, and a murmur still persists, then the tumo" if: in
all probability an abdominal aneurism, not a tumor to which aortic pulsations have been transmitted.
THE URINE. 529
qiiently the seat of these developments, although they may originate in any
mediastinal tissue. In exceptional cases the thymus gland is the original
seat of the new growths. The primary cause of their development is un-
known ; they occur at any age, but are most frequently met with between.
twenty and forty.
The symptorns of mediastinal tumors are those of pressure, e.g., aphonia,
dysphagia, cyanosis, pain, and a sense of constriction about tlie chest.
Displacement of the heart without any other recognizable cause is an almost
diagnostic symptom.
The physical signs vary with the size and site of the tumor, which may
pulsate and have a distinct hruit. Mediastinal tumors, mediastinal ab-
scesses, aneurism, pericardial or pleuritic effusions and chronic pneumonia
all produce symptoms which are strikingly similar ; and the diagnosis of a
mediastinal tumor is arrived at mainly by exclusion. The exploring trocar
is often the only means by which a diagnosis can be reached.
Prognosis. — Mediastinal tumors sooner or later terminate fatally. Lebert
states that their average duration is thirteen months. In a case of Jac-
coud's, death occurred on the eighth day.
The ^rm^mew^ is palliative.
DISEASES OF THE KIDNEYS.
THE UEESTE.
The urine in health is a clear, amber colored liquid of acid reaction,
saline taste, and having a peculiar aromatic odor. The amount voided in
twenty-four hours ranges between forty and fifty ounces. Its specific
gravity varies from 1.012 to 1.030 ; the average being about 1.020. After
exposure to the air the acidity of the urine, which is due mainly to the
presence of the acid phosphates, continues for a few days, and then an acid
or alkaline fermentation takes place. The former is caused by the growth
of a round cell vegetable ferment, and is accompanied by the ci-ystallization
of uric acid and the precipitation of the acid urate of soda. The alkaline
change is the result of the growth of the micrococcus urea, and is marked
by decomposition of the urea and the formation of carbonate of ammonia
and the triple phosphates.
Normal Cotistitnents of the Urine. — Generally speaking, these may be
regarded as the products of the metamorphosis of the tissues of the body ;
the most important organic constituents are urea, uric acid, hippuric acid,
oxalic acid, kreatinin, xanthin, and the coloring and extractive materials.
Urea. — This substance represents the result of the retrograde metamor-
phosis of the nitrogenous body tissues and the excess of the nitrogenous ele-
ments of the food. It is formed in the tissues, taken up by the blood and
lymph, filtered by the kidneys, and appears in the urine to the amount of
five to six hundred grains daily. Urea is abnormally increased in amount
in all febrile and nervous affections, in pyaemia and diabetes ; it is abnor-
mally diminished in nephritis, anasmia, cholera, and starvation, and maj
34
530 DISEASES OF THE KIDNEYS.
be entirely absent in acute yellow atrophy of the liver. TJrea is a feeble
base, extremely soluble, and cannot be detected except by chemical exami-
nation.
Uric acid is generally found in the urme combined with some base,
especially lime or soda. Its origin is similar to that of urea. In health
six to nine grains are passed every twenty-four hours ; this amount is in-
creased by a highly albuminoid diet and in certain febrile conditions. It
is diminished by out-door exercise. Uric acid appears in the urine as a
crystalline deposit, which will be described hereafter. Besides the above
constituents, the urine normally contains small quanti-
ties of kreatinin, hippuric acid and xanthin, which may
be said to represent the less completely oxidized products
of tissue change.
Coloring and extractive materials. — The normal color of
the urine is due to tbe presence of a pigment, called urohse-
matin ; a substance closely allied to the coloring matter
of the bile, and derived from the blood by the action of
Fig. 113. the livcr and spleen. Another normal pigment of the
ippuric ci . X 250. ^^j,jj^g ^g iiifjicai;,^ a peculiar substance which under certain
conditions gives rise to indigo-blue. The extractives are certain volatile
organic acids which give to the urine its peculiar aromatic odor.
The inorganic constituents of the urine are chlorine, sulphuric acid,
phosphoric acid, potassium, sodium, calcium, magnesium, oxygen, hydro-
gen and nitrogen.
Chlorine. — The average amount of chlorine passed daily is about one
hundred grains ; an increase in this amount has no special significance, but
a diminution or absence has been noticed in all acute febrile diseases with
the one exception of intermittent fever.
Sulphuric Acid. — The amount daily passed averages about thirty
grains. Sulphuric acid in the urine arises from the animal and vegetable
food taken into the system, and from changes in those tissues which con-
tain sulphur and sulphates.
Phosphoric Acid. — About fifty grains of this acid are eliminated in
the twenty-four hours. It is abnormally increased in all inflammatory
diseases of the nervous system, in severe nerve lesions and in rickets. It
is abnormally diminished in most febrile and inflammatory diseases, es-
pecially in pneumonia and Bright's disease. The rest of the inorganic con-
stituents of the urine, which amount to about one hundred grains daily,
will be considered under the head of urinary sediment, as they generally
appear in that form.
Albumen. — ^When albumen appears in the urine it may have its origin
in the kidneys or depend upon the presence of pus or free blood ; this
question can only be settled satisfactorily by the microscope. Albuminous
urine is generally of low specific gravity. In diseases of the kidney the
serum-albumen which is found in the urine has its origin in the blood,
and either by the increase or diminution of the blood pressure within the
glomeruleSj, the albumen is transuded within the capsule of Bowman, and
THE UEINE. 531
then is waslied along the uriniferous tubules with the urine. When albu-
men appears in the urine in acute and chronic Bright's disease some
structural change in the kidney is indicated ; but it may appear independ-
ent of any structural lesions under the following conditions, viz. : febrile
and inflammatory diseases, impediments to the circulation of the blood,
pregnancy and the puerperal state, saturnine intoxication, hydraemia and
atony of the tissues, after the use of certain drugs, and in some people after
taking certain articles of food.
Urinary Sugar. — When the urine contains much sugar it is of a pale,
yellow color, sweetish taste, and increased in amount. Its specific gravity
is always high, generally between 1.030 and 1.040, although cases are occa-
sionally met in which it is as low as 1.008. Sugar, except in a very small
quantity, is not found in normal urine, so when it is constantly present
in large amounts a grave pathological lesion is indicated. Diabetes mel-
litus is the only disease in which sugar is found in the urine in large quan-
tities, but traces of it appear after disturbances of the abdominal circula-
tion, after injuries to certain portions of the nervous system, after inter-
ference with respiration, in the urine of women just after weaning a child,
and sometimes it is temporarily present without any assignable cause.
Bile. — Urine containing bile varies in color from a deep reddish brown
to a dark green, and generally has an acid reaction and high specific gravity.
The coloring matter of the bile, such as bilirubin, biliverdin, and bili-
prasin, is the portion which usually appears in the urine in disease. It is
especially noticed in those who are jaundiced. The bile salts are some-
times present.
Lactic acid has been found in the urine in diabetes, acute yellow atrophy
of the liver, trichinosis and osteomalacia.
i^a^. — Fat is not very often found in the urine, but when it is present it
gives to that fluid a milky appearance, for it is held in the form of an
emulsion by the albumen present. The
O Q (-\ urine shows a tendency to spontaneous
^0 oo coagulation, and in a short time a white
^rsO'oO l^y^^' I'ises to the top which disappears
® J: o o o on the addition of ether. Under the
O
Q o Q rnicroscope mmute globules of fat, some-
times with blood and lymph corpuscles,
are seen.
Fat globules from -r • •\ m • mi
chylous nrine. Lcucin and lyrosm. — The urine
often contains large quantities of these
substances, which arise from the prolonged action of ^i*^- "s.
the pancreatic ferment upon the nitrogenous elements Leucm andTyrosm.
of the food. A. Globules of Levcin.
B. Tyrosm. x 250.
Leucin appears either in the form of white crystal-
line scales freely soluble in water, or as small, round, yellow bodies looking
something like spherical fat cells.
TyroHin is in the form of white masses consisting of long shiny needles
arranged in star-shaped groups. Leucin and tyrosin appear in those
532
DISEASES OF THE KIDKETS.
diseases in whicli oxidation is very greatly impaired, such as acute yellow
atrophyof the liver, typhoid fever, small-pox, and in hepatic diseases
generally.
UEINAEY SEDIMENTS.
A
Many deposits, in crystallizd and non-crystallized forms, appear in the
urine, some of which are passed with it, and others are separated from
it aiter its passage. The following are the most important :
Ui'ic Acid. — The strong acids which appear in the urine during the
stage of acid fermentation quickly decompose the urates, and set the uric
acid free. This is deposited in the form of yellowish-red colored crystals
which assume a multitude of forms. „The
most common are lozenge-shaped and rhom-
boidal crystals, having angles more or less round-
ed ; they also appear, especially when abun-
dant, as aggregated or flat stellate crystals.
Should any doubt arise as to the character of
the crystals, dissolve the sediment in a drop of
potassic hydrate, then add a little hydrochloric
acid, and the uric acid, if present, will recrystal-
lize into one of its numerous forms. The clinical
importance of uric acid crystals has already
been referred to.
Urates. — When the urine contains abundant
amorphous urates it is generally turbid, but
becomes clear on heating. On careful obser-
vation a fine powdery sediment will be seen,
which clings to the glass and varies in color
from a light fawn to a pink. The urates are in a
state of solution in normal urine, but when
that fluid becomes concentrated
or has lost the temperature of
the body, the urate of soda will
become deposited in an amor-
phous condition, appearing under
the microscope as mossy granu-
les. Urate of ammonia appears
only after the urine becomes
alkaline, occurring as brown-
ish spherical bodies, with or with-
out fine proiecting spiculaj. The ^'■^^e of Ammonia.
. A Cluster of BTcywn
urates may be deposited after 'spiwruies.
slight indigestion, great mental 'vie!°withmcuia-^^
and physical exertion, and in %staif'''f^^!'
acute febrile and inflammatory
diseases ; they are often the forerunner of urinary calculi, and of derange-
ments of the liver and of the other chylopoetic viscera.
Fig. 116.
Uric Acid.
A. The most crmimon form.
B. Disintegr 'ted crystals.
C. Formaiion of 7'ounded masses .
X 350.
Pig. 118.
Fig. 117.
Urate of Soda.
A. AmorpfwMS granvles in clusters
resemhling moss.
B. Granules in strings sometimes
mistaken fm^ granular casts.
X 250. ■
UEINARY SEDIMENTS.
533
o
o c?
(P
.oo
Fig. 119.
Oxalate of Calcium.
The octahedra, most fre-
quently present, are
seen on the left. The
comparatively rare
form of dumb-bells is
also shown, x 250.
Oxalate of Calcium. — Calcium oxalate is often held in solution in the
urine, but when it is precipitated it takes one of two
forms, either as small, colorless, sharp- edged, octa
hedral crystals resembling envelopes, or as dumb-
bell shaped crystals, entangled with mucus. The
presence of the oxalate of lime crystals is due
to the reduction of the compounds of oxalic and
carbonic acids which are normal to the urine, or to the
ingestion of certain articles of food. "When oxalate of
calcium occurs constantly in the urine it produces the
so-called oxaluria or oxalic acid diathesis, and is apt to
lead to- the formation of the mulberry calculi, and in
time exert its poisonous effects on the brain and spinal
cord. The crystals of calcium oxalate are found in the urine in cases
of disturbed respiration, emphysema of the lungs, rachitis, and after
epileptic convulsions.
Earthy Phosphates. — The earthy phosphates are the most common sedi-
ment met with in the urine, in fact, when the urine is alkaline they are
never absent ; they present themselves as the am-
monio-magnesian or triple phosphates, or as the
phosphate of calcium. During the stage of alkaline
fermentation, the ammonia produced combines
with the phosphate of magnesium present, and the
result is that the crystals of the triple phosphates,
being insoluble in an alkaline fluid, are thrown
down in large quantities, as also are the crystals of
the phosphate of lime, the separation of the latter de-
pending upon the presence of one of the fixed alka-
lies, as the carbonate of sodium. The crystals of the
triple phosphates vary according as they are the re-
sult of rapid or slow crystallization : in the former
case they assume a feathery form, looking some-
Ammonio-Magnesian, or Triple thing like two fcms crossing at an acute angle ; in
Phosphate. ^j^^ latter case they appear as triangular prisms with
A. Larqe colorless prisms. t^. , ,, »,. „
B. Forms rapidly deposited, bevelled edgcs. ihe pliosphatc 01 lime lorms an
amorphous transparent sediment like the urates,
but is distinguished from them by the action of heat, which causes an
increased precipitation, and by that of nitric acid, a few
drops of which clear up the urine. A sediment of the
earthy phosphates does not of necessity indicate that there
is an abnormal amount in the urine, but it does show the
alkaline state of the urine and the possible results of such
a condition, and it points out the danger of the formation
of phosphatic calculi. An increase of the earthy phos-
phates has been noted in certain diseases of the bones, such
as rachitis.
Cystine, which is a crystalline body derived from the
Fig. 120.
Fig. 121.
Phosphate of Lime.
X 350.
534
DISEASES OF THE KIDJS'BYS.
Fig. 122.
Cystine, x 250.
liver, is not often found in the urine, but when it is it presents itself in
the form of flat hexagonal plates, which are of neutral reaction and can be
dissolved by the caustic mineral alkalies. When this
substance occurs in the urine it is apt to give rise to cal-
culi. Cj^stinuria seems to run in families.
Organized Sediments. — Mucus and EpitJielium. All
urine contains a varying amount of mucus, derived from
the urinary passages and from the bladder, which sepa-
rates in the urine as a light, flaky cloud. Under the
microscope mucus presents itself in one of two forms,
either as mucous corpuscles in the form of small, round
granular cells containing one or more nuclei, or as trans-
parent masses of mucous coagula, which look very much like granular
casts and for this reason have been called mucoid casts. An abnormal
amount of mucus in the urine shows that there is irritation at some point
along the urinary tract ; this may be the re-
sult either of a local inflammation or of a
general constitutional disease, such as pneu-
monia or typhoid fever ; when there is a mu-
cous sediment in the urine, there is always
found entrapped in it a large number of
epithelial cells of different varieties, which
for convenience of description may be di-
vided into three classes. First, round,
spherical cells having distinct nuclei de-
rived from the tubules of the kidney, or from
the deep layers of the mucous membrane lin-
ing the pelvis or from the male urethra.
Second, columnar and ciliated cells derived
from the cervix of the uterus. Third, flat
cells with large distinct nuclei which have
their origin in the bladder or vagina ; in the
former case they are much larger and granu-
lar. The situation of an inflammation con-
0?
Fig. 123.
Epithelium from Urinary Deposits.
. --. Large, flat bladder cells.
fined to some portion of the urinary tract B"^. From Uadder— deeper layers.
, - . . , y- Cells from vagina.
may sometimes be determined by noting the v. cmated cells from cervix of uterus.
1 , «,, -iiTi n T-iT C*. From mucosa of uterus.
character oi the epithelial cells passed m the p. cdisfrainpeMsofkidney.
urine whenever it can be determined whether g. F7wn!prostatvcport^ of urethra.
the cells came from the tubules or pelvis of "" ^^'
the kidney, or from the bladder or lower part of the urinary passage.
Blood may appear in the urine in varying amounts, and may come from
any portion of the tract ; when the urine contains blood it will have a
reddish or smoky appearance, and deposit, on standing, a coffee-ground like
sediment, and will show by chemical analysis the presence of both albumen
and fibrin. The appearance of the urine, the amount of blood, and the
cause of its presence will vary greatly according to the portion of the
urinary passages from which it comes -.—first, when the quantity of blood
URINARY SEDIMENTS. 535
is small, and it is equally diffused throughout the urine, in all probability,
it is derived from the parenchyma of the kidneys, and especially from the
Malpighian tnfts ; this condition is met with as the result of Bright's dis-
ease, congestion of the kidney, injury, the use of certain drugs, such as
cantharides, the formation of abscesses secondary to renal infarctions, and
from the presence of adventitious growths. Second, when
the urine contains much blood and distinct clots are visi-
ble, it is safe to infer that the blood is derived from
the pelvis of the kidney, from the ureters, or from the
bladder ; in the former case it is generally the result of
pyelitis, renal calculi, parasites, or morbid growths ; in the
latter case it is present as the result of vesical calculi, or
erosions and ulcerations of the mucous membrane. Blood
may appear in the urine as the result of disease of the
urethra, but then the cause of its presence can easily be ^. sivoUen red cor-
determined. Certain constitutional causes may give rise to uHnfo/Zws^
bloody urine, for it appears in the following diseases : ^ cfmateT^^'^lmr/us-
fevers, scurvy, purpura, cholera, myelitis, and in the ^les from dense
hemorrhagic diathesis.
Pus, when present in the urine, gives to it a milky appearance, and, on
standing, a yellowish-green sediment is precipitated which, as long as the
urine is acid, can easily be mixed with it, but when the urine becomes
alkaline, the sediment will have a gelatinous, ropy appearance and soon
undergo ammoniacal decomposition. Albumen is always found in urine con-
taining pus, and varies in quantity with the amount of pus present. The
microscopical appearance of pus is sufficient to determine its presence ; for
the shape, size and granular appearance of the pus corpuscles, with their
granular nuclei rendered more distinct by the addition of acetic acid, cannot
mi g^ # ^® mistaken for anything else. Pus appears in the
t- #*" urine either as the result of some suppurative inflam-
^#?^ ^bi ® ^ mation along the genito-urinary tract or from the rup-
ture of some neighboring abscess, but it must be re-
membered that in women it may be derived from the
^ genital organs. The significance of pus in the urine
^ ^ depends upon its source, which may be determined by
^ © @ remembering the following points :— if the urine is
® © acid, when voided, the pus probably has its origin in
® the kidneys ; if it is alkaline, its origin is in the blad-
^Puf ^' ^®^ 5 ^^ ^^^ presence is accompanied by slight colicky
A. Pits corpuscles as ordi- pains ovcr the course of the ureters, probably suppu-
B. TfTfLTjrM"'wUh ration is going on in them. In inflammations of the
acetic acid, x 300. urethra pus can be pressed out of the meatus.
Casts are peculiar cylindrical bodies consisting of exudative material or
coagulated matter formed in the urinary tubules of the kidney as the
result of disease, and then washed out by the urine secreted behind them.
They vary in size and number according to the nature of the disease which
gives rise to them, but it may be rightly stated that the more numerous the
536
DISEASES OF THE KIDN"EYS.
Pig. 126.
EpiiheJial Casts.
X 250.
casts and the longer time they are present, the more extensive will be the
Etructural lesions in the kidney. The following are the principal varieties
of casts met with in the urine :
Epitlielial castn consist of tubular masses of renal epithelium, especially
from the tubules of Bellini in the medullary por-
tion of the kidneys ; they are also, at times, de-
rived from the epithelial lining of the pelvis
and calices of the kidney. Occasionally the
epithelial cells present a normal condition, but
generally they show granular degeneration. This
variety of casts indicates desquamative nephritis.
When they are found mingled with pus cor-
puscles a serious inflammatory condition is in-
dicated.
Hyaline casts are structureless, transparent cyl-
inders, having a tendency to fracture transversely,
and are derived from the fibrinous exuduation
which has passed through the degenerated walls
of the renal vessels and coagulated in the tubules
of the kidney. Large hyaline casts are met with
in the atrophied stage of all forms of Bright's
disease. Small hyaline casts are found in the
acute stage, and sometimes
when no lesion can be appreci-
ated.
Granular Casts. — These casts are solid, fibrinous cyl-
inders, which have a finely granular appearance caused
by the presence of the debris of the degenerated renal
epithelium. Blood and pus corpuscles and granular cells
are often found embedded in this granular matter. These
casts are most often found in the advanced stages of
Bright's disease, and indicate the large white or granular
kidney, or that extensive destruction of the paren-
chyma of the kidney is taking place.
Fatty casts are made up of a material supposed to
be mixture of olein with cholesterin, and some al-
buminous matter ; fat globules, varying greatly in
size, and also some epithelial
cells and granular material
may be found in them. These
casts show that the degenera-
tive changes in the kidney are
fatty, and they indicate the
same conditions as granular
casts.
Blood casts consist of coagu-
lated fibrin and red blood corpuscles. By some they are thought to indi'
Fig. 137.
Hyaline Casts.
A. Bellcate hyaline casts.
B. Dense, so-called waxy casts.
Pig. 128.
Granular Casts.
A. Large granular casts.
B. 8mall finely granular
casts. X 250.
Pig. 130.
Blood Casts.
A. Collecting -tube blood casts.
B. Mucous casts.
ACUTE UEtEMIA.
537
cate the disease of the renal blood-vessels, especially amyloid or fatty de-
generation of the Malpighian tuft.
Spermatozoa are occasionally met with in the
urine, and give to it, when present in abundance, a
milky white appearance. If a drop of the urine
be placed under the microscope the characteristic
tadpole appearance of the spermatozoa can easily
be recognized. Spermatozoa appear in the urine
after coitus, involuntary nocturnal emissions,
and occasionally after defecation. They have
also been found in the urine of typhoid fever
patients.
Animal and Vegetable Organisms. — Fully
developed hydatids and echinococci, or only
portions of these, may appear in the urine,
having been developed at some portion of the
genito-urinary tract or poured into it by tlie
rupture of some hydatid cyst. A small uni-
sexual parasite, the Bilharzia haematobia, has
been found in the urine, especially during the
epidemics of hfematuria occurring in North-
ern Africa. Bacteria, or fermentation spores,
form in urine which is undergoing decom-
A.ToruiacerevisicR.—B.PenicUmmgiau- position. Sarcinas have been observed in al-
cum.— C. Sarcince Vent, x 300. i t ■ t-» • -t i t i
kalme urine, renicilium glaucum has been
found in acid albuminous urine. Torula cerevisise often forms in diabetic
urine.
Pig. 132.
ACUTE UE^MIA.
Under the tei*m acute uraemia may be grouped two classes of symptoms,
which differ in their mode of development and in their attendant phenom-
ena. In the one, nausea, vomiting, and headache usher in twitchings and
epileptiform convulsions of the voluntary muscles, a state which has re-
ceived the name of nrcemic convulsions. In the other, headache and drowsi-
ness, a gradually advancing torpor or convulsions usher in a state of insen-
sibility, which has received the name of nrmmic coma.
The primary cause of both these conditions is to be found in a failure of
the kidneys to perform their normal function of elimination, and the con-
sequent accumulation in the circulation of some or all of the poisonous ele-
ments of the urine. This condition may occur in the course of any disease
in which suppression of the renal secretion takes place ; such arrest of the
function of the kidneys most frequently occurs in the different forms and
stages of Bright's disease, in the puerperal state, in connection with the
surgery of the urethra, cystic, tubercular and cancerous disease of the kid-
ney, and in suppurative nephritis ; by far the largest number occur in acute
Bright's disease.
538 DISEASES OF THE KIDNEYS.
A number of theories have been advanced in regard to the exact element
which acts as the poisonous agent in uraemia. The earliest accepted view
is that which attributes the symptoms of uraemia to retained urea. Although
this view at different times has been discarded, and apparently disproved by
the experiments of distinguished observers, to-day it is the one generally
received. French's theory was that urea, as urea, was innocuous, and
that the poisonous agent was carbonate of ammonia resulting from decom-
position in the blood of urea into carbonate of ammonia and water, which de-
composition was ascribed to the action of a ferment in the blood ; this theory
has been disproved. Another hypothesis which has attracted much attention
is that the phenomena of ursemia are due to cerebral anaemia and the attend-
ing cerebral oedema. This is the mecMnical theory. Still more recent ex-
perimenters have claimed that urea is formed in the kidneys from nitroge-
nous matter m the blood, and that uremic manifestations mainly depend
upon the accumulation in the blood of kreatin and kreatinin. Again,
others have claimed that the phenomena of uraemia are due to the retention
in the circulation of the products of nerve waste. It has also been claimed
that some forms of uraemia may be associated with structural changes in
the brain similar to those which occur in the retina in cases of neuro-ret-
initis.
Mahomed (Brit. Med. Jour., 1877, ii. 10-43) calls attention to the cer-
ebral lesion which, he says, accounts for the epileptiform convulsions of
uraemia, viz., numerous punctiform hemorrhages in the gray matter of the
cerebral convolutions. They are true hemorrhages. He ascribes other cer-
ebral symptoms to oedema of the brain following increased tension. Simi-
lar to oedema is the ''hyaline exudation into nervous tissue "found by
Gull and Sutton. Similarly, headache results from increased tension with-
out exudation. Gubler (Paris, 1878) describes the ''diminished number
and impaired respiratory capacity of the red blood-corpuscles " in ursemia,
due (G. states) to kreatinin and ammonium carbonate. Hence there is
more or less "asphyxiation of the nerve centres." He also believes «r^erm?
spasm to result in sudden retention of effete products. He regards the
dyspnoea as at times due to kreatinin, at times to ammonium carbonate :
in one the breathing is hurried, in the other it is the " Clieyne- Stakes'
respiration.'^
The experiments and facts upon which these theories are based, lead to
the following conclusions : that ursemic toxaemia depends upon a complete
or partial arrest of the urinary secretion. A qualitative analysis of the
constituents of the urine goes to show that urea is its only actively poison-
ous ingredient, and that it is not the special product of any particular tis-
sue or organ, but the united product of all nitrogenized effete matter.
That the tissue-changes found in the brain in acute uraemia are the results
of the action of this poison. Sometimes ten to fifteen times as much urea
is found in the blood in uraemia as in health. Again, in severe cases the
amount may be so small as to be scarcely determinable (Jacobson). And
large amounts of urea may be found in the blood witJiout the symptoms of
acute uraemia.
ACUTE URAEMIA. 539
Symptoms. — An acute ursemic attack is usually preceded by certain pre-
monitory signs, such as oedema in various parts of the body, restlessness
or an almost irresistible desire to sleep, vertigo, headache, delirium, nau-
sea, vomiting, diarrhoea, and impaired vision. The countenance has a pale,
waxy or dingy appearance, and the urine is scanty, high-colored, bloody,
albuminous, and contains casts ; the body and extremities may become
violently convulsed, or the patient may pass rapidly into a state of coma.
The convulsions may consist of a single paroxysm, or a succession of
paroxysms may follow one anotlier at intervals of a few minutes or several
hours, the patient during the interval lying in a state of more or less pro-
found insensibility. They may almost exactly simulate epilepsy, or they
may be unattended by loss of consciousness. During the convulsions
the face becomes livid, the eyes are glassy, and the pupils are contracted
or dilated ; at the commencement of the convulsive attack, they are gener-
ally contracted. Frothy mucus, which is sometimes bloody, collects around
the mouth, and there is a strong urinous odor emanating from the per-
spiration. The pulse is accelerated, and the temperature is raised in some
instances as high as 107° F. A low temperature may be present in the
aged. Sudden coma may occur with convulsions. Eestless delirium is the
chief symptom in many cases. Intense dyspnoea, and articular symptoms
are very rare.
Urmmic coma may come on gradually, twenty-four or forty- eight hours
elapsing before the stupor is complete, or the patient may fall suddenly
into a state of profound coma, its advent resembling an attack of cerebral
apoplexy. Headache, giddiness, disorders of vision, vomiting, or delirious
excitement may precede the coma. There are periods when the coma is so
profound that nothing arouses the patient ; at other times he is easily
aroused, or arouses himself and attempts to speak and sit up, swallowing
fluids with difficulty. If the system has become accustomed to the pres-
ence of the urinary poisons, a considerable excess of urea and effete uri-
nary products may exist in the blood for a long period without giving rise
to any but the premonitory symptoms of acute uremia. When once this
balance is destroyed and a certain excess of urea and its allies in the blood
is reached, the kidneys become embarrassed by the excessive demand made
on their excreting power, and rapid and intense renal congestion follows, but
either convulsions, coma, or both, result in this way ; acute uraemia may
be developed in the chronic as well as the acute stage of renal disease.
Ursemic coma is always accompanied by stertor. The stertor is peculiar :
it is not the ^'snoring" of apoplexy, but a sharp, hissing sound produced
by the rush of expired air against the teeth or hard palate. At first the
respirations are accelerated, but they soon become slow and labored ; the
pupils are dilated, but they are not irregular ; they may be normal ; they
react slowly to light. The pulse is increased in frequency and lacks firm-
ness ; at first the temperature is raised, but after a time it falls below the
normal standard ; the face is pale.
Differential Diagnosis. — Acute uraemia simulates in some of its phenom-
ena those diseases in which convulsions and coma are prominent symptoms.
540 DISEASES OF THE KIDNEYS.
The phenomena of an epileptic seizure are almost identical with those
of an uraemic convulsion, and it is exceedingly difficult to distinguish one
from the other. If the previous history is known, the chronic character
of the epilepsy will in some instances distinguish it from acute ursemia,
and an examination of the urine will generally determine the ursemic char-
acter of the convulsions ; in epilepsy one side is convulsed more violently
than the other ; while in ursemia both sides of the body are equally con-
vulsed. In epilepsy the temperature is not elevated, and although there
is a loss of consciousness, reflex sensibility continues from the beginning
to the end of the paroxysm, which is not the case in ursemia. Immedi-
ately following urgemic convulsions there is deep coma ; following an
epileptic seizure there is merely a deep sleep, from which the patient may
be aroused. The initial cry and corpse-like pallor of the face in epilepsy
are wanting in uraemia.
In cerebral apoplexy coma always precedes convulsions, and with the con-
vulsions there is facial paralysis and hemiplegia ; there is also clonic
spasm of the parsflyzed parts. The urinary symptoms of uraemia are ab-
sent and the stertor is less sharp and hissing.
In hysterical convulsions the patient falls with a scream into a convul-
sive, tetanic or cataleptic condition. Close inspection shows that the
patient, is not unconscious, and the pupils are normal, as are the pulse and
temperature. The limbs are jerked irregularly, the breathing is spasmodic
and is attended by a choking sensation ; opisthotonos is very common.
There is no lividity of the face, nor distention of cervical blood-vessels,
and the close of the paroxysm is usually accompanied by the discharge of
a large quantity of pale urine, — non-albuminous and free from casts.
OTiolcemic convulsions very closely resemble ursemia, but may be dis-
tinguished from them by the jaundice which precedes or accompanies their
development, and by the antecedent history of hepatic disease. Convul-
sions originating in meningitis and other cerebral affections are distin-
guished by the accompanying characteristic symptoms of these affections.
The points in the differential diagnosis of urcemic coma are similar to
those of ursemic convulsions. It may be distinguished from the coma of
apoplexy by the absence of paralysis.
From opium poisoning it may be distinguished by the rise in temperature.
The temperature in opium poisoning is often below the normal. In opium
coma the respiration is slow and peculiar, and the pupils are uniformly con-
tracted. Ursemic coma is distinguished from epileptic coma by the ante-
cedent history of the patient, the presence of bloody froth about the mouth,
and the indentations on the side of the tongue ; from alcoholic coma, by the
temperature, and the character of the breathing, which is "puffy" in alco-
holic coma, and a hissing stertor in uremia. In all cases of coma, an ex-
amination of the urine is important before reaching a diagnosis.
Prognosis. — From experiments as well as from the clinical history of acute
ursemia, it is evident that the primary cause of death is a poison, the exact
nature of which is obscure, but which resembles in its action narcotic
poisons. This poison acts primarily on the nerve centres, and produces*
ACUTE TJE^MIA. 541
changes in the blood which interfere with or arrest oxygenation. This
action is followed by certain structural changes in the different tissues of
the body. When this poison is introduced into the circulation in small
quantities, so that its elimination can be effected in a short time, it only
temporarily disturbs the functions of organic life ; but when it is intro-
duced in large quantities, oxygenation of the blood is arrested, and it under-
goes certain changes which render it incapable of supporting life. The
prognosis, then, in each case will depend upon the amount of the poison,
and the length of time the system is under its influence.
If the symptoms of excessive ursemic toxaemia are present, and there are
evidences that the poisoning has been going on for a considerable time, the
prognosis is much more unfavorable than when the acute uraemic symptoms
are mild and of recent date.
Treatment. — It is claimed that the most important thing to be accom-
plished in the treatment of acute uraemia, is to secure as rapidly as possible
a free eliminative action of the skin, bowels, and kidneys. The favorite
method of elimination is by diaphoresis, accomplished by the hot-air baths.
Pilocarpin has recently been used to accomplish the same results. In con-
nection with diaphoresis, a vicarious action of the bowels is induced by the
administration of drastic j)urgatives, such as elaterium, pulvis purgans and
scammony. The testimony in regard to the use of diuretics is conflicting.
Many object to their use, on the ground that inflamed organs should not
be stimulated.
Digitalis acts efficiently — is diuretic without stimulating the kidneys.
It increases the power of the heart's action and increases the tension in the
Malpighian tufts. The diminished secretion of urine is due to obstruction
in the capillary circulation of the kidneys. Digitalis, by increasing the
heart power, overcomes such obstruction. To obtain its effects in such con-
ditions, larger doses are required than are usually administered. My rule
of practice in these cases is to give half an ounce of the infusion every three
hours for twenty-four hours, or at least until its specific effect is produced.
In the majority of severe cases of acute ureemia, when the patient is in
convulsions or coma, the excretory functions of the skin, bowels and kid-
neys are completely arrested, so that diaphoresis cannot be induced, or, if
induced, it is not eliminative, and the bowels do not respond to purgatives
although the patient may swallow them in large doses, and digitalis in
large doses fails to restore the urinary secretion. At one time under such
circumstances free general blood-letting was used extensively, but the result
was unsatisfactory.
If there is acute uraemia, the avenues of elimination are shut off, and the
question arises: — what means have we to counteract this uraemic poison, and
open again the avenue of its elimination, or, at least, to hold the patient until
the normal eliminating process shall be re-established ? The first indication
is to diminish reflex sensibility, and subdue spasmodic muscular paroxysms,
for these, if continued, will either directly terminate life, or end in equally
fatal insensibility. The remedy which for some years has been employed
for the accomplishment of these results is chloroform. It has been exten-
542 DISEASES OF THE KIDNEYS.
sively used, and, I believe, is regarded as the safest and most reliable means
for controlling nrsemic convulsions. Hydrate of chloral and bromide of
potash are also more recently recommended, but their action is not swift or
powerful enough. Although many authorities recommend the use of chlo-
roform in uraemic eclampsia, few make mention of its employment in acute
uraemia independent of the puerperal state. Its only known clinical effect
is to control muscular spasm, and in a large projaortion of cases it fails to
give more than temporary relief to those patients who pass from successive
convulsions into a state of complete coma, and die without any apparent
neutralizing effect from the chloroform. In the few cases in which I have
administered chloroform in non-puerperal ursemic convulsions, it has
seemed to me to have no other effect than to arrest convulsive movements
by rapidly hastening the patient into a state of insensibility. In no in-
stance have I known its administration to be immediately followed by di-
aphoresis or a return of the urinary secretion. It has seemed to be more
diflBcult to establish diaphoresis or diuresis by diaphoretics and diuretics in
patients with urgemia to whom chloroform had been administered, than in
those who had not taken it.
Therefore, I believe that while chloroform temporarily controls muscular
spasm, it prejudices the chances of ultimate recovery by the changes its in-
halation produces in the blood, which changes increase rather than retard
the development of the ursemic toxaemia. With these impressions one nat-
urally seeks an agent which not only has the power to control muscular
spasm, but shall also at the same time tend by its action to reopen the ave-
nues of elimination, either by counteracting the effects of the ursemic poi-
son on the nerve centres, and thus facilitating the action of diuretics and
diaphoretics, or by acting itself directly as an eliminative.
I believe morphine administered hypodermically to be such an agent.
There are two questions that very naturally present themselves in con-
nection with the use of morphine in acute uraemia.
First. Can morphine in full doses be administered without danger to
patients with acute uraemia ?
Secondly. What are the effects of such administrations ?
If one turns to recognized authorities for an answer to the first of these
inquiries, he will find that nearly all make mention of the use of opium in
urasmic toxaemia only to warn against the danger attending its administra-
tion. During the first years of my professional life, I regarded opium as
one of the most dangerous remedial agents that could be administered to
urgemic patients, rarely daring to give more than five grains of Dover's
powder to a patient with albuminous urine, and if fatal coma followed
such administration, more than once do I remember to have felt that a Do-
ver's powder which I had administered might have been the cause of the
fatal coma. In 1868 I administered my first hypodermic injection of
morphine to a patient with acute uraemia. The effects which followed its
administration in this case taught me that in some cases with marked urae-
mic symptoms morphine could be administered hypodermically not only
safely, but with apparent advantage. Since that time I have used mor-
REKAL HYPEREMIA. 543
phine hypodermically in the treatment of these patients, not only during
the premonitory stage, but also during the active manifestations of ursemic
intoxication, and its administration has been uniformly followed by good
results. In no instance have I caused a fatal narcotism.
From the histories of quite a large number of puerperal and non-puerpe-
ral cases of acute uraemia, in which morphine was successfully used, T have
reached the following conclusions : ^— first, that morphine can be adminis-
tered hypodermically to some if not to all patients with acute uraemia with-
out endangering life. Secondly, that the almost uniform effect of morphine
so administered, is, first, to arrest muscular spasms ; secondly, to establish
profuse diaphoresis ; thirdly, to facilitate the action of cathartics and
diuretics, especially the diuretic action of digitalis. Thus, morphine
administered hypodermically becomes a powerful eliminating agent. The
rule is to give small doses at first, not to exceed one-sixth of a grain. If
convulsions threaten, and a small dose does not arrest the muscular spasm,
it may be increased to one-quarter or one-half of a grain, and the hypo-
dermics may be repeated as often as every two hours. It must be given
in suflBcient quantities to control convulsions ; neither the contraction of
the pupils nor the number of the respirations is a reliable guide in its
administration.
I would not discard all (perhaps none) of those means which have been
relied on for the relief of patients in acute uraemia, but would urge that
hypodermic injections of morphine not only control muscular spasms, but
aid in establishing the eliminating processes, and thus become another
means of saving life in these often fatal cases. Dry and wet cupping, leech-
ing and poulticing over the loins may be employed to aid in this re-estab-
lishment of the suppressed renal function.
DISEASES OF THE KIDNEYS
will be considered in the following order :
I. Renal Hyper cBinia. VII. Cystic Kidney.
II. Renal HemorrJiage. (Embo- VIII. Reiial Calculi.
lism and Infarction. ) IX. New Groiuths. (Cancer, etc. )
III. BrigJifs Diseases. X. Parasites. (Hydatids.)
IV. Pyelitis. XI. Perinephritic Abscess.
V. Acute Suppurative Nephritis. XII. Hcematuria.
("Surgical Kidney.") XIII. Chyluria.
VI. Hydronephrosis. XIV. Cystitis.
EENAL HYPEREMIA.
{Congestion.)
Eenal hyperaemia may be active or passive. Passive renal hyperaemia, or
congestion, is almost always due to a mechanical obstruction of the venous
circulation, and is sometimes called ''chronic renal congestion."
Morbid Anatomy. — Active renal hyper cemia has its seat mainly in tho
1 New York Med. Rec, Aug. 1, 1873.
544
DISEASES OF THE KIDN'EYS.
renal arteries and in the Malpighian tufts. The kidneys are much increased
in size ; the hyperaemia may involve the cortical or medullary portion, and
may be more intense in one portion than another ; it is usually most marked
at the base of the pyramids. The kidneys are of an unnaturally dark color,
their capsule is non-adherent, their surface is smooth, and they are softer
and moister than normal.
071 section, dark spots are noticed scattered over the cut surface which
correspond to the Malpighian tufts, and the vessels of the cones are filled
with blood. A dark fluid follows the section, which is partly serum and
partly blood. The stars of Verheyen are prominent. A microscopical ex-
amination shows that these changes are due to an engorgement of the blood-
vessels, and a more or less abundant infiltration of serum into the inter-
tubular structure of the kidneys.
Passive liypercemia, or '^chronic renal congestion," has its seat in the
veins, which are overfilled with venous blood, while the amount of blood
contained in the arteries may be even less than normal. The kidneys are
but slightly, if at all, increased in size, are firmer than normal, their cap-
sule is non-adherent, and their surface is smooth and of a uniform red color.
In chronic cases the surface is uneven. The tubular epithelium is gran-
ular, opaque and fiattened from
coagulated fibrin which may
partially fill the lumen of the
tubes. The convoluted tubules
may be filled with blood. The
stroma is unaltered. Hypersemia
of, and hemorrhages into the
mucous membrane of the pelvis
and ureters may occur in A'ery
severe cases.
Upon section, it will be noticed
that the medullary portion is of
a darker color than the cortical,
that the cortical portion has
streaks of red rather than an
uniform redness. The Malpig-
hian tufts are not prominent.
The veins are dilated, tortuous,
and varicose, the abnormal hard-
ness of the kidney being due to
the constant distended condi-
tion of the efferent capillary
vessels. The epithelium of the
convoluted tubes may have a
peculiar stiff appearance, not
the result of an inflammatory
process. Coagula of yellowish hyaline material are sometimes found in the
glomeruli, arranged in concentric layers.
Fig. 133.
Eenal Hj'pereemia.
Vertical section of part of a Malpiqhian Pyramid in Pass-
ive Hypercemia.
A, A. Collecting tubes.
B, B. Dilated, tortious vessels.
C, C Collecting tubules containing blood, x 300.
RENAL HYPERiEMIA. 545
Both these varieties of hypertemia may lead to, or be accompanied by
inflammatory processes in the tubular and intertubular structures of the
kidneys. Active hyperemia may be the stepping-stone to acute parenchy-
matous nephritis. It is only a step from congestion to some of the more
chronic inflammatory forms of kidney disease. When to passive hyperae-
mia there is added inflammatory swelling of the epithelium, of the tubules,
the kidneys will be enlarged, and the epithelium of the convoluted tubules
will be swollen, granular, fatty, and disintegrated. When the inflamma-
tion extends to the stroma the kidneys will be diminished or enlarged, but
retain the stony hardness of non-inflammatory congestion. The capsule
will be adherent, and on section the cortical portion will be slightly dimin-
ished, and there will be patches of new connective-tissue throughout its sub-
stance, — the process not being unlike the "cirrhotic" form of Bright's.
If the passive hyperaemia is due to heart disease, the kidneys will be in-
creased in size, the capsule will be non-adherent and the surface smooth.
The cortical substance will be pale instead of red, and the medullary portion
of a darker color than normal, the gross appearance very closely resembling
that of the "large white kidney." There will be well marked changes
in the epithelium of the tubules, in the stroma, and in the walls of
the arteries. These are the large stony kidneys of chronic heart dis-
ease. Chronic passive hyperaemia is sometimes called "cyanotic indura-
tion."
Etiology. — Active renal hypercemia, or fluxion, may be produced by ex-
posing the body to sudden changes of temperature, by any of the blood
poisons which give rise to the acute infectious diseases, by malaria (and it
is sometimes a prominent feature of a violent malarial paroxysm), by the
prolonged and excessive use of certain drugs which give rise to irritation of
the urinary passages, as cantharides, copaiba, turpentine, cubebs, nitrate of
potash, carbolic acid, etc., and by the irritating condition of the urine in
diabetes, cholsemia, etc. It sometimes accompanies Basedow's disease.
The early stage of acute inflammations of the kidneys is attended by active
renal hyperemia. Paralysis of the vaso-motor nerves of the kidneys (sup-
posed to occur in hysteria and allied states, polyuria, etc. ) is said to be a
cause of active renal hyperaemia.
Passive renal Tiypercemia, or renal congestion, has its most frequent
cause in organic disease of the heart. All valvular lesions of the heart, or
structural diseases of the cardiac valves which interfere with venous return,
come under this head, as well as all those forms of pulmonary disease
which interfere with the pulmonary circulation, and are followed by dilata-
tion of the right heart, e. g., emphysema and fibroid phthisis. Congestion
may also be produced by pressure on the emulgent renal veins or inferior
vena cava in pregnancy and by other abdominal tumors. The formatioa
of a thrombus is also followed by it. Some of the cases of so-called albu-
minuria in pregnancy are examples of passive hyperaemia from the pressure
of the pregnant uterus.
Symptoms. — The symptoms of both varieties of renal hypereemia are for
the most part confined to changes in the urine. In active hyperaemia the
35
54:6 DISEASES OF THE EID^TEYS.
urine is scanty, high colored, of high specific gravity, containing a large per-
centage of albumen, with few blood casts and hyaline tube casts.
In passive hyper mmia, without any structural changes in the kidneys, the
quantity of the urine is not much diminished, its specific gravity remains
about normal, the amount of albumen is small, and only small hyaline
casts are present. It is often of an acid reaction, and deposits urates. The
amount of urea is a little below normal. The simultaneous appearance of
blood and albumen in the urine is so common in renal congestion that the
presence of albumen alone, without blood globules, almost excludes it. Be-
sides the changes in the urine in active hyperemia, there is usually slight
oedema of the face and lower extremities, with nausea and a persistent
headache.
Passive hypersemia is often produced by chronic cardiac or pulmonary
disease, attended by a cough with a watery blood-stained expectoration, and
by dyspnoea that often becomes so severe as to prevent the patient from
lying down. The cougli and dyspnoea depend in part upon the accompany-
ing heart or pulmonary disease, but there is also a nervous element in it
which is characteristic of the renal complication. There is loss of appe-
tite, nausea and occasional vomiting ; there is a continuous headache, rest-
lessness and insomnia, which, added to the dyspnoea, make the patient's
condition distressing. There is loss of flesh and strength, and steadily in-
creasing ansemia. These symptoms gradually become worse, and general
dropsy develops, and the patient may die from the general anasarca, or from
convulsions and coma.
The history of these cases varies greatly : some get progressively worse,
others pass from an apparently hopeless condition to one of comparative
comfort, and these attacks are repeated at intervals for a long period.
However desperate the condition may appear, a return of a comparatively
comfortable condition is always possible. That form of renal congestion
which is so often met with in pregnancy is usually accompanied by the
presence of albumen and casts in the urine before any other symptoms are
developed ; afterward the patients become anaemic, and suffer from per-
sistent headache, vomiting, and oedema of the face, feet and legs ; they
become "water-logged." In a few cases the first symptom may be a con-
vulsion. In all cases the thing to be dreaded is the onset of convulsions,
which rapidly follow each other until coma is reached.
Differential Diagnosis. — Eenal congestion is distinguished from Briglifs
disease by the general condition of the patient, the presence or absence of
cardiac or pulmonary disease, or venous obstruction. The urine, though
scanty, is above normal in specific gravity, and always deposits blood,
renal epithelium, or tube casts.
Prognosis. — The prognosis in active renal hypersemia, when the cause is of
a transient character, is good. Eenal congestion which occurs in the ad-
vanced stage of cardiac disease and pulmonary emphysema has much to do
with causing a fatal termination, and after it is once developed it is never
recovered from. That form of active hypersemia which occurs in congestive
malarial fevers is sometimes so intense as to entirely arrest the function of
RENAL HYPERiEMIA. 547
the kidneys, and then it becomes a direct cause of death. The renal con-
gestion of pregnancy is usually relieved by the removal of its cause, which
should never be delayed if the symptoms become urgent.
Treatment. — The most important thing to be accomplished in tlie treat-
ment of active renal hypersemia is to find out, and as quickly as possible
remove its cause. The treatment is to be addressed to the kidneys. Place
the patient in bed in a room with a temperature of 80° F., and apply a dozen
wet cups over the lumbar region. Administer a powerful drastic purge,
induce free diaphoresis, and let the patient drink freely of diluted muci-
laginous drinks. The hot-air or warm vapor-bath, and even blood-letting
in intense fluxion, are to be employed. Camphor is advocated in some
cases of active hyperasmia. In passive renai hyperemia the main thing to
be accomplished is to relieve the venous congestion ; it is to remembered
that there is too much blood in the veins and too little in the arteries.
There are three ways of restoring the natural state of the circulation : —
1st. By general bleeding.
2d. By increasing the force of the heart's action.
3d. By causing the. dilatation of the capillary arterioles.
A free bleeding from one of the large veins will temporarily relieve the
venous congestion and cause a better filling of the arteries, but it exhausts
the patient, and is only admissible in the renal congestion of pregnancy
when the symptoms are urgent. By increasing the propelling power of the
heart, the amount of blood in the arteries is increased and that in the veins
diminished. This is the usual mode of procedure in the passive renal
hypersemia which depends upon chronic heart and lung disease. Digitalis
is the drug which has been most extensively employed to accomplish this.
It must be given in full doses and continued until the desired effect is in-
duced. The best mode of its administration is in the infusion ; a tablespoon-
ful of the infusion of the leaves may be given every three or four hours until
its specific effect is produced or the quantity of urine is greatly increased.
Eecently the fluid extract of convallaria in half-drachm doses has been
recommended as a substitute for digitalis. My exjoerience with it has been
very unsatisfactory ; its action is not only temporary, but far less certain
than digitalis.
The drugs that seem to have some power in dilating the capillaries and
arterioles are nitrite of amyl and nitro-glycerine. The nitrite of amyl may be
given by inhalation in doses of from three to five drops every four hours.
The nitro-glycerine may be given in a one per cent, alcoholic solution, one
drop every three or four hours. It is now two years since I first used nitro-
glycerine in renal disease, and under its use albumen has disappeared from
the urine in quite a number of instances, and remained absent so long as the
patient continued the drug.
If counter- irritation is employed it must be mildm character — a few dry
cups over the lumbar region, or some mild embrocation is all that is neces-
sary. The intestines should be occasionally unloaded by a full dose of
calomel combined with rhubarb. When the venous obstruction is directly
mechanical, as in pregnancy and fluid accumulation in the abdominal
548
DISEASES OF THE KIDNEYS.
cavity, something may be accomplished by so changing the position of the
patient as to relieve the pressure on the renal veins.
If passive renal hyperemia, especially in heart disease, is attended by
great restlessness and dyspnoea, morphine may be given hypodermically in
sufficient quantities to give relief and make the patient comfortable, even
though but a small quantity of urine is being passed.
EEKAL HEMOREHAGE.
{UmhoUsm and Infarction.)
Eenal congestion and renal hemorrhage are very often associated, for
renal hemorrhage often occurs as a result of renal congestion.
Morbid Anatomy. — The anatomical changes in a kidney which is the seat
of renal hemorrhage do not differ essentially from those already described
as present in a renal hypereemia, unless there are hemorrhagic infarctions
or renal calculi. Blood may be effused into the uriniferous tubules or the
interstitial tissue, giving rise to ecchymotic spots varying in size, from
which, on section, blood flows freely. The vessels will be found ruptured,
and the epithelia and stroma of the kidney are stained with blood pigment.
The epithelia soon become opaque, granular, and infiltrated with fat, and
finally disintegrate. Incident to the great increase in the blood pressure,
diapedesis of the red corpuscles may occur ; this is true renal hemorrhage,
having its origin in the Malpighian tufts. The blood escapes between the
vascular tuft and its capsule, which is slightly dis-
tended. '
The most frequent form of renal hemorrhage is that
which occurs in connection with renal embolism and in-
farction. Its occurrence is marked by the development
of hard uniform masses in the cortical portion of the
kidney ; these masses are usually wedge-shaped, and
have t]ieir sharp edges toward the hilus of the kidney
and their base toward its surface.^ They vary in size
according to the size of the vessel obstructed ; they may
be capillary, and then are of very small size. These in-
farctions when first formed are of a dark red color, and
are as firm as normal kidney-tissue ; very soon they be-
gin to change in color, losing their dark red hue and
becoming lighter, and their centres present a yellowish
appearance ; sometimes they undergo cheesy change,
which always commences at their centres. Around
these infarctions a zone of redness is formed ; this zone
is in the normal kidney-tissue, beyond the infarction.
mi vessels fc"'capmu; A Congestion takes place in the vessels, due to changes
liumfmiringtunmid in the urinifcrous tubes adjacent to the capillaries in
^aitofS£ti/tuMi: that portion of the kidney which surrounds the infarc-
^l$ing fmmlhf%tft ^iou ; there is also a more or less rapid production of
ana entenng the tubule, eells in this surrounding zone. If the infarction does
Fig. 134.
Eenal Hemorrhage.
Diagram showing Hem-
orrhage from the vas-
cular tufts of the glo-
meruli.
1 Cornil and Kanvier.
" Rayer's so-called " Bheiimatic Nephritis.'
RE]S"AL HEMORRHAGE.
549
by absorption, this zone-change continues until there
developed about the infarction, which
contraction of the tissue, gradually
not disappear
is more or less cicatricial tissue
shrinks in consequence of the
diminishes in size, and after a
time disappears altogether, leav-
ing only cicatricial tissue to mark
its former site. The surface of the
kidney may be depressed over an
atrophied infarction.
On the other hand, the produc-
tion of cells may be so rapid and
abundant that the entire mass
undergoes purulent transforma-
tion, producing abscesses which
will occupy the seat of the infarc-
tion. This is one of the ways in
which abscesses are formed in the
kidneys. In these cases there is
always a certain degree of sup-
puration occurring at the margin
of the affected area. Again, these
infarctions may undergo a still
more rapid degeneration, increas-
ing in size and becoming necrotic,
so that at the autopsy a gangre-
nous mass is found as the result of
the necrotic change which has
taken place in the infarction. More or less suppuration also attends it.
Again, there may be little masses found scattered throughout the substance
of the kidney, especially in the cortical portion, looking very much like
ecchymotic spots, which are simply capillary thrombi : these are usually
due to some slowing of the circulation in the capillary vessels. These
capillary thrombi may be very numerous, and they may undergo changes
similar to those which take place in the larger infarctions.
At the autopsy the kidneys may be found studded with minute abscesses ;
unquestionably these little collections of pus are nothing more than minute
capillary infarctions or thrombi which have undergone purulent transforma-
tion. Thus a single abscess or many abscesses of the kidney may form as
the result of infarctions. This form of renal hemorrhage is especially liable
to occur in passive renal hypersemia.
Etiology. — Intense hypersemia of the kidney is a cause of renal hemor-
rhage, especially in the first stage of acute nephritis. It may also result
from injuries, and in connection with the development and passage of renal
calculi. It may also occur in connection with the development of morbid
growths in the kidney, especially cancer. Blood changes, such as occur in
purpura, scurvy, etc., may cause it. Passive obstructive hypersemia from
Fm. 135
Renal UGmorrhage.
Diagram illustrating Renal Infarction.
A. Embolus in an interlobular artery.
B. Cheesy centime of the infarct.
C. C. Zone of redness.
550 DISEASES OF THE KIDNEYS.
cardiac disease may become so intense as to give rise to it, witli or without
the occurrence of infarctions.
Symptoms. — It is attended by no constant or distinctive subjective symp-
toms. Our knowledge of its occurrence, during life, rests almost exclu-
sively upon the results of an examination of the urine. Its existence can-^
not be recognized, unless the blood is effused into the uriniferous tubules
or into the hilus of the kidney and discharged in the urine. At autopsies,
large infarctions of the kidney are often found which, during life, have given
no indication of their existence, because there was no extravasation of blood
into the uriniferous tubules, and consequently no blood appeared in the
urine.
The course of a renal hemorrhage depends to a great extent upon the
cause which produces it. When dependent upon the presence of a renal
calculus, the hemorrhage occurs after every violent exertion. When it
arises from cancer or other tumors, it is generally profuse and persistent.
The bleeding which accompanies inflammation of the kidneys in the infec-
tious diseases is never severe ; it may be so slight as only to be recognized
by a microscopical examination of the urine. That form of renal hemor-
rhage which occurs in malarial districts in hot climates is usually profuse
and occurs periodically. When it is caused by an infarction, the patient is
usually seized with a chill at the time the infarction occurs, followed by
pain in the back, and more or less nausea and vomiting. If, therefore,
these symptoms are developed in connection with cardiac disease or pyae-
mia, it is evidence that renal infarctions have occurred.
When valvular disease of the heart exists with ulcerative endocarditis or
extensive calcareous degeneration of the arteries, embolic infarction may be
suspected, when in addition to the sudden appearance of blood and albu-
men in the urine there is fever and vague pains in the lumbar regions.
Small abscesses, the sequelae of infarcts and circumscribed spots of gangrene,
cannot be diagnosticated.
Prognosis. — The prognosis depends upon the conditions and circum-
stances under which the hemorrhage occurs. If it occurs in connection
with renal calculi or cancerous disease of the kidney, the prognosis is bad ;
life is endangered under these circumstances by the exhaustion produced
by the continued loss of blood. Occurring in connection with infectious dis-
eases, it has no particular significance ; it merely is an indication of intense
renal hyj^erEemia. When there is reason to believe that a hemorrhagic infarc-
tion has occurred in the kidney, the event must always be regarded as at-
tended with danger to life ; not that it is necessarily fatal, or that the prog-
nosis is necessarily unfavorable, but the fact that infarctions exist will cause
anxiety as to the development of the other degenerative changes in the kid-
neys, and as to the lodging of emboli in other parts, particularly the brain.
Treatment.— The first thing to be accomplished in its treatment is to find
out and, if possible, remove its cause. In many cases where the main causa-
tive disease is amenable to treatment, the hemorrhage does not require any
special attention. During the occurrence of the hemorrhage, the patient
should be kept absolutely at rest. If there is danger of exhaustion from
bright's diseases. 551
repeated and profuse hemorrhages, ice-bags may be applied to the lumbar
region and styptics administered internally.
The remedial agent which seems to have the greatest control over these
hemorrhages is tannic acid, it being expelled from the system through the
kidneys in the form of gallic acid ; a powerful astringent is thus brought
directly in contact with the uriniferous tubes and urinary passages. Ergot,
muriate of iron, alum, the acetate of lead, and turpentine are sometimes of
service. Ergotin given hypodermically in connection with morphia is in-
dicated if hemorrhages are profuse. If the hemorrhage is of malarial ori-
gin, large doses of quinine and arsenic are indicated. The danger from
acute renal inflammation must always be borne in mind when renal hem-
orrhage occurs in connection with the infectious diseases ; the proper meas-
ures for the subduing or arresting of such inflammations must be promptly
resorted to.
A very important, and at the same time a very common group of dis-
eases, are classed under the comprehensive term of Bright' s diseases of the
hidneys. Dr. Bright first called the attention of the profession to these
diseases in the year V^'ri, at which time he described, and represented by
colored drawings, various morbid appearances of the kidneys, which he
showed were of every-day occurrence, and were frequently associated with
general dropsy. He was the first systematic investigator in the field of
renal pathology. Dr. Bright regarded granular degeneration as the prin-
cipal, if not the only pathological lesion present in this class of diseases ;
he accordingly designated it as a granular nephritis.
Eecent and more extended investigations have shown that there are
several morbid processes in the kidneys of those who are the subjects of
this class of diseases, and that the kidneys in the course of these morbid
processes present a great variety of appearances.
A great number of terms claiming to be exj)ressive of these different
morbid appearances have been employed, such as the large white kidney,
the large granular kidney, the small fatty granular kidney, the large and
small red granular kidney, the waxy kidney, and the cirrhotic kidney ;
all these different varieties are described by different writers under the
head of Bright's disease.
Before studying the morbid changes which occur in this group of dis-
eases, it is important to remember that there are three distinct anatomical
elements in the kidney which are primarily or secondarily involved in
these changes ; namely, the uriniferous tubules, the blood-vessels, and the
intertubular tissue (or stroma). In the different kidney changes included
in Bright's diseases, the morbid processes begin in one of these three ele-
ments, and it is possible to divide this group of diseases into classes which
shall correspond to the anatomical elements primarily affected. Eor in-
stance, there is one form in which pathological changes commence in the
uriniferous tuhules ; another in which they commence in the walls of the
552 DISEASES OF THE KIDTvTEYS.
vessels, and another in which they commence in the intertubular tissue.
All these morbid changes may be present in the same kidney, but by care-
ful investigation one is enabled, in many instances, to determine in which
the primary morbid processes commenced.
I shall describe Bright's diseases under the following heads : —
First. A form in which the morbid changes commence in the uriniferous
tubules, designated parenchymatous nephritis, tubular, diffuse, catarrhal,
croupous, and desquamative nephritis.
Second. A form in which the morbid changes commence in the inter-
tubular tissue, designated the cirrhotic form of Bright's disease, the hob-
nailed, "gin-drinker's," gouty, or "red granular" kidney.
Third. A form in which the morbid changes commence in the walls
of the blood-vessels, designated the amyloid form of Bright's disease,
waxy or lardaceous degeneration of the kidney ; it were more in keeping
with modern pathology to describe this variety under the head of " de-
generations of the kidney."
Clinically there can be readily recognized two well-defined varieties of
Bright's disease, — the acute and the chronic.
ACUTE BEIGHt's DISEASE.
Acute Bright's disease is a tubular inflammation which may be wholly
recovered from, prove fatal, or lead to chronic parenchymatous nephritis.
Morbid Anatomy. — The gross and microscopical appearances of the kid-
neys in acute Bright's disease will vary according to the intensity and char-
acter of the processes which attend its development. The kidneys are
usually increased in size, their capsule non-adherent, their surface smooth
and mottled, presenting an irregular combination of red vascular engorge-
ment and unnatural pallor ; sometimes they are of a dark purplish color
dotted here and there with spots of ecchymosis. The stars of Verheyen
are more or less dilated and the kidneys are softer than normal.
On section, the cortical portion is relatively increased in size, and is dot-
ted over its entire cut surface with dark or bright red points, which cor-
respond to the situation of the Malpighian tufts, which in some instances
stand out prominently upon its cut surface. The cortical substance be-
tween the Malpighian tufts may be of a paler color than natural. Some
distinguish between a "red" and a "pale" kidney in acute Bright's.
The engorgement will usually be most marked at the base of the pyramids,
at the junction of the cortical and medullary substance — in the arterial
arcade. The medullary portion will be of a darker color than normal,
darker even than the cortical portion ; sometimes it will present a stria-
ted appearance (red and white lines alternating), the lighter lines corre-
sponding to the changed uriniferous tubes.
The lining membrane of the pelvis of the kidney is usually congested.
The inflammation of the mucous membrane of the pelvis and calicos is
attended by exudation of a turbid fluid containing cells.
When such a kidney is examined microscopically , it may be found to pre-
ACUTE BRIGHT'S DISEASE.
553
First, the epithelial lining of the tu-
sent quite a variety of appearances,
bales may become partially or
completely lifted from its nor-
mal situation, and the tubules
become more or less filled with
cells — the changes correspond-
ing to those which occur in ca-
tarrhal inflammations of the mu-
cous surfaces. The cells of the
convoluted tubes of the cortex
will have undergone cloudy
swelling ; and in them and in
the looped tubes of H e n 1 e
the epithelia are granulo-fatty.
These changes are common in
the acute Bright's of fevers.
By pressing on the top of a Mal-
pighian pyramid a turbid fluid
exudes, containing granular and Acute Bright's Disease.
fattv eoithelial cells hvaline ^^^^^on of the cortex of a Kidney sJiowing ^^ cloudy swell-
J ir ' J _ iwg'," etc.
casts and pus cells. There will a. Part of a capsule of a lUalpigMan body.
11 1 1-1 • ni JB, S. Convoluted tr/bes showing the cloudy, swollen epithe-
also be more or less cell mhl- Uum. The nuclei are obscured.
+ J-'^-r, r.-..^n-,v^/-l +!> /^ 4-1-1 1-> n 1 /^c 4 r", ^ Ascendtng Umb of Henh^ s loop.
tration arouna tne lUDUieS in 2>. SUgU round-cetl infUtralion in intertubular tissue.
the intertubular tissue.' Some "" ^^'
cases are very mild, the epithelia are "cloudy," and red and white cor-
puscles and hyaline casts are found in the tubes. ^
Again, in another class of cases the centre of the uriniferous tubes will
contain a hyaline material which resembles coagulp ,ed fibrin ; this hyaline
material may have mingled with it, or may be surrounded by, epithelium
and blood globules, and it resembles fibrinous inflammatory exudation.'
Again, in another class of cases the epithelial cells of the uriniferous
tubes become cloudy, their nuclei disappear, and they become distended
and granular ; desquamation follows, and the tubes become filled with
broken-down epithelium and fatty matter. The epithelia in a few cases
undergo simple atrophy. In some cases of acute Bright's disease all these
processes may be present at the same time in the same kidney. In addition
to these tubular changes, more or less cell development takes place in the
intertubular structure. In scarlatinal nephritis exudative processes co-
exist ; * small cells and nuclei form abundantly in the vascular tuft of the
glomerulus, and at its centre or upon the vascular loops a compact ball is
formed, wherein the small vessels of the glomerulus are matted together by
an embryonic connective-tissue, infiltrated with lymph cells In the latter
part of this stage, if the inflammatory stimulus is constant, the contents
• Celt accumulations about the glomeruli and tubuli contorti are said by Traube to be primary, and the
epithelial changes to be secondary.
2 Wagner calls this " hemorrhagic catarrhal nephritis," and Cohnheim calls it " glomerulo-nephritis."
' Reinhardt compared this form of acute Bright's disease to pneumonia.— 4«n«/. d. Gharite, Berlin-
♦Kelsch and Klebs describe peculiar morbid occurrences in scarlatinal nephritis.
554
DISEASES OF THE KIDNEYS.
Fig. 137.
Acute Bright's Disease.
Section of the Coi'tical portion of a Kidney, show-
ing advanced degenerative changes in the
parenchyma.
A, A. Convoluted t-ubules filed with broken-down
epithelium and gramdo-fatty matter.
B. Swollen epithelium of one of Henle^ s tubes.
C. A collecting tnlnde. Epithelium nearly nor- occasionally
mal.
350.
of the tubules become clianged into an amorphous mass. In some cases
swarms of micrococci are found in the blood-vessels. In most cases these
processes quickly terminate either
in recovery or death ; in a few they
become chronic. When blood extra-
vasations are abundant in acute
Bright's the name '' hemorrhagic
nephritis " has been given to it.
Etiology. — Its most common cause
in the adult is exposure of the
surface to sudden changes of tem-
perature, as is indicated by the class
of subjects in which it is most
liable to occur — bakers, firemen,
moulders, and those whose occu-
pation subjects them to sudden,
repeated changes of temperature.
Again, it occurs among those whO'
are addicted to the use of alcohol :
they may not be habitual drinkers
or greatly intemperate, but they
go on a spree," and
while in a state of intoxication expose
their surface to sudden changes of temperature, or to prolonged cold
after violent exercise. Under these circumstances it is not the alcohol
that develops the tubular inflammation, but the sudden changes of tem-
perature to which these persons subject themselves in consequence of
such indulgence. The daily use of alcohol may be indulged in for years
without leading to acute Bright's disease, provided the individual exercises
care in regard to exposure, and therefore it should not be included in the
list of its direct causes.
Occasionally it happens that a very trifling exposure to sudden changes
in temperature is sufficient to develop it, such as sitting in a draught of air
and exposing the lightly covered loins to a current of cold air while the in-
dividual is in a heated condition. In this climate, the failure to wear flan-
nel next the body throughout the year involves the risk of developing at
some time an inflammatory process in the uriniferous tubules. It is not
clear how such exposure excites tubular inflammation, Runeberg states
that congestion (e. g., passive hypergemia) and the consequent slowed cir-
culation and diminished pressure in the glomeruli is the cause of the al-
buminuria or tubular inflammation. The theory that the nephritic in-
flammation is due to the reflex influence of the nervous system — there being
a connection between the sympathetic nervous system and the surface of
the body — rests on the same basis which is employed to explain the occur-
rence of pneumonia and bronchitis after exposure to cold.
Another very common cause of acute Bright's disease is the circulation
of morbid elements in the blood ; such elements are very numerous, em-
ACUTE BEIGHT's DISEASE. 555
bracing all those poisons which give rise to specific forms of infectious dis-
eases. The infection of scarlet fever is one of its most frequent causes,
especially in childhood. Every epidemic, however, is not attended by
renal complications, for there are some seasons when a type of scarlatina
prevails, in which scarcely a case will have renal complications ; while dur-
ing other seasons almost every case will be attended by them. Such vari-
ations can only be accounted for by regarding the occurrence of nephritic
complications as dependent upon a difference in the scarlatinal infection.
Another class of causes is included under the head of renal irritants
which may be introduced into the stomach : among these are the balsam
of copaiba, spirits of turpentine, cantharides, phosphorus, arsenic, and
lead. The prolonged use of these remedies, or their administration in over-
doses, not infrequently gives rise to tubular nephritis. Another cause is
acute internal inflammations, especially inflammation of the lungs : one
should always be on the watch for its occurrence during a pneumonia.
Another frequent cause is pregnancy. It was formerly supposed that
pregnancy produced Bright's disease by interference with the renal circu-
lation from pressure on the renal veins ; but probably this is rarely its
cause. During pregnancy there is an abnormal quantity of excrementi-
tious material to be carried out of the system by the kidneys, which not
only calls upon these organs for increased labor, but the material elimi-
nated acts as an irritant on the uriniferous tubes, and tubular inflammation
is the result. It may occur at any period of pregnancy, but it is rare be-
fore the third month, and is of more frequent occurrence during the later
months. In connection with pregnancy, this form of kidney disease rarely
terminates in chronic Bright's. It often disappears rapidly and never re-
curs, or it may appear in successive pregnancies, and finally lead to the de-
velopment of chronic Bright's disease. Again, passive renal hy^DerEemia
dependent upon obstruction to the return circulation from cardiac or pul-
monary lesions, may cause acute Bright's disease.
There is a degeneration of the epithelium of the uriniferous tubes which
occurs under certain circumstances independent of inflammation. It is
not amyloid ; it is not, strictly speaking, a fatty change ; but it occurs dur-
ing the degenerative processes of old age. This epithelial degeneration of
the uriniferous tubules is a result of senile change. In this sense, extreme
old age may be regarded as a cause of tubular epithelial degeneration in the
kidneys.
Symptoms. — The presence of urea and its allies, kreatin, kreatinin, etc.,
in the blood in abnormal quantities gives rise to the phenomena which at-
tend the development of acute Bright's disease. The symptom which usu-
ally first attracts the attention of a j)atient is oedema of the face. There
may have been signs of gastric disturbance prior to its occurrence, but they
have not been distinctive in character. After exposure to sudden varia-
tions in temperature, or after an attack of some form of acute infec-
tious disease, or withor.t any known cause, there is noticed a slight puffi-
ness about the eyes in the morning ; if the patient is anaemic, the oedema
may appear in the feet and ankles at the same time This oedema usually
556 DISEASES OF THE KIDN^EYS.
increases very rapidly. With the occurrence of the oedema there is great
restlessness. Toward evening there is a little quickening of the pulse and
a slight rise in temperature — never typical ; the patient complains of head-
ache, which increases in severity from hour to hour ; at times he is very
drowsy. Complete, sudden, but temporary blindness may occur at its very
onset, the ophthalmoscope showing no morbid appearances.
If the patient is closely questioned, he will state that he has recently
noticed some change in his urine, that it has been scanty and high colored,
and he has had a frequent desire to pass it. Perhaps he has had some pain
in the back and loins ; he may complain of nausea and perhaps of vomit-
ing ; the latter is sometimes so troublesome that the physician may direct
his attention to the stomach as the seat of the disease, and treat the pa-
tient for some form of gastric lesion. There is more or less acceleration
of the pulse, which is irritable in character. The skin is usually unnatu-
rally dry ; occasionally it is moist, but when it is so the perspiration has a
peculiar urinous odor. These, in brief, are the symptoms which attend
the development of a mild form of acute Bright's disease.
In a favorable case, after the patient has reached the condition described,
he begins to improve ; the urine is increased in quantity, the oedema grad-
ually disappears, the headache moderates, the gastric disturbances disap-
pear, and in the course of two or three weeks he has entirely recovered.
In a certain proportion of cases, instead of improving, the patient steadily
grows worse ; the oedema steadily increases until the cellular tissues of the
entire body become oedematous. As a result of the pulmonary oedema there
is dyspnoea. Dyspnoea in this connection is not always dependent upon an
oedematous condition of the lung, for uraemic dyspnoea may occur inde-
pendent of any change in the lung-tissue. When there is general ana-
sarca the dyspnoea is usually due to pulmonary oedema ; it may be accom-
panied by more or less pulmonary congestion, giving rise to a watery expec-
toration, which may be streaked with blood. If the disease progresses, the
anasarca will gradually increase until the patient becomes " water-logged."
With the general anasarca the surface of the body assumes a peculiar, pale,
waxy appearance ; there is oedema of the scrotum and penis, or labia, and
more or less eifusion into the peritoneal, pleural, and pericardiac cavities.
Hydrothorax may so impede respiration as to cause death.
As the uraemia becomes more profound, a series of nervous phenomena
are developed : the patient becomes exceedingly restless, muscular twitch-
ings occur, and these may soon be followed by convulsions, coma, and
death. If this class of patients do not die from the direct toxic ejffect of
the urea, they may have complications, such as meningitis, pericarditis, en-
docarditis, pneumonia, etc., which may rapidly lead to a fatal issue. This
is the most unfavorable of all the types of acute parenchymatous nephritis.
Such cases sometimes follow scarlet fever. The same type of cases is also
met with in connection with other infectious diseases.
There is still another type of acute Bright's disease which is occasionally
met with. It is ushered in by violent symptoms : the patient is seized
with a chill, intense pain in the back and along the ureter, with retraction
ACUTE BRIGHT's DISEASE. 657
of both testicles ; there is delirium, great nervous disturbance, urgent cere-
bral symptoms, and the patient may pass quickly into a state of coma and
die within two or three days. The chill in these cases is followed by high
temperature ranging from 104° F. to 106° F.; there is often almost com-
plete suppression of urine, perhaps not more than two ounces being se-
creted in twenty-four hours. The delirium which is present so closely re-
sembles that of meningitis that it is often difficult to differentiate between
the two conditions. In these cases there is intense, active renal hyperaemia,
and the tubules are extensively filled with an inflammatory exudation.
Very soon after the accession of the ushering-in symptoms, oedema of the
face will be developed, and soon after its occurrence the patient will pass
into a state of coma, which is usually followed by death. If these patients
recover from the acute stage, the kidneys will be permanently damaged, and
they will afterward present the symptoms of chronic Bright's disease.
Connected with the history of acute Bright's, there are symptoms which
are of special imjoortance, and which I shall consider more in detail ; these
are the changes in the iirine, the dropsy, and the nervous phenomena.
These are present to a greater or less degree in all cases, and their exist-
ence is necessary for its diagnosis.
The urine in all varieties is diminished in quantity, high colored, and
sometimes smoky in appearance ; it is of high specific gravity, perhaps as
high as 1.030. A sediment, in which there are red and white blood-corpus-
cles, forms soon after the urine is voided. The amount of urea eliminated
in the twenty-four hours is diminished to one-half or one-quarter the nor-
mal amount. When tested for albumen, from one-third to one-half of the
entire bulk of the^ urine will coagulate. In testing for albumen it is well
to employ both heat and nitric acid. Albuminous urine is usually coagu-
lated by heat below the boiling point, and by nitric acid. If both of these
tests are carefully used, one will rarely be led into error ; but mistakes are
often made when only one of these agents is employed, for the reason that
heat alone Avill not coagulate albumen in urine which is neutral or alkaline ;
in such cases the addition of nitric acid coagulates and precipitates the al-
bumen. In true albuminuria, where serum-alhumen appears in the urine,
there is some kidney change. In false albuminuria, where albumen, not
serum-albumen, appears in the urine, the kidneys maybe healthy.' Ee-
cently, opinions have changed in regard to albuminuria.^ If a |)ortion of
the urinary sediment be microscopically examined, casts will be found which
' See text-books on " Urinary Analysis '" for modes of determining the different albumens ; also Appen-
dix to Foster's " Physiology."
2 Albuminuria itself is, according to Gull's statements, as common in young men and boys as spermator-
rhoea ; Moxon confirms this. Young girls from fourteen to seventeen have it. Depressing mental emo-
tions cause a lowered pressure in the vessels, and this, according to Runeberg's ingenious theory, is the
one cause of albuminuria. Leube and Purbruger incline to the opinion of an individual permeability of
membrane. Temporary nervous innervation may in some instances induce transient albuminuria, with or
without healthy kidneys. Drs. Brunton and Power (St. Barthol. Hosp. Rep., 1877) take issue with Burtel's
statement that albuminuria is always of renal origin. There are different albumens, some derived from
the blood, others from the digestive organs. Diminution and increase of blood-pressure in the glom.
eruli have both been advanced as prime causes of the albuminuria. Probably blood-pressure plays but an
unimportant part. Cohnheim legards changes in the epithelium covering the glomeruli as an important
factor. These changes are, no doubt, in part produced by the stagnant inflammatory current. The vessels
of the glomeruli unquestionably allow most of the albumen (in acute albuminuria) to exude.
558 DISEASES OP THE KIDKETS.
correspond to the contents of the urinif erous tubes already described ; these
casts consequently vary in appearance and composition. Tliose which are
most characteristic are the epithelial casts, which may contain blood-glob-
ules ; in yery active forms of the disease, the casts may be entirely composed
of coagulated blood, called hlood casts; casts of this form and composition are
found in no other form of Bright's disease, unless it is complicated by acute
tubular inflammation. In addition to epithelial and blood casts, small and
large hyaline casts may be found. The small hyaline casts are formed in tubes
the epithelium of which has not been removed. In addition to the casts, free
epithelial cells and blood -globules may be seen. Hyaline and epithelial
casts are sometimes found independent of Bright's disease, and saccharine
urine may be loaded with them. ' Distinctly formed cell elements in a cast
point to an origin in the straight or collecting tubes.
Dropsy occurs early ; there have been several theories advanced as to its
cause, but none are perfectly satisfactory. One theory is, that it is due to
the sudden removal from the body of a large amount of albumen ; whereas
in the most rapidly developed dropsies no albumen is carried out of the
body, for the reason that the patient passes little or no urine. '^ Another
cause assigned for the dropsy is, that the kidneys fail to eliminate the
watery portion of the blood in the form of urine, and that the dropsy occurs
as the result of the retention of the watery elements ; yet very extensive
dropsies occur while the patient is passing more than the normal quantity
of urine. ^ Again, it is said that dropsy occurs in consequence of the
anaemic condition of the patient. The anaemic condition undoubtedly con-
tributes to the ease with which the transudation of fluid through the walls
of the vessels takes place ; but a patient may be exceedingly anaemic and
yet no dropsy be present, and dropsy very often occurs before the patient
shows any evidence that he is in an ansemic condition.
1 regard dropsy as a necessary symptom of acute Bright's, but the exact
cause of its occurrence in many cases cannot be satisfactorily determined.
Nervous symptoms are of great importance and prominence. Undoubt-
edly these are due to the presence of some irritating poison in the circula-
tion, which acts directly upon the nerve centres." Usually the nervous
symptoms first manifest themselves by headache ; therefore headache is a
symptom which must not be lightly regarded, for it is often the precursor
of more dangerous symptoms. If persistent and severe, and permitted to
pass unrelieved, it may be followed by convulsions. The larger proportion
1 Southey regards it as an error to suppose that the larger casts are derived from the larger tortuous
lubes. Nothing but cellular elements cau pass through Henle's loops (diameter 1-1200 to 1-1000 in.); " when,"
he says, " a cast is assumed to come from the profounder renal tissue and to be of grave significance, an
error is committed, based on ignorance of anatom3^" Hyaline casts probably form in Henle's loops.
2 Cohnheim, in his work on pathology, regards inflammatory changes in the walls of the cutaneous and
subcutaneous vessels — whose causes are the same as those of acute Bright's— to be the reason of anasarca
in many instances, — the vessels being rendered more permeable.
3 Cohnheim {Virchow''s Archiv. 1877, 96, p. 106), after most elaborate experimentation, regards oedema as
the result, not of dilution of the blood or of increase in the relative amount of water, but of hydrcemit
plethoi'a, i. e., increase in the absolute amount of water. This fact, with changes in the walls of the ves-
sels, is accepted by most authorities as the most plausible and probable cause of oedema in acute
Bright's.
■» The different theories in regard to the causation I have considered under the head of acute iircemia.
ACUTE BRIGHTS DISEASE. 559
of cases in acute Bright's will suffer from more or less severe headache,
without any subsequent convulsions ; but the fact that convulsions do fol-
low it is sufficient to cause one to watch for the indications of their occur-
rence. If the poisoning goes on gradually the patient will first become
drowsy, the drowsiness passing into stupor, and frequently into coma. A
large number of patients with acute Bright's unquestionably die from the
direct effect of urea and its allies upon the nervous centres ; but a still
larger number die from complications.
DiiFerential Diagnosis. — If a patient has headache, some fever, more or
less oedema, nausea, and perhaps vomiting, with scanty, high-colored
urine of high specific gravity, containing epithelial, small hyaline, or blood
sasts, it is certain that acute Bright's disease exists. There may be other
pathological conditions existing in the kidneys at the same time, but this
train of phenomena gives unmistakable evidence that some of the urinifer-
ous tubes are the seat of acute inflammation ; — the acute may be ingrafted
upon the chronic. In every case which presents this train of symptoms
frequent examinations of the urine should be made. The general symptoms
and the changes in the urine in acute Bright's disease are so obvious
that it can scarcely be overlooked or mistaken for any other disease.
The only circumstances under which it is possible for this affection to pass
unrecognized are those in which dropsy is not a prominent symptom, and
when a careful examination of the urine has not been made.
It is not always easy to determine whether acute Bright's is primary or
secondary — that is, whether it has occurred in kidneys that were healthy
previous to its occurrence, or in those that were already the seat of chronic
Bright's. The previous history of the patient, and the presence or absence
of cardiac hypertrophy, are the only means to guide one under such cir-
cumstances.
The points of differential diagnosis between congestion of tlie hidneys
and acute Bright's disease have already been given.
Acute Bright's is distinguished from paroxysmal hcematuria and albu-
minuria by the abrupt commencement and brief duration of these affec-
tions, by the marked nervous and gastric symptoms, the slight jaundice,
and the absence of dropsy. Granular pigment in hsematuria, and a
very great quantity of albumen and tube casts in paroxysmal albuminuria
are characteristic urinary symptoms. Haematuria, with a tendency to sup-
pression, has few tube casts.
Prognosis.— The tendency of acute Bright's disease is to recovery, but
the chances of recovery are much better in the young than in those past
middle life. In those cases which terminate in recovery the characteristic
symptoms of the disease disappear within two or three months from the
commencement of the attack. So long as albumen continues in the urine,
however small in quantity, recovery cannot be regarded as complete. The
indications of a fatal termination are very scanty urine, frequent and dis-
tressing vomiting, extensive anasarca, severe and persistent headache,
convulsions, coma, tjrphoid symptoms, and the occurrence of complica-
tions.
560 DISEASES OP THE KIDKETS.
The pulmonary complications which render the prognosis imfavoraDle,
are oedema, pneumonia, and capillary bronchitis. The great danger in
pneumonia which complicates acute Bright's disease is the sudden develop-
ment of pulmonary oedema in portions of the lung not involved by the
pneumonia. Another dangerous complication is inflammation of the se-
rous surfaces, especially endocarditis and pericarditis. Acute meningitis is
a rare, but always a fatal complication. There may be complete loss of
sight ; — this form of amaurosis is usually temporary, and is unattended by
any change in the retina recognizable by the ophthalmoscope ; it is probably
due to the direct effect of the urea upon the retina. Subacute gastritis,
functional hepatic derangement, and oedema glottidis are also complicating
conditions which render the prognosis unfavorable.
In a small proportion of cases patients pass rapidly from acute into
chronic Bright's disease.' The passage from acute into chronic is indicated
by a copious secretion of paler urine containing few casts. The droj^sy
diminishes, but does not entirely disappear. The individual may be able
to resume his ordinary avocations, but the oedema of the feet and ankles
does not entirely disappear and the urine remains albuminous.
Treatment. — Formerly, general and local blood-letting was practised in
the treatment of acute Bright's disease. At the present time general blood-
letting is never resorted to, unless in the very acute form which is at-
tended by violent cerebral symptoms. As soon as its pathology was better
understood, a plan of treatment was adopted, based on the proposition that
the first essential in the treatment of an inflamed organ was rest. It was
proposed to treat an inflamed kidney upon the same principle as an inflamed
eye or an inflamed joint would be treated : that is, give the kidneys perfect
rest. With this end in view it was proposed to supplant the function of
the kidneys as far as possible by increasing the function of the skin, so that
it should perform the work of the kidneys. The so-called diaphoretic plan
of treatment, as well as the free administration of hydragogue cathartics, is
based on this principle.
The object of these two plans is to eliminate the i-etained excrementitious
materials, allowing the inflamed kidneys to rest. The usual method of
producing profuse diaphoresis is to place the patient in bed and cover him
with flannel blankets, and then by means of the hot-air apparatus in-
troduce a constant current of hot air beneath the bed-clothes, until pro-
fuse perspiration is induced and the excretory power of the skin is taxed
to its utmost. The bath should be continued from half an hour to an
hour; then the patient should be allowed to gradually become cool, and
when so, to resume his clothing and walk about the room or ward, the
temperature of which should be above 70° F. These baths may be re-
peated once or twice each day, or every other day, as the condition of the
patient may demand. The effect usually produced by these baths is a
rapid subsidence of the oedema. It may not require more than half a
dozen baths to entirely remove the dropsy from a " water-logged "
^ Of forty-one hospital cast-s, twenty-one terminated in complete recovery, twelve died, and seven
passed into chronic Bright's ; in private practice the rate of mortality is usually less.
ACUTE BRTGHT'S DISEASE. 561
patient, and as far as that one symptom is concerned to give complete
relief ; — but the relief is only temporary. Soon the patient becomes
anaemic, loses his strength, and after a time a point is reached at which
the oedema returns, although the hot-air baths are continued, and the
toxic effects of urea steadily increase. I have seen patients pass into con-
vulsions while in a hot-air bath.
In addition to the baths, it is customary to administer hydragogue ca-
thartics in sufficiently large doses to produce daily three or four watery
discharges from the bowels ; under the conjoined action of these two
plans, this class of patients for a time will appear very much relieved ; but
after a few active purgations, and a few hot-air baths, they will begin to
complain of extreme weakness, and very soon reach a point at Avhich the
combined action of these agents fails even to relieve the distressing symp-
toms, and their condition is then worse than before their administration was
commenced.
Several years ago I became convinced that this depurative plan of treat-
ment was wrong, and that it was wrong because it rapidly depleted
patients who could not bear depletion. Exhaustion can as certainly be
produced by diaphoresis and hydragogue cathartics as by repeated general
bleedings. Besides, the repeated use of hydragogue cathartics interferes
with the processes of digestion and assimilation.
In the treatment of acute Bright's disease, there are three important
things to be accomplished. First : the elimination of urea and its allies.
Second : the removal, as rapidly as possible, of the inflammatory products
which obstruct the uriniferous tubules. Third : to counteract the effect of
urea and waste j)roducts upon the nervous system.
Th9 question arises : How shall we meet these indications ? The main
thing to be done is to remove the exudation which obstructs the urinifer-
ous tubules. This exudation not only interferes with the elimination of
urea and its allies, by preventing the kidneys from performing their nor-
mal eliminative function, but if it remains in the tubules it induces de-
generative processes. If the excretory power of the kidneys can be so in-
creased that they will pour out fluid in sufficient quantity to carry off this
material, the desired result will be reached.
Digitalis is the drug which will accomplish this result, as it increases
the urinary secretion without stimulating the kidneys ; it overcomes the
obstruction in the renal circulation, and thus causes an increased flow of
the watery portion of the urine through the Malpighian tufts into the
upper portion of the uriniferous tubules. Thus the obstruction in the
tubes is washed out, and at the same time the eliminative function of the
kidneys is increased, so that urea is carried out of the system much more
rapidly and completely than it can be by the skin or bowels. If diluent
drinks are given water is the test. Spirits of nitrous ether, acetate of
potash, tincture of the perchloride of iron, or squills may often be ad-
vantageously combined with digitalis.
In connection with the administration of digitalis, I would recommend
the application of dry cups over the region of the kidneys. In order that
562 DISEASES OF THE KIDNEYS.
the dry cupping may be more effective, each cup should he removed as soon
as the vessels beneath are well filled. The object is to draw the blood
from the arteries into the capillaries, but not with sufficient force to cause
extravasation. The object of dry cupping is not to irritate the surface, but
to rapidly draw the blood from the arteries and as rapidly carry it through
the capillaries to the veins in its backward course to the heart. After dry
cupping, warm poultices over the kidneys may be applied with benefit ;
digitalis leaves may be used for a poultice, and thus applied they will
increase the diuretic effect of the drug administered internally. After the
free administration of digitalis and the application of dry cups, if the
ursemic symptoms are still urgent, hot-air baths and hydragogue cathartics
may temporarily be resorted to, to aid in carrying the patient over the
period of greatest danger ; but their use should not be continued after free
diuresis is established.
The next object to be accomplished is to relieve the nervous symptoms ;
the means to be employed to accomplish this are the same as in the treat-
ment of acute uraemia. For the successful management of acute Bright's
disease, whatever may have been its exciting cause, the patient must be
kept in bed, in a large, well-ventilated apartment, with a temperature of
75° F. Milk should be the only article of diet. Skimmed milk is advo-
cated highly ; besides being nourishing, it is a good diuretic. Dry cups
should be applied over the kidneys, and the infusion of digitalis should be
freely administered. If this plan is systematically carried out from the very
commencement, the urine soon becomes copious, the albumen gradually
diminishes, and the dropsy passes away. As soon as the flow of urine com-
mences, the administration of digitalis must be discontinued, and diluent
driuKS are to be given. If the renal secretion be not re-established in
twenty- four hours, hot-air baths, hydragogue cathartics or pilocarpin hypo-
dermically in one-eighth or one-tenth grain doses are to be used. For
the relief of convulsions or coma, hypodermics of morphine should be
^given.
CHEONIC BEIGHT'S DISEASE,
dhronic Bright's disease will be described under the following heads : —
I. Chronic Parenchymatous Nephritis.
II. Interstitial Nephritis ; or, " Cirrhotic Kidney."
III. Amyloid Degeneration ; or, " Waxy Kidney."
CHRONIC PARENCHYMATOUS NEPHRITIS.
As already stated, chronic parenchymatous nephritis may be a sequela
of the acute form, but it is oftener a chronic degenerative process from its
onset. Under this head may be included the large fatty hidney, the large
white hidney, and the small, granular, fatty hidney.
Morbid Anatomy. — Chronic parenchymatous nephritis is almost always a
legitimate consequence of depraved cell-development, and it may make its
appearance in any form of renal lesion in which there is a protracted inter-
CHRONIC PARENCHYMATOUS NEPHRITIS.
563
ference with the normal nutrition of the tubes. In the large fatty kidney,
but few of the epithelial cells of the urinifcrous tubes at first undergo
change, but as the transformation becomes general, the entire contents of
the affected tubules become loaded with minute oil globules. The mucous
membrane of the pelvis and calicos is thickened, opaque, and anaemic, or it
presents a vai-icose dilatation of its veins. The kidneys are enlarged, their
capsules are non-adherent, and their surface smooth ; their color is paler
than normal, presenting a more or less yellow appearance ; sometimes they
are mottled.
On sectifm, the enlargement of the organ will be found to be due chiefly
to an increase in the size of its cortical substance, which is of a pale yel-
loAvish color. There is but little change in the medullary portion. The
Malj)ighian tufts do not stand out prominently, for there is more or less
fatty material in the dilated portion of the uriniferous tubes around the
Malpighian tufts, which gives them a somewhat pale appearance. The vas-
cularity of the whole kidney seems to be very much diminished ; but here
and there spots of hemorrhage or congestion are seen. The principal
changes take place in the convoluted tubes of the cortical portion, esjae-
cially in those which surround the Malpighian tufts.
These sections of the cortical substance in this form of degeneration
are very opaque ; under a
low power they show little
more than uriniferous tu-
bules irregularly distended
with fatty granules, and va-
ricose. To the unaided eye
the tubules look like streaks
of sebaceous matter. At
some points they are greatly
increased in size, at others
they are of normal calibre.
In the Malpighian bodies are
found oil-globules in vary-
ing quantities, but the capil-
laries of the tuft are un-
changed. Under a high
power, fine fat granules are
seen about the nuclei in
the protoplasm of the epi-
thelial cells, and also in
the cells of the external coat
of the small vessels. Gran-
ulo-fatty material covers a
homogeneous vitreous sub-
stance in Henle's tubules.
The lacunae and cells of the
intertubular connective-tissue are also filled with fine fat granules.
Fig. 13f
Chronic Parenchymatous Nephritis.
Section from the Cortex of a Kidney.
A. Slightly thickened capsule of the glomerulus.
B. Vascular tuft, nearly normal. A small ammmt of gran-
ular matter is seen beneath the capsule.
C. C, C. Convoluted i/ulmles— epithelium nearly destroyed. Some
of the tubes are entirely filled with fatty granules. The
nuclei of the epithelia are yet plainly seen.
D. Longitudinal section of Henle's looped tube— ascending por*
Hon. '
E. A small artery. v. 350.
564 DISEASES OF THE KIDJS'ETS.
Large Wliite Kidney. — In this variety of parencliyinatous nephritis,
the kidneys may be twice their normal size, of an ' ' ivory-white " color,
their surface smooth, and their capsule non-adherent.
On section, the enlargement is found to be due to an increase in the
volume of the cortical substance. The medullary portion shows no appre-
ciable alteration. The microscope will show that the morbid changes are
confined almost exclusively to the epithelium of the convoluted tubules and
that lining the Malpighian bodies. The epithelium is granular, and so
much swollen that the lumen of the tubes is obstructed and may be dis-
tended with a hyaline material. There is a dilated and varicose condi-
tion of the tubes, with some thickening of their walls. In some cases
Henle's loops present alterations similar to those that occur in the convo-
luted tubes.
Small Granular Fatty Kidney. — The atrophic alterations in the kidney
in this variety (or stage) of parenchymatous nephritis are entirely different
from those of atrophy produced by interstitial nephritis. The epithelium
which may have been the seat of fatty or granular change, disintegrates,
liquefies, and is absorbed or passes off in the urine. The tubes, deprived of
their epithelium, collapse. Some claim that renal atrophy and granular
degeneration of the kidney are the same. That these processes are asso-
ciated is very evident. During the process of atrophy, developments occur
in the walls of the tubes and in the intertubular tissue, which lead to,
or are followed by, thickening of the tubules and blood-vessels. The
processes of inflammatory atrophy are always slowly progressive. An
atrophied white kidney is markedly diminished in size, its surface is
uneven and more or less nodular ; its capsule is adherent and slightly
thickened, and when removed portions of kidney tissue may be removed
with it ; the denuded surface is more or less granular, its color varies,
it may be white, have a stellate vascularity, or present a mottled appear-
ance.
On section, it will be found that the diminution in the size of the kid-
ney is mainly due to atrophy of its cortical substance ; the medullary por-
tion retains very nearly its normal dimensions ; the cortical substance be-
tween the pyramids will be somewhat atrophied. The kidney is firm and
jtough. The granulations on its surface and in its substance are the pyra-
mids of Ferrein. Under low power a section of the cortical substance will
show an increase in the stroma of the organ, the walls of the vessels will be
thickened and the Malpighian tufts will have lost their distinctness. The
uriniferous tubules will be denuded of their epithelium, in some places filled
with granular or fatty material, and distended ; in others they will be en-
tirely obliterated, atrophied, and more or less shrivelled. This form of
kidney degeneration may be distinguished from the contracted kidney of
interstitial nephritis by the larger size of the organ, its less firm consis-
tency, its more uneven surface, its pale yellow and large granulations not
only on its surface but throughout its substance, evidently formed by the
accumulation of fat in the tubules, and by the absence of cysts either on ibs
surface or in its substance. It is not necessary that the small atrophic
CHRONIC PABENCHYMATOUS KEPHEITIS. 565
Mdney of chronic parenchymatous Lephritis should have been preceded by
an enlarged fatty or granular kidney.
Etiology. — Chronic parenchymatous nephritis may be the sequela of
acute. It is more common in males than in females, it occurs in early
adult life rather than past middle life. Exposure, moderate alcoholism,
bad hygiene, phthisis, diabetes, arthritis deformans, emphysema, and
chronic cardiac diseases predispose to its development. The cause is
sometimes undiscoverable.
Symptoms. — This form of chronic Bright's disease may be ushered in by
acute symptoms or come on insidiously ; in either case, when once fully
developed, the symptoms are identical. There are two symptoms which
are always present, viz. : albuminuria and dropsy. If its advent is marked
by acute symptoms, its development is attended by the phenomena of acute
Bright's ; the patient rapidly reaches a condition of general anasarca ; his
countenance assumes a pallid appearance ; the pallor is not like the clear
pallor of phthisis, nor the dingy pallor of cancer, but is peculiar to the dis-
ease. When he has reached an apparently hopeless condition his urine
becomes gradually increased in quantity. His appetite returns, nausea
disappears, he suffers less from restlessness, the anasarca gradually dimin-
ishes, the sleep becomes refreshing — in short, there is a gradual improve-
ment in all his symptoms. The improvement may be continued or
relapses may occur, but after a few weeks or perhaps months he may reach
a condition of comparative health ; this class of patients never so far
recover that no traces of the disease remain. There will always be some
cedema along the line of the tibia and over the internal malleolus, and the
albumen will never entirely disappear from the urine. Patients in such a
condition are always inspired with the hope that they will reach com-
plete recovery ; but they are liable at any time to a sudden return of
their dropsy.
When the disease comes on gradually without any acute symptoms one
of its earliest indications is increased frequency of micturition ; the oedema
may not be very extensive, but it is always present ; perhaps there is at no
time pain in the back or loins ; but there is a time, early in the history of
the disease, when the urine is scanty and high colored ; afterward it be-
comes copious, of a pale color and low specific gravity. The gastric and
nervous symptoms, so prominent in acute Bright's, are never severe ; there
is gradual loss of energy with progressive emaciation ; the skin becomes
dry and harsh, the surface assumes a peculiar pale, sallow appearance, there
is often great thirst, very troublesome dyspeptic symptoms, and often marked
signs of anaemia. The pulse becomes feeble and irregular in force, and the
patient grows old rapidly.
The urine after a time becomes more abundant than normal, of low spe-
cific gravity, sometimes as low as 1.010, and the quantity of albumen is in-
creased. Fatty and hyaline casts are present ; when the stage of atrophy
is reached the urine sometimes becomes very abundant, and, although the
albumen at times may be small in quantity, it never entirely disappears,
and large hyaline and fine granular casts are always present. As the elim-
566 DISEASES OF THE KIDJSTEYS.
ination of urea is steadily diminislied, it is important to subject the urine
to frequent quantitative analyses. Cardiac lijrpertrophy develops, and albu-
minous retinitis is of frequent occurrence.
It is to be remembered that the symptoms and course of this form of
Bright's disease are not continuous ; there will be remissions, periods when
these patients seem to be recovering, and suddenly the urgent symptoms
of chronic ansemia will develop, and the patient passes into a state of list-
lessness, stupor, or coma, and death rapidly ensues.
Differential Biagnosis. — "When the urine is abundant, of a pale color, low
specific gravity, highly albuminous, and contains fatty, granular and hyaline
casts, accompanied by oedema of the lower extremities, one readily makes a
diagnosis of chronic parenchymatous nephritis, especially if a careful analy-
sis of the history of the patient corresponds to the usual course of its de-
velopments. A state of uraemic stupor, with a dry tongue and sordes on
the teeth, may be mistaken for typhoid fever, yet the history of the case,
and a careful examination of the urine will soon remove all doubts.
If the urine is carefully examined it is hardly possible for one to con-
found the anmmia and cachexia which sometimes attend the stage of
atrophy of chronic parenchymatous nephritis with the cachexia of other
clironic diseases. The mistakes that are made in diagnosis, or rather the
failures to recognize its existence, are usually due to the fact that a careful
examination of the urine has not been made. In every case of persistent
dyspepsia careful examination of the urine should be made.
Prognosis. — One of the most constant attendants of the advanced stage of
this form of Bright's disease is the development of cardiac hypertrophy.
It is probably due to interference with the systemic capillary circulation,
and it is an evidence that the renal disease has existed for a long time ; it
suggests the possible occurrence of cerebral hemorrhage, and therefore
renders the prognosis unfavorable ; visceral inflammations, especially pneu-
monia and bronchitis, are liable to occur, and often are the direct causes of
death.
The most frequent serous inflammations in this connection are pleurisy,
pericarditis, and meningitis. They are usually insidious in their develop-
ment, and always render the prognosis unfavorable. Another complication
which may render the prognosis unfavorable is subacute inflammation of
the mucous membrane of the stomach. Patients never entirely recover
from the structural changes which occur under such circumstances.
Amaurosis is first indicated by the patient's inability to see distinctly ; sub-
sequently he has more or less difficulty in reading print which formerly he
had read with ease ; lenses do not improve his vision ; after a time the
sight may be entirely lost. This amaurosis is due to a neuro-retinitis ; it
is present to a greater or less degree in a large number of these patients.
The structural changes in the kidneys in the advanced stage of this form
of Bright's disease are such that they do not admit of repair. All j)ortions
of the kidney, however, are not equally involved ; consequently the de-
purative function of the organ is not suspended, but only imperfectly
carried on. So long as the degenerative process is not progressive this class
CHRON"IC PARENCHYMATOUS NEPHRITIS. 667
of patients may get on quite comfortably, but its tendency is to progress
until it reaches a point beyond which life cannot be sustained. In a large
number of cases, long before this limit is reached, some one of the com-
plications to which reference has been made will cause death.
In the advanced stage, the most trustworthy jorognostic indications are
to be obtained by comparing the evidences furnished by examinations of
the urine with the general symptoms ; one must always be cautious in
giving a prognosis, for the uraemic symptoms may suddenly be greatly
aggravated by exposure to cold or errors in diet, and the j)atient quickly
passes from a condition of comparative good health into ursemic coma. Al-
though in all advanced cases the prognosis is unfavorable, still there is
reason to hope that by judicious management, even in the most unprom-
ising, relief may be obtained from many of the more distressing symptoms
and life be prolonged.
Treatment. — At one time mercurials were extensively employed in the
treatment of this form of Bright's disease, with the idea of keeping up its
constitutional effects for months. This plan is now abandoned ; there
are some, however, who claim that the bichloride may be employed with
benefit. I shall, in considering the cirrhotic kidney, refer to a class of
cases in which the administration of this form of mercury is admissible. It
is important that the diuretic plan of treatment should be continued when
a patient passes from acute into chronic parenchymatous nej)hritis. Digi-
talis in moderate doses, or at intervals, is always indicated ; it is imj)ortant
that the accumulations in the uriniferous tubules should be removed the
same as in the acute stage.
There is another element which enters into the treatment. The most
important thing to be accomplished in the treatment of this form of Bright's
is the establishmenfof healthy nutrition ; the nutrition of the kidneys is
always imperfectly performed, and these patients are always more or less
ansemic. For this reason it is important that the nutritive processes be
carried to their highest point ; that after the degenerated material is re-
moved from the uriniferous tubes, the degenerative inflammatory processes
maybe arrested and the epithelial lining of the tubes restored. Digitalis
combined with iron should be given in sufficient quantity to produce mod-
erate diuresis. In most instances milk is the best article of diet. Adults
will often take three or four quarts in twenty-four hours ; when taken
freely it supplies an abundance of liquid, which acts to some extent as a
diuretic. In most cases a moderate amount of stimulants will be of ser-
vice. Wines are to be preferred, and they should be taken with the food.
The patient must be placed under the best hygienic conditions, in a uni-
form temperature, and the surface of the body must be covered with flan-
nel ; over-indulgence of every kind, and exposure of the surface to cold must
be carefully avoided ; a residence in a uniformly dry climate is of the utmost
importance. The urinary secretion must be carefully watched both as to
its quantity and quality. In the stage of atrophy there will be no necessity
for the administration of diuretics, for the urinary secretion is abundant.
The disease is attended by great feebleness, and on account of their feeble
568 DISEASES OF THE KIDNEYS.
digestive power this class of patients will be compelled to take food in small
quantities and at short intervals ; they will generally be greatly benefited
by cod-liver oil, combined with iron. Wines are always indicated in
moderation. Whenever the urine becomes scanty, two or three full
doses of digitalis should be administered and dry cups applied over the
kidneys.
The urgent symptoms, such as dropsy, etc., must be relieved by an oc-
casional hot-air bath, hydragogue cathartics or stimulating diuretics, and
at the same time great care must be exercised lest the depletion be carried
too far. Jaborandi or the hydrochlorate of pilocarpin may be cautiously
used in very urgent cases ; they are prompt and efficacious, but sometimes
dangerous. Iron and cod-liver oil are the two great remedial agents in this
disease, and should be daily administered, unless the condition of the stom-
ach of the patient shall contraindicate their use. Milk should be the prin-
cipal article of diet. By living in a warm climate, by constant watchfulness,
and by following the rules given in acute Bright's, a fatal termination may
be long delayed, although complete recovery cannot be hoped for.
Let me impress this fact : — that no depleting remedies should be em-
ployed, except in times of emergency, when from some sudden renal con-
gestion the function of that portion of the kidney structure which is still
performing the work of elimination becomes suddenly arrested or impaired,
and acute uraemic symptoms are developed.
CIREHOTIC BEIGHT S DISEASE.
In the cirrhotic form of Bright's disease the morbid processes do not pass
through distinct stages. The changes consist essentially in an increase of
the intertubular structure, and a consequent atrophy of all the other struc-
tures. As has been stated, it has been called interstitial nephritis, the
gouty, hob-nailed or small red kidney.
Morbid Anatomy.— Kidneys that are the seat of interstitial nephritis are
at no time very much increased in size. The changes are characterized by
a gradual increase in the connective-tissue of the kidneys and by atrophy of
the tubules. In its early stage the capsule is somewhat adherent, its sur-
face uneven, and the stroma of the cortical substance somewhat increased.
In the advanced stage of the process the kidneys are diminished in size,
sometimes to one-fourth their normal bulk ; their capsule becomes thick-
ened and very adherent ; the thickening of the capsule is quite character-
istic, and there is more or less prolongation of the connective-tissue from
the capsule into the cortical substance, in consequence of which a portion
of the kidney structure will be removed when the capsule is torn off, leav-
ing the surface of the organ uneven and ragged, having sometimes a finely
granular appearance and of a reddish color. Such kidneys have a dense
fibrous feel, and dilated veins are sometimes seen upon their surface.
Upon section it is found that the diminution in the size is due to decrease
in the cortical substance. It is more markedly diminished in this than in
CIRREOTIO BRIGHT'S DISEASE.
569
any other form of Bright's disease ; it will also be noticed that the blood-
vessels are more distinctly visible than in the normal kidney. The Mal-
pighian tufts, however, are not as prominent ; the medullary portion retains
very nearly its normal appearance and is not markedly diminished in
size.
The principal change, so far as retraction is concerned, takes place in
the cortical portion. This portion may be reduced to one-sixth its normal
thickness. The shrinking is not only apparent in the cortical substance
beyond the bases of the pyramids, but also in the tissue between the
pyramids. Cysts are usually found m the cortical portion, especially near
its surface. These cysts are of varying size, and may be the result of a
variety of changes.
The usual anatomical changes which occur are as follows : —
First, there is cellular infiltration of the intertubular connective-tissue
of the cortical substance, most abundant around the capsule of the Mal-
pighian tufts ; this gradually develops into a fibrillated structure ; in this
stage of the process the tubes and their epithelium are but slightly, if at
all, implicated. The Malpighian tufts
are diminished in size, their capsule
thickened, and around the tufts are
laminated, concentric zones of connec-
tive-tissue, between whose lamellae are
flat, stellate, or small round cells. The
intertubular growth, by its pressure
and contraction, causes atrophy of the
tubes, which in some ]3laces are obliter-
ated, in others irregularly distended,
and they contain degenerated epithelial
products ; as the atrophy proceeds the
intertubular tissue becomes filled with
granular and fatty debris. Tlie walls
of the small arteries ' become thickened
by hypertrophy of all their coats, espe-
cially the middle, but they have an ir-
regular outline. The firm, dense mass
of connective-tissue between the Mal-
pighian tufts completely obliterates the
expanded uriniferous tubules, bringing
the tufts much nearer to each other
than in the normal kidney, but it does
not as a rule obliterate them. The
shrinking and even total disappearance
of the convoluted tubes near the tufts, cause the tufts to almost touch
one another. The Malpighian tufts are sometimes obliterated, but their
' Johnson regards induration of the arterial walls as due to an hypertrophy of the muscular coat : Gull
and Sutton regard it as a deposit of a hyal in-fibroid, or hyaline-granular mass infiltrating the walls of the
arterioles and capillaries. Cornil and Ranvier say it is neither : it is but a chronic arteritis to them, both
intima and adventitia being involved, i. e., endarteritis and periarteritis.
Fig 139.
Cirrhotic Bright"* Disease. Early.
Section from the Cortex of a Kidney in Cir-
rhosis.
A. Capsule of a Malpighian body thickened with
concentric layers of connective-tissue, con-
taining Jlat and round cells.
B. Vascular tuft of the glomerulus diminished in
size.
C. Aferent and efferent ressds of tvft.
D and E. Convoluted tubes in transverse and
longitudinal section — Epithelium, nearly
normal.
F. Small artery in longitudinal section, x 350.
570
DISEASES OF THE KID1S"BYS.
obliteration is usually due to the development of cysts. The cysts are often
"colloid cysts." '
Sometimes connective-tissue formations extend into the medullary por-
FiG. 140.
Cirrhotic Blight's Disease.
Section from tJie Cortex of a Kidney in advanced Cirrhosis.
A, A, A. Malpighian bodies with shrunken tufts and thickened capsules which fuse
with the intertubular connective-tissue.
B, B. Nearly obliterated convolvted tubes.
C, Small Arteries with thickened walls.
B. Convoluted tvbes containing colloid material, x 60.
tion, and more or less shrinking of the pyramids occurs as a result. It is
usually, however, confined to the cortical portion. Those tubes that retain
their normal diameter are filled with fatty, granular or colloid cells ;
and their lumen contains hyaline or colloid casts. Blood pigment often
stains the cells of the tubules. The tubules in an uncomplicated cirrhotic
kidney contain coagulated fibrin, which will be indicated by the presence
of hyaline casts in the urine : all the tubular changes are secondary.
The pelvis and calices are congested ; the submucous tissue is dense and
thickened ; sometimes the pelvis and calices are dilated. In the advanced
stage of this form of kidney degeneration the organs are very greatly dimin-
ished in size — their capsules exceedingly thickened, their surface finely
granular, and the vessels on the surface varicosed and much enlarged. The
1 Concerning colloid casts, Cornil and Ranvier state that " after inflammatory destruction of the nor-
mal cells of the convoluted tubules there are developed cells — not having the character of secreting cells —
but assuming the cubical or flat form ; these cells undergo colloid transformation and fuse into a colloid
mass, which is increased by the deposit of successive layers, while at the same time new cells at the perlph'
ery become colloid."
CIRRHOTIC BRIGHT'S DISEASE. 571
cortical substance is tough and fibrous ; the kidneys are of a red or buff color,
and usually a number of small cysts are scattered through their substance.
Etiology. — The two most common causes of this form of kidney degenera-
tion are gout and rheumatism. One of these causes is so frequently associ-
ated with its development that it has given the name of " gouty kidney "
to it. The constant and continued use of alcohol may be regarded as an-
other cause of cirrhotic kidney, for we not infrequently find this condition
of the kidney associated with cirrhosis of the liver ; and the same steady
and prolouged indulgence in the use of alcoholic drinks which produces
cirrhosis of the liver, may produce cirrhotic kidney. These are its three
principal causes.
It is occasionally met with in connection with lead poisoning. It has been
claimed that the passive hyperaemia of the kidneys which occurs in con-
nection with some forms of heart disease leads to the development of cir-
rhotic kidney. Cold, especially in a variable climate, exposure, poverty, and
bad hygiene are strong predisposing causes. It is met with most often in
and after middle life. Active brain workers are more liable to it than
those who are indolent and lihlegmatic.
Symptoms. — The early symptoms of the cirrhotic form of Bright's disease
are always obscure. It is so insidious in its development that its commence-
ment can rarely be determined One of its earliest and most constant signs
is a frequent desire to pass urine, which may contain neither albumen nor
casts. Dropsy may be absent, and there may be none of the symptoms
which usually mark the presence of kidney disease. Tiiere may be only
ill-defined nervous symptoms during life, and yet at the autopsy extensive
cirrhotic degeneration of the kidneys may be found.
Usually the disease is developed in the following manner : an individual
notices that he is growing feeble without any apparent cause ; he is suffering
from dyspeptic symptoms ; he notices that he is passing a larger quantity
of urine than normal, and perhaps at the same time there will be a slight
swelling of the lower extremities after prolonged exertion, such as stand-
ing or walking. This oedema comes and goes, is more marked at night on
retiring, and disapjDears in the morning on rising. The complexion assumes
a dingy hue. His disposition changes, he is morose, fretful, and his mem-
ory is treacherous. Insomnia and headache are tormenting, and there
may be sudden loss of sight. The appetite is lost or is capricious. It is
for the relief of their dyspeptic symptoms that this class of patients usu-
ally consult a physician, and a plan of treatment is adopted for their
relief, with the assurance that they will be better as soon as they can leave
off work and take rest. A single or repeated examinations of the urine
may fail to detect either albumen or casts, and the promises of speedy re-
covery become more positive. The case goes on ; the patient becomes
more and more feeble, he has a careworn look, the complexion is altered,
the eye has a peculiar expression on account of the oedema of the conjunc-
tiva, nervousness and restlessness increase, and insomnia becomes con-
stant ; suddenly under great excitement convulsions occur and the indi-
vidual passes into coma, remains insensible for twenty four hours and dies.
672 DISEASES OF THE KIDNEYS.
Perhaps the urine was examined the day before the convulsion and no al-
bumen was found ; but if it is examined at the time of the seizure both
albumen and casts are present.
The three prominent symptoms of this form of Bright's disease are
changes in the urine, the dropsy and the nervous phenomena.
The urme is increased in quantity and of low specific gravity. It is
characteristic of the urine in this form of Bright's disease that albumen is
sometimes present and sometimes absent. In the other forms, albumen is
always found in greater or less quantities. It may be necessary to examine
several specimens before casts will be found, but when found, they usu-
ally are of the large hyaline variety ; granular casts are infrequent ; often
several examinations of the urine are necessary before any satisfactory evi-
dence of the disease can be obtained.
Dropsy is never very marked. Slight oedema of the feet and ankles after
exertion is present in most cases. When oedema of the feet and ankles is
constant, and is associated with the general symptoms and conditions of the
urine which have been described, the diagnosis is readily made. When as-
cites is present, it is due to changes which have taken place in the liver
rather than to those in the kidney.
Its most prominent symptoms are associated with its nervous phenomena :
they come and go in a manner not well understood. The earliest and
most constant is headache, which is often violent ; occurring as it very
commonly does with gout and rheumatism, it is very apt to be regarded as
gouty or rheumatic in character. With these headaches there is more or
less disturbance of nerve function, such as vertigo, temporary inability to
speak, loss of sight and hearing, diplopia, myopia, presbyopia — numbness,
neuralgic pains, muscular cramps, chorea, temporary and partial paraly-
sis in one arm or leg, hemiplegia or paraplegia. Nervous dyspnoea is not
uncommon, and it may be accompanied by " Oheyne-Stokes' respira-
tion." There may be confusion of thought or impairment of memory; con-
iBrmed mania may be developed. TJraBmic vomiting inducing great prostra-
tion, and angemia — unaccompanied by dropsy — are alarming symptoms.
There may be excessive itching of the surface. These patients are al-
ways liable to convulsions after severe mental or physical exertion ; from
the convulsions they may pass directly into coma, or become delirious,
with a brown, dry tongue, dilated pupils, and thus gradually become
comatose.
It is always important to remember the dangers to which these patients
are constantly exposed. Cardiac hypertrophy is present in a greater or less
degree in the advanced stage. The hypertrophy is usully confined to the
left ventricle. The presence of left ventricular hypertrophy without val-
vular insufficiency is sufficient to direct attention to the kidneys. If, in
connection with the cardiac hypertrophy the urine is abundant and of
low sijecific gravity, containing only a trace of albumen, the evidences of
contracted kidney are almost positive. Many theories have been advanced
to explain the connection between cardiac hypertrophy and the cirrhotic
kidney ; some regard it as purely mechanical, produced by '*the obstruc-
CIRRHOTIC BRIGHT'S DISEASE. 573
tion to the renal circulation and the consequent increased pressure in the
aorta;" but there is no conditio /i ot renal obstruction that will explain
the hypertrophy. Otliers claim that the walls of the renal and of all
the other arteries progressively hypertrophy from the altered condition of
the blood and the retained urinary excretion, until the heart becomes
hypertrophied as "a result of the antagonism of forces." The order of
its occurrence seems to be, first, capillary resistance ; second, high arterial
tension ; third, cardiac and arteriole hypertrophy.'
Amaurosis is a frequent attendant of cirrhotic kidney ; the loss of sight
comes on gradually ; one eye only may be affected, but usually both eyes
are equally involved ; the cause of the loss of sight is a true neuro-retini-
tis, which can readily be recognized by an ophthalmoscopic examination.
The optic papilla is cloudy and swollen ; the retinal veins are distended
and tortuous, and there are white patches on the retina. White dots and
streaks in the perimeter of the macula lutea, are thought to be character-
istic.
Differential Diagnosis. — This variety of Bright's disease may be mistaken
for diabetes. The thirst, the large quantity of urine passed, the dyspeptic
symptoms, the progressive emaciation, the absence of casts and albumen
lead toward diabetes ; but the low specific gravity of the urine and the
absence of sugar soon settle the question. The presence of a gouty or
rheumatic diathesis, the insidious development of the disease, the large
quantity of urine, its low specific gravity, with little or no albumen and
only occasional casts, are sufficient to distinguish this from the other forms
of Bright's disease.
Prognosis. — When the anatomical changes which characterize this form
of renal disease are once established, their tendency is to progress ; and
although a long period may elapse between their commencement and the
fatal termination, yet whenever there is reason to believe that the morbid
processes are advanced the patient is constantly in danger from complica-
tions. Serous inflammations are not as liable to occur as in other varie-
ties of Bright's diseases, but mucous inflammations are more frequently
met with, especially bronchitis, which assumes a chronic type.
Its complications are pericarditis, pneumonia, acute and chronic bron-
chitis, pleurisy, chronic gastric and intestinal catarrh, cirrhosis of the
liver, atheroma and sclerosis of arteries, eczema, and psoriasis. In its
advanced stage hemorrhages from mucous and serous surfaces, as well as
into the substance of organs, are liable to occur. The most serious of
these hemorrhages are the cerebral. It is more frequently associated with
cerebral apoplexy than any other form of kidney disease. Hemorrhages
in the retina are common.^ It must be remembered that inflammation of
the uriniferous tubes may be ingrafted upon cirrhotic kidney, and that
the three forms of degeneration may be present in the same kidney.
' Dickenson regards the vascular lesion? as partly hypertrophy, and partly fibroid.
2 In 100 cases reported by Mahomed seventeen died of heart disease and fifteen of apoplexy, i. e.,
thirty-two per cent, of cardio-vas-cular changes. Of thirteen who died of surgical diseases, he says many
died indirectly from failing heart. Eighteen died of lung diseases (eleven from severe bronchitis and
emphysema, and seven from pleurisy and pneumonia).
57-± DISEASES OF THE KIDNEYS.
Treatment. — In this form of kidney disease no special plan of treatment
can be adopted. It has been claimed that the long-continued administra-
tion of mercury in small doses has the power to arrest or prevent connec-
tive-tissne dcTelopment, but there is no evidence that it has such power ;
besides, in most instances, cirrhotic kidney is developed in connection with
a gouty or rheumatic diathesis which most positively contraindicates the
prolonged use of mercurials. When it is developed in connection with lead-
poisoning, mercurials are most decidedly contraindicated. Mercurials can
be employed with possible advantage only in those cases in which cirrhotic
kidney is developed in connection with a cirrhotic liver. The bichloride
is the preparation -usually employed in such conditions. If the disease de-
velops in connection with gouty or rheumatic manifestations, the same
means which are employed to relieve gouty or rheumatic articular manifes-
tations will afford relief.
Many of these patients will derive great benefit from residing for a time in
those localities where they may constantly use water from alkaline springs.
The Germans and French recommend very extensively the use of alkaline
waters in the treatment of this class of diseases. Milk, skimmed milk, and but-
ter-milk have all been vaunted as possessing curative pro23erties ; hence the
once famous "milk cure." Although these patients appear anaemic, their
nervous symptoms are aggravated rather than relieved by the use of iron.
In a certain proportion of cases cod-liver oil will be found of service, espe-
cially when combined with the hypophosphite of soda ; diuretics are not
indicated, but when a marked diminution in the urinary secretion occurs,
their temporary employment may be of service. When the disease is devel-
oped in connection with cirrhosis of the liver, an occasional hydragogue
cathartic may be attended with benefit. It is of the utmost importance
that this class of patients should make a permanent residence in a warm
climate, and that all the exciting causes of cirrhotic development should
be carefully avoided. Although a cure cannot be hoped for, the progress
of its development may be delayed, and by carefully watching the condition
of the nervous system, and by timely interference, the development of the
graver forms of nervous disturbance may be delayed or prevented, and the
life of the patient prolonged. For symptoms or complications that demand
a narcotic or anodyne, opium is to be used in preference to all others. In
its advanced stages, inhalation of oxygen has caused disappearance of albu-
men. '
Whenever there is extensive general anasarca, and the respiration be-
comes impeded by cedema of the chest-walls, or by an oedematous condition
of the lungs, and all other means have failed to relieve the drojjsy, prompt
and sometimes permanent relief may be afforded by making free incisions
through the skin into the areolar tissue above the ankles, or by pricking
the parts with needles in many places.^ Those dyspeptic and gastric symp-
toms which are so obstinate and distressing can usually only be relieved by
a carefully regulated diet.
1 Dajardin-Beaumetz.
* See London Lancet, 1877, i. 649. Southey uses drainage tubes in anasarca.
WAXY KIDNEY.
575
WAXY KIDNEY.
(" Amyloid Form " of Bright' s Disease.)
Amyloid degeneration is always chronic ; it has no acute stage, and
usually invades several organs of the body simultaneously ; when the kid-
ney is the seat of this degeneration its tissues become infiltrated with amy-
loid material. Cornil and Ranvier found that waxy degeneration in the
kidneys was invariably associated with chronic parenchymatous nephri-
tis ; they are, moreover, convinced that the latter condition always pre-
cedes amyloid degeneration.
Morbid Anatomy. — The primary waxy changes take place in the walls
of the minute arteries ; secondarily the secreting tubes and cells are in-
volved. At first, when the walls of the vessels are principally involved, there
is little change in the appearance of the kidneys. They may be slightly
increased in size, firmer, and of a paler color than normal.
Upon section the Malpighian tufts appear more prominent than normal,
and present the appearance of gray translucent points, which reflect light
better than the surrounding tissue. Usually both the cortical and medul-
lary portions are simultaneously, but unequally, involved ; by the " iodine
test " the amyloid change, however slight, will become very distinct, and a
section under the microscope will show the change to be most marked in
the vessels in the Malpighian
tufts, the vasa recta and in the
middle coats of the small arteries.
In a more advanced stage of
the process the kidneys will be
increased in size, their capsules
be non-adherent, their surfaces
smooth and of a pale color with
stellate vascularity.
On section the increase in the
size will be found to be due to an
increase in the cortical substance,
which is denser than normal.
The medullary substance is but
slightly increased. The normal
anatomical outline of the cortical
and medullary portion is lost, the
Malpighian tufts are indistinct,
looking like little grains of boiled
sago, and the whole cortical sub-
stance has a peculiar waxy ap-
pearance. Under the microscope
an entire section will present a
shining yellow appearance, as if all the tissues of the organ were infiltrated
with amyloid material. The glomeruli, most of the arterioles, the small
Fig. 14 .
Waxy Kidney,
Section from the Cortex of a Kidney in commencing Amy
laid Degeneration.
A. Malpighian body. The lower part of the vasovlar
tvfi i,i the seat of the amyloid change.
B, B. Conholuted tubes 'containing hyaline and granulO'
fatty matter.
C, C. Arteries, with coats shmving waxy degeneration.
Z>, D. EjAthelium of convoluted 'tvbes containing granu-
lar and fatty matter. X 300.
576
DISEASES OF THE KIDKETS.
veins and the basement membrane of the tubules will be infiltrated.
The epithelial cells of the convoluted tubes are not infrequently flattened.
The contents of the tubes may be made up of broken-down epithelium and
fatty granules, mingled with a material which is fibrinous in its nature ;
this material will not, however, give the characteristic reaction of amyloid
matter. Fatty, granulo-fatty, and hyaline materials are found in all
cases in addition to the above. Usually the kidneys atrophy and become
very much diminished in size, sometimes less than one-half their normal
size; their capsules are adherent, their surfaces uneven, granular, and of
a pale color.
On microscopical examination it will be seen that the diminiition
in size is due to decrease of both the medullary and cortical portions.
The Malpighian tufts are large and prominent, and are grouped
together ; the small arteries are enlarged and at points are imper-
vious. On examination of sections from different portions of the kidney,
the tubules will be found at all points
more or less atrophied and their walls
collapsed ; some are obliterated ; the
blood-vessels will appear thickened, and
their outline will be more or less irregu-
lar. Iodine upon the degenerated Mal-
pighian tufts will give the characteristic
amyloid reaction. The degree of atrophy
may vary, but however extensive it may
be, by dipping a section in the iodine
solution, and microscopically examining
it with a low power, one will always
find abundant evidence of amyloid ma-
terial in the degenerated vessels and
tubes.
Etiology. — The primary cause of amy-
loid degeneration is still a vexed ques-
tion. It never occurs in those who
are in perfect health, and the circum-
stances under which it almost uniformly
occurs determine to a certain extent its
causation. It is most frequently met
with in syphilitic subjects. Another
frequent cause is prolonged suppura-
tion, especially when associated with
diseases of bone. A long-continued empyema may give as a result an amy-
loid kidney. It is not infrequently met with in those who die of pulmonary
phthisis, consequently chronic suppurative diseases of the lungs must be
ranked among its causes. Caries of bone, ulcers of the intestines, cancer,
and chronic rheumatism may induce it.
Symptoms. — The symptoms which attend the development of amyloid de-
generation of the kidney are never well marked. The usual manner of its
Fig. 142
Waxy Kidney.
Vertical Section from the Medullary Portion of
a Kidney in advanced Waxy Degeneration.
A, A. Collecting tubules containing fatty gran^
ules, B, and colloid matter, C.
D, D. Wall of tubules showing thickening and
irregularity, the result of waxy change.
Transverse and F longitudinal sec-
tion of blood-vessels with lumen nearly
obliterated by amyloid degeneration
of the coats. G. Ascending limb of
Henle^s loop, x 350.
E.
WAXY KIDNEY. 577
development is as follows : an individual who is suffering from tertiary
syphilis or some exhausting form of disease, notices that he is • losing
strength, that he is becoming more feeble than usual, and that he has less
mental and physical vigor than he is accustomed to have ; that he is trou-
bled with shortness of breath on exertion ; that he has an unusually pallid
countenance, and that there is a great increase in the quantity of urine
passed. He is obliged to rise two or three times during the night to pass
urine, and at times he passes large quantities. He also notices a fulness
of the abdomen which he has never before observed, and sometimes there
is a sense of weight in its upper portion. He may have detected a tumor
in the right and perhaps in the left hypochondrium. When he assumes
the recumbent posture, he must have the upper portion of the body ele-
vated to prevent dyspnoea. Doubtless the dysj^noea is partially due to the
anaemia and partially to the pressure caused by an enlarged liver and spleen.
Perhaps there is slight oedema about the ankles, especially at night. The
patient does not perspire readily, but when he does the perspiration has a
urinous odor. Certain articles of food, especially fatty substances, which
never before have disagreed with him, now give rise to dyspeptic symptoms
and he may have occasional vomitings.
This train of symptoms coming on in one who has been the subject of
any of the forms of disease to which I have referred, leads to the suspicion
that amyloid degeneration of the kidney is taking place. If, upon further
examination, a marked enlargement of the liver and spleen is found, and
the surface of the liver is smooth and its edges sharp, it is almost certain
that the amyloid form of Bright's disease exists. With these symp-
toms there will also be more or less fluid found in the abdominal cavity,
but its presence will be due to changes which have occurred in the liver and
not to changes in the kidneys. The blood is slightly altered ; the white
corpuscles are somewhat increased in number, and the red are diminished
and ill-defined ; in a large proportion of cases there is a peculiar cachexia
present which is almost characteristic. The patient has a pale, waxy com-
plexion, with little pigmentary deposits in the skin, particularly about the
eyelids. This cachexia is usually most marked in syphilitic subjects.
As in the other forms of kidney disease, there are three important symp-
toms to be considered. First, abnormal changes in the urine ; second,
dropsy ; third, nervous phenomena.
The urine is increased in quantity, the patient perhaps passing as much
as one hundred ounces in twenty-four hours. It is light colored, looking
very much like clear water, or it may have a slight amber color. It is of
low specific gravity, sometimes as low as 1.005. When tested for albumen
it will be found always to contain an appreciable quantity, never a large
quantity. The amount of urea excreted is but little if at all diminished ;
the urine will always contain casts, either large hyaline or fine granular, or
both, but tlie hyaline predominate. Casts of eitiier variety usually are
not abundant, and several examinations may be required before their pres-
ence or absence can be positively determined. Epithelial and fatty casts
are sometimes found.
37
578 DISEASES OF THE KIDNEYS.
Dropsy is never very marked in this form of Bright's disease. The gen-
eral anasarca which is so frequently met with in connection with paren-
chymatous nephritis, is never present. There may be slight oedema of the
feet, especially at night, and there may be fluid in the abdominal cavity.
The nervous symptoms are never very prominent. This class of patients
do not usually sufl:er very much from headache, and rarely have convulsions
or pass into coma. They usually die from exhaustion, or from some com-
plication, or, in other words, die from amyloid degeneration of other organs,
diarrhoea, the result of amyloid changes in the mucous membrane of the
intestine, or ascites.
Differential Diagnosis. — The diagnosis of this form of Bright's disease is
not difficult when it occurs as a late manifestation of syphilis. A copious
secretion of urine of low specific gravity containing little albumen and few
casts, in one who has a syphilitic history with an enlarged liver and spleen,
leaves little doubt as to the character of the kidney change. It is hardly
possible to confound the cachexia which attends this form of Bright's
disease with that of any other chronic disease, for a urinary examination
will give positive evidence of the renal disease, and it only remains to de-
termine its character, which is usually readily reached by the history of
the case. The large quantity of urine passed often causes the patient to
consult the physician with the idea that he has diabetes, but the urinary
examination soon settles this question.
Prognosis. — The duration of this form of Bright's disease is uncertain ;
it undoubtedly takes many years for the anatomical changes in the kidney
to reach the stage of atrophy, yet when waxy changes are once established
recovery is impossible. Eesulting as it does from a grave constitutional
cachexia, the causes which produce it are so often continuous that they are
only in a slight degree influenced by treatment.
The progress of the disease may sometimes be temporarily arrested, but
its usual course is steadily progressive to a fatal termination. Amyloid
degeneration of the kidneys may exist for many years, and yet the patient
enjoy a comparatively good degree of health. I now have the care of a
medical gentleman in whom the disease has existed certainly eight years,
yet he is in such good health as to be able to discharge the duties incum-
bent upon a large country practice.' An exhausting diarrhoea or an ab-
dominal dropsy is often the direct cause of death. Most of the com-
plications which occur are degenerative in character. Patients are not
especially liable to have pneumonia, bronchitis or pericarditis, or any of
the acute inflammations which occur in connection with other forms of
kidney disease^ Cardiac hypertrophy is rarely present in any stage of the
amyloid kidney. Its early symptoms are so obscure that it is difficult to
determine its average duration.
Treatment. — This is an incurable disease ; there are no known means for
arresting it or preventing its development. The same general principles are
to govern its treatment as govern the treatment of waxy degeneration in
other organs. First, if possible remove its cause, as diseased bones, pro-
1 Bartholow records a case where there was complete recovery from the waxy kidney.
PYELITIS. 579
longed suppuration, or purulent accumulations. If it occurs with syphilis
anti syphilitic remedies are indicated, always remembering that waxy de-
generation occurs only as a tertiary manifestation of syphilis, and that all
measures which have a tendency to debilitate the patient must be avoided.
Iodide of potassium and mercury are the most reliable remedial agents.
Both of these agents have gained some favor as remedies in the treatment
of Bright's disease, and there are those who employ indiscriminately one or
the other or both of them. The benefit derived in certain cases from their
use is undoubtedly due to their power over syphilitic manife.stations. In
such cases, the long-continued use of small doses of mercurials will gen-
erally be followed by marked improvement, but care should be exercised
that their use be not continued until the specific effect of the drug is
produced.
When these patients are in a debilitated condition iodide of potassium
with cod-liver oil will be of greater service. The form of iodine which I
have found most serviceable to this class of patients is pil. ferri iodidi.
One of these pills given three times a day, at the time of taking food, is
often followed by the most beneficial results. Diuretics and hydragogue
cathartics will rarely be required. The tincture of the perchloride of iron,
quinine, nux vomica, and sirups of the phosphates are often beneficial.
PYELITIS.
Pyelitis is an inflammation of the mucous membrane of the pelvis and
calices of the kidney, and may run an acute or chronic course. It may in-
volve the pelvis and infundibula of one or of both kidneys. Some describe
an acute catarrhal, pseudo-membranous, and calculous pyelitis and a
chronic purulent pyelitis that may or may not result in pyonephrosis.
Morbid Anatomy. — In acute pyelitis the mucous membrane of the pelvis
of the kidney is at first more or less reddened. When very hypergemic the
surface will be dotted here and there with little dark-red spots which are
minute ecchymoses ; the epithelium of the mucous surface is more or less
removed ; sometimes it is entirely removed, at others it is removed in
patches. The peculiar " tailed" cells of the pelvis are thrown off in great
quantity. As the inflammation progresses the mucous surface becomes
covered with more or less muco-pus. The urine in the |)elvis will contain
numerous desquamated epithelial and lymph cells.
In some cases a membranous exudation may be developed upon the
mucous membrane of the pelvis, called ^' pseudo-membranous" pyelitis.
It is a diphtheritic exudation occurring in connection with diphtheritic
exudations in other parts of the body, and should be called diphtheritic
pyelitis. This diphtheritic membranous exudation is liable to become de-
tached and block up the ureter. Sloughs may form, and after their re-
moval an ulcerated surface may be left.
In chronic pyelitis the mucous membrane of the pelvis of the kidney is
congested and thickened, and its surface presents small vascular granula-
tions. It assumes a grayish white or slate color and is traversed by dilated
580 DISEASES OF THE KIDI^EYS.
yeins ; the pelvis and infundibula and ureter are dilated and more or less
thickened. Pus is more or less abundantly formed, and if there is no ob-
struction it passes off with the urine. Calculi or fragments of calculi may
be found mingled with the pus.
Should there be an impediment to its escape it accumulates in the pelvis,
which it distends more and more, and at last gives rise to a condition
known as pyonephrosis. This dilatation as it progresses encroaches first
upon the papillae, which become flattened and obliterated, next on the
pyramids, and finally, by the pressure it causes, the cortical portion of the
kidney disappears. The apices of the pyramids may suppurate and ulcer-
ate. In such cases only a sacculated pouch remams containing from one
to several ounces of fluid, which may be mixed with inspissated pus, broken
down calcareous matter, ammoniacal products and calculi.
If a renal calculus is present, and the cause of the pyelitis, more or less
extensive ulcerations may be established. These ulcerations may cause
perforation of the pelvis, and give rise to extravasation of urine into the
adjacent tissues. In this (so-called) calculous pyelitis the kidneys are al-
ways the seat of interstitial nephritis, cysts, marked atrophy, etc. The
ureter of the kidney which is the seat of the pyelitis may be completely ob-
structed, and pus, blood, and urinous material may accumulate behind the
obstruction. If these obstructions are permanent an opening may be made
through the dilated ureter and the contents of the sac discharged into the
adjacent tissues, into some hollow viscus or into the abdominal cavity, or
by an adhesive inflammation reach the surface and be discharged externally.
When the obstructions are temporary the contents of the sac are dis-
charged into the bladder through the ureter when they give way, and such
obstructions or accumulations may occur repeatedly. Sometimes these re-
tained accumulations undergo entire absorption, and there remains a thick
cicatricial tissue, with the normal kidney tissue entirely obliterated, and
the ureter becomes transformed into a tendinous cord. Under such cir-
cumstances if the fellow kidney is healthy it becomes increased in size and
performs in a very satisfactory manner the function of both kidneys, and
the patient may live for many years. Again, in certain cases, the accumu-
lation in the kidney is changed into a cheesy material, and presents an ap-
pearance resembling what is known as tubercular kidney. Mingled with
this cheesy mass may be found the urine-salts which cause it to have a
sandy feel The kidney may be changed into a fibrous shell containing
pus and debris.
Etiology. — Pyelitis is seldom, if ever, a primary disease. Its most fre-
quent cause is the presence of calculi or some foreign substance in the
pelvis of the kidney, and the pyelitis is then secondary to mechanical irri-
tation. Pyelitis may result from extension of inflammation from the
bladder or ureter, or from acute interstitial nephritis, rarely from perine-
phritic abscess. It may result from the irritation produced by the decom-
position of urine retained in the pelvis of the kidney, as a consequence of
some obstruction to its normal outlet. For instance, an enlarged prostate
gland, a tumor pressing on the ureter, paralysis of the bladder, or an
PYELITIS. 581
urethral stricture which causes obstruction to the passage of urine from
the bladder. As a result of retention of urine in the bladder, cystitis is
developed, and the inflammation of the mucous surface of the bladder may-
extend to the ureters, and from the thickening of their mucous lining and
the diminution of their calibre, the passage of urine from the kidneys to
the bladder is obstructed, and there is not only retention of urine in the
bladder but also in the pelvis of the kidneys. As a result of such retention
the urine undergoes decomposition, the urea is changed into carbonate of
ammonia and vs^ater, the carbonate of ammonia acts as an irritant and ex-
cites inflammation of the lining membrane of the pelvis, and thus pyelitis
is developed.
The absorption of the ammonia resulting from the decomposition of the
urea may be sufficient to give rise to a condition which has received the
name of ammonmmia. This condition is not infrequently mistaken for
uraemia, yet they differ widely in their manifestations and the dangers
which attend their development. In ammonsemia the urine when voided
isammoniacal, as are also the breath and perspiration. The mucous mem-
brane of the mouth is dry and shining; the complexion is sallow and there
is increasing emaciation ; no dropsical accumulations are present. Con-
vulsions and vomiting are rare ; chills are frequent. Death is usually pre-
ceded by coma. The development of the train of symptoms indicative of
ammonsemia, accompanied by the evidence of obstruction to the normal
outlet of the urine, should cause one to hesitate before performing any
operation, especially an operation for relief of stricture of the urethra.
Pyelitis not infrequently occurs in connection with that class of diseases
which depend upon blood poisoning — pyaemia, diphtheria, and typhus
fever. In this connection it is generally a complication of acute Bright's
disease, which is not severe in character, but which causes bloody urine.
It is an almost diagnostic complicating symptom of myelitis. Pyelitis
occasionally occurs in consequence of over-doses, or the prolonged use, of
certain irritating drugs, as turpentine, cantharides, and other stimulating
diuretics. In very rare instances it seems to come on idiopathically from
exposure to cold and wet, or from some unknown cause.
Symptoms. — In the majority of cases the development of pyelitis is pre-
ceded or accompanied by symptoms due to the causes which produce it,
such as renal calculi, diseases of the bladder, etc' Prominent among those
symptoms which directly attend its development is pain in the back. This
is present in the mild as well as in the severe cases. This pain may have
its point of maximum intensity over one or both lumbar regions. It is
often of an aching character, and shoots down along the course of the
ureters. This pain is usually accompanied by frequent micturition, and
when it is very intense the voiding of urine is almost incessant and is
attended by severe pain. The commencement of acute pyelitis is usually
marked by rigors, and in that chronic form in which temporary obstruc-
tion of the ureter occurs, rigors are frequent.
1 It is said (Klebs) that bacteria may be carried into the bladder on unclean catheters or other instrut
mente, and that these, making their way into the pelvis, cause pyelitis.
582 DISEASES OF THE KIDNEYS.
Symptoms of hectic fever may also mark the occurrence of permanent ob-
struction of the ureter and the development of that condition termed />yo-
neplirosis. There is usually considerable lassitude attending the progress
of pyelitis, and when the disease is due to the presence of a calculus, the
patient ordinarily sufEers more or less pain on motion.
All of these symptoms are accompanied by changes in the urine, and
these changes are its most reliable signs ; — in its early stage the urine con-
tains blood mixed with mucus and epithelial cells from the pelvis and in-
fundibula : the presence of these epithelial cells, which are readily distin-
guished from epithelium of any other portion of the urinary tract by their
characteristic shape and appearance,is its most certain diagnostic indication.
The specific gravity of the urine ranges from 1.025 to 1.030, and it usually
retains its acid reaction. In the more advanced stages the characteristic
epithelium is to a great extent replaced by an abundance of pus cells, but
the urine retains its acid character. If sacculation of the kidneys is devel-
oped, the urine will become ammoniacal. More pain and hemorrhage at-
tend calculous pyelitis than the other forms. Albumen is present in pro-
portion to the amount of pus and blood. In the advanced stage of pyelitis,
if the urinary channels remain free the discharge of pus is constant. If the
ureter becomes blocked, for a time the urine may be quite normal, but the
removal of the obstruction is followed by a copious flow of purulent urine.
This may be repeated from time to time, at intervals varying from a few
days to a few months. If the pelves of both kidneys are affected, and there
is partial or complete obstruction of one side, the accumulation of pus in the
urine is diminished, but not entirely prevented. If the obstruction is long
continued or becomes permanent, a tumor develops in the lumbar region.
The development of d^pyonephrotic tumor indicates complete obstruction
of the ureter. The existence of the tumor is determined by the presence of
bulging between the crest of the ilium and the false ribs on the right or left
side, according as the right or left kidney is involved. As a consequence
the outline of the abdomen is rendered unsymmetrical. On palpation, deep-
seated fluctuation is felt over the tumor, which usually is tender on press-
ure. The area of percussion dulness will correspond to the outline of the
tumor, except where it is crossed by the colon. With these physical signs
present, and a history of pyelitis, one will be justified in resorting to the
exploring trocar to complete the diagnosis.
Differential Diagnosis. — The diagnosis of pyelitis in its first or acute stage
rests almost exclusively on the presence in the urine of the characteristic
epithelium of the pelvis and infundibula mixed with blood globules and
mucus. If the urine contains pus cells mixed with these epithelial cells it
indicates a more advanced stage of the disease. The presence of pus and
acid urine, with pain in the lumbar region, accompanied by the develop-
ment of a tumor at the seat of pain, which tumor gradually increases in
size and suddenly disappears at the same time that a copious discharge of
pus takes place from the bladder, which discharge is attended by a sense of
great relief to the patient, renders the diagnosis of pyonephrosis very cer-
tain. If the ureter of the affected kidney is permanently obstructed, the
PYELITIS. 583
lumbar tumor is liable to be mistaken for Jiydronephrosis, an hydatid cyst,
or Q. perinepJiritic abscess.
In perinephritic abscess neither pus, blood, mucus, epithelia nor albu-
men will be found in the urine ; in pyonephrosis they are common and
constant. Pain on motion, the occurrence of slight oedema over the tumor,
the delayed appearance of fluctuation — these are in contrast to the symp-
toms of pyonephrosis. The mass of tumor in perinephritic abscess may be
tilted forwards by pressure in the renal region, which is never the case with
pyonephrosis.' Fever is a marked symptom in abscess, and slight or absent
in pyoDephrosis. In women a pyonephrotic tumor has been confounded
with an ovarian cyst. The exploring trocar will very quickly remove all
doubts.
Pyelitis is distinguished from cystitis by absence of vesical pain and fre-
quent micturition, by lumbar pain, and by the intimate admixture of for-
eign materials in the urine. Pelvic epithelial cells are not found in the
urine of uncomplicated cystitis. In pyelitis the urine is acid ; in cystitis
it is alkaline. When pyelitis occurs as a complication of chronic cystitis,
an enlarged prostate gland, or urethral stricture, it is often impossible to
diagnosticate its existence if there is no tumor in the lumbar region. Under
these circumstancesthe character of the urinary constituents is not of much
assistance. If, however, the quantity of pus is large, the urine slightly
acid, the loins painful on pressure, and the febrile movement constant,
with rapid loss of flesh and strength, there is good reason to believe that
chronic pyelitis has been added to disease of the bladder and urethra.
Prognosis. — The prognosis in pyelitis depends upon the nature of its ex-
citing cause. In simple catarrhal pyelitis, not connected with extensive
disease of other portions of the urinary ajjparatus, the prognosis is good,
unless the disease affects both kidneys and has reached the purulent stage;
then, whatever may have been its cause, the prognosis is bad. When the
disease is confined to one side, recovery is possible, although one kidney
may be completely destroyed. We suspect unilateral layelitis with calculi
and with tumors that compress an ureter ; but following a cystitis, ure-
thritis, prostatitis, etc., the affection is usually bilateral, and the prognosis
is unfavorable.
Pyelitis may be regarded as a hopeless disease when it is secondary to an en-
larged prostate gland, extensive chronic cystitis, urethral stricture, creancer
of the kidney. It is exceedingly grave when it depends upon renal calculi or
hydatids, although it is not necessarily fatal. The issues of a pyonephrosis
are uncertain ; the various directions in which a sac may burst determine
to a great extent its termination. Eupture into the peritoneal or thoracic
cavity is speedily fatal. Kecovery is possible if the rupture takes place
externally or into the intestine. Sometimes, when the sac does not rupture,
patients die from the exhaustion caused by the long-continued discharge.
Eecovery may be reached by a gradual diminution of the discharge and a
final contraction and obliteration of the sac, provided the other kidney is
unaffected. Death may occur from uremia or ammonsemia.
1 London Lancet, January, February, March, 1879.
584 DISEASES OF THE KIDNEYS.
Treatment. — The first thing in the treatment of pyelitis is, if possible,
to remove its cause. If the attack is an acute one, and at the onset of the
disease the fever is considerable, the pain in the lumbar region severe, and
the urine bloody, wet cups should be freely applied to the loins, followed
by a hot bath, and a suflBciently large hypodermic of morphine to entirely
relieve pain. The patient should drink freely of alkaline fluids and should
be l\ept in bed.
In chronic pyelitis, when the secretion of pus is abundant, astringents
may be employed to diminish the purulent secretion. Balsams are here
indicated.! Attention should be paid to the general health of the patient.
Cod-liver oil and quinine should be administered with a nutritious and
non-stimulating diet. A residence at, and prolonged use of the waters of
some alkaline spring will often be found of great service. Diluent alkaline
drinks and milk should be the sole articles of diet in the acute stage.
When a tumor exists and can readily be reached through the integument,
aspiration may be performed, after which the question of a free permanent
external opening will present itself, and must be decided by the peculiarities
of the case.
ARTEEIO-CAPILLAET FIBROSIS, WITH CONTRACTED KIDNEYS.
Dr. Bright himself and most pathologists since his time noticed that
the granular contracted kidney, the ''small red kidney" of the English
writers, was usually associated with morbid changes in other organs, and
it was generally held that, under these circumstances, the kidney was the
organ primarily affected, and that tbe other changes were the result of the
cachexia produced thereby.
In 1872, Sir Wm. W. Gull and Wm. Henry Sutton'^ denied the correct-
ness of this latter opinion, and claimed that all the morbid changes,
those found in the kidney, as well as those of the other organs, were
equally dependent upon a fibroid degeneration of the walls of the smaller
arterioles and capillaries. To this degeneration they gave the name
arterio-capillary fibrosis, and while admitting that it commonly began in
the kidneys, they claimed that there was evidence of its primary appear-
ance in other organs, and also of its occasional localization elsewhere,
to the entire exclusion of the kidney. The theory then advanced has
been very thoroughly worked out by subsequent writers, whose arguments
and proofs are very strong, although, perhaps, not yet entirely demon-
strated. The supporters of this theory maintain the existence of a general
fibroid degeneration usually occurring during, or after middle life, but
sometimes also at earlier periods, and deserving to be classified with the
other recognized degenerations, the fatty, amyloid, etc.^ The morbid
changes peculiar to this degeneration have long been recognized by patholo-
gists, as have also the corresponding clinical facts, but the connection be-
1 TJva ursi, buchu, copaiba, pareira brava, and sandal-wood oil are regarded as beneficial, and are to be
given with allialine waters.
^ Medico-Chirurg. Transactions, 1872.
3 Mahomed, London Lancet, August, 1877.
ARTERIO-CAPILLARY FIBROSIS, WITH CONTRACTED KIDNEYS.
585
tween them was not understood. It is this connection, this grouping to-
gether, with a more detailed knowledge of the minute changes, that con-
stitutes the theory.
The cause of the degeneration is attributed to some form of blood-
poisoning, either temporary or chronic, such as gout, alcoholism, preg-
nancy, scarlet fever, lead poisoning, and certain forms of dyspepsia, mal-
assimilation and functional disorders of the liver, which act by producing
first a functional and then an organic increase of the arterial tension.
The pathological changes consist in a general increase in the amount of
fibroid tissue throughout the body, especially marked in the excretory
organs, together with hypertrophy of the left and dilatation of the right
ventricle. The increase of fibrous tissue usually begins in the outer coat
of the smallest arteries, and spreads thence through the connective-tissue
stroma of the organ involved. It is seen under the microscope as a more
or less thick granular and generally structureless (" hyalin-fibroid ") border
on the outside of the vessel staining deeply with carmine. The inner coat
is also sometimes much swollen, granular and thickened. In the capillaries
the new tissue is granular and without any fibroid appearance. According
to Gull and Sutton the muscular coat of the artery is atrophied. The re-
sult of these changes is to diminish the calibre and destroy the elasticity
of the vessels. This alteration in the vessels is the primary and essential
morbid process ; by its reaction upon the heart and by its spreading to
the adjoining tissues, it produces the following secondary changes. By
the formation and retraction of
new connective-tissue, especially
in the kidneys, gastro-intestinal
tract, and skin, these organs di-
minish in size and lose more or
less of their granular epithelial
elements.
The lungs are firm with promi-
nent bronchi and often show well-
marked vesicular emphysema.
There is atheroma of the aorta
and of the cardiac valves, opacity
of the arachnoid, and increase
in the amount of the sub-arach-
noid liquid.
The kidneys are small, red,
and granular with adherent cap-
sules, and with small cysts scat-
tered through them. This con-
dition of the kidney must be
distinguished from the mixed
or yellrnv granular kidney, which,
according to this theory, is either
a large white kidney that has shrunk and become granular, or else is the
Fig. 143.
Arterio-Capillary Fibrosis.
Section from the Cortex of a contracted Kidney, showing
two Glomeruli.
A. Capsule of a Malpighian body thicTcened with lamin-
ated connective tissue.
B. Vascvlar tuft deqenerated into a fibrous nodule.
C. Capsule of another Malpighian body, ivith fibrous
tMclcfning, smaller in amount than at A.
D. Vascular tuft, adherent to capsule, with round cell
infiltration. _
E. Nucleated fibrous tissue surrounding the atrophied
glomeruli, x 300.
586 DISEASES OF THE KIDISTEYS.
consequence of an attack of acute parenchymatous nephritis supervening
upon the chronic interstitial change. The microscopical appearance of the
kidney is such as has been described in interstitial nephritis. There is
increase of intertubular connective-tissue, especially around the Malpighian
bodies, and in and around the walls of the minute arteries. The urinif-
erous tubules present all the degrees or changes between an almost com-
plete destruction and the normal condition. The changes when found seem
due to a fibroid thickening of the wall of the tubule, with destruction of
the epithelium and diminution of the lumen of the tube, although some-
times the tubes are irregularly dilated. The importance of the granular
condition of the epithelium is claimed by Gull and Sutton to have been
greatly exaggerated, and they attribute this appearance either to post-mor-
tem change, or to a simple venous congestion preceding death. The in-
crease in the amount of intertubular connective-tissue and the thickening
of the walls of the minute arteries have been long recognized, but the
interpretation given to the latter change has been explained differently
heretofore, and its general distribution has not been known. It was sup-
posed to be due to an increase of the muscular coat, and to indicate an in-
creased ability on the part of the vessels to propel the blood through them.
According to the present view, the change is entirely different, and the
flow of blood is impeded by the diminution of the lumen and the lack of
elasticity in the wall of the vessel. The hypertrophy of the heart, which
is found so constantly in connection with the small red kidney, is readily
explained on this theory. The heart is called upon for greater effort, in
order to overcome the obstruction to the blood-current created by the change
in the arterioles and capillaries, and, as in the case of other muscles, the
heart increases in size and strength to meet the additional calls made upon
it. The increase of arterial pressure is also felt within the heart, and ulti-
mately produces the other changes seen upon the valves, changes which are
found at the points subjected to great pressure.
This explanation is in harmony with the following facts observed by Gull
and Sutton : hypertrophy of the left ventricle existed in all cases in which
the vessels were generally thickened by the hyalin-fibroid change, and its
degree varied directly with the degree or the extent of the change. They
argue that it is due not to renal disease, but to the morbid changes in the
vessels, because (1) it is often absent in cases of large white kidney, in
lardaceous disease, and in scrofulous pyelitis with almost complete destruc-
tion of the organ ; (2) whenever hy23ertro23hy of the heart coexisted with
large white kidney the hyalin-fibroid change was also present ; and (3)
hypertrophy is found at a very early period of the kidney affection when
the excretory function is not greatly altered.
Symptoms. — The symptoms vary with the organ chiefly affected and the
period of the disease. The first in order of time, and the one upon which
Mahomed places the most reliance as a means of diagnosis is the in-
crease of arterial tension, recognized by the pulse, or better by the sphyg-
mograph. During this stage, if the pressure has increased rapidly, dropsy
and albuminuria may be present, but ordinarily these two symptoms denota
AKTERIO-CAPILLARY FIBROSIS, WITH CONTRACTED KIDNEYS. 587
accompanying epithelial change in the kidney or an exaccrljation in the
progress of the disease. Albuminuria is not itself a symptom of arterio-
capillary fibrosis with contracted kidney ; on the contrary, the affection
may run its course without the aj)pearance of this symj)tom. In such
cases the vascular changes have involved other organs, and have left the
kidney unchanged or but slightly affected ; such patients die with symp-
toms of pulmonary or gastro-intestinal troubles or of cerebral hemorrhage
or aneurism.
The condition begins as a diathesis in early life, gaining ground every
year, and betraying itself by the pulse, pulmonary emjDhysema, or dyspep-
sia, and if at any time a serious exacerbation occurs death may be caused
with symjDtoms referable more directly to the kidneys.
Diagnosis. — The diagnosis, therefore, is to be made mainly by a considera-
tion of the character of the pulse, and it is claimed that heretofore, in the
majority of cases, the disease has passed unrecognized,' the diagnosis being
made only when the kidneys were sufficiently involved to give rise to
albuminuria. The important point, therefore, is to recognize the condition
of high arterial tension. The sphygmograph alone can always do this
with certainty, but careful examination of the heart and pulse will usually
suffice. The pulse of high pressure has been variously described as hard,
cord-like, persistent, long or slow. The most constant and characteristic
quality is that designated as persistent or slow (not infrequent). The
artery feels full under the finger during diastole as well as systole of the
heart, and its systolic expansion is prolonged, — the so-called pulsus tardus,
shown on the sphygmograph by a prolongation of the elevation of the trace.
The heart signs of high arterial pressure are, according to Mahomed, a.
long or reduplicated first sound heard over the inter-veutricular septum,
and an accentuated second sound.
The following conclusions, taken from Grull and Sutton's first paper and
Mahomed's last upon the subject, present the points in convenient form.
There is a disease characterized byhyalin-fibroid formation in the arterioles
and capillaries, attended with atrophy of the adjacent tissues. This morbid
change in the vessels is the primary and essential condition of the morbid
state called arterio-capillary fibrosis with contracted kidney. The kidneys,
however, may be little if at all affected, while the morbid change is far
advanced in other organs. The blood condition which produces the high
arterial pressure is the primary condition, and is not secondary to deficient
renal excretion as heretofore held. The cardio-vascular changes, when
found alone, may be taken as evidence of the existence of the disease. The
condition of high pressure is almost constantly present in old age, and in
one form or another brings about a large proportion of the deaths of those
over fifty years. Tlie existence of high arterial tension in the pulse of
young persons indicates a diathesis, and is of grave importance. The same
1 Mahomed says: "How often patients are allowed to die— nay, more, even killed— when their
hearts are failing from the terrible arterial pressure they can no longer overcome. Their flagging, over-
taxed ventricles dilate ; the wretched, feeble, laboring pulse is thought to mean weakness which requires
stimulation, its persistence (indicating over-distention) is passed unnoticed, and the struggling heart,
failing at last in its work, stops and the patient dies for want of a lancet or purge."
688 DISEASES OF THE KIDNEYS.
condition being of frequent occurrence after the age of fifty is not of such
great importance, unless present in an excessive degree. It then produces
serious symptoms and calls for active treatment.
ACUTE SUPPUEATIVE INTERSTITIAL NEPHRITIS.
{Surgical Kidney.)
Morbid Anatomy. — The kidney is intensely hypersemic, softer than nor-
mal, and the fat about it is oedematous. When the thickened and opaque
capsule is stripped off, pus often flows from beneath it. The surface shows
arborescent injection.
On section, several purulent foci are seen in the cortex and pyramids,
about the size of a pea ; these, coalescing, may form a large abscess. When
pygemia is its cause, the abscesses are wedge-shaped, and colonies of bacteria
are found surrounding the shreddy necrotic tissue, and in the centre of
the suppurating mass the epithelium is cloudy and desquamated. Cell-
infiltration takes place in the adjacent connective-tissue, and secondary
thrombi are found in the small veins. Micrococci are found in the arteri-
oles.' When the abscesses are wedge-shaped they are called "^ metastatic;^'
but when circular they are merely spots of "suppuration in foci."
In cJironic suppurative nephritis, decomposing pus, calcareous salts, and
a serous, fetid fluid are contained in a sac whose wall is connective-tissue.
With these (so-called) chronic abscesses, cysts and renal atrophy are present.
In large pysemic or non-pygemic abscess ulceration may take place at the
tips of the pyramids, and the abscess may open into the pelvis, the intestine,
externally, or into the peritoneum. The liver has been involved from the
breaking of a renal abscess into its softened parenchyma (Rayer).
Diffuse purulent infiltration " is of rare occurrence ; then the whole kid-
ney seems to be a mass of pus ; the surface and cut section are homogene-
ous looking. Pus is readily scraped off, and ecchymoses are seen studding
its surface.'
Etiology. — Any of the causes of pyelitis may be, secondarily, causes of
surgical kidney. Pyaemia, ulcerative endocarditis, typhoid fever, and puer-
peral fever may be complicated by it. Wounds, blows, and severe contu-
sions cause it. Eeflex irritation and some, as yet unknown, nervous con-
ditions are supposed by many to be the cause. Certain spinal diseases are
attended by it, — perhaps from disturbance of "trophic influences."
Symptoms. — There is lumbar pain, tenderness on pressure over the kid-
ney, recurring chills, fever, languor, anorexia, emaciation, perhaps diar-
rhcBa, nausea and vomiting ; the mouth and skin become clammy, sordes
may collect on the teeth, the breath becomes offensive, and there is drowsi-
' This is Kleb's parasitic nephritis ; the infecting particles or spores ascend ("presumably from the blad-
der) to the pelvis thence up the tubules. Hyaline casts in " parasitic nephritis " have spores and algse on
their periphery. Coriiil and Ranvier think they may be formed in the kidney during life.
2 Full descriptions are given in Ei'ichsen's Surgery, p. 712, etseq., vol. ii.
3 Marcus Beck (in " Qiiain's Diet, of Med.," pp. 1563-5) describes acute interstitial nephritis without eup-
pnration as one variety of the surgical kidney ; infiltration of small round cells in the intertubular struc-
ture and about the Malpighian tufts being the chief pathological event. An acute or sub-acute interstitial
(non-suppurative) nephritis I have already described.
HYDRONEPHROSIS. 589
ness whicli rarely passes into coma.' These symptoms (especially the chills
and febrile movement) are often severe, and then the disease is of short
duration. The patient passes rapidly into a state of stupor without con-
vulsions and with a subnormal temperature. The urine may be in excess
of the normal quantity or be scanty ; albumen is present in varying quan-
tities ; hyaline and pus casts and renal epithelia are also present in A^arying
amounts. Blood is always found in the acute cases. The specific gravity
is never very high. The urine is in many cases ammoniacal. Should a
tumor be felt, it will fluctuate ; but rarely is there a distinct tumor.
Differential Diagnosis. — From pymmia it is distinguished by the absence
of recurring chills and sweats ; by its lower temperature ; by absence of
joint and lung symptoms, and by the purulent bloody urine. It is often
diflScult to distinguish it from septiccemia.
A perinephritic abscess is distinguished from suppurative nephritis by its
tumor, and by the fact that in uncomplicated perinephritis urinary symp-
toms are absent.
Pyelitis has the characteristic angular "■ tailed " cells from the mucous
membrane of the pelvis in the urine, and the constitutional symptoms are
insignificant compared with those of suppurative nephritis.
Prognosis.— The prognosis is always grave. The free discharge of a large
abscess may prolong life, and, if unilateral, be followed by recovery. Death
from complications is its frequent termination. In the aged it is almost
necessarily fatal. Asthenia, ursemia, and complications cause death.
Treatment. — The treatment is for the most part surgical. Tonics, stim-
ulants, and condensed nutriment are indicated from its onset. A pure milk
diet is advantageous. Dry cupping, fomentations and poultices or leech-
ing over the loins are of service. The bladder is to be washed out with
quinine, Condy's fluid and sulphuric acid, or thymol water. Benzoic acid
or benzoate of ammonia may be given to relieve the offensiveness of the
urine.
HYDRONEPHEOSIS .
Hydronephrosis is a chronic, non-inflammatory affection of the pelvis
of the kidneys. Whenever the flow of urine through the ureters into the
bladder is permanently obstructed, the urine collects in the pelvis and in-
fundibula, compressing the renal substance, which becomes partially or
completely atrophied, so that after a time the kidney is converted into a
sac or pouch. This condition has received the name of hydronephrosis,
or dropsy of the kidney. The dilatation may affect the ureter and pel-
vis, or only the pelvis.
Morbid Anatomy.— In a kidney that is the seat of moderate hydronephro-
sis following simple dilatation of the pelvis, the papillse will become flat-
tened, hardened and shrunken, and gradually disappear. The remaining
portion of the renal substance gradually diminishes from the pressure and
becomes more or less tough and resistant. In extreme cases the kidney
substance finally entirely disappears and the kidney is converted into a large
1 There is a frequent desire to micturate. Suppression of urine may occur.
590 DISEASES OF THE KIDNEYS.
multilocular cyst ; sometimes it is unilocular. At times sucli a cyst at-
tains a size as large as a child's head ; there is a case recorded where the
whole abdominal cavity was occupied by an enormous tumor containing
sixty pounds of fluid. Some healthy kidney substance will nearly always
be found in its walls. That portion of the ureter which is the seat of dila-
tation may reach the size of a small intestine, has a blue-white color, its
walls become greatly thickened, and it may become convoluted.
The fluid contained in hydronephrotic cysts is generally altered urine.
It is much more watery than normal urine, containing more or less of the
urinary salts ; it may also contain blood, pus, epithelium and some albu-
men. Sometimes it is perfectly clear ; it is usually alkaline. Adhesions
frequently form between the enlarged kidney and neighboring organs.
Etiology.— Closure of a ureter which gives rise to hydronephrosis may
be due to compression by a tumor external to its walls, especially rectal or
uterine, or to the impaction of a calculus, blood-clot, or mass of echi-
nococci within it, or to inflammation which has caused adhesion of its
walls and complete obliteration of its lumen. A moderate degree of dila-
tation of the ureter sometimes results from obstruction to the free dis-
charge of urine from the bladder ; when this is the case the pelvic dilata-
tion is bilateral, and can never become very extensive without destroying
life, for when the pressure becomes equal to that within the blood-vessels
the urinary secretion is entirely suppressed. Congenital defects often
cause it.
Symptoms. — The symptoms of hydronephrosis depend upon the nature
of its cause and the extent of dilatation. If the sac is small and the op-
posite kidney healthy, there may be no symptoms to indicate its existence ;
there will be no diminution in the urinary secretion, as the healthy (usu-
ally hypertrophied) kidney performs the work of its diseased fellow.
There may be pain in the lumbar region.
As soon, however, as the tumor attains suflficient size to be readily felt,
the existence of hydronephrosis may be determined by it. This tumor
causes no pain or inconvenience except by its pressure. "With double hy-
dronephrosis ursemic symptoms may develop suddenly. The nephritic
tumor is fluctuating, usually lobulated, and gives a tympanitic resonance
in front on percussion unless the colon has been pushed aside. If the ob-
struction to the escape of urine from the kidney is temporarily removed,
its removal will be followed by a sudden diminution and disappearance of
the tumor, coincident with a sudden discharge of a large quantity of pale
urine. Such an occurrence is almost pathognomonic of hydronephrosis.
Constipation, from pressure of the tumor on some portion of the intestine,
is not infrequent.
Differential Diagnosis. — Hydronephrotic tumors may be confounded with
ovarian cysts, ascites, hydatid cysts, and pyonephrosis.
They are distinguished from ovarian cysts by the presence of the colon
in front of the tumors, by the absence of tympanitic percussion in the lum-
bar region, and by a vaginal and rectal examination.
Single hydronephrosis is distinguished from ascites by the non-existence
CYSTIC KIDNEYS. 591
of dulness in both lumbar regions. In ascites, when the position of the
patient is changed, there is a change in the level of dulness, which never
occurs in hydronephrosis.
It is quite impossible to distinguish hydronephrosis from an hydatid
cyst, unless the hydatid vesicles are found in the urine, or the hydatid fre-
mitus is present.
It is distinguished from pyonephrosis by the non-purulent character of
the urine, aud by the absence of constitutional symptoms. An aspirating
needle will generally decide the diagnosis, for the watery urine withdrawn
differs, chemically and microscopically, from the fluid obtained from hy-
datid or ovarian cysts or the pus of a pyonephrosis or a perinephritic ab-
scess.
Prognosis. — The prognosis is more favorable in this than in any other
form of renal tumor ; yet it is always serious. When only one kidney is
involved life may be indefinitely prolonged, and there is always a possibility
that spontaneous evacuation of the sac may occur. But cases are recorded
where — one kidney only being involved — it caused death by pressure on
neighboring parts. If the healthy kidney becomes the seat of any form of
nephritic degeneration, the prognosis becomes unfavorable ; complete sup-
pression of the urine may then occur at any moment; or if the impedi-
ment which has obstructed one ureter extends so as to prevent the flow of
urine from both kidneys, urgemic symptoms will be developed, and death
speedily follow.
Treatment. — In hydronephrosis the principal thing to be accomplished is
the evacuation of the tumor. To accomplish this result it should be care-
fully manipulated. This can readily be done, as the tumor generally causes
no pain. If this does not cause its evacuation, aspiration should be re-
sorted to. I now have a case under observation in which aspiration has
twice been performed with complete relief to the patient, and the aspira-
tion has not been followed by any unpleasant symptoms ; nothing is to be
expected from medicinal treatment.
CYSTIC KIDNEYS.
Oysts of the kidneys are very frequently met with at autopsies, but they
are of very little clinical importance, for if the cysts are of small size
they give no symptoms during life. Cystic degeneration may have a con-
genital origin, and both kidneys may be converted into a mass of cysts of
sufficient size to entirely fill the abdominal cavity ; such conditions are
usually associated with other congenital malformations. It is claimed that
cysts originate in the epithelia or even in the fibrous stroma of the kid-
ney. They are often found scattered through kidneys that are otherwise
healthy. It is difficult to make any practical distinction between the
cysts of a true cystic kidney and those occurring with cirrhotic kidney.
They are usually situated in the cortical substance near the surface.
Colloid cysts of the glomeruli are freqiiently surrounded by laminae of
fibrin from hemorrhages within the capsule.
a93
DISEASES OF THE KIDNEYS.
The contents of kidney-cysts vary in character even in the true cyst.
They may contain a clear albuminous fluid ; sometimes it is gelatinous,
containing phosphates, carbonates, cholesterin, and very rarely urea and
uric acid. The vascular tuft in
a glomerulus that is transformed
into a cyst, is flattened against the
wall of the thickened capsule, and
the cyst may be lined with pavement
epithelia.
Fia. 144.
Cystic Kidney.
Drawing sliotoing a Vertical Median Section of a
Kidney containing Cysts.
Fig. 145.
Cystic Kidney.
Section from the Cortex of a Cirrhotic Kidney, show-
ing the Epithelial lining of a small Cyst-
A. Cirrhotic intertubular tissue.
B. A small artery in. transverse section sJiowing the
thickened coats.
C. Cavity of a small cyst.
D. EpitJielial lining of the last, partly detached.
(The extreme temiity of this lining cannot be
well shown in a wood-cut.) x 300.
The origin of these cysts is obscure, although there is reason to believe
that they are the results of dilatation of the kidney tubules and Malpighian
bodies. Congenital cysts have their origin, as a rule, in the Malpighian
bodies. Serous cysts are often found in kidneys that have undergone senile
atrophy. They may be developed in the connective-tissue by an enlarge-
ment of a lacunar lymph-space.
RENAL CALCULI.
Eenal concretions vary greatly in shape and differ in their composition.
They may be deposited in the tubes of the pyramids, in the cortical sub-
stance, or in the pelvis of the kidney. Their development occurs at any
age ; they are met with in the kidney of the foetus in utero and in the
kidneys of the vei-y aged.
Morbid Anatomy. — In the kidneys of infants dying within forty-eight
hours after birth, brownish striae of amorphous urates will invariably be
found running from the papillae to the base of the pyramids. In adults,
urate of soda, in the form of crystals, may be found deposited in the
RENAL CALCULI.
593
■white lines in the pyramids and cortical substance, both in the tubular and
intertubular structure ; this is always associated with a gouty diathesis.
Carbonate and phosphate of lime may be found deposited in the tubes and
l^yramids of the kidneys of old people, or in connection with diseases of the
bones. By far the most frequent variety is uric acid. Some think that
oxalate of lime forms the starting-point of uric acid deposits. Cystine,
ammonio-magnesian phosphate, or urate of ammonia and the mixed urates
may form nuclei of renal calculi. Mixed calculi are not uncommon.
These different varieties of urinary concretions may be permanently im-
pacted in the uriniferous tubes, and render them impervious and cause
cysts to be developed, or they
may be washed down the tubes
by the urine, and finally de-
posit in the infundibula and
pelvis of the kidney. They
vary in number and size. A
kidney may contain one or a
large number of concretions.
They usually vary in size from
a pin's head to a hazel nut ;
the larger ones may fill the
whole pelvis ; the smallest con-
stitute " kidney gravel.'^ If a
concretion becomes impacted
in the pelvis, it may attain a
very large size, weighing one
or two ounces. The smaller
calculi pass through the
ureters into the bladder and
are discharged ; the larger
ones may permanently ob-
struct the ureters and become
the cause of pyo- or hydro-
nephrosis.
The anatomical
produced by renal concretions
vary: they may cause pyelitis, pyonephrosis, hydronephrosis, or abscess,
or they may excite parenchymatous nephritis.
Etiology. — The causes of the different concretions found in the kidneys
are very obscure. Uric acid is most frequently met with in infants. The
deposits of lime and triple phosphates are most frequently met with in
adults. They are caused by the precipitation (in the nascent state) of uric
acid or oxalate of lime due to renal excess of insoluble uric acid, or to de-
ficiency in water of the urine. A colloid material composed of mucus or
blood globules or other animal base exists in all. They increase by accre-
tion. Certain constitutional conditions are supposed to be favorable to their
development, but the exact nature of the urinary changes has not as yet
Fig. 146.
Renal Calculi.
changes Drawing showing an Impcmted Eenal {Mulberiif) Calculus, A.
=> B. 'Cysts.
594 DISEASES OE THE KIDNEYS.
been determined. In most cases, calculi that develop in the pelyis of the
kidney have some foreign substance as a nucleus. These nuclei may be
pus, blood, epithelium, or grains of pigment. The composition of the re-
maining portions of the calculi depends upon the varying conditions of the
urine which attend their development.
Symptoms. — The symptoms which indicate the presence of renal calculi
vary. In some instances they are well marked, in others very obscure.
Usually, the existence of renal calculi is indicated by an aching pain in the
lumbar region and loins, which frequently shoots into the testicles or labia
and down the thighs,— by an itching at the end of the penis, and by a fre-
quent desire to urinate. The urine often contains pus, blood and " tailed "
epithelium from the pelvis of the kidney. These symptoms are usually
aggravated by anything that disturbs the position of the calculus, espe-
cially by violent exercise, or by jolting in driving or horseback riding.
The symptoms often assume the characteristics of ''renal colic," due to
the passage of the calculus along the ureter to the bladder ; this may occur
after violent exercise or without any assignable cause. The attack may be
sudden, or there may have been uneasiness in the loins for some time. The
passage of a calculus along the ureter into the bladder is marked by sudden
and intense pain in the region of the affected kidney. This pain radiates
in various directions, but mainly toward thehypogastrium, testis, inside of
the thigh and end of the penis. There is a constant desire to micturate, —
*' tenesmus of the bladder," — but the urine is scanty or suppressed, and
what is passed is of a smoky, high color, often bloody, and is discharged in.
drops, the individual at the time experiencing a painful burning sensation.
When hemorrhage is profuse, elongated blood clots are not infrequently
found in the urine. The testicle of the affected side is retracted. As the
pain increases in severity the patient rolls from side to side and shrieks
with pain. His countenance becomes pale and the surface of the body is
covered with a cold perspiration. The pulse is small and the hands and
Jeet are cool. The severe paroxysms of pain are often attended by violent
and frequent vomitings. There is great anxiety, and if the patient is of a
Tery nervous temperament convulsions may occur. If the attack is pro-
longed there is a slight rise in the temperature. Syncope is common dur-
ing the attack.
The duration of these attacks varies. Sometimes they are only of a few
hours' duration, at other times they may be prolonged for days ; again,
temporary remissions may occur, followed by violent exacerbations.
As the calculus reaches the bladder the pain suddenly subsides, with a
sense of relief, and the patient is often conscious of its passage into the
bladder. After the passage of a calculus into the bladder it will soon be
found in the urine voided. Occasionally calculi become impacted in some
portion of the ureter. In such cases the subsidence of the pain is more
gradual and less complete, and signs of hydronephrosis follow, and a tumor
may be felt in the region of the kidney. By placing the patient on his
back with his knees drawn up, the enlarged kidney may be pressed forward,
and with the other hand in front it may be pressed backward and below
RENAL CALCULI. 595
the margin of the ribs. In the young and in those who are thin this method
will aid very much in the diagnosis. Renal calculi may attain a large
size and destroy extensive portions of the kidney, and yet not a single symp-
tom may be present to indicate their existence. Again, tlie signs of renal
calculi may exist for a long time, and finally atrophy of the kidney occurs,
or they may become encysted and cease to give any indication of their
presence.
Differential Diagnosis. — Eenal calculi may be confounded with neuralgia ;
the seat of pain is the same, and the neuralgic pains are often severe and
paroxysmal ; but the urinary symptoms and an examination of the urine
will make the differential diagnosis.
The passage of hlood-clots or hydatids through the ureter, causing renal
colic, cannot be distinguislied from the passage of renal calculi, unless the
antecedent history is known and appreciated, and a subsequent urinary
analysis is made.
The irritation produced by an impacted calculus on the right side will
not long be mistaken for peritypfiUtis, if careful and repeated examinations
of the urine are made. Frequently, the abnormal conditions of the urine
which indicate the presence of renal concretions are j)resent only after vio-
lent exercise.
Prognosis. — The prognosis in renal calculus is good, unless the calculi
become impacted and obstruct the ureter, or are of too large size to pass
through the ureter to the bladder. In these conditions the prognosis is the
same as in similar conditions in pyelitis, pyonephrosis and hydronephrosis.
Should both kidneys be involved, the prognosis is exceedingly unfavorable.
Treatment. — The treatment of the general condition is considered under
the head of Urinary Sediments. The treatment during the interval be-
tween the paroxysms which mark the passage of renal calculi will depend
upon the changes which have occurred in the kidneys ; different theories
have been advanced in regard to the dissolving of these concretions, but
none of them are of practical importance. The surgical treatment of im-
pacted calculi with extensively diseased kidney is now attracting much at-
tention. The means to be employed for the relief of the kidney changes
due to irritation produced by calculi, have been considered under pyelitis
and pyonephrosis.
The paroxysms which attend the passage of renal calculi, or so-called
nephritic colic, must be relieved by the free administration of mori^hine
hypodermatically, warm baths, and the application of hot poultices to the
loins and abdomen. In some instances, when the pain is intense and the
vomiting constant, inhalation of chloroform will be found to give the most
speedy and sometimes permanent relief. Change in the position of the pa-
tient, and manipulation of the abdomen along the course of the ureters,
may sometimes dislodge a calculus and facilitate its passage into the blad-
der.
696 DISEASES OF THE KIDNEYS.
ITOW GEOWTHS 11^ THE KIDNTET.
{Benal Cancer.)
Renal Cancer may occur as a primary or secondary affection. When seC'
ondary, its developments usually are of small size, and may occur in both
kidneys. "When primary, it is limited to one kidney, which soon forms an
enormous tumor.
Morbid Anatomy. — Both primary and secondary cancer of the kidney are
generally of the medullary variety, and develop in the form of circumscribed
nodules in the cortical substance, or occur as a diffuse infiltration. The
medullary cancer, however, may be nearly as hard as scirrhus. Colloid can-
cer is rare. It develops from the fibrous stroma of the cortical substance.
Sometimes a whole kidney is transformed into a cancerous mass, which at-
tains an enormous size, filling up a large portion of the abdominal cavity.
The average weight of a cancerous kidney is over eight pounds ; it has
weighed thirty-one pounds in children. Secondary cancer (bilateral) never
reaches a very large size. The kidney tissue is always intensely congested ;
it is often associated with cancer of the testicle.
The pelvis, ureters, the veins, the peritoneum, colon, and even the skin
adjacent to the neoplasm may be involved. The lymphatics and adjacent
glands are always enlarged. With the growth of the cancer all traces of
renal structure become obliterated and the diseased organ becomes adher-
ent to the adjacent tissue. Hemorrhages occurring in the mass at varying
points give an appearance called "fungus haematodes." Sometimes a can-
cerous kidney is movable, no adhesions taking place with surrounding
parts. The minute anatomical changes that take place in cancerous devel-
opments in the kidney, are similar to those which occur in cancerous devel-
opments in the other organs of the body.
Etiology. — The etiology of renal cancer is as obscure as the general eti-
ology of cancer. In a large proportion of cases it depends either upon
hereditary taint or local infection. Primary cancer occurs oftenest iefore
the tenth and after the fiftieth year of life.^ Secondary cancer may occur
by continuity or from metastasis; e.g., mamma, uterus, liver, stomach,
testis or supra-renal capsules. Males suffer oftener than females ; the right
kidney oftener than the left.
Symptoms. — Cancer of the kidney often remains latent for a long time.
Its development is marked by gradual emaciation, for which no cause can
be assigned. It may not be attended by pain in the lumbar region ; if
pain is present it is not characteristic. There may be no change in the
renal secretion ; but as the disease advances more or less profuse hemor-
rhages occur ; sometimes the blood appears in the urine in clots, in which
elements of the neoplasm may be found.
As the disease advances, and the cancerous mass reaches a large size, it
can be felt through the abdominal walls. The form of the tumor and its
immobility will enable one to distinguish it from enlargements of the liver
1 Out of Rohre's 107 cases of primary renal carcinoma, 37 were under ten ; 30 were over fifty years of
age.
NEW GEOWTHS IN THE KIDNEY. 597
or spleen. Very large cancers of the right kidney may displace the liver
upward. The tumor is usually nodulated and firm, gives a dull or tym-
panitic note on percussion, and can be tilted forward. The colon lies in
front of it. Aortic impulse may cause it to pulsate. When haematuria is
present it is constant. In its advanced stage the countenance assumes the
characteristic cancerous cachexia.
Differential Diagnosis. — Cancer of the left kidney is distinguished from
splenic tumors by its lower site, absence of splenic notch, absence of blood
changes, by its nodulated outline, and by haematuria.
From perinephritic abscess it is distinguished by absence of febrile
symptoms, by its slow growth, and absence of fluctuation.
Cancer of the right kidney may be distinguished from hepatic tumors by
an area of tympanitic percussion between the liver and the tumor. Reli-
ance is also to be placed on signs peculiar either to hepatic or renal
lesions.
Tumors of the liver or spleen are carried down on full inspiration ; renal
cancer is not. Faecal and ovarian tumors have peculiar characteristics.'
Abscess and hydatid tumors are distinguished by introducing an aspirat-
ing needle, which withdraws either pus or a saline fluid containing por-
tions of the echinococci.
An ovarian tumor when tapped is found to contain a peculiar ovarian
fluid ; fluid from a hydronephrosis contains some urinary elements.
Prognosis. — The prognosis is always bad. But cancer of the kidney is
tolerated longer than that of any other organ. Death is reached either by
the exhaustion produced by repeated and profuse hemorrhages, or as a con-
sequence of some intercurrent disease, as parenchymatous nephritis in the
unaffected organ. The lungs, retro- peritoneal glands, and liver may be
secondarily invaded. A year in children and two years in adults is its
average duration. Intestinal fistulas may be formed, and the skin may be
ulcerated, as sequelas to cancer of the kidney. Dropsy may result from
compression of the vena cava. The vertebrae may be eroded.
Treatment. — Its treatment is palliative. The principal things to be ac-
complished are to relieve pain by hypodermatics of morphine and to sustain
the patient.
Of the new growths met with in the kidney, cancer is the only one which
has any special clinical significance.
Leukcemic tumors are occasionally met with as small whitish masses, de-
veloped in the intertubular tissue. They are composed of lymphoid cells,
and are always associated with similar growths in the other viscera. These
" lymphadenomata''^ are developed in connective-tissue ; the liver is usually
simultaneously involved.
Syphilitic gummata are also met with in the kidneys in the form of small
nodules, in connection with similar developments in the other organs ;
cicatrices may be left, usually in the cortex, but sometimes in the medulla
of the organ. Gummata destroy the tubules. Patches of ''fibrous tissue"
independent of gummata occur in kidneys of those who are syphilitic.
' See " Intestinal Obstruction.'-'
598 DISEASES OF THE KIDN"ETS.
Fibromata may appear in the pyramids of kidneys in the form of small,
white, fibrous nodules. The remaining portion of the kidney will be nor-
mal, or the seat of parenchymatous nephritis.
Lipomata include those accumulations of fatty tissue which are some-
times developed around the capsule of the kidney and in the pelvis of
atrophied kidneys ; sometimes in the cortical substance beneath the cap-
sule small, rounded, fatty tumors are found. Growths of ho7iy, muscular,
and glandular tissue have also been met with in a few instances.
Sarcomata have been found in young children.
TUBEECULAE DISEASE OF THE KIDISTEY.
Tubercles are developed in the kidneys as an advanced lesion of gen-
eral tuberculosis. Primary tuberculosis of the kidneys is occasionally met
with in young subjects.
Morbid Anatomy. — At first, gray miliary tubercles are found throughout
the affected kidney, principally in the pyramids. The tubercles may origi-
nate in the stroma or in the cortex, in the arterioles separating the pyra-
mids of Ferrein, or on the surface of the kidney. Later, solid, cheesy, yel-
low masses are found in the pyramids and in the cortex. The organ is en-
larged and lobulated. The mucous membrane of the pelvis and ureters is
thickened, infiltrated, and often ulcerated. When the ureter is involved
diminution of its lumen may result in hydro- or pyonephrosis. The larger
yellow masses are found at the junction of the cortex and medulla ; they
are usually softened at their centres, containing a puriform debris ; the pel-
vis and calices are also dilated and filled with caseous pus or with a semi-
fluid pulp rich in cholesterin. The tubules are compressed, and their epi-
thelium undergoes gi'anular and fatty change. An inflammatory process
may coexist {strumous nephritis, of English authors), and the entire mu-
cous membrane of the genito-urinary tract may be involved. Calcareous
nodules and incrustations are found mingled with tubercle granules. Every
portion of the genito-urinary tract, especially in the male, may show tu-
bercle granulations.
Etiology. — Eenal tuberculosis generally occurs in the young. Men are
far oftener affected than women, the right kidney oftener than the left. It
may occur as a primary tuberculosis, as part of acute miliary tuberculosis,
or it may complicate chronic pulmonary phthisis.
Symptoms. — The symptoms are essentially those of pyelitis ; such as pain
and tenderness in the loins, an irritable bladder, and scalding urine, which
contains mucus, pus and blood. As the disease advances hectic fever de-
velops, with the coexistent symptoms of intestinal or pulmonary tubercu-
losis. The urine will contain albumen [no casts), and under the microscope
it is found loaded with fatty granules, lymph cells, blood corpuscles,
and debris of connective-tissue infiltrated with small and fatty granular
cells. A flaky, cloudy deposit always occurs in this urine, unless the ureter
from the affected side is impermeable. If masses of cheesy material are
HYDATIDS OF THE KIDNEY. 59^
found they establisli the diagnosis. A renal tumor may sometimes be
detected.
Differential Diagnosis. — The diagnosis rests upon the hereditary history,
the presence of tubercles in lungs or prostate, on lymphatic enlargements,
cheesy, puriform urinary debris, and the presence of a painful renal tumor.
Prognosis. — The prognosis is very unfavorable ; the complications are
tubercle in any or all of the other organs of the body, cystitis, pyelitis,
pyelo-nephritis, abscess, hydro- and pyonephrosis, waxy kidney, peritoni-
tis, and urinary suppression.
The Treatment is altogether palliative.
PARASITES IN THE KIDISTET.
Renal parasites are occasionally met with ; the most frequent is the echi-
nococcus. The cysticercus cellulosus, strongylus gigas, pentastoma denti-
culatum, distoma haematobium,' spiroptera hominis, and dactylus aculeatus
are parasites of rare occurrence. They are sometimes found embedded in
the kidney. The symptoms which attend their development, and the man-
ner in which they gain entrance into the kidney, are obscure.
HYDATIDS OF THE KIDNEY.
While hydatids of the kidney are less common than hydatids of the
liver, the affection occurs under similar conditions.
Morbid Anatomy. — A kidney the seat of hydatids is sometimes enor-
mously enlarged ; as. a rule, a spherical cyst projects from the surface whose
fibrous wall is derived from the kidney. The inner cyst wall may or may
not be covered with daughter vesicles contaiuing scolices, but a clear saline
fluid always distends it ; the pressure of the cyst causes atrophy of the kid-
ney structure. These cysts may suppurate and be changed into a shriv-
elled cyst with caseous contents in which are embedded echinococci hook-
lets. They may rupture into the perinephritic tissue and give rise to a
lumbar abscess, or into the lungs, intestine, stomach, peritoneum, or pel-
vis of the kidney.
Symptoms. — A nephritic tumor is the first noticeable sign. A vesicle
passing from the pelvis to the bladder gives rise to the symptoms of renal
colic. An examination of the urine may reveal echinococci booklets. In
all cases the exploring trocar will withdraw a clear saline fluid containing
booklets.
Percussion may elicit the hydatid fremitus. If pus or blood appears in
the urine it results from complicating inflammation or suppuration set up
by the cyst or its contents.
Prognosis. — This is always uncertain. It is possible for a cyst to grow
so rapidly as to cause death of the echinococci by pressure, or the fluid
1 The Bilharzia hsematobia in the nrirary vessels is the cause of tropical endemic haematnria. The ova
get into the syntem through foul drinking water, and their development often causes grave lesions of the
mucous membrane of the genito-urinary tract. Diarrhcea, typhoid and septic symptoms are developed.
600 DISEASES OF THE KIDNEYS.
necessary to their life may be insufficient, or it may become so altered that
calcareous changes will occur and then a calcareous mass may remain for
life and cause no further harm. An echinococcus may be the nucleus of
a stone in the bladder or in the pelvis of the kidney.
Treatment. — Aspiration should always be practised, and if it is not fol-
lowed by adhesive inflammation, iodine should be injected into the cyst.
PEEINEPHEITIS.
{Perinephritic Abscess.)
This is an inflammation of the connective-tissue surrounding the kidney :
it may terminate in suppuration, or in the formation of fibroid tissue.
Morbid Anatomy. — The cellular tissue about the kidney becomes cede-
matous and the seat of inflammatory exudation, causing the cellular, adi-
pose and adjacent retro-peritoneal tissues to become solid and firm. Sup-
puration may commence at the centre of the mass, leading to the formation
of one large abscess ; or, if it commences at numerous points and gradu-
ally extends, a number of circumscribed abscesses are formed. The tu-
mor formed may become so large as to reach from the level of the liver or
spleen to the iliac fossa, and may project forward and cause bulging of the
abdominal wall. The pus contained in the abscess may be odorless, or thin,
fetid and ichorous, especially if mixed with urine. The pus may have an
odop of faeces independent of perforation from the 'bowel into the abscess
cavity. This process may end in gangrene. The peritoneum over the tu-
mor is thickened.
A perinephritic abscess may open into the lung, pleural cavity, or bron-
chi, by extending into the retro-peritoneal tissue and then through the dia-
phragm. The pus may burrow along the psoas muscle and appear as a
psoas abscess on the thigh, or abdomen. Spontaneous opening usually
occurs, externally, in the lumbar region. The bladder, ureter, pelvis of the
kidney, peritoneum, and colon have all been perforated by perinephritic
abscesses. Sometimes inflammation of the perinephritic tissue is not fol-
lowed by suppuration, but at the autopsy a thick, tough, fibrous mass is
found occupying the place of the (so-called) adipose capsule of the kid-
ney. The same result may follow discharge of the abscess and cicatriza-
tion.
Etiology. — Perinephritis may be caused by pyelitis, suppurative nephri-
tis, blows, falls, strains, parasites, or wounds of the kidney or the tis-
sue about it. It may occur in pyaemia or in the course of any of the ex-
anthems or specific fevers. It may also complicate pelvic cellulitis, psoas
abscess, and perityphlitis. It occurs more frequently in men than in
women.
Symptoms. — Eecurring rigors are among the first symptoms, followed or
accompanied by pain in the lumbar region — which is increased by move-
ment and firm pressure — shooting down toward the testicle. The pulse is
rapid and feeble. The temperature rises to 100°-105° F. The skin at first
is dry, but later it is covered with a profuse perspiration. There is ano-
ELOATIKG OR MOVABLE KIDNEY. 601
rexia, great thirst, and constipation. The urine is usually slightly dimin-
ished in quantity ; otherwise it is normal, unless pyelitis or nephritis should
coexist.
Physical Signs. — A tumor forms in, or a little below, the lumbar region ;
it rapidly increases in size ; at first it is hard ; later it gives signs of deep
fluctuation. The skin over it is oedematous and pale. The tumor is im-
movable and cannot be separated from the kidney, but can readily be dis-
tinguished from the spleen or liver enlargements. An exploring trocar
will establish the diagnosis.
Differential Diagnosis. — The differential diagnosis between perinephritic
abscess and -pyoneplirosis and hydronephrosis has already been given.
It is distinguished from suppurative nephritis by the presence of a tumor,
and by the absence of casts, albumen, blood or mucus in the urine.
From extravasation of blood due to rupture of an aneurism, it is distin-
guished by fever, rigors, ajluctuating tumor, and the absence of the causes
and physical signs of aneurism.
Prognosis, — A perinephritic abscess is always serious. Its duration is
usually from two to four weeks ; in some cases several months have elapsed
before the tumor has subsided. Its discharge into the intestine or bladder,
or the establishment of an external opening, may be regarded as favorable.
With an early diagnosis and prompt surgical interference the prognosis is
good. Some regard many " cures" of hip-joint disease without deformity,
as in reality cases of suppurative perinephritis. '
Treatment. — A free opening should be made as soon as the diagnosis is
established. Grainger Stewart states that early counter-irritation by blister-
ing is useful, and that iodide of potassium internally and iodine externally
may prevent suppuration ; my experience does not sustain this statement.
Yet incision is safer than aspiration ; after an opening is made the finger
should be introduced into the abscess-cavity and any adhesions that may be
present should be broken down. Then a drainage tube should be intro-
duced. Antisepsis should be practised during the operation and with
subsequent dressings. Stimulants and concentrated fluid nutrition should
be freely administered.
FLOATIlSrG OE MOVABLE KTOISrEY.
As a congenital peculiarity one or both kidneys may be movable, and in-
stead of occupyiiig their normal position may lie upon the brim of the
pelvis, or be freely movable in the loose retro-peritoneal connective-tissue
which surrounds them, and the peritoneum may be so reflected in front
and behind them as to allow their free motion. The displacement of the
kidney under any one of these conditions may follow parturition or a severe
shock from a fall. It is met with more frequently in females than in males.
Morbid Anatomy.— A congenital displacement is distinguished from an
acquired displacement by the abnormal arrangement of the vessels of the
kidney and its peritoneal coverings. The extent of the mobility in any
> Afner. Jour. Med. Scieiwes, April, 1877, and Oct., 1878. V. P. Gibney, M.D.
602 DISEASES OF THE KIDNEYS.
case is determined by the length of the vessels which form the pedicle.
Movable kidneys are almost always surrounded by connective-tissue forma-
tions, and after having been once movable they may become firmly fixed
again in their normal or in an abnormal position.
Symptoms. — A displaced kidney is usually felt midway between the free
border of the ribs and the umbilicus. If the right kidney is displaced it is
apt to make its appearance just below the liver ; it may be pushed upward
and backward into its normal position, but it will return as soon as the
support is withdrawn.
If a displaced kidney can be grasped its pressure causes a sickening sen-
sation. If it gets compressed or otherwise injured, it may become painful,
tender, and swollen. Otherwise it may give rise to no symptoms and be
recognized only by accident.
Differential Diagnosis. — Its diagnosis rests — 1st, on the shape and size of
a tumor corresponding to that of a normal kidney ; 2d, when the tumor
can be felt in front there will be an abnormal tympanitic resonance over
the normal position of the kidney ; 3d, the tumor can be pressed back into
the normal kidney region ; 4th, the peculiar sickening sensation produced
by its manipulation.
Prognosis. — Such kidneys are never a cause of death. Many observers
have doubts in regard to the probable occurrence of a floating kidney.
There is little post-mortem evidence in its favor. I have never made but
one diagnosis of this condition during life that was sustained by a post-
mortem examination.
Treatment. — When a movable kidney is painful, rest is indicated, and a
concave abdominal pad so adjusted as to fit the form and position of the
kidney tumor should be worn.
HEMATURIA.
Hgematuria is the passage of urine containing blood. The blood may
have its origin at any point from the Malpighian tuft to the orifice of the
urethra. As it is a symptom, it has no morbid anatomy ; its causes con-
stitute its pathology.
Etiology. — Local causes. — (1) In the kidney the conditions which induce
hsematuria are active and passive hypersemia, acute (rarely, if ever, chronic)
suppurative nephritis, or surgical kidney, infarctions (including embolism
and thrombosis), tuberculosis, a single or multiple pygemic abscess, pyeli-
tis (especially when the pyelitis is calculous), stone in the kidney, or in the
pelvis of the kidney, and, in a few cases, hydro- and pyonephrosis. Crystals
in the tubules may induce it. Among kidney causes may be included the
drugs which cause hsematuria, e. g., turpentine, cubebs, copaiba, canthar-
ides, etc.
(2) The causes that have their seat in the ureters are ureteritis, cancer,
polypi, ulcers, and calculi.
(3) The bladder causes are cystitis (but only when very acute and accom-
panied by erosion and ulceration), cancer, abscesses in the vesical walls, poly-
H^MATUEIA. 603
pus of the bladder, stone in the bladder, rupture of the bladder, tubercu-
losis, specific or non-specific ulcers. Dilatation and varicosity of the vesical
veins may cause it, called oftentimes "hemorrhoids of the bladder."
(4) The urethral causes are many : urethritis (non-specific and specific),
peri-urethral abscess, chordee, cancer, fracture of penis, rupture of prostatic
abscess, an enlarged prostate, urethral polypi (especially in females), caustic
injections, chancre and chancroids, phimosis, impacted stone, and new-
growths in the prostate.
The general causes of haematuria are acute infectious diseases, fevers,
especially malarial, scurvy, purpura, the condition know^n as hgemophilia
(the bleeders), and certain central nervous diseases (see Mj'Clitis).'
Symptoms. — The urine may be almost black and loaded with clots, or it
may be only slightly smoky or pinkish in color. It is albuminous ; under
the microscope swollen or shrunken corpuscles are found, the degree of al-
teration depending on the time they have remained in the urine. If equal
parts of tincture of guiacum and oil of turpentine are shaken together to
form an emulsion, an intense blue color will arise when bloody urine is
slowly added to it.
To determine the source of the hemorrhages the following rules may be
observed : — urethral hemorrhages are independent of micturition, as only
a residue of blood is washed out at the beginning of the flow of urine. The
history will aid and inspection will probably reveal the true state of affairs ;
albumen, casts and epithelial cells are not often found in urine when it
becomes bloody in the urethra. The Madder may be suspected as the seat
of the hemorrhage when blood flows only at the time of micturition, and
follows the discharge of urine ; should the stream suddenly cease, a stone
or blood-clot blocks up the opening of the urethra into the bladder, and
this will be well-nigh diagnostic. Clots following the flow of urine indicate
cystic disease. When they precede the flow or occur with it, urethral dis-
ease is indicated. Should blood globules, albumen, casts, and blood moulded
in the form of renal tubules be found in the urine, renal disease may be re-
garded as the cause of the hsematuria. In renal hemorrhage blood is
mingled with the urine, and is commonly as profuse at the commencement
as at the end of micturition.
Should liEematuria be combined with the symptoms of stone in the blad-
der, of pyelitis, or of cystitis, the source of the hemorrhage is then no longer
a matter of doubt. Sir Thomas Watson states "that slender cylinders of
fibrin in the ureter indicate renal disease or commencing inflammation of
the ureter."
In "endemic" haematuria the diagnosis rests on discovering the trema-
tode or its ova in the urine or faeces ; it causes pain along and over the
genito-urinary tract.
' There is a variety of haematuria which occurs in tropical countries (Egypt, Brazil and Cape of Good!
Hope especially) caused by a fluke called Bilharzia hsematobia, aparasite (atrematodchrematozoon), which
is endemic. Dr. John Harley discovered this parasite in the blood of a patient in South America. It is^
one-half to three-quarters in. long, and is found chiefly in the vessels of the portal system and of the blad-
der. The eggs are found in the urine ; they are 1-100 to 1-180 in. in length, and are peculiarly pointed at
one end, the whole contour, however, being ovoid. This parasite causes thickening, ulceration, ecchy-
moses and large blood extravasations iu the mucous membrane in whose vessels it is lodged.
^04 DISEASES OF THE KIDNEYS.
In the so-called false hsematuria the urine contains only haemoglobin,,
the microscope failing to discover any corpuscular elements in the urine.
It is also called limmoglobinuria, hcBmathmria, and (when occurring peri-
odically), intermittent or paroxysmal hmniaturia. The haemoglobin of the
blood is set free in one of two ways : either the extravasated corpuscles dis-
integrate or the haemoglobin escapes without rupture of the capillary walls.
Once free in the blood the kidneys eliminate the haemoglobin. Fevers,
poisons, gases, and cold are said to cause this condition.
When intermittent it is usually dependent on malaria, but a malarial
cause need not necessarily exist for the paroxysm to occur. Chills, sweat-
ings, and, at times, a rise in temperature attend the discharge of the red-
dish urine, which soon shows a granular, brownish sediment. Albumen,
and hyaline and granular casts are very often present, independent of renal
disease. In severe cases the patient becomes anaemic and cachectic.
Quite recently a disease has been described called "melaBnic fever,"
resembling somewhat in its constitutional symptoms acute yellow atrophy
■of the liver and yellow fever. The urine is brown-black and contains al-
bumen, casts, and a large quantity of blood cori)uscles (not haemoglobin
alone). Suppression often occurs, and the case ends fatally.'
Differential Diagnosis. — The points of differential diagnosis have been suf-
ficiently considered in its etiology. First, care must be taken by micro-
scopical examination and spectrum analysis to positively determine that
blood corpuscles or haemoglobin are actually present in the urine. Then
a study of its causes and accompanying symptoms renders the diagnosis
comparatively easy.
Prognosis. — The prognosis in haematuria depends on its cause. Endemic
haematuria is never the direct cause of death, but it may lead to extreme
anaemia. Paroxysmal haemoglobinuria is rarely fatal.
Treatment. — When the haematuria is slight and of short duration no
special treatment is required ; if profuse or persistent the patient should
be placed in a recumbent position, ice-bags applied over the seat of the
hemorrhage, and haemostatic remedies used, such as gallic or tannic acid,
ergot, acetate of lead, and astringent ferric preparations. If the haema-
turia is of parasitic origin prophylaxis demands that the drinking water
be filtered and boiled ; to expel the parasites male-fern or chloroform may
be given internally. Harley advises belladonna and henbane. Quinine is
indicated in all forms of paroxysmal haematuria or haemoglobinuria. If
the hemorrhage is from the bladder persistent weak astringent injections
may be employed.
CHYLURIA.
Chyluria is characterized by the occasional or continuous discharge of
urine which resembles milk when passed and coagulates into a jelly mass on
standing.
Morbid Anatomy and Etiology. — The kidneys are usually found free from
1 Virginia Med. Monthly, February, 1880.
CHTLURIA. 605
disease, and the affection is attended by no known constant pathological
lesions. At one time it was regarded as a disease of defective assimilation
which permitted the chyle to miugle with the blood; at another, a fault of
the kidneys which allowed the unchanged chyle to be transuded with the
urine. Neither of these explanations has been sustained by observation.
There are at present many theories in regard to its causation : first, that
there is a direct communication between the chyle-carrying vessels and the
urinary tract ; second, that it is a symptom of piarrhsemia due to a de-
ranged liver function ; third, that it is caused by an eczema along the
urinary tract ; fourth, that it is due to hypertrophy of the lymph channels
and their subsequent assumption of glandular functions ; fifth, that it is
due to a parasite, but whether the action of the entozoon is on the function
of the liver or causes irritation and rupture of the lymph and chyle chan-
nels is not determined.
Symptoms. — No disease pursues a more irregular course : no two cases
exactly resemble each other. There may be pain in the loins and along the
gerii to-urinary tract, depression of spirits, and debility, before the urine
becomes chylous ; or, the first sign may be a sudden flow of milky urine,
having a whey-like or milky odor, made more perceptible by warmth. It
soon coagulates on standing, but the trembling. Jelly-like clot breaks down
and the urine decomposes in a few hours. Bloody coagula, usually shreddy,
may also form. White and red blood discs are found in varying quantity.
Clots may form in the bladder, and during micturition the flow may sud-
denly stop from blocking of the urethra. The sp. gr. of the urine varies,
(1.007-1.030). Heat and nitric acid cause a precipitate. Shaken with
ether the urine loses its milkiness. Fat, albumen, and fibrin are all present.
Blood analyses vary ; but when the filaria sanguinis hominis is not found
in chylous urine it is found in a drop of blood taken from the finger, and
vice versd. Hoppe-Seyler says blood in this disease resembles human
lymph in its composition. Chylo-serous discharges take place also from
axilla, groin, scrotum, and surface of the abdomen or inner corner of the
eye. Chyluria is an intermittent disease, but there is no periodicity or
regularity to it.
Prognosis. — The disease runs a chronic course. Men have suffered on and
off for fifty years. Change of climate does not seem to improve the out-
look when the disease is once established. Sudden death may occur at any
moment, even in those with fair health. Elephantiasis, phlebitis, haema-
turia, "lymph-scrotum," craw-craw, leprosy, and furuncles are not infre-
quent complications.
Treatment— This has been unsatisfactory. Turpentine and gallic acid
are recommended. Iodide of potash and perchloride of iron are claimed to
be highly beneficial. Mangrove and nigella sativa are used by the natives
in places where chyluria prevails; sometimes they effect a cure, oftener not,
however. Prophylaxis demands care in drinking water in a tropical re-
gion, and first boiling or filtering it.
606 DISEASES OF THE KIDiS'ETS.
CYSTITIS.
Cystitis is an inflammation of the mucous membrane lining the urinary
bladder. It is acute or chronic; aud it may be either catarrhal, croupous,
or diphtheritic. The whole or part of the bladder may be involved j
when " partial," it is limited to the neck and bas-fond.
Morbid Anatomy. — In acate catarrhal cystitis the appearances are in no
wise different from those observed when any mucous surface is inflamed.
The small glands at the base of the bladder are enlarged and filled with a
pearly secretion. The interior portion of the trigone is also studded with
these pearly masses. They may form a circle about the neck of the blad-
der. Intense (acute) cystitis may end in suppuration of the submucous
connective-tissue, and ulceration of the mucous membrane may allow
these submucous abscesses to empty into the bladder.
When cystitis results in paralysis of the bladder, gangrene of the mu-
cous membrane may occur ; then brownish-black, irregular patches are
seen mingled with debris and phosphatic incrustations on the surface of
the bladder. When the mucous layer is thus destroyed by gangrene, the
urine infiltrates the neighboring tissue, and local or general peritonitis may
result. An acute cystitis may lead to a pyelo-nephritis. Ulcerating cys-
titis occurs in typhoid and low eruptive fevers, in diphtheria, pyasmia,
etc. It is called by some diphtheritic. The lesions in this form and in
croupous cystitis are similar to those which take place in diphtheritic
exudations on other mucous surfaces. [See Inflammation.)
In chronic cystitis the mucous membrane is thick, blue-gray in color,
and very tough. Muco-pus and viscid mucus are formed in large quanti-
ties upon its surface. As the disease progresses a peri-cystitis consolidates
the bladder with the neighboring organs and parts. Chronic catarrhal
ulcers may form, and perforation of the bladder may result, and the
vagina, rectum, or abdominal cavity may be entered, or an external open-
ing may be formed through which pus is discharged. The muscular wall
of the bladder may sometimes be half an inch thick, and the fasciculi
give a ribbed appearance to the internal surface, called the "columnar
bladder." The hypertrophy of chronic cystitis may be eccentric or con-
centric. In some cases diverticuli are formed, in whose walls are dilated
and tortuous veins. Some of these cysts are in the form of hernial protru-
sions. In nearly all cases bacteria are found in abundance.
Etiology. — Acute cystitis is rarely idiopathic.
It may result from the presence of foreign bodies, especially calculi.
Blows may cause it. Protracted retention of urine has set up a rapidly
fatal cystitis.
It may be caused by some unknown blood condition, such as occurs in
scarlet, typhus, and typhoid fevers, pyaemia, septicaemia, small-pox, and
diphtheria ; it is a frequent complication of certain grave lesions of the
nervous system, especially myelitis.
Cystitis may result from the extension of an urethritis, a pyelitis, or a
pelvic cellulitis.
CYSTITIS. 607
Chronic cystitis may be the sequela of acute cystitis or result from the
retention of urine caused by an enlarged prostate or urethral stricture.
Over-distention, atony or paralysis of the bladder, calculi, polypi, and
neoplasms of all l<;inds cause it. Gout and some forms of kidney disease
are accompanied by chronic cystitis.
Symptoms. — Acute cystitis is always accompanied by frequent micturi-
tion, only a few drops being voided at each attempt. After its passage
the patient strains (as in the tenesmus of dysentery) to pass what he
imagines is still retained in the bladder. There are dull, aching pains
over the pubis ; sometimes the pains in the vesical region are agoniz-
ing, and there is a constant burning sensation along the urethra. These
local symptoms are not infrequently accompanied by rigors, and the tem-
perature rises to 100°-] 01° F., with loss of appetite, sleeplessness, and a
feeling of great anxiety or depression.
The urine is cloudy, deposits mucus on standing, is alkaline, and some-
times fetid. Microscopically, epithelium, pus and red blood-corpuscles
are found. Membranous exudations may be found, especially in females.
JSTiemeyer states that in the " croupous cystitis following cantharides
poisoning and forcible forceps deliveries large tenacious false membranes
are discharged " with the urine.
Chronic cystitis is often only indicated by a frequent desire to pass urine.
Usually there is a constant, dull, aching pain, or a sense of weakness over
the bladder. The bladder is nearly always intolerant of its contents, no
matter how long the catarrh has persisted. Hence only a small amount of
urine will be passed with each act. Distention and muscular hypertrophy
of the bladder often give rise to an abdominal tumor reaching as high as
the umbilicus ; it may contain from two to eight pints of urine ; as large
a quantity as this, in some cases, may constantly remain in the bladder,
only so much urine being passed as exceeds this amount, and then a patient
will be passing very nearly a normal quantity, and the introduction of the
catheter may remove a quart of stinking, alkaline urine, which, when it
stands, divides into two parts, a lower thick, turbid, gelatinous, coherent
and opaque mass — the supernatant layer being clear. The "glairy mucus "
so frequently described in this connection is only met with when the urine
is ammoniacal and also contains pus ; it is formed by the reaction of the
alkali upon the pus. Chronic cystitis accompanied by enlargement and
atony of the bladder often eventuates in ammonaemia, and then typhoid
symptoms are developed. Great local pain, emaciation and occasional
bloody urine indicate ulceration. Acute suppurative inflammation of the
bladder, accompanied by hectic, rigors, and extreme exhaustion, may accom-
pany acute suppurative nephritis.
DiflFerential Diagnosis. — Pyelitis often resembles cystitis closely in its sub-
jective symptoms ; there may be the same pain referred to the bladder,
and the same frequent desire to micturate. In pyelitis the lumbar j)ain,
the "tailed " cells in the urine, the even admixture of pus with the urine,
the acid reaction, and the absence of ropy, gelatinous mucus, are symptoms
in marked contrast to those of cystitis.
608 DISEASES OF THE KIDNEYS.
Prognosis. — The prognosis depends upon the cause ; in general it is good.
Chronic cystitis may continue for years ; the longer it continues the less
chance there is of recovery. Acute cystitis is usually recovered from in
about a week.
Treatment. — In acute cystitis the patient must have perfect rest. Warm
hip-baths give relief. Leeching or cupping over the bladder is often of
service. Suppositories of opium and belladonna or rectal injections of the
same are always indicated, with large poultices and very hot, peppery fo-
mentations over the bladder. The bowels should be kept free with the
mildest cathartics. An anodyne internally may be demanded for the
relief of pain; I have found chlorodyne the best. Twenty minims of liquor
potassse in mucilage may be given three times in the twenty-four hours.
Half drachm doses of fluid extract of Indian hemp are highly recommended.
The diet should be nutritious ; milk is to be preferred. No form of alcohol
should be allowed ; the patient may drink freely of flax-seed or linseed tea,
barley water, or decoction of triticum repens. In all cases the cause should
be sought for and if possible removed.
In chronic cystitis the catheter is to be regularly and persistently used.
The bladder should be washed out ; lime water and glycerine, very weak
solutions of nitrate of silver, sulphate of copper, either in water or in
glycerine, are often of service. Very weak solutions of salicylic acid, car-
bolic acid, permanganate of potash, and chloride of sodium are also recom-
mended. The daily use of a mineral water, like Vichy, is beneficial in
many cases of chronic cystitis, I have found more benefit from the daily
use (drachm doses after each meal) of the " Lafayette mixture " in chronic
cystitis than from all other remedies. All stimulating drinks are forbidden.
The injection of quinine into the bladder has recently been very success-
fully practised for the cure of chronic cystitis.'
» Lmdon Lancet, Feb. 23, 1878, and June 1, 1878.
SECTION ly.
ACUTE GEKERAL DISEASES.
Under this head I shall include those acute infectious diseases which de-
pend upon poisons developed outside the body of the affected person.
These poisons possess two distinctive characteristics. First, each poison is
specific and distinct from every other in its action, and hence inferentially
in its nature, so that the pathological processes which it incites are always
identical in kind and associated with that one etiological element, and with
no other. These processes thus become the means of differentiating this
class of poisons. Second, all these poisons possess the power of indefinite
reproduction when jDlaced under favorable circumstances, and their result-
ing diseases are therefore generally endemic, when permanent sources of
infection have become established, or epidemic, when the poison affects
large numbers at the same time, rather than sporadic. Such a poison is
termed a virus, and has its origin either in the bodies of diseased living
beings or in decomposing organic matter.
Every virus is more or less diffusible and may be conveyed by air, fluids,
or solids ; while in some diseases it becomes so localized that it can be
transmitted by inoculation. These morbific agents give rise to distinctive
diseases either by changes which they produce in the blood or by their di-
rect action upon the cellular elements of the different organs and tissues.
When a virus originates and attains its full development only in a living
animal and is excreted in an active state it is called a contagion, and the
disease which it produces is contagious.
"When the morbific agent is solely the product of decomposing organic
matter it is termed a miasm, and the affection it develops is a miasmatic
or malarial disease. Contagions may be transmitted mediately or imme-
diately, and are reproduced with each infection. Miasms are conveyed only
by diffusion, generally through air or water, and their activity is limited
to a single infection.
A third form of virus originates solely in diseased animal organisms, but
is excreted in a passive condition and becomes active only in the presence
of decomposing organic matter. The diseases in whose development such
a poison is the etiological factor are termed miasmatic- contagions.
As to the exact nature of any infectious poison, or its element of power
in the production of disease, we have no positive knowledge. At present,
there are two prominent theories. The first is based, upon chemical pro-
cesses ; the second, upon tlie multiplication of living organisms. The
chemical theory maintains that after the infectious element has been re-
39
610 ACUTE GENERAL DISEASES.
ceived into the blood it acts as a ferment, and gives rise to certain morbid
processes upon the principle of catalysis.
The theory of organisms, or the germ theory, maintains that the in-
fections poisons are living organisms, which, being received into the blood,
reproduce themselves indefinitely, and excite morbid processes which are
characteristic of certain types of disease. This theory, at the present time,
is quite extensively adopted, as it so readily explains very many remarkable
facts connected with the development and reproduction of this class of dis-
eases. It is readily understood, and there are so many animal poisons
which appear to act in this manner, that to one whose opinions are not
based upon clinical experience and actual contact with disease, the argu-
ments in its favor seem conclusive. According to this theory all the dif-
ferent forms of disease included under the head of infections may be re-
duced to two classes : first, infectious diseases which depend for their de-
velopment upon a living animal organism. Second, those which depend
for their production upon a living vegetable organism. At j^resent the
proofs of this theory have not extended beyond the demonstration of the
presence of bacteria in the pathological products of some infectious dis-
eases. Observers are not agreed as to the identity of the individual germs
of any infectious disease, nor is their etiological relation to diseases estab-
lished as yet even in the most general way. That bacteria are the exciting
cause of some diseases in animals has been very conclusively proven, but
thus far the strongest proofs of any such relation to human diseases are in-
sufficient to warrant our general acceptance of the germ theory.
I shall adopt the etiological classification of acute infectious diseases.
I. Miasmatic Contagions Diseases, due to a virus originating in a living
being and developed in decomposing organic matter.
1. Typhoid Fever. 5. Oerebro-spinal Meningitis.
2. Yellow Fever. 6. SepticaBmia.
3. Cholera. 7. Pyaemia.
4. Diphtheria. 8. Erysipelas.
9. Acute Miliary Tuberculosis.
II. Acute Contagious Diseases, due to a virus originating and developed
solely in a living being.
1. Typhus Fever. 6. Measles.
2. Eelapsing Fever. 7. Grerman Measles.
3. Small-pox. 8. Miliary Fever.
4. Varicella. 9. Influenza.
5. Scarlet Fever. 10. Whooping Cough.
11. Hydrophobia.
III. Malarial Diseases, due to a virus originating and developed solely
in decomposing vegetable organic matter.
1. Intermittent Fever. 4. Pernicious Fever.
2. Eemittent Fever. 5. Dengue Fever.
3. Continued Malarial Fever. 6. Chronic Malarial Infection.
"^n their pathology and clinical histories the fevers of the first class have
TYPHOID FEVER. 611
many things in common with those of each of the other classes, and will
be first considered.
TYPHOID FEVER.
This is the most prevalent of all fevers except malarial. So far as we
know, there is no place where it may not be developed and spread. It more
frequently prevails in the temperate zones than in the torrid or frigid, but
it is possible for it to be developed in all latitudes and in all countries.
This disease, which is essentially the same in all countries, is designated by
different names. American writers describe it under the name of typhoid
fever. The French call it the typhoid ajfect ion, or dothinenteria. English
writers describe the same form of disease under the head of enteric fever.
The Germans call it abdominal typhus, or gastric fever, I prefer the name
typhoid fever.
Morbid Anatomy. — As soon as the disease is fully established a change in
the hlood occurs. It becomes darker in color, coagulating imperfectly, and
the serum is of an unnaturally yellow color. The question arises : — did
these changes take place in the blood prior to the occurrence of the fever,
between the exposure and the period of attack ? It is certain that as
soon as the characteristic symptoms of the disease are present, the diminu-
tion in the fibrin of the blood is in exact proportion to the severity of the
fever, and the number of white globules is increased in a similar ratio.
In connection with these blood changes, a series of changes take place in
those organs and tissues of the body in which the jDrocess of waste and re-
pair are most rapidly going on. They are of the nature of parenchyma-
tous degeneration, the essential constituents of the affected organs and
tissues being involved. Similar parenchymatous changes are met with to a
greater or less extent in other acute infectious diseases.
Spleen. — The organ in which parenchymatous degeneration occurs ear-
liest and most extensively is the spleen. We find this organ undergoing
three distinct changes : —
First. It is increased in size, sometimes enormously. The enlargement
commences soon aftpr the beginning of the disease, and goes on rapidly
until the third week, after which it ceases, and within a few days begins to
diminish. If recovery takes place, by the time it is reached, the spleen will
have returned to its normal size. The splenic enlargement is apparently
due to congestion and to an increase of normal elements.
Second. As soon as the spleen reaches its maximum size, its consistency
diminishes, and this softening is sometimes so marked that, if a post-mortem
be made at the end of the third week, it will present the appearance of a
dark, jelly-like mass, which is easily broken down.
Third. The organ becomes almost black in color, owing to the intense
congestion which attends its enlargement, and to the deposit of a brown
pigment in its substance. These changes in the spleen take place, in a
greater or less degree, in ninety-eight cases out of every hundred. At the
post-mortem of those who have died of typhoid fever infarctions are some-
612 ACUTE GENEEAL DISEASES.
times found, alfhough there is nothing peculiar about them. In rare in-
stances, rupture of the spleen occurs without infarctions.
Liver. — Changes in the liver are by no means as common as those in the
spleen. The liver may be found presenting its normal appearance, or it
may be soft and flabby. When soft and flabby, a microscopic examination
shows the liver cells more or less granular and fatty ; the nuclei of the cells
can no longer be seen, and the degeneration may become so extensive that
the outline of the hepatic cells is lost, and nothing but a mass of granules
remains. Occasionally there will be found in the liver small grayish nod-
ules situated along the course of the small veins ; these bodies consist of
lymphoid cells. The lining membrane of the gall-bladder sometimes pre-
sents evidences of catarrhal or diphtheritic inflammation, when there has
been no evidence of its existence during life ; cases are recorded where it
has been found ulcerated.
Kidneys. — Degenerative changes in the kidneys are of not infrequent oc-
currence in the course of typhoid fever ; they vary in extent with the dura-
tion and severity of the fever. When present, they are more marked in
the cortical than in the medullary portion of the organ. In some cases
they are confined to the epithelial elements, while in other cases degenera-
tion of all the anatomical elements of the organs can be found. Such ex-
tensive changes are less liable to occur in typhoid than in typhus fever.
Small gray nodules, similar to those referred to as occurring in the liver, are
sometimes found. If the epithelial degeneration of the cortical substance
is extensive, the cells finally break down into a granular detritus, and the
cut surface assumes a yellow color and is softer than normal. Infarctions
are sometimes met with in the kidneys of those dying of typhoid fever.
Heart. — The parenchymatous changes which take place in the heart are
more marked than those in any other organ except the spleen. In a large
proportion of cases it becomes soft and flabby, and is of a grayish or brown
color. Sometimes it is so much changed that its tissue is easily broken
down by moderate pressure ; it loses its" normal outline, and when removed
from the body the walls of its cavities readily fall together. When its mus-
cular tissue is examined microscopically, in many instances it will be found
that granular changes, affecting the ultimate muscular fibres, have oc-
curred ; this granular muscular degeneration may be general or local. Oc-
casionally the muscular fibres are infiltrated with brown pigment. If, as
is sometimes the case, the heart retains its normal outline, is friable, and
its cut surface glistens, the muscular fibres will be found to have undergone
a change which closely resembles amyloid degeneration ; they will be filled
with a material which presents the same shining appearance as the amy-
loid substance, but on applying the iodine test the amyloid reaction does
not take place. It is a form of degeneration which is not confined to the
muscular tissue of the heart, but is found to a greater or less extent in the
voluntary muscles throughout the body. Thrombi are sometimes found in
the heart, and vegetations adhering to the valves and chordae tendinese.
These may give rise to infarctions in the different organs. The existence
of these degenerative changes in the heart may be recognized during the
TYPHOID FEVEE. 613
life of the patient, for the heart-sounds become feeble according to the ex-
tent of the degeneration, and in some cases the first sound of the heart will
be absent.
Lungs. — The lungs undergo changes which have received the name of
splenization, from the close resemblance which the affected portion of lung
then bears to the spleen. The affected tissue is of a darker color than nor-
mal, and scattered through its substance will be seen minute red or yellow-
ish-white points ; these points are scanty blood extravasations. It is of a
reddish-blue, brown, or black color ; its consistence is firmer than normal,
it crepitates less freely, has a more homogeneous appearance upon its cut
surface, and is less moist than normal lung-tissue ; a dark fluid will some-
times ooze from its cut surface, but not as freely as in hypersemia, and the
fluid is more watery in appearance. A microscopical examination of lung-
tissue in this condition shows the capillary vessels filled with blood, and the
alveoli containing a variable number of cells. It is a condition closely re-
sembling that condition known as static pneumonia, but no inflammatory
process exists ; it is simply a stasis in the capillary circulation, accom-
panied by a slight increase in the cell elements in the alveoli.
So constantly is catarrhal bronchitis present in this fever, that Dr. Stokes
proposed to call typhoid fever Ironcliial typhus. In most cases this catarrh
is not extensive, but affects only the larger bronchi ; it may, however, ex-
tend to the smaller tubes and give rise to capillary bronchitis and broncho-
pneumonia. Pulmonary infarctions are frequently found in the lungs of
those who have died of typhoid fever. They are sometimes quite numerous,
are usually of small size, and vary in appearance according to the stage of
their development. When recent they are of dark color, and feel like con-
solidated lung-tissue ; later, the color changes to yellow ; they may soften
and break down.
Larynx. — The larynx, as well as the bronchial tubes, is frequently the
seat of catarrhal inflammation ; less frequently it is the seat of diphtheritic
inflammation. In connection with these laryngeal inflammations, ulcers
appear in the larynx ; these have received the name of " typhoid ulcers of
the larynx : " sometimes they give rise to quite extensive hemorrhages.
In connection with, or independent of, these laryngeal ulcers, ulceration of
the mucous membrane of the mouth and pharynx may occur; at times it
involves the epiglottis in such a manner as to clip off its edges. These
ulcers may develop on the mucous membrane of the Eustachian tubes. In
those cases where permanent deafness follows an attack of typhoid fever,
it will usually be due to ulceration of the mucous membrane of the Eus-
tachian tube.
Brain and Nervous System. — As yet we have not been able to determine
whether there are any structural changes in the brain or nervous system
so constant that they may be regarded as lesions of typhoid fever, although
it is reasonable to infer that in a disease where such severe functional dis-
turbances of the cerebro-spinal system exist there must be constant and
definite parenchymatous changes. (Edema of the pia mater and of the
brain substance, with occasionally quite extensive adhesions of the dura
614 ACUTE GEISTEKAL DISEASES.
mater to the cranium, not infrequently exists. Punctate extravasations
into the brain substance are found in a certain number of cases, but even
in severe cases they are not always present.
Stomach. — The changes which occur in the stomach are equally impor-
tant with those which occur in the other internal organs, and are degenera-
tive in their nature. Softening and degeneration of its glandular struc-
ture are sometimes so extensive that, if recovery from the fever takes place,
a very long time must elapse before the organ can perform its normal func-
tion. It is the existence of these degenerative changes that gives rise to
the disturbance in digestion which is present in so many cases, not onlj
during the continuance of the fever, but during convalescence.
Muscles. — Muscular degeneration is of two varieties -.—first, a granulai
degeneration, which corresponds to ordinary fatty degeneration. Secondly,
a waxy or vitreous degeneration, which consists in the conversion of the
contractile substance of the primitive bundles into a homogeneous, waxy
shining mass. Often both forms of degeneration occur together, one or the
other predominating. In both forms of degeneration the muscular fibres
become thicker and more brittle than normal. In the highest degree of de-
generation the muscular fibres are entirely lost, and the muscle may present
a yellowish or whitish appearance, so that hardly any traces of its normal
color remain. This muscular degeneration, however, is not peculiar to
typhoid fever, but is met with in all severe infectious diseases. The want
of muscular power, which is so prominent a symptom during the height
of the fever, may depend on the disturbances of the nervous system, but
the excessive loss of muscular power which is so often present during con-
valescence is due almost entirely to the muscular changes. The physical
strength returns gradually during convalescence as the muscles are re-
generated, and it may be months before it is fully re-established. The
muscles of the tongue undergo degeneration in the same way as the other
voluntary muscles, which accounts in some degree for the interference
with the function of that organ, so often a prominent phenomenon of the
disease.
The salivary glands enlarge, become firm and tense, and assume a more
or less brown-yellow color. They have the consistence of cartilage. Late
in the disease the hardness diminishes, and they assume a red color. These
changes are due to a parenchymatous degeneration, which has been pre-
ceded by a cellular hyperplasia. It accounts to a certain extent for the
diminution of the salivary secretion, which is so marked and constant an
attendant of the fever. Similar cellular and parenchymatous changes take
place in the pancreas. Changes similar to these occur in other febrile
diseases, so that they cannot be regarded as characteristic of typhoid
fever.
Intestines. — The essential and characteristic lesions of typhoid fever are
found in the lymph structures of the intestines. They vary only in degree
and not in character with the duration of the fever and their proximity to
the ileo-csecal valve. Although changes closely resembling them may be
present in other diseases, there is no other disease in which they follow a
TYPnOID FEVEE.
615
regular course of development, with stages limited by days and weeks.
These changes in typlioid fever correspond very closely in their different
stages with the four weeks of the disease. During the first week they are
confined to a catarrhal inflammation of the intestinal mucous membrane,
most marked about the Peyerian jiatches, with a medullary infiltration of
these and the solitary glands, which extends in some cases into the adja-
cent tissues. Tlie infiltrated cells are mostly lymphoid cells, though large,
round and polygonal cells with multiple nuclei are also present. These lat-
ter are swollen epithelial cells from the reticulated tissue of the mucous
membrane and lymph follicles. As a result of these processes, there is
hyperasmia and swelling of the mucous membrane, and the affected glands
become enlarged and elevated from one to two lines above the mucous sur-
face. They assume a dark red or reddish-gray color marked with fine white
striations, and present the so-called
"shaven beard" aj^pearance. Their
consistence varies with the severity of
the process. When moderately swollen,
they are soft and present a spongy ap-
pearance, but in the severer types the
entire gland becomes hard and smooth.
These changes begin and are most ex-
tensive in the glands nearest the ileo-
csecal valve ; they are generally well
marked within forty-eight hours after
the commencement of the disease, but
are not fully developed until the end of
the first week, when all the glands are
involved which are likely to undergo
change. The number of patches in-
volved varies from four to five near the
valve to twenty or thirty throughout
the whole intestine. The solitary fol-
licles do not participate in the infiltra- mucou
tion and swelling to the same extent as
fbp Ho-Tm'nfltpfl o-lfliidc? ^- ^^yf patch showing the reticulated or
Liit! aguiiiifiueu gxaiiub. shaven-beard appearance.
Tn +1t<3 QPrnnrI oiwol- tlia lTTrnor5»miQ The mitcovs membrane is hyper cemie, and the
in xne secona WeeiC ine nyperaemia solitary folUcles, B, are only slightly involved.
and catarrh of the mucous membrane
subside, leaving the agminated and solitary glands more elevated ; the
white lines upon their surface disappear, and they assume a uniformly red
color. An unusually rapid cellular hyperplasia takes place in the follicles,
by which they beco"me swollen in all directions. Usually the new cell
growth extends beyond the limit of the follicles, so that the adjoining
mucous membrane is also infiltrated with cells. The new cells distend the
glands, and a vertical section of a patch in this stage shows the villi in-
creased in length and width, and fused together at their bases or through-
out their, entire length by the embryonic tissue. These newly formed
cells may wander through the muscular coat or penetrate the sub-serous
Fig. 147.
surface of a portion of the Ileum
during the first week of Typhoid Fever.
616
ACUTE GENERAL DISEASES.
tissue.
Thus hyperplasia of the adenoid tissue is the essential patho-
logical change in the second week.
By the middle or latter part of the
second week the process passes into
its third stage, and necrotic changes
are established in the newly formed
tissue.
These morbid changes may ter-
minate in three ways : first, the new
elements in these ductless glands may
become disintegrated and undergo
absorption, and in this way they may
gradually undergo resolution ; second,
either the tissue between the follicles
remains infiltrated and elevated while
their contents are absorbed, or indi-
vidual follicles of the agminated
glands rupture and discharge their
Mucous surface ofthe Ileum during the second week Contents into the intestine, leaving
. ^ , of Typhoid Fever. dcprcssious which givc the gland a
A. Peyer s patch thickened and raised— from hype.r- '^ ^
jyiasio,. reticulated appearance ; third, the
B. Solitary follicles much enlarged. , „ , t i • , ■ ,
most irequent and cliaracteristic ter-
mination of the typhoid process is the separation of the dead tissue as a
«longh, or by ulceration and the
formation of the typhoid ulcer. ,^ . ,^___ ,^:b
Ulceration which begins at the
most elevated portion of a patch,
already stained yellow or yellow-
ish green by intestinal fluids or
darker by sanguineous infiltration
advances gradually until a small
irregular ulcer has enlarged to
one covering the whole gland, or
the entire gland may slough uni-
formly, and at once form the com-
plete ulcer.
Usually the sloughing and re-
moval of the necrotic tissue does
not take place until the third
■week of the disease. As the
sloughs gradually loosen and fall
ofi:, there is a loss of substance
which extends to the deeper
layer of the mucous membrane,
removing the entire gland and
the mucous tissue surrounding it,
laying bare the muscular coat of
ABm
Fig. 149
Mucous surf ace of a portion of the Ileum in the third week
of Typhoid Fever.
A. Peyer's patch, ulcerated, showing the overhangirig
edges and the roughened base.
B. Solitanj follicles ulcerated at their apices.
C. A small oval ulcer.
D. Pe7f oration of the intestine.
TYPHOID FEVER.
617
the intestine. The necrotic process may extend and involve the muscular
tissue, and end in perforation of the peritoneal covering. These ulcers
may be developed in the jejunum, the ileum, the stomach, and the large
intestine. In the lower part of the ileum, at the ileo-csecal valve, they are
usually of large size— so large that only small portions of healthy mucous
membrane are left between them ; in the jejunum, stomach, and large
intestine they are usually round and of small size. The form of the
ulceration corresponds to that of the necrotic tissue ; if an entire
Peyerian patch is necrotic, an elliptical ulcer is formed, with its long axis
corresponding to that of the intestine. In the jejunum and large intes-
tine, the ulcers are usually small and round. The edges of the ulcer are
sharp, tumid, and overhang the floor of the ulcer. Sometimes the ulcers
are hemorrhagic.
In the fourth week the process of cicatrization is commenced. Gradually
the swollen edges of the ulcers subside, granulation-tissue springs up from
their base, connective-tissue membrane is formed, and the edges of the ul-
cer become united by a cicatrix which is covered with a layer of e]3ithelium.
The gland structure is never regenerated. The cicatrix which is formed
by the healing of these ulcers is slightly depressed, and less vascular than
the surrounding mucous membrane. During the healing process the cica-
trix becomes more or less pigmented, and these pigmented scars may be
recognized years after cicatrization has taken place. They seldom cause any
puckering or diminu-
tion in the calibre of the
intestine. In many cases
the process does not
pursue this regular
course ; while one por-
tion of the ulcer is
cicatrizing, ulceration
in another part may
be extending ; such
long-continued ulcera-
tion prolongs convales-
cence, and may even
cause death from ex-
haustion.
Mesenteric Glands. —
Associated with these
intestinal changes, anal-
ogous processes take
place in the mesenteric
glands. These mesen-
teric changes are also
most marked in the
glands situated nearest
the ileo-caecal valve ; they are secondary to the changes in the intestinal
Fig. 150.
Sketch ehowiug Enlargement of the Mesenteric Lymphatic Glands
in Typhoid Fever.
A, A. Portion of Small Intestine.
B. Mesentery.
O. Glands enlarged. At Da gland is shown in section.
618 ACUTE GElifEEAL DISEASES."
glands, and usually in a degree corresponding to the extent of the intestinal
lesions. The glands are first congested, then there is a production of lym-
phoid and large cells similar to those which are found in the enlarged
intestinal follicles ; the glands become enlarged, and are the seat of an
acute cellular hyperplasia. When the enlargement has attained its full
size, the hypergemia diminishes, and the cellular elements begin to disin-
tegrate and are absorbed. In about one-half the cases the enlargement
reaches its maximum size by the middle of the second or at the commence-
ment of the third week. The enlarged glands vary in size from that of
a hazel-nut to a small hen's egg. In the stage of retrogression some of
the glands simply shrink and return to their normal condition; in others,
partial softening takes place and afterward absorption, leaying a fibrous
cicatrix. If the glands reach a very large size, absorption is incomplete,
and dry, yellow, cheesy masses are left, which after a time become calca-
reous and enclosed in a fibrous capsule. In rare instances the glands be-
come fluid, their capsules are destroyed, and the softened masses escape into
the peritoneal cavity and cause peritonitis. A calcareous condition of
the mesenteric glands, like the pigmented cicatrices of the solitary and
agminated glands, gives evidence of a previous severe attack of typhoid
fever.
Another lesion of typhoid fever occurring during convalescence, is sup-
purative inflammation in the subcutaneous cellular tissue. The inflamma-
tion is not of an active type, but is accompanied by some redness and pain.
Gradually a tumor is formed at the seat of the inflammation, usually where
there has been the greatest amount of pressure, and after a time fluctuation
becomes distinct as the swelling increases ; sometimes two or inore of these
swellings coalesce, and finally an immense abscess may be formed contain-
ing a pint or more of pus. Eetro-pharyngeal ulcers are the result of sup-
purative inflammation of the connective-tissue.
Etiology. — According to the classification which I have adopted, typhoid
fever is included in the list of miasmatic-contagious diseases. Usually it
has been regarded as an endemic form of disease. There seems to be no
connection between its development and destitution. It may occur as an
isolated case, or whole households and neighborhoods may be stricken down
with the disease. "We must therefore regard the causes of its production
as local and limited, not widespread. It is possible for it to prevail as an
epidemic, but it must first have been endemic.
In studying the etiology of this fever, two prominent questions present
themselves : —
First : is it a contagious form of disease ?
Second : is it ever of spontaneous origin ?
After years of careful investigation, I think it may be now unhesitatingly
stated that facts do not sustain the opinion that typhoid fever is ever,
strictly speaking, a contagious disease. Persons sick with this fever are
now admitted into our general hospitals, and are placed by the side of
patients with pneumonia or any form of chronic disease, without endanger-
ing the lives of such patients. This fact shows how generally the pro-
TYPHOID FEVER. 619
fession regard this disease as non-contagious. Typhoid fever is no longer
restricted by quarantine regulations.
The question of spontaneous origin has strong advocates on both sides.
Some of those who believe that it may have a spontaneous origin maintain
that the poison which gives rise to it is developed by the decomposition of
organic matter, and that the specific character of the fever is due to the
particular substances which are undergoing decomposition. Others main-
tain that decomposing human excrement is necessary for the production
of the peculiar poison which gives rise to typhoid fever. Again, others
believe that the presence of vegetable matter in certain conditions is neces-
sary for its production, and that these conditions are similar to those which
exist when miasmatic fevers are developed, the difference in the two poisons
depending rabher upon the temperature than upon the character of the in-
gredients.
There is a view, recently advanced, that sewer gases contain the poison
which has the power of developing the disease. On the other hand, it is
maintained by those who do not believe in the spontaneous origin of this
fever that, in addition to decomposing animal and vegetable matter, it is
necessary that the specific typhoid poison be incorporated in the decom-
posing mass. Observations prove clearly that vegetable or animal decom-
position alone is not sufficient for the development of this disease, and facts
do not sustain the claim of those who say that sewer gases contain the
typhoid poison, for those cities in which the sewerage is most imperfect,
and those houses most frequently permeated Avith sewer gases, are not the
hotbeds of typhoid fever. Moreover, this fever is more prevalent in the
country than in the city, in places where there are no sewer gases ; indeed,
well-marked cases of typhoid fever are of quite rare occurrence in the city,
and when they do occur seem to be develoj)ed independently of defective
sewerage. In other words, all the elements which favor its production
may be present, such as animal and vegetable decomposition or sewer gases,
and yet not a single case of typhoid fever be developed, until the typhoid
poison is brought Avithin the boundaries favorable to its development ; then
a severe epidemic of the disease may be developed, but decomposition is
simply the soil in which the specific poison is developed.
The question now arises : — what is the real nature of that poison derived
from a person sick with typhoid fever, which has the power of indefinitely
reproducing itself outside of the body in connection with decomposing or-
ganic matter and thus becoming the infecting agent when individuals are
brought within its influence ? The history of epidemics of typhoid fever
leads to the conclusion that the poison is contained in \\\q f cecal discharges
of the sick. When such excrement is in fresh condition the poison is not
active ; it must go through a stage of development outside of the body.
This may take place in the excrement itself, but it goes on more rapidly
and abundantly if the excrement is collected in privies or in earth that is
already saturated with organic matter. In this way we can readily explain
how a typhoid fever patient coming into a locality previously free from the
disease can establish there a focus of infection, from which many persons
630 ACUTE GEXBRAL DISEASES.
may become diseased. It is evident that this poison is not active in its
fresh state, from the fact that the disease is not carried directly from one
individual to another ; — attendants, nurses, and physicians are no more
liable to the disease than those who are in no way exposed to the disease
and live in a healthy locality.
It is difficult to determine the period of incubation, or length of time
the poison must remain in the body before symptoms of the disease are
manifest. The histories of isolated cases would lead to the conclusion that
the period varies from fourteen to twenty days. Undoubtedly there are
two principal channels of infection, namely, the air we breathe and the
water we drink. This fever may be developed by gases which emanate
from privies, sewers, etc., which have been the receptacle of excrement
from typhoid patients, and also, by drinking water from springs and wells
which have become contaminated by matters from adjoining privies and
cess-pools. It is an established fact that water remains contaminated,
though far remote from the point where it came in contact with a defective
sewer or water-closet. Soil pipes and sewerage may be defective for a
long time and no case of typhoid fever occur, when suddenly an endemic
of typhoid fever breaks out, and careful investigation shows that its de-
velopment was preceded by the introduction of the excrement of a single
individual sick with the disease. It is the belief of some that milk may
convey the typhoid poison, and there is evidence in favor of this opinion ;
but there is stronger evidence that the water used to dilute the milk, and
not the milk itself, is the medium through which the poison is transmitted.
This poison has great vitality. Typhoid fever frequently occurs in the
same locality year after year, when the surrounding conditions are favor-
able to its development. Those conditions are more frequently present in
the autumn than in any other season of the year, and for this reason it
has been called autumnal fever. Usually it makes its appearance in a
locality, each year, at about the same time ; case after case is developed
until entire households and neighborhoods become its victims. Individu-
als who come to care for the sick may contract the disease, and even per-
sons who visit houses in which the disease is prevailing may afterward de-
velop the fever, contracting it, not from the sick, but from the infected
atmosphere of the locality.
Age must be regarded as a predisposing cause of typhoid fever. It is
much more likely to occur in young than in old persons ; it occurs most fre-
quently between the ages of fifteen and twenty-five, and is rarely met with
in persons over fifty. There are also individual idiosyncrasies which seem
to predispose to this fever. Some contract it upon the slightest exposure
to the influence of the poison, while others, frequently brought in contact
with it for a long time, escape. Again, an individual may have repeated
attacks of typhoid fever.
Symptoms. — I shall first consider the prominent symptoms of a typical
case, and discuss in detail these symptoms, without special regard to the
time of their occurrence.
This fever is usually insidious in its approach, and comes on with a cer-
TYPHOID FEVER. 621
tain degree of uneasiness throughout the system ; the patient feels uncom-
fortable, has no pain, but feels thab he is about to be sick. He complains
of a grumbling headache, more or less aching of the limbs, " a tired feeling
all over," chilly sensations, alternating with flashes of heat and loss of
appetite ; — not infrequently nausea and vomiting are present. The pre-
monitory symptoms gradually increasing in severity, by the fifth or sixth
day the patient is compelled to i;ake to his bed. At this early period there
may be a slight diarrhoea. In very mild cases the disease comes on so in-
sidiously, and with symptoms so mild, that the patient is often able to
pursue his ordinary avocations, complaining only of an undefined indispo-
sition. In very many severe cases it is impossible for the patient to accu-
rately fix upon tlie time when the fever commenced ; and in no case will
an early positive diagnosis be possible. 'Typhoid fever may be suspected,
but that is as far as one can safely go.
In all cases variation in temperature is one of the most important early
symptoms. Such variations in temperature in a typical case may be divided
into four periods, of one week each, which correspond to the four weeks of
the disease. In the first week there is a gradual and steady rise in tem-
perature, with regular morning and evening variations, each evening tem-
perature being about 2° F. higher than that of the morning, and 1^ F.
higher than the previous night, so that at the end of the first week it
is at its maximum, — 104° or 105° F. This is one of the most character-
istic features of the disease. This gradual rise of, and these variations in,
temperature are not present in every case, but when they are present
they will greatly assist in making an early diagnosis. It has been said that
tj^phoid fever is the only disease, except double quotidian intermittent
fever, that gives two full thermometrical curves within twenty-four hours;
that is, two remissions and two exacerbations. If this is true, it helps to
explain certain high temperatures in the morning, and afPords valuable
assistance in making a diagnosis.
During the second week the variations in temperature are slight, retain-
ing, however, the same maximum as was reached at the end of the first
week. The variations during the third week are remittent in character.
During the fourth week they become intermittent, and the range of tem-
perature in the exacerbations is lower. The variations in pulse correspond
to those in temperature. During the first week the pulse gradually be-
comes more and more frequent, and remains at the height reached at the
end of the first week ; throughout the second and third weeks there are
distinct morning and evening remissions ; during the fourth week it falls
to its normal standard. Diarrhoea generally comes on during the first
week or is continued from the prodromal stage. In some cases it may have
ceased by the second week.
On the seventh day, or between it and the twelfth day, the characteristic
eruption appears. About this time the headache abates and more or less
somnolence and delirium come on. The delirium at first is slight, and is
only observed during the night. Day by day the patient loses flesh and
strength, and becomes more and more unconscious, and all the phenomena
622 ACTJTE GENEEAL DISEASES.
of the typhoid state are developed, viz. : a dry brown tongue, feeble pulse,
low muttei-ing delirium, stupor, tremors, subsultus, involuntary evacua-
tions, and the other phenomena of great prostration. If the disease is to
terminate favorably, the amendment is usually gradual. The first sign of
improvement is a decided remission of the fever.
Such, in brief, are the phenomena which attend the ushering-in and de-
velopment of an ordinary case of typhoid fever ; they are, however, sub-
ject to numerous modifications. Some cases are mild throughout their
entire course ; some are severe at first and mild afterward ; some are mild
at first and severe afterward ; while others are severe throughout their en-
tire course.
The Physiognomy. — As a rule, the countenance has nothing peculiar in
its appearance ; but if the disease is of a severe type, by the second week
the countenance assumes a characteristic appearance — there is a pale, olive,
leaden look, the eye becomes dull and the conjunctiva congested, and usu-
ally there is a small, rose-colored spot in the centre of each cheek. The
face does not assume the dark mahogany color seen in typhus, but in the
advanced stage of the fever it has more of the hectic flush of phthisis.
Tongue. — From the very outset, the tongue is covered with a light, white
coat, but there is nothing special in its appearance before the end of the
first week ; then it may become red upon its sides and tip, and show a
slight disposition to dryness in its centre. As the disease passes into its
second and third weeks, the tongue becomes more heavily coated, the
coating becomes brown and dry, and sordes collect upon the teeth and
sides of the mouth in sufficient quantities to form crusts. These crusts
may become thicker and more abundant as the disease progresses. At any
period in the course of the disease the tongue may suddenly clear off, and
present a shiny red, " beef-colored " appearance. The tongue and lips may
become dry, cracked and fissured. As the sordes are removed from the
lips, they will often bleed ; and in certain cases, more especially in the
severer forms of the disease, the entire mouth and tongue may be covered
with dark-colored incrustations. Such incrustations are seen early in con-
nection with those cases where there are extensive blood changes ; when
present they are of grave significance. One of the first indications of con-
valescence is a moist condition of the tongue about its edges ; gradually
its entire surface becomes moist, and by the time convalescence is fully
established it is restored to its natural condition.
Gastric symptoms are always more or less prominent ; loss of appetite is
one of the earliest symptoms, and nausea and vomiting are quite common
during the first week of the fever. The vomited matters usually consist of
a greenish fluid. When vomiting comes on late in the fever, it is either
due to sub-acute gastric catarrh, or is symptomatic of local or general peri-
tonitis. In a large proportion of cases thirst is excessive. The lips are
parched, and in severe cases crack and bleed. In some cases hemorrhage
from the gums occurs.
Diarrhoea. — Although not invariably present, diarrhoea is so frequent an
attendant of this fever that it is considered one of its characteristic symp-
TYPHOID FEVEK. 623
toms. It varies with the severity of the attack, the date of its commence-
ment, and its duration. The characteristic typhoid discharges are of a
yellowish -green color, described as -'pea-soup discliarges." Sometimes
they are of a dark color, resembling coffee-grounds ; their react;on is alka-
line. In some cases diarrhcea is present at the very outset of the disease,
and continues throughout the entire course. In others, it does not appear
until the third week. The second week is the ordinary time for its ap-
pearance. When the diarrhoea appears late in the course of the disease,
the discharges are more copious than when it appears early. A mild
diarrhoea throughout the entire course of the fever is a favorable rather than
an unfavorable symj)tom. In mild cases diarrhoea is sometimes absent.
Intestinal Hemorrhage. — This occurs in about one in twenty cases, and
varies in quantity from a mere trace of blood in the stools to a profuse dis-
charge of from sixteen to eighteen ounces. The slight hemorrhages which
occur early in the disease simply indicate a hemorrhagic tendency, the same
as the epistaxis, which is very frequently among the early symj^toms. In
both instances the bleeding comes from the capillaries of the mucous mem-
brane. The more profuse hemorrhages are due to the opening of an artery
in some intestinal ulcer. Hemorrhages due to this cause may be sudden
and profuse, and may destroy the life of the patient. The usual time for
the occurrence of these profuse intestinal hemorrhages is the latter part of
the second and during the third week. These hemorrhages are usually
accompanied by a sudden fall in temperature, perhaps two or three degrees ;
if then in a patient severely ill of typhoid fever a sudden fall in temjDcra-
ture occurs daring the second or third week, accomjDanied by extreme
prostration, it is very conclusive evidence that intestinal hemorrhage has
occurred, although externally the hemorrhage may not have made its
appearance. The blood is usually fluid, rarely clotted ; generally it is of a
bright red color^ owing to the alkaline condition of the intestinal contents.
Copious intestinal hemorrhages are more frequent in severe cases that have
been attended by profuse diarrhoea. Patients may die of intestinal hem-
orrhage before any blood has been voided externally. If the joatient sur-
vive a profuse intestinal hemorrhage, there is great danger of his dying
from peritonitis. He may die unexpectedly by syncope a number of hours
after a profuse intestinal hemorrhage.
Abdominal fain and tenderness are not usually present at the very outset
of typhoid fever, but generally, and almost without exception in the
severer cases, by the sixth day of the disease some pain and tenderness will
be present in the right iliac fossa. The pain and tenderness usually in-
crease as the disease progresses, and in the advanced stages it is sometimes
so marked that slight pressure over this region is unbearable. While ex-
amining this region in order to determine the presence or absence of pain
and tenderness, the pressure should be made with the palm of the hand ;
the expression of the countenance will indicate the presence of ten-
derness, long before an audible complaint is made by the patient. It is
important to bear in mind the possible occurrence of a more severe ab-
dominal pain arising from intestinal perforation. The following are the
624 ACUTE GENERAL DISEASES.
characteristic symptoms of this lesion : if in the course of a slight op
severe form of this fever, or even when the disease has been latent and the
diagnosis of typhoid fever has not been clear, the patient should be suddenly
seized with diarrhoea, pain in the abdomen, aggravated by pressure, per-
haps at first localized in the right iliac fossa, but soon extending over the
entire abdominal cavity, attended by rapid tympanitic distention of the
abdomen, and symptoms of great prostration, a rapid, feeble pulse, a sunken,
anxious expression of countenance, nausea and vomiting, quickly followed
by coldness and blueness of the extremities, and the other signs of sudden
collapse, it is almost certain that perforation of the intestine has occurred.
I have known this accident to occur when convalescence was apparently
progressing satisfactorily.
Tympanitis is another very common symptom of typhoid fever.
Usually it is not present during the first week, but by the end of the first
or the commencement of the second week a fulness of the abdomen will
be noticed. As the fever advances, the distention often becomes extreme;
this is due to a collection of gas in the large intestine, developed
through some change in the mucous membrane, the exact nature of
which we do not fully understand. When once it is developed it remains
until convalescence is fully established, and is always an important diag-
nostic sign of this fever.
In connection with the development of the tympanitis, when firm press-
ure is made over the right iliac fossa, a gurgling sound is produced ; but
gurgling in the right iliac fossa cannot by any means be regarded as a
positive symptom of typhoid fever, as it may occur in any disease where
there is distention of the abdomen due to accumulation of gas in the intes-
tines. In typhoid fever, so long as the abdomen remains tympanitic, no
matter what the temperature and pulse of the patient may be, he is in
more or less danger, for it shows that there are intestinal changes still in
progress, and the reparative processes are not complete ; this is more espe-
cially the case when the tympanitis has continued from the active period
of the disease into the period of convalescence.
JJrine. — Extended and very careful analyses of the urine of typhoid
fever patients have been frequently made, without giving any very practi-
cal results. Usually during the first two weeks of the fever the urine
is diminished in quantity, and its color is dark and its specific gravity high;
after the second week it is increased, and when convalescence is estab-
lished, it becomes pale, and its specific gravity is lowered. The amount of
urine excreted daily throughout the active period of the fever is increased.
The increase is in proportion to the intensity of the fever, subject in some
degree to the quantity and quality of the food taken. It will be greater
when large quantities of strong beef-tea are taken than when the diet
consists of milk. So long as the kidneys are able to eliminate the excess
of urea, no harm results ; but if the quantity exceeds their power of elimi-
nation, or if their function is interfered with, uraemic symptoms will be de-
veloped, such as delirium, stupor and coma. Albumen in the urine is
only of occasional occurrence in the course of typhoid fever. When
TYPHOID FEVEE. G25
present the quantity is usually small, and is only temporary. It rarely
appears before the third week. Its appearance is often marked by the oc-
currence of cerebral symptoms. Renal epithelium and casts may or may
not be present with the albumen.
Nervous Phenomena. — The symptoms referable to the nervous system
are not so prominent in typhoid as in typhus fever ; yet there are many
cases in which these symptoms form an important part of the history. One
of the most constant is headache. In the majority of cases it is one of the
ushering-in symptoms of the disease. It is present in mild as well as in
severe cases ; sometimes it is confined to the forehead and temples ; more
often it extends over the whole head ; it is not violent, but a dull, heavy pain.
It usually increases in severity until the middle period of the disease, cer-
tainly until the close of the first week ; and generally associated with it
there is intolerance of light and conjunctival injection, pain in the back
and limbs, and a general aching of the whole body.
Somnolence is present to a greater or less degree in all cases. In mild
cases it does not appear until late, and usually is not long continued. In
the severer cases it appears early and continues until convalescence begins ;
in fatal cases it passes into a state of coma. It is often interrupted by de-
lirium. In children this symptom is especially prominent, and is very val-
uable as a means of diagnosis.
Delirium is more frequently present than absent in typhoid fever. The
character of the delirium varies ; the usual form is known as the "low-
muttering " delirium, and is rather characteristic of this type of fever, al-
though in very many cases the delirium is violent in character, and may
become maniacal to such an extent as to I'equire physical restraint. Not
infrequently typhoid fever patients attempt to jump out of a window, or
injure themselves or their attendants in their endeavors to escape from fan-
cied dangers. It is very common for the minds of this class of patients to
be occupied with those things which engaged their attention just prior to
their illness. The delirium rarely comes on until the second week of the
fever, and it commences and is most active at night. After it has once ap-
peared, it usually continues until convalescence is established, and generally
disappears during a sound sleep which attends the early stage of convales-
cence. The maniacal form of delirium in typhoid fever is usually most
marked at night. During the low-muttering delirium, if the patient is
asked questions he will generally answer correctly.
Muscular Prostration and Paralysis. — In all severe cases of typhoid fe-
ver, muscular prostration is noticeable in the early stages, and increases
with the progress of the fever. It is generally most marked during the
third week. Where there is marked muscular paralysis, the urine and fas-
ces are passed involuntarily, there is inability to protrude the tongue, and
more or less difficulty in deglutition, or inability to articulate distinctly.
Retention of the urine may also occur from vesical paralysis.
Muscular Tremors. — Tremors of the hands, tongue, or lips are most
often met with in young subjects and those who are addicted to the use of
spirits. Severe tremors unaccompanied by much mental disturbance often.
40
626 ACUTE GENERAL DISEASES.
attend extensive intestinal changes. Spasmodic movements, such as sub-
sultus, hiccough, etc., and rigid contraction of the muscles of the neck or
extremities are sometimes present in severe cases. General convulsions are
of rare occurrence, except in very young children, and when they occur
have no special significance.
Special Senses. — The symptoms referable to the special senses require lit-
tle more than enumeration. As regards the sense of sight, there is nothing
worthy of note, except that the eye assumes a dull expression and that the
pnpil is dilated ; some patients complain of haziness of vision, which is in-
creased when they assume a sitting posture. The setise of hearing is always
Inore or less impaired. This is most marked about the middle period of
the fever ; then it is impossible for the patient to hear ordinary conversa-
tion. Ringing and buzzing sounds in the ears are often complained of in
the early stage of the fever. When the loss of hearing is confined to one
ear, it is generally caused by ulceration of the mucous lining of the Eusta-
chian tube, or by suppuration of the middle ear. The sense of taste usually
is altered or perverted ; articles of food are tasteless, or have an unnatural
flavor. When the tongue and mouth are covered with a heavy coating of
sordes, the patient is unable to distinguish between bitter and sweet, and
swallows the most disgusting doses without complaint.
Hypermsthesia is another disturbance of a special sense. The surface of
the body of a typhoid fever patient may become so sensitive that he will cry
out with pain from the slightest touch. This hypergesthesia may be present
during the first week, or may not be present until convalescence is estab-
lished. It is most marked over the abdomen and lower extremities, and
usually occurs in females of an hysterical tendency. It is of importance to
discriminate between cutaneous tenderness in the abdominal region, and
the tenderness of peritoneal inflammation.
Epistaxis. — When this occurs during the first week, in most cases it is
of little importance except as a diagnostic sign of this type of fever ; when
it occurs during the third week it becomes important as an element of
prognosis, as it may be sufficiently profuse to destroy the life of the patient.
■Occurring late in the disease, unless it can be promptly arrested, it always
jeopardizes the life of the patient.
Emaciation is perhaps more marked and rapid in this than in any other
form of fever. It commences early and is progressive. By the time a
patient has reached the fourth week of a typhoid fever of even moderate
severity he is usually in a condition of extreme emaciation. In this par-
ticular he markedly differs from a patient ill with typhus fevp»\ for in the
latter case emaciation to any great extent does not occur.
Temperature. — In making thermometrical observations in this as well as
in ^li other forms of fever, the thermometer may be placed in the axilla,
the mouth, or the rectum. I shall refer to axillary temperature whenever
I speak of temperature without qualification. Usually in a typical case
the temperature begins to rise about noon on the first day of the develop-
ment of the fever, and continues so to do until between six and eight
o'clock in the evening, when it reaches its maximum for that day ; then
TYPHOID FEVEE.
627
there is no change until midnight, when it begins to decline, and by six
or eight o'clock in the morning it has reached its minimum, which is a de-
gree higher than on the morning of the preceding day. After six or eight
o'clock in the morning the temperature does not vary much until noon ;
then it again begins to rise, and by six o'clock in the evening it has reached
its maximum for that day, which is one degree higher than on the even-
ing of the preceding day. Again, at midnight it begins to fall, and by
morning it has fallen a degree, which leaves the minimum, and the aver-
age for the day a degree higher than on the preceding day. Thus it rises
a degree each day, with regular morning and evening variations, until the
eighth day of the fever, when, in most cases, it has reached its maximum
for the whole course of the disease.
Fig. 151.
Temperature Record in a Typical Case of Mild Typhoid
Fever. Eecovery.
During the second loeeTc the temperature remains at about the same maxi-
mum degree which it has reached at the end of the first week. There are
morning and evening variations of a degree or more, but the maximum of
the evening exacerbation remains the same.
During the third weeh the remission becomes more and more marked,
while during the exacerbation the temperature retains nearly the same
standard as during the second week. By the end of the third week the
morning temperature during the remission will be two or three degrees be-
low the maximum of the second week.
By the time the fourth weeh is reached, or at least by the middle of that
week, the temperature becomes intermittent, and with each exacerbation it
falls lower and lower, until by the end of the week the normal standard of
temperature has been reached, or it may fall a little below the normal
standard. These are the typical thermometrical variations of typhoid
fever, yet they are not always present, and there are many things which
will materially modify them. The fever does not always follow this typi-
cal course. Marked deviations from the record may be produced by com-
plications which would never have been discovered but for the irregular
thermometrical variations. By treatment, the temperature can, for a time, be
628
ACUTE GENERAL DISEASES.
Tery much lowered ; but if the treatment be discontinued, it will rise again.
In some cases it is not possible to detect the cause of the irregularity.
Pulse. — The pulse is also subject to variations, which correspond very
nearly with the variations in temperature, and occur not only on different
days, but at different hours on the same day. During the first week the
pulse becomes more and more frequent ; in the second and third weeks it
Sa,^. L 12. a 4. 5. 6. 7. 8. 9. m /J.
12. /3. /^. J5. 16. /7. \IS. 19. 20. 21. 22
/O^ ^ ^ ^ ^:
l--f^-f:
n e m e 7n e rri e 7n\e m e Jfi e m.\e fit e m e^WL €'.
''^f 1 1 |i H Ml
J 1
„ ^ ^g.
9S°i^ ^
— V it
()■/ \z :
-^ 1
\
© An intestinal hemorrhage occurred here.
Fig. 152.
Temperature Record in a Non-typical Case of Typhoid Eever.
remains at its height, and during the fourth week sinks to its normal aver-
age. Throughout the whole course of the disease it is less frequent in the
morning than in the evening. If, at the commencement of the fever, the
pulse is 98, by the end of the first week it will have reached 100, or 110
per minute, and there it remains during the second week ; after that time
it may become as frequent as 120, or 140.. During the first and second
weeks the rate of the pulse and the temperature range correspond, but
after this time the parallelism ceases as the failure of heart-power begins
to manifest itself. This failure of heart-power is indicated by an increase
in the frequency and feebleness of the pulse, which at this time may reach
140 per minute and yet the temperature show no alarming variation.
Under these circumstances, the pulse may become irregular and intermit-
ting. Should these irregularities and intermissions occur during the third
week, in most cases they are followed by death. With an irregular and
intermitting pulse, the first sound of the heart will usually be inaudible
over the precordial space, and this indicates that prompt and judicious
means must be employed to restore the heart's normal action and to avert
a fatal issue.
The severity of the disease during the first and second weeks of its devel-
opment is, to a great extent, indicated by the frequency of the pulse and
the height of the temperature. Although delirium and extensive tym-
panitis are important symptoms they do not determine the result ; but if a
patient during the first, or at the commencement of the second week of the
TYPHOID FEVER. 629
disease, has a pulse of 120 per minute, and a temperature of one hundred
and six, it is very doubtful whether convalescence can ever be established.
The pulse may increase in frequency from feeble heart-power alone while the
temperature is steadily falling. On the other hand, the pulse sometimes
falls almost to a normal standard, while the temj^erature remains high.
Eruption. — Some have claimed that this should be considered as a lesion
of the disease, but I prefer to class it among the symptoms. It makes its
appearance between the sixth and twelfth days, dating from the commence-
ment of the fever, and it is not attended by any unusual sensation. It re-
mains visible from eight to fourteen days, leaving no stain or mark on the
surface after its disappearance. It consists of isolated, lenticular spots
scattered more or less abundantly over the surface of any part of the body,
but usually most abundant upon the chest and abdomen. There may be
only a few spots visible at a time, or they may be so profuse as to cover the
body like a rash. Two or three well-defined spots of the eruption are suf-
ficient to establish the existence of the fever. Each spot is circular in
shape, and varies in diameter from a point to a line and a half, rarely
reaching two lines. It is slightly elevated above the surface of the sur-
rounding cuticle, is of a bright rose color, disappears upon slight pressure,
and returns as soon as the pressure is removed. Each spot remains visible
for three days, and then disappears. Sometimes, as one crop of the erup-
tion disappears another is developed, and this may go on for eight, twelve
or fourteen days. There are many cases in which only one crop appears.
As soon as one spot makes its appearance, it is well to mark it with tinc-
ture of iodine or nitrate of silver, so that observations will be always made
upon the one point. If it is a spot of typhoid eruption, and one crop of
eruption is to follow another, it will disappear within three days from the
time at which it was first seen, and other spots will take its place. It is
this feature which distinguishes the typhoid eruption from that of all other
fevers.
The question may be asked : — is this eruption essential to the diagnosis of
typhoid fever ? Many observers mention that the eruption is not constant,
and consequently not necessary for its diagnosis ; while others, equally
competent, maintain that, unless the eruption be present at some period
during the progress of the disease, the diagnosis of typhoid fever cannot be
made with certainty. Jenner states that he found the eruption present in
one hundred and forty-eight out of one hundred and fifty-two cases. I
would not say that it is possible for typhoid fever to occu,r without the
eruption ; neither would I affirm that scarlet fever ever exists without the
characteristic rash of the disease ; but as regards these respective fevers, if
no eruption was present, I would make the diagnosis with equal hesitancy
in the one case as in the other. The eruption is usually most marked in
cases of typhoid fever which occur between the ages of ten and thirty. Be-
fore ten and after thirty years it is usually not as well marked, and may be
readily overlooked unless careful search is made.
The typhoid poison, in its operation on the human body, does not always
effect the series of changes and symptoms just described. On the contrary.
630 ACUTE GENERAL DISEASES.
there are cases which run so mild a course that they can scarcely be digni.
fied by the name of fever, and, besides, there are imperfectly developed
cases which show a great diversity in their course, but they all can be in-
cluded under two heads.
First. — Mild typhoid fever, in which the symptoms are all mild.
Second. — Abortive typhoid fever, in which the duration of the disease is
markedly shortened.
In the 7nild tyjie, the fever runs its regular course, but is of low grade.
The temperature rises regularly until its maximum is reached, which rarely
exceeds 103° F., then it remains stationary for a time, generally about a
week ; the decline follows in the same manner as in a typical case. This
is the regular course of these cases if left to themselves, and, as a rule,
they should be left to themselves. Some of these cases are so mild that the
patients are not confined to the bed, or even to their rooms, and perhaps
throughout the entire course of the disease are able to transact a certain
amount of business. Such cases have been called " walking cases " of ty-
phoid fever. The eruption appears in these cases early, is of short dura-
tion and only a few spots appear ; usually there is only one crop. Diar-
rhoea is also present in most cases of this class, but it is of a mild type and
the discharges from the bowels apparently give relief to the patient. In
some cases the diarrhoea alternates with constipation, or constipation may
be present throughout the entire course of the disease, and the cases go on
exhibiting a varying amount of fever for from twenty to thirty days, until
gradual convalescence is established. This class of cases, if properly man-
aged, rarely prove fatal ; but if improperly managed, there is great danger.
If a patient walks about while he is suffering from one of these so-called
mild attacks of typhoid fever, he does it at great risk to life ; there should
be no " walking cases " of typhoid fever. A patient sick with typhoid
fever, however mild the type, should take to his bed and remain there
until convalescence is fully established, as it is impossible to say just how
extensive the changes may be that have occurred in the intestinal tract,
and in the mildest type of the disease they may be of such a nature that
very little physical exertion will cause intestinal perforation which will be
followed by a fatal peritonitis.
The abortive form of typhoid fever is ushered in with all the symptoms
of a typical case — headache, lassitude, pain in the limbs, nausea, etc., —
and the temperature during the first week follows the regular variations of
the fever. At the onset the disease has every appearance of a severe form
of typhoid fever ; the temperature may rise as high as 105° F. or 106° F.
by the end of the first week ; delirium is often active, and diarrhcea is
present. By the end of the second week, certainly by its close, if recovery
occurs, the fever is cut short, and abruptly disappears ; the temperature
falls to the normal standard, and the patient passes on to a state of rapid
and complete convalescence. The eruption, diarrhoea, and all the urgent
symptoms of the disease may be present, and yet before the end of the
second week the patient may be fully convalescent. That it is the typhoid
poison which thus acts upon the system, and gives rise to the characteristic
TYPHOID FEVER. 631
symptoms of typhoid fever in these abortive cases, is evidenced by the fact
that at the post-mortem examinations the characteristic typhoid intestinal
lesions are found, and these, taken in connection with the presence during
life of the typhoid eruption, establish the diagnosis beyond question.
There can be no doubt but that an individual may be affected, overwhelmed
as it were, by typhoid poison, and yet not develop well-marked typhoid fever.
So, if only a moderate amount of typhoid poison is introduced into the sys-
tem, a mild or an abortive type of fever will be developed. The natural
power of the individual to resist the action of such poisons must always be re-
garded, and should be taken into consideration in the treatment of a case.
Differential Diagnosis. — In a typical case, after the fever is fully developed,
the diagnosis is not diflBcult. The presence of febrile excitement, marked
by evening exacerbations and morning remissions, headache, diarrhcsa, ab-
dominal tenderness, and other abdominal symptoms, and the presence of
the characteristic rose-colored spots are sufficient for a diagnosis. In tha
mild type of the disease, or when the symptoms are developed irregularly,
or during the first week of a typical case, the diagnosis is often difficult,
and sometimes impossible.
The principal diseases which are liable to be confounded with typhoid
fever are typhus and relapsing fevers, continued malarial (so-called typho-
malarial) /ever, acute tuberculosis, py(Bmia, septiccsmia, pneumonia, gastro-
enteritis, trichinosis, and diffuse parenchymatous hepatitis. The differen-
tial diagnosis between typhoid fever and g astro-enteritis and diffuse hepa-
titis have already been given. The points of differential diagnosis between
typhoid and typhus, relapsing and continued malarial (so-called typho-
malarial) fevers, will be considered in connection with the history of these
fevers.
Acute Tuherculosis. — This disease is attended by many of the symptoms
which are present in, and supj)osed to be characteristic of, typhoid fever.
The fever of acute tuberculosis is of a remittent type, attended by evening
exacerbations and morning remissions, delirium, a dry, brown tongue, a
tendency to stupor, great prostration, rapid emaciation, and sometimes by
a diarrhoea, with abdominal tenderness and tympanitis. All of these are
among the prominent symptoms of typhoid fever. More than once have
patients in Bellevue Hospital, with the diagnosis of typhoid fever, pre-
sented at the post-mortem examination the characteristic lesions of acute
tuberculosis. If, therefore, patients with acute tuberculosis may go through
a large general hospital, under the observation of diagnosticians, — who cer-
tainly are not men of inferior ability, — and be supposed to have typhoid
fever, there evidently is great danger of a mistake in diagnosis. The higher
range of temperature in acute tuberculosis than in typhoid fever is one of
the distinguishing characteristics of the disease. Usually, early in the
progress of the disease, it reaches 106° or 107° F., while in typhoid fever
the temperature rarely reaches 106° F., or if it does, in most cases it is not
before the end of the second week and after the typical rise. There is no
eruption, neither is there enlargement of the spleen in acute tuberculosis,
while both are very constant attendants of typhoid fever ; yet their absence
632 ACUTE GENEEAL DISEASES.
is not positive proof that typhoid fever does not exist. Quinine will reduce
the temperature of typhoid fevor from three to four degrees, while it has
but little influence over that of tuberculosis. Pulmonary consolidation is
at the apex in tuberculosis, at the base in typhoid fever. According to
Bouchut, the ophthalmoscope reveals the presence of tubercular granula-
tions in the choroid in all cases of acute tuberculosis. In all doubtful
cases the family history of the patient, his immediate surroundings, whether
typhoid fever is prevailing at the time, and whether the patient has been
exposed to typhoid poison, become important points in diagnosis ; after
the first week of the disease, the presence of the rose-colored spots is neces-
sary for a diagnosis of typhoid fever.
Pymmia and Septiccemia. — In most cases these diseases will be readily
recognized, as the surface of the body has a jaundiced hue, there are no
lenticular spots, and the febrile symptoms are irregular in their develop-
ment. There are exacerbations and remissions, but their appearance and
disappearance are not marked by any regularity, and usually there is more
than one exacerbation and remission in the twenty-four hours. Not only
are the variations in temperature irregular, but the temperature reaches a
high degree much sooner, and ranges higher throughout its entire course
in pyaemia and septicaemia than in typhoid fever. In pyasmia and sep-
ticaemia there are early in the disease recurring chills followed by profuse
sweatings, great prostration, rapid emaciation, delirium, subsultus, tym-
panitis and diarrhoea, while in typhoid fever these do not come on until
late in the disease. Moreover, the history which precedes and attends the
development of pyaemia and septicaemia differs widely from that of typhoid
fever. In pyaemia, thrombi, infarctions and multiple abscesses establish
the diagnosis.
There is a condition of septic poisoning occasionally met with resulting
from the introduction into the system of septic poison through the drink-
ing water, which so closely resembles that which is the result of typhoid
poisoning that it is almost impossible to make a differential diagnosis. In
these cases the absence of the rose-colored spots is almost the only distin-
guishing feature.
Pneumonia. — Pneumonia, with typhoid symptoms, is sometimes mis-
taken for typhoid fever. The pneumonia which complicates typhoid fever
does not come on until late in the fever, and is preceded by the regular
history of typhoid fever. On the other hand, when the typhoid symptoms
are present from the beginning, or come on at the end of the second
stage of the pneumonia, the physical signs of the pneumonia will attend
or precede the typhoid symptoms. There will be cough and the character-
istic pneumonic expectoration ; there will be no eruption, and no typical
variation in temperature. If a patient who is over sixty years of age with
this type of pneumonia is not seen until the second or third week of its
progress, although evidences of lung consolidation may be present, it will
frequently be very difficult to decide whether the pneumonia is or is not
complicating a typhoid fever. The diagnosis must be based upon the his-
tory of the case.
TYPHOID FEVEK. 633
Gastro-Enteritis. — In the adult this disease is quite readily distinguished
from typhoid fever, as the diarrhoea and vomiting precede the febrile move-
ment ; the fever is irregular in its development and progress, and the tem-
perature rarely rises higher than 103° F. In a child between two and six
years of age it is very difficult to distinguish gastro-enteritis from typhoid
fever. The typhoid eruption is not so prominent or constant a symptom
in the child as in the adult, and with both diseases we have diarrhoea,
tympanitis, and typhoid symptoms. When all the symptoms precede the
fever, and there is a history of the case, and a thermometricai record from
the beginning of the fever, in most cases the diagnosis can readily be made ;
but if the case is not seen until it has reached the second week of its prog-
ress, and there is no accurate or reliable history of its development, a posi-
tive diagnosis is impossible.
Trichinous Disease. — This condition is not infrequently attended by
diarrhoea, vomiting, and the development of other typhoid symptoms ; but
with poisoning by trichinae there are almost constantly present intense
muscular pains and oedema of the eyelids, which will be sufficient to arrest
attention. There will be wanting the typical temperature trace and the
rose rash, and a microscopic examination of small portions of the muscular
tissue will afford a positive diagnosis.
Prognosis. — Death may occur at any stage of this fever. A typhoid
patient is not out of danger until all tympanitis, diarrhoea, and other ab-
dominal symptoms which indicate that intestinal changes are still progress-
ing, have disappeared. Independent of complications, the duration, type,
and intensity of the febrile excitement have more to do than all the other
elements in determining the prognosis in any case of typhoid fever. The
height of the temperature on the eighth day determines the range of tem-
perature that may be expected on each succeeding day. If upon that day
it is not higher than 104° or 105° F., and has been regular in its devel-
opment (independent of complications), the prognosis is good; in uncom-
plicated cases it very rarely rises higher than the degree it has reached at
that time. A prolonged high temperature (above 105° F.) after the first
week renders the prognosis unfavorable. In mild cases, during the second
week, a marked morning remission occurs, which begins early and continues
until midday; the evening exacerbation is late, and by the end of the sec-
ond week there is a marked and permanent fall in the temperature. In
severe cases, the opposite conditions are observed. A sudden rise in tem-
perature, or a rapid and extreme fall at any period of the fever is a very
bad omen ; the latter often precedes the occurrence of a severe intestinal
hemorrhage. Marked variation from the typical temperature of the disease
indicates the existence of complications. Slight decline accompanied by
great fluctuation of temperature, during the third week, is an unfavorable
symptom. The natural power of an individual to resist disease, especially
the effects of prolonged high temperature, is a very important element in
prognosis. The organ which is the surest indicator of such power (espe-
cially in typhoid fever) is the heart.
If the pulse is full and regular, perhaps beating at the rate of 130 or 115
634 ACUTE GEl^ERAL DISEASES.
per minute, if the cardiac inipulse is good, and a distinct first sound can
be heard, even though at the end of the second week the temperature stands
as high as 106° F., the prognosis is favorable. If, however, the pulse has
risen to 120 or 130 per minute, if the apex-beat is feeble or imperceptible,
and the first sound of the heart is indistinct or altogether obscured, with a
tendency to cyanosis and pulmonary oedema, the indications are that the
patient's powers of resistance are failing, and under such circumstances the
prognosis must be unfavorable. It is not so much i-apidity as irregularity,
a sudden falling and a sudden rising of the pulse, that indicates impending
danger. The rapid rising of the pulse upon the slightest excitement is the
most unfavorable indication, as it shows extensive heart-failure and a rapid
giving way of vital power. A sudden fall of the pulse from any cause must
always be regarded as an unfavorable indication. The abundance or color
of the eruption does not influence the prognosis. Excessive tympanitis and
severe abdominal pains are unfavorable symptoms. Severe and protracted
muscular tremors, with subsultus, indicate danger. Sudden collapse
during the second and third weeks of the fever is always attended with
danger, as it is very likely to be due to copious intestinal hemorrhages
or intestinal perforation. It sometimes occurs independently of either of
these causes, but nevertheless is very apt to be soon followed by a fatal
result.
The prognosis is always bad in those who are very fat, and in those
who are the subjects of gout, disease of the kidney, or any other severe form
of chronic disease. In all such persons, during the second and third weeks
of the disease, it is necessary to be constantly on the watch for the occur-
rence of sudden collapse. My own experience leads me to the belief that
when intestinal hemorrhage is scanty it has little influence on the final re-
sult. When it occurs before the twelfth day of the fever, it is often of ad-
vantage by relieving the intestinal congestion. But when profuse, or even
slight, after the twelfth day, it is an unfavorable symptom and renders the
prognosis unfavorable. The occurrence of the hemorrhage renders it prob-
able that ulceration has extended to the vessels beneath the transverse mus-
cular fibres of the intestine, and such ulceration is very apt to go on to per-
foration and a fatal peritonitis.
The influence of age is very great in determining the prognosis in any
case of typhoid fever. It is much better in children than in adults ; and in
persons over forty years of age the prognosis is decidedly unfavorable, even
though the symptoms may not indicate a severe type of the disease. In the
case of those individuals who habitually use alcoholic stimulants, whose
power of resistance to high temperature is diminished, the rate of mortality
is very great. The puerperal state renders the prognosis especially unfa-
vorable. The danger to the patient is equally great, whether the fever
comes on prior to delivery or during puerperal convalescence. The paren-
chymatous changes which take place in the different organs of the body
during the progress of this fever, necessarily influence the prognosis. The
muscular degenerations of the cardiac walls, and consequent loss of heart-
power, which favor pulmonary and other hypostatic congestions, and the
TYPHOID FEVEK. 635
diminished quantity of blood sent to the various tissues of the body, inter-
fere more or less with their nutrition. Necrotic and gangrenous processes,
sometimes met with in the cellular tissue of the surface and along the line
of the intestines, as also the venous thrombi which so frequently develop in
a protracted case of this fever, are, to a certain extent, the result of this
cardiac weakness, and render the prognosis unfavorable. Excessive cardiac
weakness also favors the development of blood-clots in the heart-cavities ;
these may break up and cause embolism somewhere in the course of the
general circulation, and thus lead to changes which may destroy life. In-
testinal perforations, one of the results of the intestinal changes incident to
the fever, render the prognosis most unfavorable.
Complications. — Slight bronchial catarrh can hardly be regarded as a
complication, it is so much a part of the clinical history of the disease,
but another much more serious bronchial complication is capillary bron-
chitis. This usually comes on during the second or third week of the
disease, and, if extensive, greatly endangers the life of the patient. It is
indicated by subcrepitant rdles suddenly developed over the whole of both
lungs, accompanied by great dyspnoea and an abundant expectoration of
stringy mucus. Its advent renders the prognosis most unfavorable. Ex-
tensive osdema of the lungs, occurring with, or independent of, capil-
lary bronchitis and pulmonary congestion, sometimes comes on suddenly
during the third week of typhoid fever, and indicates great failing in
heart-power. The slighest indication of its occurrence would always be
regarded with suspicion. It is not infrequently accompanied by more or
less extensive hemorrhagic infarctions of the lungs. These depend on
embolism of some of the branches of the pulmonary artery due to frag-
ments of clots which have formed in the right side of the heart, the re-
sult of the cardiac weakness, and often lead to gangrene of the lung. It
is sometimes impossible to diagnosticate their existence during life.
Pneumonia, when it complicates typhoid fever, is generally latent. It
comes on very insidiously, and will be recognized only by the most care-
ful physical examination. It is more frequently developed during the
third and fourth weeks of the fever, and usually is lobular rather than lobar
in character. At first only single lobules are involved, but after a time
an entire lobe becomes consolidated. When irregular variations m
temperature occur during convalescence, or during the third or fourth
week of the fever, there is reason to suspect the development of pneumonia.
In the majority of cases the characteristic pneumonic cough and expecto-
ration are absent. Whenever an extensive pneumonia complicates typhoid
fever, the prognosis is especially unfavorable.
Pleurisy is not so frequently a complication of typhoid fever as is
pneumonia or bronchitis. When it does occur, the almost invariable prod-
uct of the inflammatory process is pus. Usually it comes on insidiously,
late in the disease, and is quite likely to pass unrecognized unless frequent
physical examinations are made. In many instances it is really a sequela
of the fever, not developing until three or four weeks after the fever has
run its course. Its occurrence must always be regarded as unfavorable.
636 ACUTE GENEKAL DISEASES. ',
for a year, or even longer time, must elapse before recoyery can take place,
and even then complete recovery is doubtful.
Occasionally laryngitis is a serious complication of this fever. It gene-
rally occurs in those cases where the fever has been very protracted, and
there is great prostration. Its presence is marked by sudden and very
intense inflammation of the mucous membrane of the glottis, which is
liable to become oedematous, when death may suddenly occur. It may
lead to ulceration of the mucous membrane. PycBmia may be met with
as a complication during convalescence from typhoid fever, but it is not of
as frequent occurrence as septicaemia. Whenever septic poisoning is de-
veloped, with extensive sloughs in the intestines, the prognosis is exceed-
ingly unfavorable. Acute gastric catarrh is another complication of this
fever. During the fourth week, or in early convalescence, imprudence in
diet, either in quantity or quality, may produce irritation and inflamma-
tion of the weakened gastric mucous membrane and endanger or destroy
the life of an already enfeebled patient.
The greatest care must be exercised in regard to the diet of patients con-
valescing from typhoid fever. They should be restricted to milk and
nutritious broths, in moderate quantity, until all danger from complica-
tions shall have passed. Disturbances of nerve-function have been con-
sidered under' the head of symptoms, but not infrequently certain brain
and nerve lesions are developed which cannot be classed under that head.
Cerebral oedema may complicate a typhoid fever during its third week, and
give rise to symptoms of a grave character. A decided enfeebling of the
mental powers and a tendency to stupor announce its occurrence. Hemor-
rhagic extravasations on the surface and into the substance of the brain,
the result of degeneration of the walls of the cerebral vessels, occasionally
occur during the height of the fever. If the effusion is moderate, no
marked symptoms are developed ; but if a considerable extravasation takes
place, it gives rise to symptoms of cerebral compression. Meningeal in-
flammation is a rare complication. The occurrence of any of these com-
plications in any case renders the prognosis unfavorable.
During the second and third weeks of the fever certain cerebral disturb-
ances may occur which seem to indicate the existence of some one of
these complications, when no cerebral lesion exists. Usually, they are
present in patients who have had a continuously high temperature, and in
favorable cases they disappear after a few days. Various other disturb-
ances of the nervous system, such as hemiplegia, paraplegia, etc., which
may simulate those due to lesions of the nerve-centres, or forms of local
paralysis and anesthesia which seem to be confined to individual nerves
are met with, but as these functional disturbances do not depend upon any
anatomical changes, the prognosis in such cases is good. Those changes in
the kidney, due to parenchymatous degeneration, which usually attend this
fever have already been noticed ; but occasionally nephritis is developed
as a sequela. The urine becomes scanty, is loaded with albumen, and con-
tains blood and casts ; the face and extremities become oedematous, and
death may occur from uraemia. The occurrence of this complication
TYPHOID FKVER. 637
necessarily renders the prognosis bad. In a few instances under my ob-
servation, severe catarrh of the bladder has developed during convalescence,
greatly complicating the case ; in one instance the cystitis was accompa-
nied by pyelitis. Cellulitis, especially of the surface, often complicates
convalescence, and in some cases causes death. Occasionally it is met with
in the pharynx and along the line of the lymphatics. Accompanying this
cellular inflammation, or occurring independently of it, gangrenous inflam-
mations of the integument not infrequently occur, giving rise to hed-sores.
These gangrenous processes are most frequently developed at those points
which have been subjected to the greatest pressure, on account of the po-
sition of the patient in bed, such as the sacrum, nates, heels, and shoulder-
blades. In the simplest form of hed-sores there is only a superficial loss
of substance ; in more severe cases the subcutaneous cellular tissue is in-
volved ; and in the worst cases the muscles and fibrous tissues. I have
met with cases where Xhe slough had involved the connective-tissue and
muscles, and laid bare the bone. A considerable number of typhoid pa-
tients who have lived through the fever die either from the exhausting ef-
fects of these bed-sores or from the resulting septic poisoning. The possi-
ble occurrence of these complications must enter into the prognosis in every
severe case, and the earlier they make their appearance the greater the
danger.
The average duration of typhoid fever is from three to four weeks. It
may terminate in death or recovery at an earlier date. A typical case ex-
tends over a period of four weeks. The period of invasion lasts from one
to five days. The period of glandular enlargement continues until about
the fourteenth day. The period of ulceration extends from the twelfth or
fourteenth day to between the twenty-first and twenty-eighth. When the
fever is protracted beyond the middle of the fourth week, in most in-
stances this is due to some complication, or to an extension of the intestinal
ulceration. The period of greatest danger is at the close of the third week.
Death rarely occurs before the fourteenth day. The prominent direct
causes of death are : toxmmia ; asthemia ; suppression of the excretory
function of the kidneys ; hypercemia and oedema of the lungs ; intestinal
hemorrhage ; exhaustive diarrhoea ; intestinal perforation ; and peritonitis
with or without intestinal perforation. In nearly all cases the failure of
heart-power is directly or indirectly the cause of death. In no case can
convalescence be said to be fairly established until the temperature remains
normal for two successive evenings. The termination, like the commence-
ment, is gradual, and is not marked by any critical evacuation or day of
crisis.
Relapses. — After typhoid fever has run its course, and the patient is en-
tirely free from fever, quite frequently there is a new development of the
fever ; these new developments are called relapses. Their course corre-
sponds with that of the primary attack, only they are of shorter duration.
The temperature rises more rapidly, the eruption reappears, the spleen en-
larges, the intestinal and abdominal symptoms return, and all the promi-
nent symptoms of the primary fever are rapidly developed. As a rule, the
638 ACUTE GEKERAL DISEASES.
relapse is milder than the primary attack. If it terminates fatally, the post-
mortem examination shows, in addition to the cicatrizing intestinal ulcers
of the primary attack, the recent intestinal changes of the relapse. The
lesions of the relapse, although of the same character as those of the primary
attack, are less extensive.
It is very diflBcult to give a satisfactory explanation of these relapses.
Some claim that they are the result of certain plans of treatment, especially
the cold-water plan. This assertion lacks proof. Others hold that all re-
lapses depend upon a new infection. Perhaps this is possible if the patient
remains in the same locality and has the same surroundings as when he had
the primary attack ; but it does not explain relapses in those who are re-
moved from all the sources of the primary infecdon. Another explanation
offered is that a part of the typhoid poison has remained in the system,
undeveloped during the primary attack, and that some time after this has
passed the poison reproduces itself and sets up a second fever. A more
recent theory is that the typhoid poison thrown off in the faeces of the
patient is reabsorbed and causes the relapse. Unquestionably, it is possible
for healthy glands to become inoculated by sloughs thrown off from those
first affected. In many cases it is impossible to account for the occurrence
of the relapse, and all of these explanations as to the cause in any case are
more or less unsatisfactory. In those cases which have come under my
own observation, I have noticed that the splenic enlargement which has
existed during the course of the fever does not subside with its decline ;
and that the tenderness along the line of the intestines, especially in the
right iliac region, continues during the period between the original attack
and the relapse. In some instances, apparently, the relapse has been
brought on by indiscretion in diet, or by injudicious exercise on the part of
the convalescent patient. Occasionally relapses have occurred when great
care had been taken against any indiscretion or over-exertion. There is
little doubt but that relapses are of much more frequent occurrence in those
cases that are treated with cathartics during the first week of the fever,
than in those where cathartics are not employed.
Treatment. — Accepting the theory that the specific poison of typhoid
fever is contained in the excrements of typhoid patients, the j^rs^ indication
in prophylaxis is to destroy this poison as soon as it is discharged from the
body. For this purpose the intestinal discharges should be received into
a porcelain bed-pan, the bottom of which is covered with a thin layer of
powdered sulphate of iron ; immediately after the discharge, crude muriatic
acid, equal in quantity to one-third of the faecal mass, should be poured
over it. The discharges of a typhoid patient (no matter how thoroughly
they may have been disinfected) should never be emptied into a privy or
water-closet. Trenches should be dug for their reception, and new trenches
should be opened every few days ; the greatest care must be taken that
these trenches are not so situated that the drainage from them can con-
taminate wells or springs which furnish drinking water.
All underclothing or bed-clothing that may have become soiled by the
discharges from the bowels should be immediately immersed in chlorine
TYPHOID FEVEK. 639
water, and thoroughly boiled within twenty-four hours. These procedures
will certainly destroy the infective power of the typhoid poison contained
in the intestinal discharges, and in the majority of instances will prevent
the spread of the fever. Kepeated observations show that when one mem-
ber of a family has typhoid fever, not infrequently it is developed in every
other member. This spread of the disease can be prevented, unless there
is some local cause for its development which cannot be reached. When
its origin is not apparent, the wells, springs, and all the sources from
whence water is derived for drinking and cooking purposes should be care-
fully and thoroughly inspected. Care must be taken that the waste-pipes
from wells and springs do not pass directly into cess-pools or sewers, and
thus become a means for the conveyance of impure gases into the springs
and wells. The greatest care must be exercised in regard to house drains
and sewer pipes, that they shall be free from leakage and obstruction, and
that all water-closets, sinks, and other openings into them be provided with
suitable traps. When unpleasant odors are constantly present in dwellings,
especially in sleeping apartments, disinfectants should be emjaloyed, and
the house be thoroughly ventilated. When it is necessary to open drains
and cess-pools in a dwelling for purposes of repairing or cleansing, the same
precautions should be exercised ; they are especially of importance during
the summer and autumn.
The question naturally arises : — is it not possible to counteract or neutral-
ize the effects of the fever-poison after it has gained admission into the sys-
tem, and thus prevent the development of typhoid fever ? To accomplish
this, blood-letting, emetics and diaphoretics have all been employed ; but
there is not the slightest proof that typhoid or any fever-poison was ever
removed from the system by these or any other agents. A patient with
some of the premonitory symptoms of fever may perspire, be relieved, and
at once recover, but such a patient had not received the typhoid poison into
the system, and was not, as is sometimes said, " threatened with typhoid
fever." Notwithstanding the bold affirmation of the author of the cold
afPusionplan of treatment, that if it were resorted to before the third day
of the disease, it would invariably arrest its development, it has failed to
stand the test of practical experience. More recently, sulphate of quinine,
administered in large doses, has been thought to have the power of arrest-
ing the development of tjnphoid fever in the same way that it arrests mal-
arial fever, by its anti -periodic power ; but there is no evidence that it has
any such power, and as a prophylactic remedy it has been abandoned.
After the poison has once gained entrance into the system, no means
has as yet been discovered by which it can be counteracted or neutralized
so as to prevent the development of the disease. The duty of the physician
is to guide the disease, so far as he may be able, to a favorable issue, and
prevent injury to organs essential to life, keeping in mind that a certain
definite period must elapse before this result can be accomplished.
The arrangement of the sick-room of fever patients, though often over-
looked, is a matter of no inconsiderable importance, not only as regards the
comfort of the patient, but also the successful issue of the case. It is of
640 ACUTE GENERAL DISEASES.
the greatest importance that a properly qualified nurse be selected ; one
who has had experience in the care of fever-patients is to be preferred. The
patient should be placed in a large and well- ventilated apartment. All fur-
niture should be removed from the sick-room except those articles which
are necessary for the comfort of the patient and the convenience of the at-
tendants. The carpets should be removed from the floor and the patient
placed in a bed of moderate size in the centre of the room. Free ventila
tion during both day and night, is of the utmost importance. The tem-
perature of the apartment should be kept below 60° F. The bed and body
linen of the patient should be changed daily, and at once removed from the
sick-room and placed in a weak solution of chlorinated soda ; especially
is this important if the patient is having frequent discharges from the
bowels. The apartment should be kept perfectly quiet, the light subdued,
and only the attendants should be allowed in the room. Any medicinal in-
terference in a mild type is unnecessary. The treatment resolves itself into
the arrangement of the sick-room and proper diet ; milk is the most suit-
able food, Siud fruits are not to he alloioed in any case. Even in the mild-
est case this care in diet is important, and the patient should be kept in
bed until convalescence is fully established. This should be insisted upon
in the mild as well as in the severe cases.
The temperature in a mild type of this fever rarely rises above 103° F. ;
therefore there is no necessity for resorting to antipyretic measures ; fre-
quent sponging of the surface with cold or tepid water, as is most agree-
able to the patient, will be found of service. By far the larger number of
cases of this fever, however, are of a more severe type, and though the
treatment must be regulated by the circumstances which attend each indi-
vidual case, more decided measures will usually be necessary. Typhoid
fever is a disease that has certain stages to pass through, and there is
great doubt whether the physician can shorten its duration by a single day,
but experience warrants the belief that many lives may be saved by reme-
dial measures, used at the proper time, and combined with judicious hy-
gienic management.
Unquestionably one of the most important things to be accomplished ia
the reduction of temperature, or rather the keeping of the temperature be-
low a certain standard. The agents which have been employed more re-
cently for this purpose, namely, sulphate of quinine and cold applications
to the surface, act powerfully in reducing the temperature and lessen-
ing the severity of the disease. It is claimed by many distinguished ob-
servers of the present day that the parenchymatous degenerations of the
different organs and tissues of the body which are found in those who die
of typhoid fever are due to the prolonged high temperature which is pres-
ent during the course of this disease ; but as yet there are no facts to prove
this assertion, for the same parenchymatous changes are found in the bodies
of those who have died of diseases the course of which was not marked by
high temperature, and did not extend over a period of more than forty-
eight hours. So far as we are able to determine by analogy upon what
these parenchymatous changes depend, we are led to believe that the spe-
TYPHOID FEVER. 641
cific poison of the disease lias more to do with their development than the
high rate of temperature. One thing must be apparent to every clin-
ical observer : that the injurious effects of a prolonged high temperature
are early and most markedly shown by disturbances of the cerebro-spinal
system, it is still an unsettled question whether these disturbances are due
to the primary changes in the constituents of the blood, which always ac-
company a high range of temperature, or to the direct effects of the high
temperature or of the peculiar poison on the nerve centres. Whichever view
we adopt, the employment of those means which have the power of safely
reducing temperature is indicated, and when judiciously used they have
much to do with the safety of the j^atient.
All those means which have been employed for the reduction of tempera-
ture are included under the general term of antipyretics, and the treatment
of disease by the use of these agents has received the name of antipyretic
treatment. Unquestionably the most efficient and reliable of the antipyretic
agents are the external application of cold by means of baths, packs and af-
fusions, and the internal administration of the sulphate of quinine. The
quinine is not administered to produce any specific action upon the typhoid
fever poison, but is employed for its antij)yretic power. There are other
antipyretic agents besides these two, but they are of so little importance
that it is necessary to give them only a passing notice after we shall have
considered these two important ones.
At the present time the opinion prevails, to a great extent, that the ap-
plication of cold to the surface is the great antipyretic in the treatment of
fever. This is no new teaching. Long ago Dr. Currie recommended the
application of cold to the surface of tiie body for the purpose of rapidly re-
ducing temperature, and proved that it had such an effect ; yet it was never
very generally practised, and soon fell into disuse, as there were no reliable
indications to guide one in its application. As we now have the thermome-
ter as such a guide, it has been resorted to more recently with considerable
Buccess. It is employed in the following manner. As soon as the axillary
temperature in the evening rises above 103° F., the patient is placed in a
water-bath having a temperature of 70° E. or 80° P., which is gradually
lowered, by the addition of cold water or ice, until the temperature of the
patient begins to fall. It may be necessary to lower the temperature of the
bath to 60° P. before the temperature of the patient is affected. When the
temperature begins to fall, thermonietrical observations should be made
every two or three minutes, by placing the thermometer in the rectum. If
it falls rapidly — that is, two or three degrcQS in five or six minutes — as soon
as the temperature has reached 103° F. the patient is to be removed from
the bath ; if it falls slowly, as soon as it reaches 101° F. he should be re-
moved and immediately placed in bed. It is never safe to keep the patient
in the bath until the temperature shall have reached the normal standard ;
for he may pass into a state of collapse, since the temperature continues to
fall for some time after his removal from the bath. While in the bath, cold
should be applied to the head by means of a sponge wet in cold water, or
by an ice-bag. The cold pack is much less effective than the bath ; but if
41
(J43 ACUTE GENERAL DISEASES.
the patient is too feeble to be removed, it may be employed with benefit.
The patient is wrapped in a sheet wrung out of tepid water, and over this
one wrung out of cold water is applied. The latter may be removed as it
becomes warmed, and its application and removal continued until the de-
sired fall in temperature shall be obtained. In severe cases, during the
first and second weeks, after the temperature has been reduced by the ap-
plication of cold to the surface, it will soon begin to rise, and continue to do
so until it reaches its former height. Usually one to three hours will elapse
before it begins to rise, and from two to six before it reaches its former
height. It will then be necessary to repeat the baths or packs, and to con-
tinue their use, both day and night, from three to six times during the
twenty-four hours, in order to keep the temperature below 103° F., and ac-
complish anything by this plan of treatment.
My experience in the use of cold applications leads me to believe that
unless it is possible to maintain a low range of temperature after four or
five baths very little is gained by their continuance. I am also convinced
that, after the second week of typhoid fever, cold baths should not be em-
ployed to reduce temperature. The condition of a typhoid patient during
the first and second weeks of the fever is very different from that during the
third and fourth weeks. During this latter period there is great danger of
collapse after a cold bath, and in several instances I am confident that pul-
monary complications have been the result. In a few instances the tem-
perature can be very rapidly lowered by the application of ice-bags to the
abdomen. In some cases when the patient is placed in the cold bath, the
temperature will immediately begin to fall ; in other cases there will be a
gradual reduction of temperature as the water is made cooler. In certain
severe cases, a patient may be kept in a bath of the temperature of 60° F.
for the space of half an hour without the temperature falling a degree.
These cases are exceedingly grave in character, and the bath should be used
with great care.
There is no remedial agent wMcJi requires greater care and judgment in
its use than the cold bath, yet, doubtless, when Judiciously employed, the
lives of many typhoid patients may be saved, and it is equally certain that
when injudiciously employed many lives may be destroyed. The general
condition of a patient and the stage of the fever must be considered ; also
the effects of the first few baths must be carefully noted. Should a pa-
tient's temperature range at 104° F. or 105° F., it is no positive indication
for the resort to a cold bath, or that a cold bath is the best agent to be em-
ployed for its reduction. If the patient after the second or third bath is
more quiet, has less delirium (if delirium previously existed), if his breath-
ing becomes easy and natural, if the heart's action is more regular and
forcible, and he falls asleep and perspires, there can be no question in re-
gard to the beneficial effects of the bath. If, on the other hand, the bath
is followed by feebler heart's action, by dusky cheeks, by rapid respiration,
and by coldness of the extremities, from which condition the patient
rallies slowly and imperfectly, it is certain that, however high the tem-
perature may range, harm will be done by continuing the baths. When
TYPHOID PEVEE. 643
the extremities are cold, or there is j)rofuse hemorrhage from the bowels,
or when from any cause there is great feebleness of the heart's action, and
especially in the case of aged persons, cold baths are contraindicated.
Cold compressions or ice-bags applied to the abdomen, in addition to
their beneficial effect on tlie intestinal changes which constitute such an
important element in the history of this fever, often have great power in
reducing the general heat of the body. I have also in some instances
found the body temperature rapidly lowered by injections of ice-water into
the rectum. Care must be exercised that the cold injections are not ad-
ministered too rapidly or in too large quantities. Although this mode of
aostracting heat and lowering the body temperature is never so effective as
by baths and paclcs, still it has this advantage, that no such compensating
increase in the production of heat follows the use of the cold injections as
follows the cooling of the external surface by the baths. In many cases the
extreme obstinacy of the fever, which resists the most systematic use of
cold, as well as the fact that some patients cannot bear a sufficiently fre-
quent repetition of the baths as to effect the desired result, or that there
may be contraindications to their use, necessitates the employment of other
means for the reduction of the body temperature.
The antipyretic power of sulphate of quinine is established beyond ques-
tion. When quinine is employed as an antipyretic, however, it must be
given in large doses ; the administration of two grains every two hours, or
a larger quantity administered in divided doses within a period of twenty-
four hours, will not act as an antipyretic ; but thirty or forty grains must
be administered within a period of two hours. If the stomach is irritable,
and a large dose produces vomiting, ten grains may be given every half
hour until the desired quantity has been administered. Usually from four
to six hours after the antipyretic dose has been taken, the temperature
will begin to fall and in about twelve hours it will reach its minimum ;
then it will remain stationary from twelve to twenty-four hours. After the
temperature has once been reduced by the quinine, its administration may
be discontinued until the temperature shall again rise to 105° F. As a
rule, the temperature rarely ranges as high as before the quinine was ad-
ministered. This mode of administering quinine in antipyretic doses to
fever patients rarely produces any symptom of cinchonism, other than a
transient deafness after the first dose. In a large number of cases the
temperature can be kept below 103° F. by the sulphate of quinine ; but in
very severe cases it will be advisable, sometimes it will be absolutely neces-
sary, to employ not only the quinine, but at the same time the cold baths.
My rule is, after I have reduced the temperature to 101° F. or 102° F.,
by a cold bath, to administer an antipyretic dose of quinine, and thus delay
the recurring rise of temperature. While the cold bath more rapidly re-
duces temperature, the effect of the quinine is more lasting ; consequently
by making use of both of these reliable antipyretics during the first two
weeks it is possible to control the temperature during that time. After this
period it is not safe to resort to cold baths ; but when the temperature
rises above 103° F., occasionally the cold pack may be used in connection
644 ACUTE GE]SrEEAL DISEASES.
with antipyretic doses of quinine. If during the third and fourth weeks,
these means fail to reduce the temperature, from ten to twenty grains of
powdered digitalis may be administered within twenty-four hours, unless
the pulse is very frequent and irregular — when its use is contraindicated.
As an antipyretic, digitalis should be employed only when quinine is
given. It seems to increase the antipyretic power of the quinine, but has
little or no power when administered alone. The use of all antipyretic
remedies must be persisted in until the desired end — the reduction of tem-
perature — is accomplished ; but the peculiarities of each patient must be
studied, and these agents must be so administered as to suit each individual
case. The satisfactory results obtained by the systematic use of these
remedies justifies their employment ; but the exact rules which are to gov-
ern one in their use, as to manner and time, can only be determined by ex-
perience.
If the temperature of a patient can be kept below 103° F., during the
first two weeks of the fever, the first and perhaps the most important
thing in the treatment of this disease will be accomplished.
Toward the end of the second, or during the third week, signs of failure
of heart-power begin to manifest themselves ; although the temperature
may not rise higher than 101° F., the pulse frequently becomes extremely
feeble and irregular and reaches 140 per minute, while the first sound of
the heart becomes inaudible at times ; the surface is cool and moist ; the
patient complains of a sense of exhaustion, and perhaps is unable to turn in
bed ; muscular tremors, dry, brown tongue, and all the symptoms which,
indicate failure of vital power are present.
Under these circumstances the use of stimulants seems to be urgently
demanded.
A few simple rules govern their administration.
First. They should never be administered indiscriminately — that is,
simply because the patient has typhoid fever.
Second. When there is reasonable doubt as to the propriety of giving or
withholding stimulants, it is safer to withhold them, at least until the signs
which indicate their use become more marked.
Third. In every case, but especially when stimulants are not clearly in-
dicated, the effect of the first few doses should be carefully noted. There
are few whose experience in the treatment of typhoid fever is such as to-
enable them to determine positively, from the appearance of the patient,
when the administration of stimulants should be commenced.
If under their use the tongue becomes dry, the patient more restless, the
delirium more active, the temperature higher, and the pulse more fre-
quent, it is very certain that stimulants are contraindicated. If, on the
other hand, the pulse becomes fuller and more regular, if the first sound
of the heart is more distinctly heard, or if, having been absent, it returns,
if the restlessness and delirium are less marked, the tongue more moist,
and the patient more intelligent, it is equally certain that the time for ad-
ministering stimulants has arrived. When their use is once begun, it is of
the greatest importance to administer them at stated intervals, especially
TYPHOID FEVER. 645
during the night. In a severe case of typhoid fever, free stimulation, just
at a critical period (which may not lust more than twenty-four hours),
will often be followed by a refreshing sleep, and the patient may rapidly
pass from an apparently hopeless condition to one of convalescence.
The third important thing to be accomplished in the management of
typhoid fever patients is the maintenance of nutrition. The principal
effects of the typhoid poison are manifested in the changes which take
place in the lymphatics of the gastro-intestinal tract. Experience has
taught us that the enfeeblement of the digestive and assimilative powers,
due to these glandular changes, which is manifested from the very com-
mencement of the fever, renders the digestion of solid food impossible, and
for a long time it has been the rule of the profession to allow typhoid fever
patients only liquid food. There has been, and still is, great diversity of
opinion in regard to the special articles of diet best suited to this class of
patients. There is no disease in which a waste of all the tissues of the body
goes on so rapidly as in typhoid fever.
Milk is an article of diet which furnishes the elements of nutrition neces-
sary to repair this rapid waste, and there are not the objections to its use
which are against animal broths and gruels. Although there have been,
and still are, in some quarters, strong objections against its use as an article
of diet in fevers, recently it has been regarded with more favor, and those
who have had most extended opportunities for testing its nutritive qualities
have come to regard it as the only article of diet required by typhoid
patients. In it we not only find all the elements required for repairing the
rapidly wasting tissues, but they are in a condition to be most readily
assimilated by the enfeebled digestive apparatus. In order that it shall not
become distasteful to the patient some variations must be made in its
preparation. It may be simply curdled, boiled, frozen, slightly fermented,
or mixed with lime-water, seltzer, or some other mineral water, and various
palatable preparations can be made from milk which has been partially
digested with pepsin or pancreatin. If agreeable, buttermilk may be sub-
stituted for a time. The quantity of milk is not limited ; the patient may
take all his stomach will digest — usually j^atients will take from four to
six quarts in the twenty-four hours. After the patient has passed into the
fourth week of the disease it may be necessary to administer cream and the
yolks of eggs in connection with the milk.
I now come to the treatment of the accidents of the disease.
Diarrlima. — The poison which produces this fever unquestionably has a
specific action upon the intestinal glands and lymphatics. It is here that
we find the characteristic lesions of the disease, and it is scarcely ques-
tioned that the typhoid poison, to a great extent, gains entrance to the
system through these glands and lymphatics, and here produces the primary
irritation. Following the irritation and inflammation of the follicles, other
portions of the mucous membrane become involved, and a catarrhal inflam-
mation of the mucous membrane of the intestinal tract follows. The nec-
essary consequence of this is a diarrliffial discharge, which is simply an in-
dication that these intestinal changes are going on ; it is not due to the
646 ACUTE GENERAL DISEASES.
elimination of the typhoid fever poison, but to the inflammation which the
fever poison has excited in the intestinal glands. When the diarrhoea is
present in the earlier period of the disease, it is better to let it alone, as
during the first and second weeks the danger is very slight. It has been
proposed to treat this diarrhoea, which makes its appearance early in the
disease, with alkalies, bismuth, pepsin, etc. It is claimed that if these
remedies be administered, diarrhoea can be prevented, or, if it already
exists, that it can be controlled. Theoretically, I see no reason for employing
alkaline remedies, for the diarrhoeal discharges are always alkaline, and
from clinical observation, I am convinced that bismuth, pepsin, etc., have
little or no effect either in controlling the diarrhoea or in preventing the
intestinal changes which produce it.
When diarrhoea commences late in the disease (during the latter part of
the third, or during the fourth week of the fever), it is of a very different
character from that which occurs during the first and second weeks. Ul-
ceration of the intestinal glands, and perhaps sloughing has been estab-
lished, and, in addition to the extensive local changes, there is a septic ele-
ment which enters into the causation of the diarrhoea at this stage. Be-
sides, the increased peristaltic action of the intestines, which attends the
diarrhoea, favors an extension of the inflammatory processes to the peri-
toneum, especially that portion which covers Peyer's patches. In view of
these facts, the diarrhoea should be arrested or held in check. For the
accomplishment of this, there is but one remedy which can be relied upon
— that is opium. My experience is against the use of astringents, if
opium will not arrest it, one may expect little aid from astringents com-
bined with opium as they are usually administered. The use of opium is
objected to by some, who claim that it diminishes the power of the heart's
action ; but in this disease, when administered in small doses, it seems to
me to increase rather than diminish the heart-power. It is acknowledged
that opium, more than any other drug, arrests the peristaltic action of the
intestines ; and that is what we wish to accomplish when diarrhoea is pres-
ent during the third and fourth week of typhoid fever.
When during convalescence diarrhoea is persistent, the patient should be
kept in bed and some of the vegetable astringents, as catechu or hasmatoxy-
lon, may be employed.
Tympanitis. — When this has proved a distressing symptom, I have
usually found relief to be obtained by the application of turpentine stupes
to the abdomen. Some claim that if turpentine be administered internally
from the beginning to the end of typhoid fever, tympanitis and the intes-
tinal changes which lead to it and to the diarrhoea are much less severe. I
am confident that the turpentine treatment, as it is called, does not have
the controlling influence over this fever which has been claimed for it ; but
I am certain that it is our most reliable agent for the relief of the tym-
panitis.
Intestinal Hemorrhage. — When this occurs early in the fever, it usually
requires no treatment ; but when it occurs during the third or fourth week,
or after convalescence is apparently fully established, it must be arrested as
TYPHOID FEVER. 647
promptly as possible. The occurrence of severe intestinal hemorrhages
may sometimes be prevented by keeping the patient in bed. A typhoid
fever patient should not be allowed to get out of bed from the beginning of
the attack until convalescence is fully established. Especially is this of
importance if the case is a severe one, and attended by symptoms that indi-
cate extensive intestinal lesions. When hemorrhage from the intestines
occurs during the third or fourth week of the fever, it is most surely con-
trolled by the administration of opium in small doses at short intervals.
Absolute rest of the body must be insisted on, the patient must not be
turned on the side or moved in bed,, and an ice-bag should be applied
over the abdomen. I doubt if any good results can be accomplished by
the use of astringents, either by enemata or by the mouth, as it is not
known that they even reach the seat of the hemorrhage, although gallic
acid and the persulphate of iron are usually recommended in cases of in-
testinal hemorrhage occurring in typhoid fever. If the hemorrhage is pro-
fuse, it may be necessary to keep the patient under the influence of opium
for a week or ten days ; in such cases the internal use of turpentine in con-
nection with the opium will be found of service.
Peritonitis. — When perforation of the intestine occurs, the case may be
regarded as hopeless ; death takes place usually within twenty-four hours,
as the result of general peritonitis ; no plan of treatment avails anything.
If the peritonitis occur without perforation, from extension of the inflam-
matory process from the intestinal ulcers, bringing the patient rapidly into
a state of semi-narcotism and holding him there for five or six days may
prevent the occurrence of the perforation, and thus save life. Such a case is
to be treated in every respect as one of localized peritonitis. After recovery
from an intestinal hemorrhage or a localized peritonitis in typhoid fever
great care should be exercised in the administration of cathartics or ene-
mata. The bowels will move spontaneously after a time, even though the
use of opium be continued, and no harm will follow should two or three
weeks pass before they do so. When the stomach is irritable, the hypodermic
injection of morphine is preferable to opium administered by the mouth.
Broncldtis. — For the catarrh of the larger bronchial tubes no special
treatment is required ; but, if the bronchitis becomes capillary, great relief
will be obtained from the application of dry cups to the chest and the in-
ternal administration of carbonate of ammonia. Vapor inhalations will
also be found of service in severe cases.
Pneumonia. — The pneumonia which complicates typhoid fever in nearly
every case is lobular in character. The signs which indicate its occurrence
are sudden rise of temperature, increased frequency of respiration, and the
physical signs of localized pulmonary consolidation ; cough and expectora-
tion are rarely present. Its occurrence is always an indication that stimu-
lants should be administered. If they are being administered, they should
be increased in quantity. To prevent or relieve the hypostatic congestion
of other portions of the lung, which frequently accompanies pneumonic de-
velopment, the heart-power must be increased, and the position of the
patient changed.
648 ACUTE GENEEAL DISEASES.
Laryngitis. — T'or the relief of the laryngitis which occasionally compli-
cates typhoid fever, a small blister may be applied on either side below the
angle of the jaw, and the whole neck enyeloped in a poultice. If these
measures fail, and suffocation aj)pears imminent, tracheotomy should be
resorted to without delay.
Sui-acute gastric catarrh, occurring as a complication during conva-
lescence from the fever, can only be managed successfully by giving the
stomach rest as far as possible, restricting the diet to a single tablespoonful
of milk at a time, and applying hot fomentations over the epigastrium.
Bed-sores. — The severer forms of bed-sores are the most intractable com-
plications one has to combat. Fortunately the severer forms are much less
frequently met with under the more recent plan of treatment. Scrupu-
lous cleanliness is the principal means for preventing their development.
So long as there are no erosions, the parts should be frequently bathed in
spirits of camphor, and the points of attack should be relieved from all
pressure. If the sores penetrate the integument, they should be frequently
washed with a weak solution of carbolic acid, or brushed over with equal
parts of balsam of Peru and balsam copaiva, and afterward covered with dry
lint, or lint covered with vaseline. The most unfavorable cases are those in
which the point of pressure caused by the weight of the body becomes gan-
grenous. In such cases, a continuous warm bath is recommended by some.
As soon as sloughing takes jDlace, and the parts separate, they should be
dressed with lint saturated with balsam of Peru and carbolic acid.
Constipation. — As already stated, diarrhoea is usually present in the early
period of this fever ; but sometimes there is constipation. The question
arises : — is the administration of cathartics ever admissible in typhoid fever ?
Quite diverse views are still held in regard to this question. Eecently,
certain observers of extended experience have claimed that there is suffi-
cient reason for the belief that a portion of the typhoid jDoison lodged in the
alimentary tract, may be expelled by the timely administration of cathar-
tics, and thus the severity of the fever be mitigated and its duration short-
ened. Eecent German writers claim that calomel acts beneficially only as
a cathartic. Those who favor the administration of cathartics recommend
their use mainly during the first week of the disease. On the other hand,
equally competent observers maintain that the intestinal changes are aug-
mented and rendered more extensive by the action of cathartics, that the
normal course of the fever is interfered with, and that in a large proportion
of cases where intestinal and peritoneal complications occur, hypercatharsis
has been induced at an early period of the fever by the administration of
cathartics for the purpose of shortening its duration. My own experience
leads me to exercise the greatest caution in the administration of cathartics
in any stage of this fever.
I am confident that the routine practice of administering purgative
medicines in the early stage of tyjDhoid fever can only be followed by
a threefold injury '.—first, the patient is weakened. Secondly, the local
intestinal lesions are increased. Thirdly, perforation and peritonitis are more
liable to occur.
TYPHOID FEVEE. 649
Kervous Phenomena. — Should headache be severe, not readily relieved
by fomenting the forehead and temples with warm water, or should it give
place to active delirium and other severe nervous disturbances, the ques-
tion presents itself : — shall anodynes be administered ? If they are to be
used the most reliable is opium, and usually the condition of the pupil
of the eye will serve to indicate whether opium shall or shall not be ad-
ministered. A contracted or ''pin-hole" pupil maybe considered to contra-
indicate its use, though there are exceptional cases in which opium acts
favorably, notwithstanding this condition of the iiuj)il. Opium should be
given with great caution whenever signs of cyanosis are present. In all
cases of typhoid fever, it is safer to administer opium in small and repeated
doses than to venture upon the administration of one large dose. There
are other anodynes which will sometimes be of service, such as hyoscyamus,
chloral and the bromides. Chloral is said to have a special value in
quieting active delirium, which is sometimes so troublesome, but my
own experience in its use has not been favorable.
When anodynes have failed to give relief to typhoid fever patients, who
have been delirious and somnolent for days, they will sometimes become
quiet and fall asleejD immediately after the free administration of stimu-
lants. Those cases in which the nervous symptoms are due to an anaemic
condition of the brain, associated with a weak heart and a flagging circu-
lation, are most likely to be benefited by the use of stimulants. In those
cases in which subsultus becomes very marked, and there is general
tremor, jactitation and restlessness, I have seen most hapjoy effects pro-
duced by the use of hypodermic injections of sulphuric ether. I would
use, as an average quantity, four drachms, given in injections of one drachm
each, in different places. The same watchful care should be taken of a
typhoid fever patient during convalescence as during the active period of
the fever. The number of typhoid patients who die during convalescence
is relatively large.
Death is often due to the fact that the physician has laid down no
strict rules to be observed as to diet and exercise, and frequently from the
non-observance of such rules when they have been given. The diet of
fever patients during convalescence should be carefully watched. Only
small quantities of food should be taken at a time, so that the gastric
juice secreted by the enfeebled stomach may be sufficient for its complete
digestion. All indigestible articles of food, and those which furnish a
large amount of waste, should be strictly forbidden. An apparently in-
significant disturbance of tne stomach, a slight vomiting, or a moder-
ate diarrhoea occurring during the period of convalescence, should be
regarded as dangerous, for any one of these may induce a sub-acute
gastritis, or lead to intestinal perforation and a fatal peritonitis. It is
obvious that while the intestinal ulcers are healing much mischief may be
done by improper diet. Notwithstanding the cravings of the patient's
appetite, the diet must be restricted to such articles as milk, cream, gruels,
jellies, and animal broths. Solid food must be strictly forbidden, espe-
cially meats, vegetables, and fruits. If diarrhoea is present during conva-
650 ACUTE GENERAL DISEASES.
,a!sceiice it is far safer to restrict the patient to milk and cream. All ex-
ercise, except simple walking around the sick-room, should be prohibited.
It is of the greatest importance that this class of patients should keep in
the recumbent or semi-recumbent posture until the cicatrization of the in-
testinal ulcers is completed, which in some instances does not take place
until two or three weeks after convalescence is well established. If con-
valescence is ."^low, small doses of quinine, iron, and cod-liver oil are of
service. They should be given after the patient has taken food. In many
cases it is important to take the evening temperature for at least two weeks
after the commencement of convalescence, for by its range it will be pos-
sible to more accurately determine the exact condition of the patient.
When convalescence is delayed, so that at the end of four or five weeks the
patient has not regained strength, change of air is indicated.
YELLOW FEVEE.
Yellow fever is a mias^natic contagious disease, usually epidemic ; it pre-
vails most in tropical regions, and is characterized by a yellowish discolora-
tion of the skin. From some of its more prominent symptoms it has been
called typhus iderodes, hlack-vomit or Jicemo-gasiric fever, fehris Jiava, and
also mal de Siam.
Morbid Anatomy. — The pathological changes of yellow fever have much
that is common both to contagious and miasmatic diseases. Its most con-
stant and characteristic lesion is to be found in the changes which take place
in the liver.
The liver is usually slightly enlarged ; it may, however, be normal, or even
slightly diminished in size. The most striking change is in its color, which
has been described as butter-, cheese-, mustard-, or chamois-yellow. Some-
times it is of a chocolate or bright orange color. The change in color
may be uniform throughout the entire organ, or it may occur in ir-
regular patches of different hues. Slight extravasations of blood are
sometimes found on its surface. In some few instances this change will be
confined to a single lobe or a circumscribed portion of the organ. The
liver-tissue breaks down readily on firm pressure, and on section is drier
than normal, containing less blood. Small points of extravasation some-
times stud its substance.
Under the microscope the liver cells, while unaltered in shape, are seen
to be filled with oil-globules, so large that at times one globule occupies an
entire cell. Sometimes the change is a granular one, the nuclei of the
hepatic cells being obscured; or they have entirely disappeared.' This
change is an acute fatty degeneration, and not an infiltration, as many sup-
pose. The organ in its gross as well as in its minute anatomical changes
resembles the fatty degeneration of the drinker's liver. Cornil and Ean-
vier^ say this degeneration is secondary to a congested and ecchymosed state
of the liver.
1 Yellow Fever considered in its Histoi'ical, Pathological, Etiological^ and Therapeutical Relations, R.
La Roche. Philadelphia, 1855. Yellow Fever. Fritz Haeniscb. Ziemssen's Cyc. Prac. Med., vol. 1.
* Patholog. Histology.
TELLOW FEVEE. 651
^~fie heart is lighter in color than normal, soft, friable and flabby. It
creaks down readily under firm pressure, and resembles strongly in its gross
and microscopical characters the heart of typhoid fever. The muscular
elements undergo the same granular degeneration, which cannot be ascribed
to prolonged high temperature, for in yellow fever the temperature is neither
high nor does it persist above normal for a long time. As in typhoid, so here
we are inclined to regard the degenerative changes as the result of the
specific poison of the disease. The cavity of the ^pericardium usually con-
tains one or two ounces of blood-stained serum. Long coagula or partly
organized clots extend from the heart cavities quite a distance into the ves-
sels. These coagula are tlie result of the heart-failure, and are formed
during the few last hours of life. Sometimes the blood in the heart is fluid,
varying in color and reaction.
The Mood-changes are similar to those of typhoid and typhus fever, yet
are more extensive than in either ; the blood is of a darker color than
normal, and coagulates very much more slowly and imperfectly than
normal ; a fact due either to a diminution in, or to a j)artial loss of the
coagulating power of the fibrin-factors. The red blood globules are de-
stroyed, or they are serrated and shrivelled, and in many instances broken
down — this explains the yellow color of the surface which gave the name
to the disease. A solution of part of the red corpuscles occurs, and the
hsematin is changed into bile pigment. This condition of the blood also
explains to a certain extent the degenerations which are found in the dif-
ferent organs of the body. Very soon after withdrawal the blood under-
goes ammoniacal decomposition, due in part to the altered relation of its
salty constituents. Some affirm that the blood contains free ammonia. It
contains no free pigment.
The mucous memhrane of the oesoiDhagus, stomach and small intestine is
always the seat of a more or less acute catarrh. The veins are varicose and
turgid, often giving rise to arborescent injection of the membrane ; and
ecchymotic spots of extravasation irregularly stud its surface. Hemorrhagic
erosion of the stomach is sometimes present, and throughout the whole in-
testinal tract there is often a considerable quantity of dark-colored fluid
blood, the stomach, however, containing matters similar to those vomited
during life. The gastric mucous membrane is aloO not infrequently found
thickened, softened, .and reddened. The mucous membrane lining the
larynx also suft'ers a catarrhal inflammation ; and ecchymotic sjDots are found
on the lining membrane of the bladder.
The lungs are almost constantly the seat of infarctions, and these are
occasionally quite numerous. When diffuse, pulmonary apoplexy occurs,
and when a large portion of a lobe is involved, the lung-tissue will be
broken down and large blood-clots will occupy the space.
The pleurcB are sometimes covered with ecchymotic spots, and occasionally
there is a blood-stained serous exudation into the pleural cavity.
The brain and cord if at all altered are only slightly hypergemic. Punc-
tate extravasations may occur in the meninges; and some affirm that an
abundant serous exudation is often present in the lumbar and sacral regions.
653 ACUTE GENERAL DISEASES.
attended by an inflammation of the membranes of the cord at the same
point, with more or less intense inflammation of the neurilemma of the
nerves in the coeliac and hepatic plexuses.
The Mdneys are the seat of parenchymatous inflammation, which rap-
idly passes to the stage of fatty metamorphosis. There are sometimes
small abscesses in the parenchyma. On microscopical examination oil-
globules are seen to till the tubules, whose epithelium is sometimes desqua-
mated, or the seat of fatty or granular change. Occasionally the tubules
are filled with broken-down epithelium. The pelves of the kidneys and
the ureters are frequently the seat of an acute catarrh.
The spleen may be slightly enlarged ; but is usually softer, more friable,
and darker than normal.
The shin varies in color from a bright golden-yellow to a dark orange.
Petechise, ecchymoses, vesicles, pustules, and large patches of extravasation
may be found upon the surface of the body. The mucous membranes are
not infrequently oi a distinctly yellowish tinge.
The gall-bladder may or may not be increased in size ; it commonly con-
tains a moderate quantity of dark-colored bile, and its mucous surface ex-
hibits spots of punctate extravasation as well as arborescent vascularity.
The ovaries and uterus verj frequently contain a considerable quantity
of extravasated blood.'
Etiology. — There is no part of the disease so uncertain and confusing as
its etiology. Equally competent observers hold diametrically opposite views
in regard to it. I shall confine my statements regarding it to well-authen-
ticated facts, avoiding the many controversies on this subject.
Yellow fever is rarely met with beyond the limits of 40° North and 20°
South latitude ; it prevails in the West Indies and eastern part of the West-
ern Hemisphere far more frequently than any other region, and the locus,
if we may say so, of the malady is the Antilles. In these places it is en-
demic, and to a comparatively slight extent it is so in certain portions of
Europe and Africa. Commercial seaports are pre-eminently the starting-
points of great epidemics ; it is sometimes circumscribed within very nar-
row limits in the seaports. Crowding is one of the essentials to its develop-
ment. The average temperature of the locality where it prevails must be
at least 73° E.; there must be a certain amount of moisture ; and animal
and vegetable matter must undergo decomposition, either on the surface or
in the substance of the soil. On ship-board there may be the greatest un-
cleanliness, yet the fever will not appear on the vessel till it has touched
land in an affected port or been brought into communication with a ship
already contaminated.
The time of year during which the fever prevails varies with the climate
and temperature ; in the United States it usually appears in July and
August, to disappear with the first frost. The epidemic in New York City
in 1795 began in August and terminated in October. When the prevailing
winds are southeasterly, the development and spread of an epidemic are fa-
1 Traite des Maladies Infedieuses : Maladie des Marais, Fievre Jaime, Maladies Typhoides, Fievre
Typhus des Abnees. Willielm Griesinger, Paris, 1868.
TELLOW FEVEE. 653
vored ; northwesterly winds check or arrest it. As has been mentioned, a
severe frost or a "freeze" puts an end to the further progress of the dis-
ease when it preA'ails under the most propitious circumstances for its devel-
opment.
There is much reason in the arguments of those who contend that yellow
fever is an "acclimation" disease. First (and here, however, it should be
remarked that the disease is indigenous in some regions), certain islands and
seaport towns along our Southern coast always suffer from an ej)idemic when-
ever certain atmospheric conditions exist; a resident of one of these places
where yellow fever is indigenous is far less liable to have the disease than a
stranger, esjDecially one from the North. One attack is usually, not ab-
solutely, a protection against a second. The disease is especially liable to
appear in those localities where a severe, type of pernicious fever has pre-
vailed, and after a warm, rainy season rather than after a dry, cool one.
Whether the fever is epidemic or endemic, and whether the locality is one
frequently visited or one in which the disease is indigenous, sporadic cases
are of very rare occurrence.
The negro race has a marked immunity from this fever. Age and sex
exercise no influence upon the etiology. Occupation seems to have some
effect in its production, since those who work over, or near, hot fires are
stricken much oftener than those who work in unhealthy, filthy surround-
ings. Exposure to cold and wet, alcoholismus, and venereal excesses here,
as elsewhere, render individuals more liable to the fever.
In regard to the nature of yellow fever poison, some assert that it is a
malarial miasm, modified by the person in whom it lodges. It is in many
respects similar to the poison of typhoid, both in etiology and the manner
of its conveyance. It is unquestionably a specific poison, which differs es-
sentially from the poison of every other fever. Typhoid, malarial and yel-
low fever may all prevail at the same time in the same locality, bat one will
never merge into the other; each runs its own individual and peculiar course.
All chemical and microscopical research has, as yet, failed to discover ivhat
the poison is ; but we are led from its mode of conveyance and from the
conditions of its development to believe that it has the elements both of a
miasm and a contagion.
There are three leading doctrines in regard to the contagious character of
yellow fever -.—first, that it is contagious, like small-pox and scarlatina ;
second, that it is non-contagious, and never directly transmitted from the
sick to the healthy; and third, that when yellow fever is prevailing in a lo-
cality, it may be carried from one person to another in that locality. The
last is the doctrine of contingent contagion. One who has seen the fever
in hospitals needs no argument to prove that it is not directly contagious.
Some claim that yellow fever poison, though not directly transmissible from
the sick to the healthy, becomes infectious when brought in contact with
decomposing animal and vegetable matter. It is well established that epi-
demics of yellow fever only occur in those localities where decomposing ani-
mal and vegetable matter is present ; and when men are crowded together
in shops and around the docks and wharves of seaports, or in the filthy
654 ACUTE GENERAL DISEASES.
streets and dwellings of such localities. In some few instances evidences
exist that yellow fever breaking out in the hold of vessels has been circum-
scribed to well-defined and very narrow limits by free ventilation. There
are ample facts to sustain the belief that this fever is infectious only when
the atmosphere has become loaded with the emanations of animal and veg
etable decomposition to which has been added the specific yellow fever poi-
son. Under such circumstances, the disease may be propagated from the
sick to the healthy.
Whatever view is taken of the contagious or non-contagious character of
yellow fever, all observers agree that it \& portable, that it can be conveyed
from one place to another by means of clothing and merchandise and in
the holds of vessels. That whenever the poison is thus introduced into
healthy localities which are suited by temperature to its reproduction, and
where there is animal and vegetable decomposition, it rapidly reproduces
itself, and thus epidemics of yellow fever occur in localities that otherwise
would be free from the disease.
There is no-doubt that the poison of yellow fever retains its vitality for
a very long period ; and with favoring conditions may cause an epidemic
in places very remote from the origin of the poison. The poison is also
cajjable of great concentration, for short exposure to the contaminated
air that often fills the holds of ships on which yellow fever is prevail-
ing will be followed by the fever in a few hours. Ordinarily there is little
danger in visiting those sick of yellow fever if there is free ventilation, and
one does not remain in the infected locality for a long time. The period
of incubation varies in duration from twelve hours to four or five days ;
when the exposure is followed in a few hours by the fever, the fever poison
must necessarily be very concentrated. The activity of yellow fever poison
is destroyed by cold ; one or two hard frosts will arrest a yellow fever
epidemic. Some claim that epidemics of yellow fever are self-limiting,
rarely exceeding sixty or seventy days in their duration. There is not,
however, sufficient proof to establish this statement. ^
Symptoms. — As in typhoid fever, there are mild and severe cases of yel-
low fever ; but they differ only in degree, not in kind ; the clinical his-
tory of both is the same.
Prodromata may occur ; but headache, anorexia, lassitude and pains in
the limbs cannot be reckoned as characteristic of the fever, and only
when these occur during an epidemic are they especially significant.
Whether premonitory signs have or have not been present, the disease com-
mences with a chill, distinct and severe. In a few instances a series of
rigors takes the place of distinct chills. Sometimes persons while ap-
pearing in perfect health are seized with a severe chill, and immediately
become seriously ill and take to their beds in a most dejected manner. Fol-
lowing the chill there is nausea and vomiting, the face is flushed, the con-
1 In this connection see : The Cause and Prevention of Yellow Fever, in the Beport of the Sanitary Com-
mission of New Orleans. Dr. E. H. Barton, New York, 1857. 3Ie?)ioire sur la Fievre Jaune qui en 1857, a
Decime la Population de Monteviedo. A. Brunei, Paris, 1860. Account of the Yellow Fever which occurred
in the City of Neiv York in the year 1822. Dr. James Hardie, New York, 1823. Remarks on the Epidemic
Yeilow Fever on the South Coasts of Spain. Dr. K. Jackson, London, 1821.
YELLOW FEVER.
Go5
junctivae are injected, there is circumorbital headache, and violent pains
in the bones, back and limbs, especially in the calves of the legs. The eye
has a peculiar lustre and a staring look. The course of the fever is the
same in the severe and in the mild cases.
The temperature rises rapidly after the chill to 103° or 104°F. ; the limits
vary, but yellow fever is not a disease of high temperature. In a few epi-
demics the initial rise in temperature has been as great as 110° F., but these
are jDhenomenal occurrences. At the end, or beginning, of the third day
the maximum fever will have been attained ; in our country this is rarely
more than 104° or 105° F. Between this period and the fourth day of the
disease slight variations, hardly amounting to distinct remissions are pres-
ent ; on the fourth day there is a rapid defervescence ; it is not an inter-
mission but a remission, for the temperature only falls to 100° or 101°F.
The period of remission lasts
from a few hours to two or
three days, after which a sec-
ond rise begins, one that does
not take place quite as rapidly
as the first, and is not usually
|)receded by a chill or rigors ;
and a temperature of 104° or
105° is again reached. The
temperature now remains sta-
tionary from one to two days,
it then falls to normal and
remains so. This last fall is,
like the first, marked by a very
sharp temperature curve. The
range of temperature is impor-
tant, for it divides this dis-
ease into three parts; first,
the stage of invasion, the
febrile stage or period of ex-
acerbation ; second, the stage
of remission, calm or passive ]3eriod ; and, third, the stage of the second
exacerbation or collapse.
The piilse in yellow fever is peculiar. It rarely exceeds 110 beats per min-
ute, thus differing from that of other fevers in which the rule is an in-
crease of five beats for every one degree rise of temperature. Indeed, in
mild cases the pulse-rate may only be five or six beats above the normal. It
has been observed to fall much below the normal, as low as 40 and some-
times 30 in a minute. The " feel " of the pulse is as if the arteries were dis-
tended with gas, and hence the name, '' gaseous pulse,-" is not inajjpro-
priate. It is compressible and of an uncertain volume, offering no resist-
ance, so to speak, to the touch.
The skin, as soon as the temperature begins to rise, maybe either dry or
bathed in a cojjious perspiration. Following the chill there is sometimes an
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Fis. 153.
Temperature Record in a Case of Yellow Fever.
656 ACUTE GENERAL DISEASES.
abnormal coldness on the surface, while rectal thermometry shows a marked
rise in the temperature. At the close of the first, or beginning of the sec-
ond day, the body emits a peculiar corpse-like odor. About the third day
the skin begins tc assume a jaundiced hue, noticed first in the sclera and
then spreading over the whole body. It is a dark jaundice, like that of py-
aemia, and is to be regarded as hematogenous and not hepatogenous. Those
who maintain that the jaundice is due to retention and reabsorption of bile
have no proof to offer, since evidences of mechanical obstruction to the out-
flow of the bile are among the rarest post-mortem appearances. The true
etiology is found in the change which takes place in the blood. The pig-
ment thus formed is deposited in the tissues, and is a true hematogenous
icterus. The perspiration now stains the linen yellow. This jaundice is
not always present in yellow fever, but when it becomes a symptom it does
not run into the period of convalescence. In the third stage the jaundice
assumes a mahogany hue.
Vomiting. — Immediately following the chill, nausea and vomiting are
present. First the contents of the stomach are voided, then a yellowish
green matter ; when the latter color is present the vomiting becomes pro-
jectile in character, and the ejected matter has an alkaline reaction and is
fluid. The alkalinity is due to ammoniacal decomposition. The vomiting
is accompanied by burning pains at the xiphoid cartilage. If the vomiting
comes without any other change in the matter vomited, it is an evidence
that the fever is going on to recovery ; in severe cases the characteristic
** black vomit " is present, the result of hemorrhage into the stomach. Thisi
vomit is brownish black, semi-fluid, with a glistening reflection, and varies
in amount from a mere trace to many pints. It may occur on the second
or third day of the fever, but usually it does not come on until about forty-
eight hours before death, or on the day of death ; it occurs only in about
one-third of the fatal cases. It undoubtedly occurs more frequently in yel-
low fever than in any other disease, but it differs in none of its constituents.
from a similar material which is sometimes vomited in other diseases where
small capillary hemorrhages occur in the stomach.
Microscopically ' it is seen to be made up of blood corpuscles, degenerated
lymphoid cells, fat cells, epithelial cells from the raucous membrane of
the stomach, fine granules of pigment, aggregated non-granular masses,
and serous fluid. The action of the gastric juice is such that the color-
ing matter escapes from the corpuscles as small granular or rounded
masses. It is claimed that the black vomit of yellow fever is specific, in
that it contains a peculiar microscopic vegetable organism. This is yet
lacking confirmation. The enfeeblement of the walls of the capillary ves-
sels results from the pathological blood-conditions, and as qualitative al-
terations are likewise added, hemorrhagic extravasations occur in the
stomach, and on other mucous surfaces. The hemorrhages from the nose
and gums that so frequently occur, and fluid blood in the discharges from
the bowels are caused by the same changes as cause the gastric hemor-
rhages. Very rarely hemorrhagic extravasations occur during life from
1 Mcroscoplc Researches in the Black Vmnit of Yellow Fever. Dr. M. Michell. Chariest. Med. Jour., 1853.
YELLOW FEVEE. 657
the respiratory organs, the genitals, the skin, and the meatus auditorius
extern us.
Urine. — Early in the disease the urine is scanty, acid, and slight traces
of albumen may be found. Later, when the jaundice appears, its reaction
is alkaline, and bile pigment is present ; as the disease progresses it be-
comes more abundant ; if not present before, it makes its appearance dur-
ing the stage of remission ; in all severe cases, leucin, tyrosin and fatty
casts will likewise be found. Entire suppression of urine is of frequent oc-
currence in severe cases. Patients with black vomit may recover, but a
fatal result almost certainly follows urinary suppression. In cases where
the yellow fever poison is concentrated and the nervous symptoms are prom-
inent, suppression of urine may exist from the onset, but it usually does
not take jjlace until the second exacerbation. Urgemic toxtemia is then
added to the yellow fever poison, and the condition is almost necessarily
hopeless. The perspiration in this condition has a urinous odor.
. The countenance in some cases is almost diagnostic : the eyes are lustrous
and staring, the face is flushed, the conjunctivae are injected, the intense
conjunctival congestion giving the eyes the appearance of two balls of fire
set in a face of a dusky, deathly hue ; this gives to the countenance a re-
markable expression of dejection and dulness.
The tongue is covered at the outset of the fever with a thick, yellowish
white coating, except at the tip and edges, which remain red. It is often
indented by the teeth ; and as the disease advances may become dry, brown,
cracked and fissured, resembling the typhoid tongue. The buccal mu-
cous membrane is bright red at first, subsequently becoming oedematous.
The bowels are usually constipated, but when diarrhoea does occur, fluid
blood is apt to be mingled with the discharges. Sometimes when intense
jaundice is present, the stools are clay colored, but this is an accidental
circumstance.
TJie mind is usually clear to the last, but when delirium sets in it will
be wild and accompanied by a desire to get out of bed. The patient lies
in a state resembling collapse, his features shrunken, indifferent both to
his own condition and to what is occurring about him.
Pain is quite severe over the lumbar and epigastric regions ; they are ex-
quisitely sensitive to pressure ; convulsive twitchings of the muscles, and
diaphragmatic contractions are often present before death. In favorable
cases all the severe symptoms distinctly remit on the second day after the
beginning of the stage of the second exacerbation, and then follows a pro-
tracted convalescence, and it is with the greatest difficulty that the stom-
ach will retain the blandest food. When death is to follow, the vomiting
persists, the urine becomes less and less in amount and richer in albumen,
and uraemic coma, or wild delirium ends the scene. Just before death,
in some epidemics, the temperature falls; hence the name algid yellow
fever. But whether coma, algidity, delirium, suppression of urine, or
black vomit is the predominant symptom in an epidemic, the disease is the
same specific fever. The mortality varies as much in different epidemics
as the prominent symptoms do.
42
658 ACUTE GENERAL DISEASES.
Differential Diagnosis. — Yellow fever may be confounded with acute yel-
low atropliy of the liver, relapsing, bilious remittent, continued malarial
fever, and the icteric variety of pernicious fever.
The diagnoses of acute yellow atrophy of the liver and yellow fever have
already been considered.
Relapsing fever is an inland disease, as a rule, while yellow fever is
essentially a coast disease. In relapsing fever the temperature rises to a
high point, often 107° or 108°, the pulse keeping pace and running up to
140 or 150 beats per minute ; in yellow fever a pulse of over 110 is very
rare, and the temperature averages 104°, often lower. Jaundice and the
peculiar-colored "yellow fever face" are early symptoms in this disease;
while there is no change in the face in relapsing fever and jaundice is a
very late symptom. Eelapsing fever has a true intermission, while yellow
fever has only a remission. The spleen is markedly enlarged and tender
in relapsing fever ; in yellow fever it is normal. During the pyrexial
period spirilli are found in the blood in all cases of relapsing fever, and are
absent from yellow fever. Bronchitis is a very common complication of
relapsing fever, while pulmonary complications are very rare in yellow
fever. Finally, relapsing fever is propagated by contagion, and yellow is
not.
Yellow fever is a portable disease, and usually prevails in cities and
along the coast ; bilious remittent fever is not portable, and is a disease of
the country and inland towns. The pulse-rate is 120 or 130 in bilious re-
mittent ; in yellow fever it is rarely over 110 ; the temperature is 105° or
106° in bilious remittent, and rarely exceeds 104° in yellow fever. The
liver is enlarged in yellow fever, and normal in size in bilious remittent ;
the spleen is invariably enlarged in remittent and unchanged in yellow
fever. There is projectile vomiting in yellow fever, while in bilious re-
mittent it is retching in character. In twenty-four hours a remission
occurs in bilious remittent, while in yellow fever the remission does not
occur until the fourth day. The urine is rarely albuminous in remittent
fever, while even in mild cases of yellow fever albumen is rarely absent.
The mind is clear in yellow fever, while a patient with bilious remittent is
dull and delirious. The difference in the invasion of the two diseases, the
countenance, the existence of the hemorrhagic tendency, and the history of
the epidemic are sufficient to distinguish yellow fever from the so-called
yellow type of remittent fever.
Id continued malarial (so-called typho-malarial) fever the temperature
is higher than in yellow ; there is diarrhoea, which is absent from yellow
fever, and the spleen undergoes marked enlargement. Yellow fever, on the
other hand, is attended by albuminuria and a peculiar facial aspect that
are both absent from all cases of continued malarial fever. There is
periodicity in the variations in temperature in continued malarial fever,
and the disease is continuous over two or three weeks ; while in yellow
fever there are slight and irregular variations in the fever, and a distinct
remission on the fourth day, which removes all doubt. Pain in the right
iliac fossa is much more marked in continued malarial than in yellow
TELLOW FEVER. 659
fever. The history of the epidemic, the portability, and other etiological
points will also often greatly aid in making the diagnosis.
Prognosis. — The mortality-rate differs in different epidemics ; the high-
est mortality is given as one out of every three ; while in mild epidemics
only one out of fifteen or twenty dies. The average duration is six
days, but in cases where a concentration of the poison overwhelms the
system at the very onset, death may occur within twenty-four hours, and
between this time and six days there is a varying number of fatal cases.
The conditions that render the prognosis unfavorable are early high tem-
perature, a severe period of invasion, deej) jaundice, scanty urine contain-
ing albumen and casts, black vomit, intense pains over and irritability of
the stomach, a gaseous pulse, delirium, and, worst of all, suppression of
urine.
Among the favorable signs are diminution in the quantity of albumen, a
quiet stomach, slight and late jaundice, a moderate degree of fever, and
fewer attacks of black vomit. A positive prognosis is best withheld ; but
"black vomit" and complete suppression render a case hopeless. Yellow
fever, in some epidemics, is complicated by numerous boils and abscesses,
and by cellulitis and inflammation of the parotid gland, perhaps termi-
nating in suppuration. Eegarding convalescence, it may be said, however
quickly it may be established, it is longer than in any other disease in
proportion to the length of the fever. Indeed it is often two weeks after
the final fall in temperature before the patient begins to mend, and five
or six months may have to elapse before he is entirely well. Death may
result from rapid overwhelming of the system with the poison, i.e., from
the effects of the blood change, from uraamia, black vomit, suppression,
exhaustion or asthenia.^
Treatment. — Prophylaxis is, in a great measure, summed up in the word
quarantine. A strict quarantine, that should include not only individuals
but also all articles that have been near the infected person or spot, would
be very desirable. This does no harm to the sick ; they may be removed
to a hospital at once, after disinfection, for the disease is not contagious.
To go into the details of quarantine, of ship and hospital disinfection,
would be out of the domain of this work. A person who is in the yellow
fever region can take the best prophylactic measure — removal from the
neighborhood. When this is impracticable, sulphate of quinine may be
taken and all predisposing causes avoided as far as possible. Mercury is by
some regarded as an efficient means of j)rophylaxis.^ The variability of the
mortality-rate has been referred to. Blood-letting, mercurials, stimulants,
and quinine, — these are the four chief methods that have been tried. ^
Blood-letting, to the extent sometimes of 180 oz. at a time, was formerly
practised, but has been abandoned, as not only wrong in theory but harm-
1 " Relati/m de la Fievre Jaune survenve a Saint-Nazaire en 1861." M. F. Melier, Paris.
2 Yellmv Fever; Us origin, improper treatment, prevention and cure. Dr. W. A. Shubert, Savannah, 1860.
A dissertation on the sources of malignant., bilious or yellow fever, and means of preventing it. Dr. W. G.
Chalmell, Philadelphia, 1799.
' Das Gelhe Fieher heurtheilt und behandelt nach einer neuen Aussicht vom Wesen der Fieher in Allge-
meinen. G. Eichbom, Berlin, 18.?3. The history of yellow fever, with themost successful method of treatment
Dr. J. Mackrill, Baltimore, 1796.
660 ACUTE GENEEAL DISEASES.
ful in practice. Mercurials are exhibited to-day only for catharsis at the
commencement. Stimulation is bad in excess ; and quinine is of no avail
for any but prophylactic measures, if even here it possesses as much
efficacy as theory attributes to it. Eecently carbolic acid has been added
to this list, but it has had so slight a trial that nothing can be said joro or
con, except that it is likely to go the way of all specifics.
The plan of treatment which seems, at the present state of our knowl-
edge, most reasonable, may be called a diaphoretic and expectant plan, the
diaphoresis looking toward the relief of the grave kidney trouble, and
hence tiding over the most serious point in the fever. When a patient is
stricken with the fever, apply counter-irritation over the kidneys, and at the
same time administer ten grains of quinine along with fifteen or twenty
grains of calomel. The body should be covered with flannel and slightly
heated, moderate diaphoresis being continually kept up by these methods.
At the same time the air must always be fresh ; close quarters are always
contraindicated. The nausea and vomiting may be controlled by eating
cracked ice, drinking milk and lime-water, or by small hypodermic doses
of morphia. The restlessness, tossing, and jactitation which are so ex-
hausting in some cases, and which probably arise from the action of the
urea in the circulation on the nerve centres, are best controlled by hypo-
dermic injections of morphine. Full doses of opium, producing as they do
free diaphoresis, may also be administered, unless the kidney lesions are
very grave. Suppression is treated by the usual methods, large doses of
turpentine being given. In the last epidemic 3j of turpentine in sugared
water was given every four hours in the case of a negro, and recovery
followed.
In copious ha3matemesis styptics can be given cautiously, and cold com-
presses may be applied over the epigastrium. When the various discharges
have caused much exhaustion the judicious use of stimulants is often
beneficial. When the opportunity offers, it might be well to try hypo-
dermic injections of the sulpho-carbolate of quinine. Yellow fever runs its
course in five or six days ; hence the vital powers must be sustained until
the defervescence, and this is found to be extremely difficult on account of
the extreme gastric irritability. A bland and highly nourishing diet is to
be prescribed as soon as convalescence occurs, and tonics form an essential
part of treatment at this period. ^
EPIDEMIC CHOLEEA.
Epidemic cholera is an acute general disease, which prevails epidemically,
and in certain localities is endemic. It is characterized by copious watery
discharges from the alimentary canal, by cramps, and by suppression
of the excretions. It has also received the names of cholera Asiatica,
cholera asphyxia, and epidemic, malignant, algid, or blue cholera.
Morbid Anatomy. — The post-mortem appearances vary with the period at
which death takes place ; in the stage of collapse or in that of reaction,
1 Tdlow Fever in Charleston, 1871, with Remarks upon its Treatment. Dr. F. P. Porcher, Charleston,
1872, (Trans. S. C. Med. Asso.)
EPIDEMIC CHOLERA 6G1
there is usually marked emaciation ; the extremities are noticeably shriv-
elled, and the surface of the body in the dependent portions is bluish or
mottled ; sub-conjunctival ecchymoses are often observed. The face has a
pinched and drawn expression, and the eyes are deeply sunken. The body
cools slowly after death, and frequently there is a post-mortem rise in tem-
perature of two or three degrees Fahr.
Rigor mortis is marked immediately after death, and muscular contrac-
tions often cause changes in the position of the limbs and body. The skin
is often so shrivelled as to resemble the condition called "parboiled,"
■which is best marked upon the extremities. Putrefaction commences much
later than in other diseases, on account of the withdrawal of large quantities
of fluid from the body.
The visceral lesions are as follows. The small intestine is distended and
of a bright red color ; its muscular coat is somewhat relaxed. Its mucous
membrane is injected with a fine aborescent vascularity ; it is sometimes
oedematous and its folds are often prominent, especially around the lower
part of the ileum. Peyer's patches- and the solitary follicles are at first en-
larged, the latter more than the former ; if the solitary glands rupture, the
membrane presents a reticulated appearance. Ulcerations resembling ty-
phoid ulceration may occur, the glands become flattened and pigmented.
There is an almost complete detachment of the epithelium; if any patch is
left undenuded there is a sub-epithelial exudation which loosens its attach-
ment to the villi. The intestine may be partially or comiDletely filled with
a "rice-water," whey-like fluid, alkaline in reaction, which contains an
abundance of cast-off epithelium, and varies in consistency from the ordi-
nary cholera stool to that of putty. The mucous surface may be of a
bright red, grayish or, rarer than all, a greenish color. In some instances
the intestine contains a moderate quantity of dark grumous blood. Dur-
ing the fever of reaction gray diphtheritic patches, very difficult of re-
moval, which later become dry, brown sloughs, are sometimes found in
both the small and large intestine. Similar patches have also occasion-
ally been observed upon the mucous membrane of the biliary passages,
vulva, and vagina. In severe cases the basement membrane is wholly
denuded.
The peritoneum of the small intestine is of a rosy color and dry, or is
covered with a thin layer of plastic matter.
The glands of the large intestine are sometimes congested, swollen and
prominent ; while the mucous surface has large ecchymoses and patches of
extravasation upon its substance. Diphtheritic ulcerations may be present
in the colon.
The oesophagus is sometimes congested and ecchymosed, and its glands
are swollen. It may have its epithelium detached, and at times it is cov-
ered with a diphtheritic exudation.
The stomach is at first distended and filled with fluids similar to those
which are found in the small intestine ; later its mucous lining is hyper-
semic, swollen, often relaxed and ecchymotic. Still later it is collapsed
and empty.
662 ACUTE GElfEKAL DISEASES.
The Tcidneys are intensely congested and enlarged, the capsule is adlier*
ent, the surface presents a stellate or "marbled " vascularity, and on longi-
tudinal section both cortical and medullary portions exhibit punctate or
striped blood injections, and numerous ecchymoses. The small veins, es-
pecially around the glomeruli, are engorged, and the cortical portion of
the kidney is more or less discolored. The uriniferous tubules have their
epithelium loosened, and the cells are cloudy, swollen and filled with a
granular albuminoid material ; often transparent cylinders fill the lumen
of the uriniferous tubes. For the most part the lesions resemble those of
acute croupous nephritis. All these changes may occur during the first day
of the choleraic attack. Later, during the secondary fever, the discolora-
tion and tubular changes are increased ; the size of the kidney being one-
sixth to one-third greater than normal, and the epithelial cells undergo pro-
gressive fatty degeneration, and the whole organ becomes soft and friable.
Chemical examinations have shown the kidneys to contain an abnormal
quantity of urea, uric acid, leucin, and some bile-pigment.
Tlie hlaclder is at first contracted and empty ; but later it may be par-
tially filled with albuminous, milky urine. Its mucous membrane and
that of the ureters and pelvis of the kidneys undergo changes similar to
the other mucous surfaces ; — viz. : hyperemia, ecchymoses, and perhaps
diphtheritic processes.
The lungs are engorged at the entrance of the pulmonary artery ; but
the parenchyma of the lung is collapsed and exsanguinated, and crepitates
less than normal luug-tissue. If death occurs during or after the reaction-
ary fever, extensive oedema, hypostatic congestion and hemorrhagic infarc-
tions may be found. Capillary bronchitis, lobular and lobar pneumonia,
and emphysema are present in those cases where death occurs during con-
valescence. Pulmonary gangrene is a rare lesion. The trachea and
bronchi are engorged and covered with a muco-pus, while later a second-
ary diphtheritic process may be established upon their mucous surface.
The pericardium is dry, and its visceral layer is ecchymotic, while the
parietal is coated with a sticky, pasty material.
Tlie heart is hard, dry and contracted, containing in its right cavity,
which may be distended, soft clots, which sometimes extend into the
pulmonary artery and into the veins. The left cavity is empty, or has
only a few small black, loose coagula in it.
The tlood is darker and thicker than normal, there is an increase in
its albumen and corpuscles, as well as in its specific gravity and in
organic solids ; while there is a. decrease in its saline elements and in its
coagulating power. Urea is occasionally present.
The spleen is small, wrinkled, flabby and shrunken, though when typhoid
symptoms co-exist, or when it is the seat of blood extravasations it is en-
larged and softened.
The liver is usually pale, containing patches of commencing fatty de-
generation, and the large veins are distended with blood. There is ex-
foliation of the epithelium of the mucous surface of the gall-bladder,
which causes plugging and distention of the ducts.
EPIDEMIC CHOLERA. 663
The meningeal vessels of the brain and the sinuses are engorged, while
the cerebro-spinal fluid is frequently absent. Medullary hyperaemia is
common. But when death has occurred late, the brain contains less blood
and is often superficially osdematous.
The suh-cntcmeous connective-tissue is hard and dry. Parotid swellings,
furuncles, purj^uric and scorbutic spots, ulcerations of the cornea, and
bed-sores are often present.
Etiology. — Cholera is an acute, infectious, non-contagious disease, prob-
ably of miasmatic origin. It prevails epidemically and may be endemic.
It first appeared in the East, and thence spread in all directions, follow-
ing the routes of commerce without regard to climate. Xo country
has been entirely exempt from its ravages. It has prevailed, how-
ever, chiefly in hot climates, during wet seasons. In this country it
prevails most in mid-summer. It is more liable to occur in low lands
than in mountain regions. Badly drained malarial districts favor its de-
velopment, especially where a cup-shaped rock or clay substratum is cov-
ered by a thin layer of permeable earth, favoring the decomposition of
vegetable matter. Bad food, overcrowding, mental depression, excesses in
venery and alcohol drinking, predispose to cholera. Epidemics of cholera
occur most when the atmosphere is moist and sultry, or when a sultry
period follows a warm rain storm. Districts where these conditions pre-
vail are regarded as favoring the development of the cholera germ.
As soon as the cholera discharges undergo decomposition the specific in-
fection of the disease is developed and may be conveyed from one locality
to another by the wind, by rivers, and in clothing. From experiments made
by Dr. Sanderson, it is evident that the specific poison of cholera is
contained in the discharges from the mucous surface of the alimentary
canal, that it is not infectious when fresh, but that it acquires virulent in-
fectious properties in from two to four days, and that it is rendered in-
nocuous by cold. There is no evidence that the bodies of cholera patients
are infectious. The establishment of these facts readily accounts for its
sudden appearance in diSerent places remote from one another. An in-
dividual travelling rapidly from one place to another becomes the carrier
of the germ, which is to develop the infection in those localities in which
the conditions favor its reproduction.
Symptoms. — The length of the stage of incubation of cholera is not de-
termined, but it undoubtedly varies from a few hours to as many days.
Its symptoms may be divided into four stages. These divisions are arbi-
trary ; first, the stage of invasion, or premonitory stage ; second, the stage
of painless diarrhoea ; third, the algid or collapse stage ; fourth, the stage
of reaction.
The prodromal symptoms are a feeling of weight in the precordium,
rumbling of the bowels, general malaise, a peculiar pallid anxious counte-
nance, and nervous phenomena, such as vertigo, tinnitus aurium, head-
ache, and tremor. Sometimes there is apathy, again a condition of ex-
hilaration. Not infrequently, for a couple of days, there are frequent and
moderately fluid dejections, sometimes accompanied by exhaustion, rarely
664 ACUTE GENERAL DISEASES.
by griping. This is called the cholera diarrhoea. Theise premonitory
symptoms continue from a few hours to a week ; usually, however, about
two days. They may be, and frequently are, absent, the disease commenc-
ing precipitately with a painless diarrhoea. Occasionally the prodromata
assume the character of cholera morbus, but cramps are more prominent,
and there is little or no fgecal odor to the discharge.
The second stage is characterized by a profuse diarrhoea, generally com-
mencing in the morning or in the middle of the night, and the patient
describes the dejection as passing from him in a stream. These painless
discharges sometimes, after the second evacuation, lose their faecal odor
and color, and assume a light straw-colored or whey-like appearance. They
vary in number from three to twenty a day, and are often accompanied
by attacks of regurgitative vomiting with each evacuation. The average
amount of fluid discharged in this stage by a cholera patient in twenty-
four hours is about sixty ounces ; the patient becomes exhausted and as-
sumes a peculiar apathetic condition; dizziness, headache, and vertigo some-
times are present. Complete anorexia is present from the onset, and the
thirst is tormenting and constant. Bile pigment disappears from the
stools, and the rice-water appearance is assumed ; there may be a pinkish
tint on account of the admixture of blood. The rice-water discharges
often have a whey-like appearance consisting of the watery elements of
the blood; their specific gravity varies from 1.005 to 1.012, and they con-
tain a small proportion of albumen and an excess of sodium chloride. On
standing, the rice-water fluid deposits a sediment holding fine granular
cells, amorphous granular matter, shreds of tissue, minate nucleated cells,
epithelium and blood globules. Occasionally the blood globules are so
numerous that the vomited matters are red. Vibriones, bacteria, urea,
triple phosphates and a few leucocytes are also not infrequent ingredients.
The vomited matter, after the contents of the stomach and bilious matters
have been ejected, is a clear, watery fluid containing urea and carbonate of
ammonia ; it is ejected in a stream, without nausea or effort, and is char-
acteristic of cholera. Everything introduced into the stomach causes vom-
iting.
The tongue is dry and covered with a thick white coating ; the coun-
tenance becomes pinched and of a leaden hue, the expression is staring
and dull ; as the exhaustion verges on collapse, the pulse becomes imper-
ceptible at the wrist. Often there is distressing hiccough, and more or
less dyspnoea. In rare instances the abdomen is tense, hard and sensitive
to pressure ; it may be retracted. Suppression of the urine is not of infre-
quent occurrence at this stage.
The algid stage commences with a well-marked fall of temperature ; first
in the hands, feet, and face, but soon over the entire body. The axillary
temperature may fall as low as 72° F., or even lower, while the rectal tem-
perature registers 101° or 102° F. The accompanying sweat makes the sur-
face feel colder than it really is ; the patient himself rarely complains of be-
ing cold. The skin is in distinct, hard folds {" washerwoman's skin") and
of a bluish oi livid color. The features and extremities are pinched, the
EPIDEMIC CHOLERA. 665
eyes are deeply sunken, and have purplish rings about them. The patient
is in a state of apathy or stupor ; and is roused therefrom only by the
severe cramps, which cause him to shriek and throw himself about the
bed. These cramps chiefly afl:"ect the muscles of the calf of the leg.
In the last portion of this stage (called the asphyxial) the condition of
the patient is apparently hopeless ; the deadly coldness is so marked in the
tongue and mouth that the thermometer may show a temperature of only
79° F. The lividity and cyanosis, the imperceptible heart sounds, the ab-
sence of the radial pulse, the "cholera face, "and the hoarse sepulchral
"^cholera whisper," the agonizing cramps that now recur oftener than at
first, complete the desperate picture of the disease. The vomiting and di-
arrhoea now markedly diminish and the discharges are less fluid when they
do occur. The stools are passed involuntarily or heedlessly.
The urine is either completely suj)pressed, or a few highly albuminous
drops are passed. The respirations are shallow and hurried, often being
40 per minute, and alternate very often with paroxysms of intense dysp-
noea. There is a loss in weight during this period, and so drained is the
blood that there is an absorption of pathological fluid accumulations as in
pleurisy and synovitis. The saliva and all secretions are suppressed. Late
in this stage of cholera the stools, from being odorless, change, and assume
a smell something like decayed fish. The state of collapse may last forty-
eight hours, and yet recovery take place ; or death may occur in two or
three hours from the onset of this algid condition.
The mind is clear throughout, and consciousness is retained till the last ;
it is even recorded that insane p)atients have, in ''cholera collai^se," re-
gained (temporarily) their sanity. »
The " reactive stage," when reached, is often marked by as speedy a re-
turli of favorable signs as was the algid stage by unfavorable ones. The
pulse appears in the carotids and at the wrists, and the heart-sounds be-
come distinct and regular. The temperature rises, the skin becomes warm,
the face looses its " deathly" look, the cramps cease, and the diarrhoea con-
tinues ; the stools soon acquire a faecal odor and a brown color ; although
in cases where the algid stage is prolonged, foul-smelling, greenish, fluid
discharges continue for some time. The urine next appears, although its
return may be delayed from ten to thirty hours ; at first it is scanty, high-
colored and albuminous, containing casts, and turning pinkish with nitric
acid. Soon it becomes copious and normal in character. The duration of
this period varies from one to ten days. This is a history of a tj^oical case
of cholera. I shall now briefly consider some of the more common var-ia-
tions.
Cholera typhoid is perhaps the commonest sequela of the collapse stage.
After a few days, in some cases a week, of well-marked reactive symptoms,
when the secretions are fully established and excretion is being normally
performed, a quickening of the pulse is noticed, usually toward evening,
and soon a febrile movement is established, which recurs with regular
paroxysms. These are accompanied by adynamic symptoms, such as low,
muttering delirium, a dry tongue, injected conjunctivse, coma, and often
666 ACUTE GENERAL DISEASES.
bed-sores and purpuric spots. The patient sinks into a state of extreme ex-
haustion, and gradually the coma deepens, the bowels and bladder are in-
voluntarily evacuated and death occurs. If patients recover from cholera
typhoid, the convalescence is very protracted and uncertain.
Urmmia is a frequent condition ; following the stage of collapse no urine
is secreted in the reactive stage ; and in about thirty-six or forty-eight
hours the pulse becomes abnormally slow, the face slightly flushed, and the
eyes darkly injected. The urine is entirely suppressed or very scanty, and
will be found to contain albumen and casts in abundance. There is con-
stant headache, rarely a mild delirium. The patient becomes drowsy and
listless, vomiting a spinach-green material. Epileptiform convulsions are
followed by coma and death. The bowels are constipated, and the febrile
symptoms are negative.
A " cholera eruption," so-called, sometimes makes its appearance either
in the typhoid variety, or in the stage of reaction. This eruption varies in
character : it may be an erythema, or resemble urticaria or roseola. It ap-
pears first on the hands and feet, then spreads to the trunk, the face being
very slightly affected. Macular, papular and vesicular eruptions sometim_es
occur ; in all cases the appearance of a cholera eruption is a favorable
symptom. The eruption lasts about two days, and is often accompanied by
a "burning" sensation. Although va. children the disease runs the same
general course, collapse supervenes much more rapidly, and death often oc-
curs after a few choleraic discharges.
Cholerine is a mild form of cholera occurring during a cholera epidemic,
and attended by all the characteristic symptoms of the disease, except that
there is no algid stage. There is often a slight coolness of the extremities
and cramps in the calves of the legs. Eecovery is usually rapid. It may
be followed by a severe and well-marked attack of cholera.
Differential Diagnosis. — During an epidemic, cholera is not likely to be
mistaken for any other disease ; but when it occurs in isolated cases, it may
be confounded with acute poisoning, as from arsenic or antimony, and with
the g astro-enteric variety of pernicious fever.
In cases of poisoning there will be the evidences of the action of the
poison on the mouth and pharynx which are absent in cholera. The
vomiting in cholera is regurgitative and painless, whereas in cases of
poisoning it is distressing, and is preceded by an intense burning pain
in the oesophagus and stomach. Diarrhoea, if it occurs in poisoning,
is never of a " rice-iuater'' character, but mucous and blood-stained. A
chemical analysis of the ejected matters will detect the presence of a
poison.
In the g astro-enteric variety of pernicious fever the first two or three
discharges from the bowels are bloody ; while in cholera they are never
bloody at first, and soon assume the "rice-water" appearance. In gastro-
enteric pernicious fever vomiting is rare, but if present, is painful and
retching in character; while in cholera it is regurgitative. The temperature
in pernicious fever is high, often reaching 106° or 107° F., while febrile
movement in cholera is slight. There is free pigment in the blood in per-
EPIDEMIC CHOLERA. 667
nicious gastro-enteric fever, which is never found in the blood of a cholera
patient.
Prognosis. — The mortality-rate varies in different epidemics from 20 to 80
per cent. ; generally one-half recover. The more dense the population in
any locality and the nearer the sea-coast the higher the mortality-rate.
The mortality-rate is always less toward the end than at the commence-
ment of an epidemic ; it is greatest in those under one or over fifty years of
age. Habits of life and hygienic surroundings influence very greatly the
prognosis. The duration of an attack varies from a few hours to two weeks.
Fatal cases usually terminate within two or three days, while the aver-
age duration of those that recover is nine days. Each ej^idemic in this
country has been milder than the preceding.
The symptoms which indicate recovery are a general improvement in the
appearance of the patient ; he becomes less restless, his breathing slower
and more natural, the radial pulse returns, the lividity of the surface dis-
appears, the shrunken tissues expand, the temperature rises to normal, the
urinary secretions are re-established, the discharges from the bowels are
again stained with bile, and the patient falls into a quiet sleep. The un-
favorable symptoms are involuntary pinkish discharges from the bowels,
absence of the radial pulse and the second sound of the heart, extreme cy-
anosis, a complete suppression of urine, coma, persistency of the vomiting
and diarrhoea, and the occurrence of complications.
Cholera may be complicated by capillary bronchitis, lobular pneumonia,
oedema and congestion of the lungs, pericarditis, peritonitis, and pleurisy.
The sequelse are uraemia, membranous enteritis, cerebral oedema and
hypersemia, gangrenous or purpuric patches, ulcerated corner, furuncles,
bed-sores, and gangrene of the lungs. Death may result from the direct
effects of the cholera poison without the occurrence of the diarrhoea, from
the exhaustion produced by the diarrhoea, from heart-failure, and from any
of its complications or sequelse.
Treatment. — Prophylactic and hygienic measures may limit the duration,
extent, and the mortality-rate of a cholera epidemic. When a cholera
epidemic is prevailing quarantine regulations must be vigorously enforced,
and those attacked by the disease should be isolated. All cess-pools,
privies, and bodies of stagnant water in the neighborhood should be drained
or disinfected, and each member of the community should be placed under
the best hygienic conditions, and his diet carefully regulated. All excesses
in food and drink, and all sources of intestinal ii'ritation should be avoided.
A diarrhoea occurring during a cholera epidemic should be immediately
checked.
Cholera stools should be immediately disinfected and buried in trenches,
as in typhoid fever. The linen and all tin utensils used in the sick room
must also be thoroughly disinfected. Instead of sulphate of iron and hydro-
chloric acid mingled with the faeces, carbolic acid may be used . indeed,
many regard it as superior to any other disinfectant for the purpose. All
persons, who are able, should be inimediately removed from the infected
district.
668 ACUTE GENERAL DISEASES.
The first great object of medicinal treatment is to control the prodrO'
mal diarrhoea. For the accomplishment of this, opium is the most reliable
drug ; it may be combined with nitrate of silver, sulj)huric acid, small
doses of calomel, or with vegetable astringents. Brown-Sequard states that
morphine hypodermically in sufficient doses at the onset will jjr event
cliolera. The patient is to be at once placed in bed, kept absolutely quiet,
and the abdomen swathed in flannel bandages. If there are slight signs of ex-
haustion early, stimulants may be given carefully. Turpentine stupes over
the stomach and bowels in the early stage, when the symptoms are urgent,
are often serviceable. Nausea in the premonitory stage is often allayed by
carbonic-acid water, cracked ice, or effervescing draughts.
When the disease is fully established, as indicated by the projectile vomit
and rice-water stools, the treatment becomes "symptomatic" or "ex-
pectant." To relieve the agonizing thirst patients may take freely of
cracked ice, very cold seltzer water, or carbonic-acid water combined with
lime water. If the pulse becomes imperceptible at the wrist, indicating
heart insufficiency, stimulants are indicated, but they must be carefully
administered. English physicians in India give opium, calomel, and acetate
of lead (or tannin) during the stage of painless diarrhoea. If the cramps
are not severe, they may be relieved by friction. But when they become
severe, hypodermics of morphia combined with chloral are indicated. If
the extremities become cold they should be wrapped in hot cloths, or hot
water bags may be placed around them, or they may be rubbed with stim-
ulating liniments or capsicum preparations. In the stage of collapse iced
brandy or champagne given repeatedly and in small doses is the best stimu-
lant ; musk and ammonia are also recommended. The inhalation of amyJ
nitrite has been tried, and found very efficient in combination with alcohol,
in the advanced stage of collapse. When death is impending, whiskey
may be injected hypodermically, or milk maybe administered intravenously.
In the use of stimulants one must be guided by the pulse, and the effects
of the stimulation. The India cholera pills, given in the collapse, are
made of camphor, asafoetida, pepper, and the essential oils or ether.
As the reactionary fever comes on, and the temperature begins to rise,
nourishment must be given with the greatest care ; the rule being to post,
pone a solid diet as long as consistent with maintenance of strength j
milk, beef -juice, and very light broths are the only articles of diet admis-
sible for some time. When the stomach is weak and irritable, and there
is a tendency to vomiting, bismuth and cherry-laurel water can be given ■
with advantage. Cerebral symptoms must be promptly treated by ice-bags
about the head, heat to the feet, and bromide of potassium internally.
The surroundings of the patient, the maintenance of cheerfulness and
calm, and even temperature — these are important points to be observed.
DIPHTHERIA,
Diphtheria is a specific constitutional disease, characterized by a granular,
fibrinous exudation upon the surface and into the substance of mucous mem-
DIPHTHERIA. G6D
branes, and upon abraded surfaces. Various countries of Europe were
visited by epidemics of diphtheria in the sixteenth and seventeenth cen-
turies. In the middle of the last century it reached England, and in the
early part of the present century it prevailed at different points in the Xew
England States.
Dr. Samuel Bard, of New York, gave the first accurate description of
the disease in this country, and brought clearly before the profession its
specific contagious character; his clear accounts tally perfectly with the
experience of the present day.' The labors and investigations of Louis,
Trousseau, Rilliet, Graefe, and Virchow have done more than those of any
Qther investigators to perfect our knoAvledge of diphtheria.
Morbid Anatomy. — The characteristic pathological lesion of diphtheria'
consists in a membranous or granular infiltration of some mucous surface.
Of the mucous surfaces, those of the pharynx, tonsils, uvula, and nasal
passages are its most usual seats ; beginning on the tonsil and anterior
wall of the pharynx the diphtheritic process may extend upward into the
posterior nares, forward into the anterior nares, or pass down the larynx,
larger bronchi, bronchioles, and even enter the air-cells. From the pharynx
it may pass down into the oesophagus, the larynx often escaping ; or it may
first appear in the larynx and extend upward into the pharynx ; — this latter
is rare. Occasionally the mucous membrane of the mouth, stomach, va-
gina, rectum, and biliary passages is the seat of the diphtheritic process.
If the skin is abraded it may become covered with diphtheritic exuda-
tion.
The first change in the part that is to be the seat of this exudation, is a
passive hypercemia ; the capillary vessels are gorged, and the mucous mem-
brane is of a dark, purplish-red color ; somewhat swollen at the point
where the membrane is to develop. The hyperaemia is not active, the color
is not the bright red of active inflammation, but dark, livid, and ''angry."
The amount of serous infiltration of the sub-adjacent tissues determines, in
each case, the amount of tumefaction. On the surface of the afPected part
there is an abnormal secretion of mucus, and the epithelial cells covering
it become enlarged and cloudy, from exudation into them. Little by little
they lose their nuclei and become transformed into a homogeneous mass,
presenting numerous ramifications — in other words, the metamor|)hosed
epithelium-cells form a reticulated membrane.
The first and most superficial diphtheritic exudation is into the epi-
thelium. The cells of the deeper structures may be simultaneously or
secondarily involved. The surface exudation becomes thicker and of a
grayish color as the sub-epithelial mucous and sub-mucous coats become
successively involved. In mild cases the membrane first resembles a gauzy
film, then it assumes a light yellow color, or occurs as white patches of
varying size. In severe cases a leathery, gray exudation from one-eighth
to one-fourth of an inch in thickness will form in five or six hours, which
can be removed, and when removed leaves a raw bleeding surface which will
immediately be covered by a "(v^a^ exudation. The membranous exudation
1 He publisht;d his pamphlet iu 1812.
670 ACUTE GEISTERAL DISEASES.
may become infiltrated with blood, and 'assume a black color ; this is not a
condition of gangrene, but gives evidence of great blood changes. Absorp-
tion of the exudation is only possible when the epithelial layer is alone in-
volved ; when the mucous and submucous tissue is involved, the mem-
branous exudation can only be removed by a suppurative or gangrenous
process.
As the exudation is taking place into the epithelium, micrococci, or
spherical bacteria will be found ; as the diphtheritic process involves the
deeper tissues, the bacteria greatly increase in number. Some regard the
bacteria originating within the epithelial cells as the result of the path-
ological processes; others that they cause the pathological changes. ' It
seems reasonable to regard the diphtheritic exudation as a granular fibrin of
low vitality, which possesses no power of organization.
The arrest of the diphtheritic process may be first by suppuration. Un-
derneath the diphtheritic exudation, there may be a suppurative process
established, which separates the layer of exudation from the tissues which
it involves. In such a case the membranous exudation becomes more
sharply defined at its boundary, the tumefaction of the surrounding mucous
membrane subsides, the inflammatory zone draws closer and closer to the
margin of the patch, whose edges curl up, and finally the mass is removed
from its base, and is thrown off spontaneously. The duration of this exfo-
liative process varies from two to five days. In some cases the diphtheritic
process is so mild that while the exudation occupying the epithelium is
thrown off, that in the subjacent structures is absorbed, no suppurative
process occurring. In this, the mildest form, there is absorption accom-
panied by a simple epithelial desquamation.
Another termination of the local diphtheritic process is in gangrene.
The nutrition of the tissues is so extensively and rapidly interfered with
by the abundant exudation that the blood supply is cut off and death of the
parts is the result. Some observers claim that gangrene is caused by the ob-
struction of the lymphatics with bacteria. With the gangrenous process
large numbers of putrefactive bacteria develop in the membrane and in the
tissues underneath, which break down into a semi-fluid, dark mass, which
has the peculiar odor of gangrene. Sometimes the sloughs are quite
firmly attached to the adjacent tissues. The so-called septic variety is
characterized by the formation of an extensive necrotic membrane, the
color of which is a dark gray, or brown with streaks of capillary hemor-
rhages throughout its entire extent. Larger colonies of micrococci are
found in its deeper layers, and pressing against the fibrinous bands they
form alveoli, in which myriads of the bacteria lie. The exudation in this
variety occurs most frequently in the nasak cavities, where in and beneath
the Schneiderian mucous membrane is an extremely rich j)lexus of lym-
phatic and blood-vessels. This variety may involve tissues other than the
1 Zahn thinks he can distinguish three varieties of diphtheritic membrane : (1) one that is the result of
morbid processes situate in the pavement epithelium ; (2) one that arises from solidification of a muco-
fibrinous exudation ; (3) and one that is the result of solidification of a fibrino-puruloid exudation. This
careful histolo-pathologist states further that any or all forms of the bacteria rnay be found in each of Ms
varieties, that they may also be absent, and that they are not an essential factor in diphtheria.
DIPHTHERIA. G71
mucous and submucous layers ; cases are recorded where the vomer was
eroded, and little depressions in it were filled with nests of micrococci.
A piece of membrane on examination will be found soft and friable,
breaking down into an ichorous, semi-fluid, dirty brown pulp. If a por-
tion of "septic" diphtheritic membrane is removed, ulcers are found in
the tissue beneath, which may be shallow or deep. When shallow, they
bleed very readily ; when deep, they are covered by dirty gray sloughs.
The variety of the epithelium, and the number of mucous glands in the
mucous membrane involved in the dij^htheritic process, modify the patho-
logical course of the exudation. When diphtheria invades the bronchioles
and alveoli, the characteristic microscopical appearances of the exudation
are discovered, and some air cells are filled with micrococci.
The heart is pale, flabby, and friable, presenting changes similar to those
in typhoid fever. The right heart is often filled with clots ; and the peri-
cardium may be the seat of numerojis ecchymotic sjDots, rarely of large
size. Endocarditis is not an infrequent complication, and when present it
is in many cases ulcerative, particularly if the disease has been severe and
there are extensive blood changes.
The hlood sometimes is but slightly altered ; in the severer forms it is
thick, of a dirty brown color, slightly coagulable, and after death contains
micrococci. The arteries and veins are equally filled. A transient increase
in the number of the white blood corpuscles is very common.
The spleen is usually enlarged, the capsule is tense, shining, and covered
with numerous points of capillary hemorrhage. The splenic parenchyma is
congested, softened, and friable, darker than normal, and often the seat
of multiple infarctions.
The lymphatic glands become swollen and inflamed on account of their
free communication with the infected parts. The hyperj^lasia occurring
within the gland causes a swelling which may be tense and hard or doughy.
This doughy feel results from oedema of the peri-glandular and subcutaneous
connective-tissue, in which vegetable parasites are frequently found. The
lymph vessels are often clogged with micrococci. Suppuration in the
lymphatics is of very rare occurrence.
The kidneys are congested or the seat, in severe cases, of parenchymatous
nephritis, differing in no respect from that occurring in scarlatina, which
has received the name of scarlatinal nephritis. Those who favor the para-
sitic origin of diphtheria regard the micrococci as the starting-point of the
morbid nephritic processes ; yet they state that if a child die rapidly from
suffocation, only a cloudy swelling of the epithelium exists; but if the disease
shall have progressed for several days, attended by severe symptoms of in-
tense blood poisoning, then the micrococci are discovered. Thus the
morbid processes, by their own statements, are shown to be primary and
not secondary to bacterian developments or migration.
The Brain and Cord. — In severe cases there are numerous small spots of
capillary hemorrhage scattered throughout the meninges of both brain and
cord. These extravasations may sometimes be large enough to form clots,
and then softening of the brain in localized spots will occur. Cells and
672 ACUTE GEKEEAL DISEASES.
nuclei swell the spinal nerves at the point where their roots join so that
their thickness may be twice the normal ; blood may be extravasated at
this point and then the swelling will be distinctly red. Punctate hemor-
rhages into nerve centres where white matter is predominant are said to be
the cause of diphtheritic paralysis, and after degenerative processes have
occurred in these hemorrhagic spots the paralysis gradually disappears.'
Etiology. — Diphtheria is a miasmatic contagious disease, often prevailing
epidemically. Many of its etiological conditions are identical with those
of typhoid fever :— filth, bad sewerage, over-crowding, etc., — and yet we
are not prepared to state that either of these diseases is of spontaneous
origin. I have met with diphtheria in houses where the water and sewer-
age pipes were defective, and where no other causative factor could be
found ; nevertheless I have a belief that the miasm of diphtheria must
be present with the other etiological conditions before diphtheria will be
developed. Trousseau claims that the infectious element is confined to
the exudation, but many clinical facts indicate that it is present in the ex-
halations and in the excretions, as well as in the exudation itself. Di|)h-
theritic contagion clings to the objects that have been in contact with the
diseased individual, and may thus be carried a long distance.
Another vexed question in its etiology : — is it first local, and then consti-
tutional, or vice versd f From a clinical stand-point it seems that the
disease starts locally ; that some particle, for instance, of the exudation,
too small to be detected with the unaided eye, is received upon the mu-
cous membrane of the pharynx, nose, mouth, larynx, trachea, vagina, or
upon a cut or abraded surface ; and thence contaminates the whole system.
The point of infection cannot be determined until after constitutional in-
fection has taken place. It seems to be well established that when the lo-
cal signs of diphtheria are present, there is already a constitutional infec-
tion. The experiments of Oertel ^ and others show that the point of inoc-
ulation is the point from whence radiates the disease. Experiments are
now being made which tend to show that in virulent fluids it is not the
bacteria but the chemical element which is capable of inducing the grave
symptoms which sometimes follow inoculation.
The stage of incubation usually varies from one to eight days ; it may last
one month; when the disease is directly communicated, as in some recorded
instances when a piece of diphtheritic membrane is dislodged and coughed
into the mouth, nose, or eye of the physician or attendant, the disease has
developed within twenty-four hours. Bat the question arises:— may not the
one thus attacked have been under the influence of the diphtheritic poison
for some time, and thus be prepared for the rapid reception of the local
poison ? During epidemics the period of incubation is shorter, and there
is reason to believe that the more virulent the poison the less time elapses
between exposure and the initial symptoms. As a rule, the latent period
of diphtheria rarely exceeds five days.
1 Einidex iiber Biphthene. L. Buhl, Zeit. fur Berl., iii., 4. 1867.
2 ExpeHmentaUe UnUrsuchungen iiber Diphtlierie. M. J. Oertel, Deutsch. Arch, fur klin. Med., viiu
1871.
DIPHTHERIA. 673
Diphtheria may prevail as an epidemic, or be endemic. It also occurs
sporadically. Sporadic cases occur most frequently in those localities
where the disease has prevailed as an epidemic. Climatic influences have
little to do with its development, but autumn and spring are the seasons
when the disease is most fatal. Age is a powerful predisposing cause ;
from the second to the fifth year is the period of greatest susceptibility ;
but no age is exempt. Previous attacks afford no immunity against sub-
sequent ones ; certain individuals seem to be perfectly proof against the
diphtheritic infection. Filth, bad sewerage and drainage, over-crowding
and a general bad hygienic condition favor the development and spread of
diphtheria. Exposure to cold and wet, and sudden chilling of the body,
may bring on, or hasten an attack of diphtheria during an epidemic. In a
region where the soil is porous, the spread of the disease is much less ex-
tensive than in clay soil.
Symptoms. — The symptoms of diphtheria are local and constitutional.
The constitutional may precede the local ; or both may appear at the same
time. In some cases the local are the primary, and for a time the only
signs of the disease. The ushering-in symptoms vary not only in different
epidemics, but in different cases during the same epidemic. It is a dis-
ease which has no typical course.
The local symptoms begin with a sensation of dryness and prickling in
the throat, with, perhaps, slight pain independent of attempts to swallow.
There is more or less stiffness along the angle of the jaw. Deglutition be-
comes more and more painful; solids do not cause as much dysphagia as
fluids. There may be marked and painful swelling of the glands at the
angle of the Jaw — in the bifurcation of the common carotid artery — but
many severe and fatal cases are accompanied by only slight glandular en-
largement, and occasionally the disease runs its entire course without any
glandular swellings. In some epidemics most of the cases will be attended
by extensive glandular swellings, while others, of equal severity, only
exhibit this symptom in a slight degree. However the disease may com-
mence, when fully established there will be noticed upon the anterior pil-
lars of the soft palate, the velum, and tonsils, sometimes also upon the
posterior pharyngeal wall, whitish patches, surrounded by a livid, tumefied
and congested mucous membrane. At this early stage the exudation can
be removed without causing even punctate hemorrhage ; and under the
microscope the epithelial cells will exhibit the appearances that have
already been described. The sub-epithelial tissue becomes oedematous, and
later, both tonsils, the uvula, and the anterior part of the soft palate will
become oedematous. At this period the membrane may be easily removed,
but soon after its removal it will reappear in the same situation, and
have the same extent. As a rule the more extensive the exudation, the
thicker will be the membrane and the firmer its attachment.
When the posterior nares are involved it is usually the 'result of the ex-
tension of the diphtheritic process upward : the tonsils, uvula, and pos-
terior pharyngeal wall having been the primary seat of the exudation. A
coryza is soon developed, and the sanious, ichorous discharge irritates, red-
674 ACUTE GENERAL DISEASES.
dens, and excoriates the surfaces over which it flows. At the same time
rapid swelling of the cervical, lymphatic, and sub-maxillary glands occurs ;
and there is undoubtedly a special connection between enlargement of the
glands at the angle of the jaw, and diphtheria of the nares and posterior
wall of the pharynx. The nostrils are soon clogged, often completely so,
and repeated attacks of epistaxis may mark the later stages of nasal diph-
theria. When the disease extends upward the parotid is not infrequently
swollen and tender. Xasal diphtheria is in a few instances primary. The
nose, in cases of invasion of the posterior nares, is often swollen and red, or
shining and oedematous ; the parts excoriated by the flow from the nostrils
are soon covered with ulcers, and the latter are often covered with the gray
diphtheritic exudation.
When the Eustachian tubes are involved, there will be tinnitus aurium,
darting pains on attempts to swallow, marked loss of hearing, and perhaps
otitis ; perforation of the tympanum, and caries of the adjacent bones may
result. The external ear has in rare cases been the seat of secondary and
also of primary diphtheria. The middle ear has also sometimes been im-
plicated. The eye may be invaded in diphtheria when the nasal duct is
the seat of the exudation ; or a piece of membranous exudation being
coughed into the eye of the examiner may excite a diphtheritic conjunc-
tivitis. If the diphtheritic process passes downward it may enter either
the digestive or the respiratory tract.
If the cesopliagus is involved there will be a marked dysphagia, and fluids
■will be regurgitated ; accompanying paralysis of the muscles of deglutition
in many instances increases the dysphagia. If no special signs of pharyn-
geal exudation are present in a suspected case of oesophageal diphtheria,
portions of the exudation may appear in the vomited matters, for vomiting
is an important sign of oesophageal diphtheria. Portions of membrane in
the fgecal discharges point to the existence of the oesophageal diphtheria
when there are evidences of tonsillar and pharyngeal exudation.
When the vagina, rectum or ktbia is involved there will be more or less
swelling of the inguinal glands in the immediate neighborhood.
The diphtheritic process may extend from the pharynx into the larynx
and trachea. Sometimes laryngeal diphtheria is developed when the pri-
mary seat of the diphtheria is in the nasal passages, or in the mouth.
Laryngeal diphtheria occurs most frequently in children ; the younger the
child the greater the liability to laryngeal comj)lication ; when adults are
attacked, it is the weak and feeble and the aged. The epiglottis becomes
hypergemic, livid, and swollen, its edges are harder than the remainder of
its substance, and the diphtheritic patches are developed irregularly upon
its surface.
The first symptom indicative of laryngeal diphtheria is a change in the
voice, which loses its volume, becomes hoarse, rough and indistinct,
then falls to an inarticulate whisper. The respirations become noisy and
whistling, and dyspnoea becomes more and more urgent as the exudation
advances. The cough is first dry and stridulous — " brassy," — but soon
changes, losing the brassy tone, and, indeed, it has no distinct tone what-
DIPHTHERIA. (,-i/5
ever, and is so peculiar as to be almost diagnostic of laryngeal diphtheria.
In children the invasion of the larynx is often sudden. In a short time
there is complete aplionia ; a cough is developed that is '^ barking" or
" croupy " in character, but (as in adults) it soon becomes abortive. The
dyspnoea is extreme ; all the auxiliary muscles of respiration are called
into play. The attacks of difficult breathing assume a paroxysmal form,
and in one of the paroxysms death may occur. If the upper part of the
larynx only is involved there is difficulty of inspiration, but when the
whole larynx is involved expiration is also affected. There is falling in of
the supra- and infra-clavicular sjiaces during inspiration, showing that im-
perfect inflation of the lungs results from the mechanical obstruction to
the entrance of the air into them. Cyanosis becomes marked, and there
is either stupor, or restlessness and Jactitation. When the child dies it is
with all the symptoms of croup {q. v.). Death is not from the action of
the poison but from local obstruction which has mechanically forestalled
its constitutional effects.
A laryngoscopic examination shows epiglottis, vocal cords, and the in-
terior of larynx to be the seat of a diphtheritic exudation, the ventricle being
usually wholly obliterated.
Auscultation reveals abnormal laryngeal sounds, together with rales of
various kinds, and a loss of vesicular respiration. In some instances the
diphtheritic process may have its primary seat in the larynx, and then ex-
tend upward, the same processes occurring upon the tonsils, uvula, and soft
palate, as when they are the primary seat of the disease. In such cases
laryngeal symptoms are present from the onset of the disease.
Constitutional Symptoms. — There are no regular stages in the develop-
ment of diphtheria, therefore no typical clinical sketch can be given which
shall include all cases. The division of diphtheria into the catarrhal,
croupous, gangrenous and septic forms can only be made at the expense of
facts, for they may rapidly merge into each other, and are only stages of
one and the same diseased process. Diphtheria may begin with well-
marked, active symptoms, as a chill, fever, pain in the head and back,
nausea, vomiting, and even convulsions. Or it may come on insidiously,
the patient complaining only of the throat symptoms. It may run so mild
a course that the patient at no time feels sick ; the throat symptoms are
not marked ; and there is a small patch of exudation upon the tonsils, but
it does not extend.
There is little or no febrile movement, and at the end of a week the
patient is fully convalescent. In those cases where well-marked symptoms
usher in the disease, the temperature ranges higher than in any other form
of the disease ; in rare cases it may reach 105° F. by the end of the second
day. Insidious cases are marked by a gradual rise in temperature, 102°
or 103° F. being the highest point reached during the whole course of the
disease. Mild and severe cases often occur in the same household during
the same epidemic.
In whatever manner diphtheria is established, the constitutional and local
symptoms do not always progress with the same severity. In some cases
676 ACUTE GE^STEEAL DISEASES.
while the exudation is rapidly extending the temperature falls to normal,
the pulse diminishes in frequency, the patient seemingly having decidedly
improved in every respect — in fact, the constitutional symptoms remit if
they do not intermit. The pulse, however, will show the influence of the
poison on the nervous system, either in irregularity or abnormal frequency,
or both. But during all this time the membranous exudation is spreading.
After a time the temperature rises to 103" or 104° ¥., the pulse to 120 or 130,
and all the severe constitutional symptoms reappear. Death often occurs
early in such cases. In another class of cases the constitutional symptoms
are severe from the onset, while the local manifestations of the disease are
but slight and not progressive. In some cases the nervous system may be
overwhelmed by the intensity of the diphtheritic poison at the onset of the
disease, and death result before any local manifestations of the disease have
had time to make their appearance.
In the more common forms of diphtheria the first symptom will usually
be the soreness of the throat, which will be found congested ; and either
upon a tonsil or at some point in the pharynx, a small white patch of ex-
udation will be seen. Slight febrile movement may accompany the throat
symptom, or it may not come on for forty-eight hours. The exudation
gradually extends until a large surface is covered with a thick layer of
membrane, which assumes a gray or brown color. The sub-maxillary glands
become more or less swollen. There is always some obstruction in the
throat and difficulty in swallowing. As the disease becomes fully developed,
patients are unable to sit up. There is nausea and often vomiting. The
urine is usually albuminous. The pulse becomes frequent and feeble ; the
temperature ranges from 101° to 103° P. The membranous exudation
continues to extend, involving more and more of the throat. The patient's
general condition becomes worse each day until about the end of a week ;
when the membrane is thrown off, the pulse becomes less frequent and the
patient slowly recovers. Or, as happens in some instances, as the exuda-
tion disappears from the tonsils it extends into the larynx : then are de-
veloped all the symptoms of laryngeal obstruction, the breathing becomes
difficult, cerebral symptoms are prominent, and patients die in a few days
after the laryngeal symptoms appear. Occasionally after the local mani-
festations of diphtheria have disappeared, patients experience a degree of
prostration and feebleness that is met with in no other disease. The pulse
becomes feeble, frequent and intermitting : and the heart-sounds are
muffled and indistinct. Death occurs in such cases as if a poison — such
as prussic acid for instance — had been taken.
Symptoms luMch indicate danger. —Diarrhoea, although not often present
in diphtheria, may be so profuse as to cause exhaustion which will hasten the
fatal termination. Nausea and vomiting coming on late are most unfavor-
able symptoms. Albuminuria occurs in mild as well as in severe cases,
rarely lasting longer than a week, except in those severe cases where oedema
is present, and where epithelial, granular, small hyaline and exudative
casts are found in the urine. It is stated by some that the amount of
albumen in the urine is in direct proportion to the intensity of the diph-
DIPHTHEfllA. 677
theritic infection. In a few rare instances diphtheritic nephritis has been
so intense that death has resulted from it, before either the constitutional
or local symptoms of the disease were present. Albuminuria generally
comes on toward the end of the first week of the disease. Coma may occur
as the result of the nej)hritis. An erythematous eruption sometimes makes
its appearance in diphtheria between the first and third days. Its usual seat
is the upper part of the chest and back.
The pulse is peculiar- and varies greatly in different cases. There are
three distinct varieties :
I. In a large number of cases the pulse from the very commencement is
feeble, small, and rapid, ranging from 120 to 160, or, in young children,
even to 170 in the minute.
II. There is a class of cases where the pulse rises to 120 or 130 early in
the disease, but falls to 60 or even 40 within twenty-four or forty-eight
hours from its onset.
III. There is a class of cases in which the pulse is irregular and inter-
mittent throughout the entire course of the disease. The prognosis in the
latter variety is always bad.
If the temperature falls to normal, or below, and the exudation shows
no signs of exfoliating, no matter how trifling its amount, or how
slight the glandular swelling, the case is grave and death is not usually
long delayed. Convulsions occurring late in diphtheria are always un-
favorable symptoms, while as usheriug-in symptoms they have no special
significance. Swelling of the lymphatic glands, although not present in
all cases, is so frequently present that it must be regarded as one of the
symptoms of the disease. If it is extensive so as to interfere with degluti-
tion and respiration, the prognosis is unfavorable.
After the exudation disappears and convalescence is apparently estab-
lished, sequelae may develop, which may continue for months and even
years. The commonest h paralysis of some of the voluntary muscles ; the
muscles most frequently affected are those of the soft palate and pharynx.
Usually the first thing indicating the occurrence of this paralysis will be
difficulty in swallowing — first fluid and then solid food — with an inability
to articulate clearly. "When paralysis is unilateral the velum is drawn' to
the healthy side ; when both sides are involved the velum hangs pendulous
and motionless ; there is also a loss of sensation as well as of motion, for
pricking it causes no pain. The voice is altered, and children cry as with
a cleft-palate, while adults have a sort of nasal twang. These changes come
from paralysis of the velum, anterior pillars of soft palate, and pharyngeal
wall. Fluids are only partially swallowed, the greater portion being re-
gurgitated through the nose, especially if the individual is standing or
leaning forward while drinking. This variety of paralysis sometimes comes
on while the exudation is yet visible in the fauces, just as it is disappear-
ing, or in a week or ten days after it has entirely disappeared. With the
dysphagia there is sometimes difficulty in expectorating ; the patient will
choke, cough and strangle in vain endeavors to get rid of mucus that has
collected in the pharynx.
€78 ACUTE GENERAL DISEASES.
As the pharyngeal paralysis is disappearing, — or from two to ten days
after, — the muscles of some other part of the body will be involved — the
lower extremities being much more frequently affected than the upper.
Though usually beginning in the feet, diphtheritic paralysis follows no
regular order ; a hand may first be affected, then a leg, and subsequently
the other hand, arm and leg. Before the occurrence of the paralysis there
will be a sensation of coldness, pricking, crawling (formication) and
numbness in the part about to be affected. The patient cannot determine
precisely where he has placed his foot — on the floor or some object higher
than the floor ; movements are ungainly and hesitatingly made, the gait
becomes tottering, and finally he cannot stand, the paralysis becoming com-
plete. Sensation is likewise more or less impaired. The hand loses its
usual dexterity ; the patient being unable to button his coat, or even write
his name. When the muscles of the neck are involved the, head
" wobbles," or is held upright with the greatest diflficulty. The neck is
usually the last part to be attacked. The power of ocular accommodation
is often seriously interfered with on account of the paralysis of some of the
ocular muscles. The ciliary and recti suffer oftenest. First, sight is
diminished or lost for objects close at hand ; and later, distant objects be-
come invisible. There is always diminished refraction, and there may be
strabismus and double vision.
When diphtheritic paralysis is general the laryngeal muscles will usually
be wholly or partially involved. The voice is hoarse, non-resonant, and
often there is complete aphonia. There is no loss of sensation until the
superior laryngeal branch of the pneumogastric is involved ; this is attended
with danger, for particles of food may pass into the bronchi, and suffocative
dyspnoea may result in death. In nearly all forms of laryngeal paralysis
there is more or less dyspnoea, greatly increased by exercise. If the paraly-
sis involves the sphincters there will be involuntary discharges from the
bladder and rectum. The genital organs may be paralyzed, and all sexual
desire and power may be lost for months. Paralysis of the muscles of the
thorax, trunk and diaphragm gives rise to grave symptoms, pulmonary
oedema and death usually resulting. Finally, paralysis of the heart may
occur.
Diphtheritic paralysis is always entirely recovered from. In mild cases
its duration is two or three weeks, while in others it has continued one
or two years. Another sequel of diphtheria is parenchymatous nephritis.
When developed during the exudative stage it usually ends in complete re-
covery. Earely does it directly cause death. When so developed it may
be regarded as part of the active history of the disease. But when it
occurs during convalescence it may lead to chronic Bright's disease. In-
flammation of a serous membrane may complicate or be a sequel of diph-
theria ; the most frequent serous inflammation is endocarditis.
Pleurisy, peritonitis and pericarditis are of rare occurrence. Chronic
pharyngitis is a sequela only in those cases wliere there has been paralysis
of the pharyngeal muscles.
Differential Diagnosis. — The diagnosis of diphtheria rests on the presence
DIPHTHEKIA. 679
of a membranous exudation. When it prevails as an epidemic, a form of
" sore throat," a pharyngeal catarrh usually prevails at the same time,
sometimes called ''diphtheritic sore throat."
This sore throat is ushered in by a chill, followed by a more or less in-
tense febrile movement. There is a sense of fulness in the throat with
swelling of the sub-maxillary glands, and more or less dysphagia. The
mucous membrane over the tonsils is intensely congested, the uvula is
oedematous, and a few points of whitish exudation stud the mucous
membrane. If these little dots are examined closely they are found to
be mucus, exuded from the enlarged follicles. The process is purely
catarrhal, and not membranous. This is called by some "catarrhal diph-
theria," but is nothing more than a catarrhal pharyngitis. It is never
contagious, but is due to atmospheric influence, and has none of the char-
acteristic local or constitutional features of diphtheria.
The points of differential diagnosis between diphtheria and croupous
laryngitis are the following : croupous laryngitis, or membranous croup, is
a local affection, while diphtheria is a constitutional disease. Croup is
not contagious or inoculable ; while dij)htheria is markedly so. In croup
the exudation is 07i the surface of the mucous membrane ; in diphtheria it
is in its substance as well as on its surface. Laryngeal symptoms are
primary in croup, while in diphtheria they usually follow severe con-
stitutional symptoms, and in the majority of cases also follow the ap-
pearance of the exudation upon the nasal or pharyngeal membranes.
Croup rarely attacks those who have passed the age of puberty ; diph-
theria attacks all ages. Croup is sporadic ; diphtheria is often epidemic.
The sub-maxillary glands may be, and often are, enlarged in diphtheria,
but never in croup.' From a clinical standpoint they must be regarded as
distinct diseases.
Diphtheria may be distinguished from scarlatinal sore throat by the
following points : — in scarlatina there is a diffuse redness of the mouth
and pharynx ; in diphtheria the redness is local and of a darker color. In
scarlatina the exudation is mucus, and on the surface of the tonsils soft
palate and pharynx ; in diphtheria it commences at one point, and spreads,
is adherent and tough, and has a grayish or brown color. When an erup-
tion occurs in diphtheria it will have the characteristics already referred
to, will last but a few days, and will appear on the trunh only. In scarlet
fever the characteristic eruption rapidly spreads over the whole surface,
lasts three to four days and is followed by desquamation. In dijihtheria
there is no characteristic eruption, only occasionally transient roseola. The
temperature is far higher in scarlet fever than in diphtheria, the ushering-
in symptoms more severe, and there is the peculiar strawberry tongue in
scarlatina which is not present in diphtheria.
Typhoid or typhus fever may be suspected when intestinal diphtheria
exists. The only means of diagnosis is to watch the passages for the mem-
brane, and take the temperature carefully ; in typhoid there will be the
1 The Bides of the neck are to be examined for enlarged glands ; those at the anterior border of the
Kterno-mastoid are always palpable, but it is important to note that the glands at the angle of the jaw are
not enlarged.
680 ACUTE GENEEAL DISEASES.
typical range, and in typhus the rise will be sudden and higher. Finally
idiopathic erysipelas of the throat is very difficult to distinguish from diph-
theria. In erysipelas the tongue is blackish brown, dry and fissured ; and
there is more puffy swelling of the parts than in diphtheria. The glands
are not enlarged and the process is limited in its extent in erysipelas.
Prognosis. — The prognosis in diphtheria yaries with different epidemics,
and with the type of the disease. The prognosis is more unfavorable the
younger the subject, since extension into the larynx is more frequent in
the young child. The death rate varies in different epidemics from twenty
to fifty per cent. A peculiar fact, and one to be remembered, is that a
mild case — one where all things are progressing favorably — is liable to as-
sume, in a few hours, a most malignant type. The system may be over-
whelmed with the poison even when the exudation shall have disappeared ;
and, again, in convalescence heart-paralysis may suddenly occur ; all of
these points make a very guarded prognosis not only safest but necessary.
Its duration varies from three to twelve or fourteen days, but death may
occur within thirty-six hours ; and again the disease may continue three or
four weeks.
The symptoms which may be regarded as unfavorable are extreme gland-
ular swellings, huskiness of the voice, a dark-colored extensive exudation,
and, above all, laryngeal implication ; when diphtheria extends into the
larynx, about 95 per cent, of the cases end fatally. Repeated convulsions
are unfavorable ; and a pulse that is irregular and intermittent, or one that
drops to 60 after having been rapid at the onset, indicates danger. When
at the same time that the exudation is extensive, it has a dark gray, green,
or black color, and when it emits a gangrenous or sickly, sweet odor, the
prognosis is unfavorable. JSTausea, vomiting, diarrhoea and epistaxis, when
they occur late in the disease are very serious symptoms. Coma, ac-
companied by casts and albumen in the urine, or by entire suppres-
sion of urine, is a most dangerous occurrence. If pharyngeal paralysis
occurs before the exudation has disappeared, the case is a very serious
one ; the future course will be troublesome, owing to intense involve-
ment of the nervous system, and these cases are often fatal. The
temperature is not a reliable element in prognosis : in the most malig-
nant types of the disease it may range low, between 101° and 102' F. A
sudden rise or a sudden fall, especially to sub-normal limits, is exceedingly
unfavorable. Primary diphtheria of a wound, in which the throat shows
no manifestations of the disease, generally runs a favorable course. Pri-
mary infection of a wound with diphtheria, in which the throat becomes
secondarily involved, is always unfavorable. Secondary wound infection,
•during the course of a pharyngeal diphtheria, shows an intense degree of
poisoning, and is a bad prognostic omen.
All complications render the prognosis unfavorable. Among the com-
plications are meningitis, endocarditis (usually ulcerative), pleurisy, peri-
tonitis, pericarditis, pneumonia, bronchitis, tracheitis, laryngitis, pulmon-
ary cedema and congestion, oedema glottidis, acute Bright's disease, and a
septic fever that ordinarily complicates the malignant form. Septicaemia
DIPHTHERIA. G81
and pyasmia may occur, and intestinal hemorrhage, purpura and jaundice
are occasional and very grave complicatioas. Deatli may occur from any
of these complications, from paralysis of tho heart, from inanition, espe-
cially in children where deglutition is interfered with, or from asthenia.
The nervous system may be overwhelmed with the poison at the onset. The
exhaustion from vomiting, diarrhoea or hemorrhage may sometimes be so
great as to cause death. The patient may be asphyxiated from intercostal
and diaphragmatic paralysis or from getting a bit of solid food in the
larynx or trachea.
Treatment. — The treatment of diphtheria will be considered under four
heads : I. Hygienic ; II. External local ; III. Internal local ; IV. Inter-
nal constitutional treatment.
Hygienic. — A patient sick with diphtheria should be kept in bed from
the advent of its first symptom until convalescence is fully established,
and the pulse is normal in frequency and regular in its rhythm and force.
The membranous disappearance is not the guide ; it is the exhausted and
anemic condition which demands absolute rest in bed. Only attendants
that are agreeable to, and can manage the child well should be admitted
into the sick room, which must be large, well ventilated, and have a tem-
perature of 70" to 75° F. Perhaps one of the most important indications is
cleanliness ; the patient should be kept scrupulously clean, — eyes, nose,
ears and mouth, as well as the face and limbs. All utensils of whatever
kind, all clothing and linen, must be frequently cleansed and disinfected.
The disinfection may be accomplished as in typhoid (q. v.). The patient
must be strictly quarantined, the attendants must mingle as little as jDossi-
ble with the rest of the household, and must avoid taking the breath of,
and unnecessary manipulation of, the patient. The rule is, not to disturb
a diphtheritic patient except so far as it is necessary for cleanliness. The
physician should be careful not to make unnecessary examinations of the
throat. The instruments used in the examination should be thoroughly
cleansed after each examination. Freshly slacked lime mixed with pow-
dered charcoal may be placed about the room as disinfectants. Fresh
air and sunlight are important, and should be so admitted into the sick
room so as to avoid draughts. A grate fire in cold weather is the best
method to attain ventilation.
External Local Treatment. — This treatment may be considered under
four heads : — 1. llood-letting by means of leeches at the angle of the jaw ;
2. cold applications — ice-bags — to the throat ; 3. counter -irritation —
blisters, etc. — over the neck and enlarged glands ; and 4, Jiot poultices or
other hot applications to the throat.
Blood-letting, local or general, while it does not arrest the exudative
process, diminishes the resisting power of the patient ; clinical experience
teaches us that all antiphlogistic remedies are contraindicated in the
treatment of this disease.
Ice to the throat is with some a favorite plan of local treatment. It is
to be remembered that the exudation is a local manifestation of a consti-
tutional disease, and that its extension is arrested and its removal accom-
682 ACUTE GENEEAL DISEASES.
plished by the establishment of a suppurative process ; and for this reason
the local application of cold is contraindicated. It may relieve pain, but
it does not arrest the diphtheritic process.
Counter-irritation is also powerless to check the membranous exuda-
tion ; besides, whenever a surface becomes abraded, the diphtheritic process
is liable to be established upon it.
If the diphtheritic exudation is arrested and removed by a suppurative
process, the external application of heat is indicated, and may be of service.
Hot fomentations must be regarded as the safest and best means of hasten-
ing the removal of the membrane, and they afford the greatest relief to the
patient.
Internal Local Treatment may be considered under three heads : — 1. Me-
chanical means employed for removing the membrane. 2. Escharotics
employed for its destruction. 3. Astringents to prevent an extension of
the exudation by their action on the unaffected mucous membrane.
It is not diflBcult to pull off a patch of diphtheritic exudation hj mechan-
ical means ; but the membrane will reappear as soon as the removal is
effected ; and the second membrane has a deeper intimacy with the tis-
sues than the primary. For this reason no attempt should be made to re-
move a diphtheritic exudation unless it hangs loosely detached, and then
the dependent portion may be carefully snipped off. Any irritation pro-
duced by instruments favors the extension of the diphtheritic process. It
is to be remembered that, however pleasant it may be for parents and
friends to see patches of the membrane removed, after each removal the
diphtheritic process is increased both in depth and extent.
The powerful escharotics which have been used for the destruction of
the diphtheritic exudation are hydrochloric and nitric acids, nitrate of
silver, bromine, chromic acid, etc. It is claimed by partisans of this plan
that, when seen very early, and when the diphtheritic patches are small,
extension of the exudation may be arrested by the destruction of its local
manifestations. There seems no more reason for the use of escharotics
than for the mechanical removal of the exudation ; for each one of the
escharotic sloughs leaves an ulcer, which is a favorite spot for the develop-
ment of a new membrane in the deeper tissues.
Astringents, by constringing the mucous membrane about a diphtheritic
patch, thus prevent the spread of the exudation. But as the primary
action of all astringents is to cause irritation of the mucous surface, and
as the irritation favors the development of the diphtheritic membrane,
their use is contraindicated.
The thing to be accomplished by local internal treatment is to hasten
the suppurative process ; the locajl means which will aid the process of
suppuration is the inhalation of the vapor of hot water. The external and
internal local treatment of diphtheria resolves itself into the application
of poultices externally and vapor inhalations internally. The vapor in-
halations should be commenced as soon as the exudation is detected, and
continued until all signs of it have disappeared. As the steam inhalation
increases mucous secretion, it favors the removal of the membrane, and
DIPHTHERIA. 683
furnishes another reason for its use. To jorevent or limit septic poisoning
antiseptics are to be used, and those that are non-irritating are to be pre-
ferred. The diphtheritic surfaces should be frequently sprayed with chlo-
rine water, or with weak solutions of carbolic and salicylic acid, boric acid,
benzoate of soda, or muriated tincture of iron. Lime water, glycerine,
and lactic acid have been used with benefit ; and when an atomizer is
not at hand, disinfectant gargles and washes may be substituted. It is
especially important that disinfectants should be employed in nasal diph-
theria, after thoroughly cleansing the nasal cavities.
The constitutional treatment of diphtheria consists essentially in sup-
porting the vital powers of the patient. There are no specifics for its
treatment, any more than for scarlet fever or smallpox. All-depressing
remedies are contraindicated. The alcoholic treatment is a favorite j^lan
with a large number of practitioners ; under this plan alcohol is given, not
merely to sustain the patient, but for its constitutional effects. With this
end in view, it is given in large quantities ; one-half an ounce of brandy
may be given to an adult every half hour ; to a child two years old from
one-half to one drachm every hour. The amount to be given must be de-
termined only by its effects. The object is to get the physiological effects
of the alcohol as quickly as possible. The beneficial effect of the stimulants
will be indicated by the pulse becoming slower after its use, by a diminu-
tion in its tremulousness, by an increased desire for food, and by a manifest
feeling of general amelioration. The stimulating plan should be carried
out more strictly in diphtheria than in any other infectious disease. An
intermittent and irregular pulse demands freer stimulation than a rajDid
and feeble, but regular, pulse. An increasing apathy, a feeble pulse, ir-
regular at times, a dry tongue, a dark and offensive-smelling exudation,
often indicate a crisis that may be tided over by crowding stimulants.
The diet should be milk and yolk of eggs ; when there is great dysphagia,
food may be administered per rectum. Ether, musk, and camphor are re-
garded by some as valuable adjuncts to the alcoholic plan of treatment. When
the temperature ranges high, quinine and cold sponging may be emjDloyed.
The tincture of the chloride of iron and chlorate of potassa are favorite in-
ternal remedies in the treatment of diphtheria. From five to twenty drops
of the tincture of iron are given in glycerine or water every hour ; and
from two to twenty grains of the chlorate of potassa every two hours. The
use of these drugs, given either alternately or in connection, is at the pres-
ent time a ruling practice in the profession. The internal use of the ben-
zoate of soda, and solution of the bromides, to neutralize the dij^hth critic
poison, although strongly advocated by some, is not sustained by the ex-
perience of the profession generally.
If nutrition be kept at a high standard, and if the use of tonics be per-
sistently kept up, the paralyses that are the chief sequelae of diphtheria
will usually soon be recovered from. Porter is one of the best tonics in
the treatment of the sequelae of diphtheria, especially the paralyses. When
pharyngeal paralysis occurs, the food is to be given through an oesophageal
tube.
684 ACUTE GENEKAL DISEASES.
When the nose is the seat of diphtheritic exudation, the nasal chambers
must be thoroughly cleansed. Lime water or dilute carbolic acid are the
best washes to accomplish this, the washings must he frequently and care-
fully employed.
When the larynx is invaded, exudations may be mechanically removed,
if suffocation is imminent. Inhalations of alkalies, lactic acid, etc., are
beneficial only in theory. Tracheotomy, if performed at all, should be
performed early, as soon as suffocative symptoms or signs of asphyxia be-
gin to show themselves. The hypersesthesia which is often so troublesome
is best relieved by large doses of bromide of potassium, and if restlessness
and jactitation are marked, moderate opium narcosis may be beneficial.
To sum up :— a diphtheritic patient should be quarantined in a large,
well-ventilated apartment, attended by a well-trained nurse; poultices
should be applied externally to the throat ; steam inhalation should be con-
stant from the onset of the disease until the exudation has disappeared ;
iron and brandy should be given freely ; the diet should be fluid,— milk
preferably,— and the patient kept in bed until the convalescence is com-
plete.
EPIDEMIC CEREBRO-SPIlSrAL MENINGITIS.
Epidemic cerebro-spinal meningitis, or cerebro- spinal fever, historically
belongs exclusively to the nineteenth century, although it unquestionably
prevailed prior to this period. French writers were the first to accu-
rately describe it.- It is a continued fever belonging to the class of mias-
matic-contagious diseases, which generally prevails in quite limited areas.
It has received various names ; as spotted, petechial and congestive fever ;
malignant purpuric fever ; cerebro-spinal and syncopal typhus.
Morbid Anatomy. — Pathologically as well as etiologically there are two
forms of cerebro-spinal meningitis ; the first is simply an acute inflam-
mation involving the meninges of the brain, spinal cord and medulla.
Its local symptoms predominate over the constitutional, and it occurs
exclusively as a sporadic disease ; the second, — epidemic cerebro-spinal
meningitis, — is accompanied by all the signs of an infectious disease, and,
at the autopsy, are found, in addition to lesions that are the counterpart of
those occurring in simple cerebro-spinal meningitis, those grave visceral
and sanguineous changes, which are present in other acute infectious diseases.
On examining the brain of one who has died of epidemic cerebro-spinal
meningitis, the convexity and base will be found most extensively involved.
Its dura mater is tense, shining, and studded with numerous punctate spots
of extravasation. The cerebral convolutions are flattened and the sulci
deepened. The pia mater of the brain and spinal cord is thickened. The
vessels of the pia mater are always more or less intensely injected and the
surface of the membrane roughened. In some cases extreme hypersemia
may be the only discoverable lesion. The exudation is the characteristic
lesion of this disease. A more or less abundant sero-fibrinous or sero-
purulent exudation takes place into the meshes of the pia mater. Clear
serum is first effused, then it becomes milky and clouded, then yellowish,
EPIDEMIC CEREBKO-SPIXAL MENINGITIS. 685
and finally a thick, viscid, greenish -yellow mass, consisting of granular
fibrin, pus-cells and red blood globules, which gives to the surface a " leek-
green " color. In the severest cases the fibrin and pus form a continuous
sheet in the sub-arachnoidean space, always thickened above the sulci. The
vessels are inclosed in the exudation, looking like red threads in a gelatin-
ous filmy mass. When the layer is removed, the subjacent gray substance
is dotted with red points. In rare cases the exudation is deeply stained
with blood ; at other times it is a thin, colorless fluid. The sinuses are
full of dark, soft coagula, or thin fluid blood. Hard thrombi are occa-
sionally found in them. '
The brain substance is frequently softened, especially near the largest
patches of exudations. This is the "mechanical softening" of French
authors.
On sectiofi there is more or less congestion and punctate extravasation
in the brain substance, and the ventricles are usually full of serum ; more
rarely of pus ; and this pus enters the ventricles by means of the velum in-
terpositum, or along the cerebellar or choroid plexuses.^ All the local changes
have their primary starting point in the pia mater. Finally, if absorption
occur, the pia mater often remains thickened. In prolonged cases cheesy
metamorphosis occurs in various spots in the thickened pia mater.
The changes in the spinal canal are similar to those within the cranium.
The dura nmter is injected, and extravasations of blood are often found
upon its parietal surface ; it is tense and shining. The meshes of the
spinal pia mater are occupied by the exudation, which occurs either as
stringy, interlacing bands forming a network, or in the form of a thick
sheet completely enveloping the cord's substance. The color and char-
acter of the exudation are the same as that in the cranial cavity. The largest
collections of pus are about the second and last dorsal and the lumbar ver-
tebrae. The posterior portion of the cord is the part most involved; the
anterior portion suffering only in those cases where the whole cerebro-
spinal tract is involved. The pia mater itself is hypersemic ; it may be
thicker than normal, shaggy and adherent to the cord. In some instances
the exudation occurs in the form of lozenge-shaped, irregular masses whose
ends are connected to one another by bands of fibrino-pus. In the severest
cases suppuration is so rapid that a complete sheath of pus is formed about
the whole cord in a few hours after the onset of the malady. The gray
substance of the cord is of a pinkish color, and may be infiltrated with
serum. It is sometimes reduced to a mere pultaceous mass.
In addition to these local changes there are blood and visceral changes.
The fibrin-factors of the blood are diminished, and hence there is a loss in
its coagulating power. The number of white corpuscles is increased, and
the red ones are shrivelled, serrated and partly disorganized. The blood
is darker than normal, fluid, and rapidly decomposes when taken from the
body. '
• Merkel states that he has found " a nuclear proliferation in the vessels, extending from the cerebral
meninges to the spinal cord."
2 Virchow'B Arch. Be. 34, Ileft 31, 866.
> The ventricular fluid contains chloride of sodium, phosphate of soda and ammonia and oxalate of urea.
—Meschede.
686 ACUTE GENERAL DISEASES.
The heart and the voluntary muscles undergo the same degeneration and
present the same appearances as in typhoid fever.
The lungs are frequently the seat of oedema, and hypostatic congestion
is present when the disease is prolonged. Passive hypersemia, lobular,
and, less frequently, lobar pneumonia, are often found at the post-mortem.
The liver is congested. The liver-cells are often cloudy and granular —
i.e., there is albuminoid or fatty degeneration.
The spleen is enlarged and softened ; the lymphatics are usually hyper-
semic, having a fleshy look.
The intestinal mucous membrane is hyperaBmic and the follicles are con-
gested. The projecting agminated glands are sometimes ulcerated. There
is more or less congestion of the kidneys ; the microscopical changes are
those of the first stage of acute Bright's. Abscesses (as in typhoid) often
form in the subcutaneous connective tissue. Bed-sores are not rare in those
parts subjected to pressure, and gangrene is sometimes present.
The integument is often the seat of petechial spots, and large, irregular,
discolored patches are sometimes seen over the body. Herpetic spots are
frequently seen on the surface of the body, on the face, and about the lips
especially. Rigor mortis is marked and very much prolonged. Finally
the serous membranes are frequently all covered with petechial spots and
small extravasations.
Etiology. — I have included cerebro-spinal meningitis in the list of mias-
matic contagious diseases, as it has more in common with this class than
with any other. It has prevailed as an epidemic and as an endemic dis-
ease, and occasionally sporadic cases have occurred in localities where it has
been epidemic. Epidemics have occurred at all seasons ; by far the greater
number, however, occur in cold weather. All classes and ages are subject
to it, but it is most likely to attack those between ten and eighteen years of
age. Young troops on the march are especially liable to it. ' Its strongest
predisposing causes are over-crowding, bad ventilation, insufficient or im-
proper food, dampness, and all other bad hygienic surroundings. Mental
excitement, excessive brain-work or bodily fatigue, exposure to excessive
cold or heat, are also predisposing causes. Cerebro-spinal meningitis is in
no sense a contagious disease. It is more closely allied etiologically to lobar
pneumonia than to any other disease, although some have regarded it as a
variety of typhus fever ; others of malarial fever.
Symptoms. — Cerebro-spinal fever follows no regular order, either in its
prodromata or in its subjective symptoms. Arbitrary classifications and
many subdivisions have been made, such as the typhoid, the paralytic, the
adynamic, the intermittent, the petechial, etc. Such classifications are
useless and confusing, for cases differ in the same epidemic. If the gene-
ral phenomena of the disease be known, the accidental circumstances that
are the basis of this complex nomenclature will be of very little impor-
tance.
The premonitory symptoms of cerebro-spinal meningitis vary in differ-
ent epidemics. In some the invasion is abrupt ; the patient, apparently in
1 Out of forty-seven French epidemics, Hirsch attributes forty-six to the military population.
EPIDEMIC CEREBRO-SPI-NTAL MENIISTGITIS. 687
perfect health, is suddenly seized with a chill, loss of consciousness, becomes
comatose and dies in a few hours. In others a feeling of lassitude, dull
headache, pains in the joints and muscles, and sometimes nausea and
vomiting precede its development. Again, patients complain of pains in
the back of the head and neck — they have no chills, but after twenty-four
hours a febrile movement is developed and they pass raj)idly into the
active symptoms of the disease. The prodromata may last from a few
hours to three or four days. In sporadic or endemic cases there is
generally a period preceding its invasion during which patients suffer
from a feeling of general indisposition.
When its onset is sudden its advent is marked by a distinct chill, in-
tense headache, pain in the back and upper part of the spine, nausea,
vomiting, a rise in temperature and an acceleration of pulse. The chill
may last an hour or more, but is usually of short duration. The skin is
abnormally cool and dry in its early stage.
Headache in most cases is a prominent, agonizing and persistent symp-
tom, and the pain, even in a condition of coma, causes the patient to groan.
In rare instances the headache intermits, and frequently it remits. Ver-
tigo almost always is an attendant, and the patient may suddenly stagger
and fall during the period of the headache.
Pain in the hach and upper part of the spine is a characteristic symp-
tom of the disease ; attempts to flex the head on the chest increase the
pain during the first twenty-four hours of the disease, and pressure np
under the ligamentwm nuchce, against the cord, often induces excruciating
agony. Soon the muscles at the back of the neck become stiff, then
rigid, the neck becoming fixed, and the head extremely extended — opistho-
tonos. So intense may be the opisthotonos that attempts to swallow are
so painful that the sufferer soon ceases to make the effort. The signs of
prostration are present early.
The temperature, as a rule, is loiv ; although 107°, 109° and 110° ¥.,
are recorded by trustworthy observers. It may rise rapidly to 104° or 105°
F., and then suddenly fall to 102° or 103° F., there to remain, with un-
important and irregular variations until a gradual return to normal marks
the beginning of convalescence. Often, before death — and an almost sure
indication of it — a low temperature will suddenly give place to a high one,
and death will occur during the time of the highest temperature. In
children the febrile movement is less marked than in adults.
The pulse at first is slightly accelerated, beating from 90 to 100 per
minute ; but in twenty-four hours after the commencement of the attack
it may range between 120 and 150, It bears no relation to the range of
temperature, often varying 40 or 50 beats in a few hours. It is feeble,
rapid and compressible in those cases where there are early symptoms of
exhaustion. In many cases it is small and wiry in character ; sometimes it
is dicrotic. In children the pulse is more accelerated and much more ex-
citable than in adults. In a few cases the pulse is slow at the onset of the
attack, but soon becomes accelerated, irregular and intermittent. Pho-
tophobia, contracted pupils, great and increasing restlessness, nausea
bob ACUTE GENEBAL DISEASES.
and urgent vomiting, and abdominal neuralgia, are among the early
symiDtoms.
The pu-pils are often unequal in size, and usually respond slowly to light.
The face is pale and anxious, and the features have a fixed, rigid expres-
sion ; in some the countenance has a dusky hue like that of one who is
tinder the influence of narcotic poison ; indeed, in some instances, the
patient believes, from the severity and suddenness of the attack, that he is
the victim of wilf al poisoning. About the second or third day of the
disease, if the headache has been very severe, delirium comes on ; it may
be mild and muttering, wild and uncontrollable, or "■ maudlin," like that
of a drunken man. In women the delirium may be attended by, or merge
into, a form of hysteria. The most fanciful hallucinations often visit the
minds of such patients, and if left to themselves they are constantly getting
out of bed. These patients are frequently roused from their wanderings by
excruciating pains in the head and extremities. Muscular contraction is
rarely absent even in the mildest cases.
By the third or fourth day a tetanic and contracted state of the muscles
of the extremities begins, and then the arms become flexed on the chest,
the forearm on the arm, the thumb on the palm, the knee on the abdomen,
and the leg on the thigh. When these excito-motor spasms of a tonic
character are marked in the groups of muscles in the back of the neck and
in the back, trismus may occur, and then the case is hopeless. Twitching
of groups of muscles often causes the patient to start from a state of semi-
stupor. General convulsions are absent in. adults, but are frequent in
children. Pains in the extremities and in the abdominal region are always
more or less severe. They are shooting and lancinating in character.
Pains when located over the abdominal region cause vomiting, and dyspnoea
when in the thoracic region. The skin may be hyper- or anaesthetic, and is
early the seat of an eruption. In the majority of cases the surface is so
sensitive that palpation and percussion are exceedingly painful ; the patient
cries out and starts at every attempt, and will usually say that it is that
particular spot which is the "sorest." Voluntary movements cause pain.
Cutaneous ansesthesia rarely exists throughout the course of the disease,
but follows the hyper-sensitiveness.
The eruption is usually limited to the face, neck, and lips ; it is herpetic
in character. It may appear on the trunk and limbs. Vesicles appear
earliest on and about the lips, and may be confined to them. Sometimes
the eruption is mottled like that of typhus, and covers the body ; it may
have a distinctly petechial character. Ecchymotic spots are often scattered
irregularly over the body, especially on those parts that are subjected to
pressure. Purpuric maculae, erythema and urticaria are sometimes present
(indeed, there are many varieties of the eruption), but herpetic and pete-
chial spots are the most common. As there is no definite time for the
appearance of these eruptions, so their duration varies ; sometimes they last
only for a day — at other times they are visible throughout the whole
course of the disease. Epidemics in which eruptions are marked have
given ric to the name of spotted fever.
EPIDEMIC CEREBKO-SPIKAL MENINGITIS. 689
With the photophobia the eye is subject to many disturbances. Paralysis
of the orbicularis palpebrarum may result in keratitis ; there may be more
or less intense conjunctivitis ; or a neuro-retinitis or choroiditis, the result
of an impIi<3ation of the optic nerve, may occur. Ptosis is present in
nearly every case. Temporary or permanent blindness, squint, double
vision, and nystagmus are not infrequent optical lesions. Atroj^hy of the
eyeball and cataract are occasional sequelae.
Taste is perverted or entirely lost ; yet the jiatient will often take with avid-
ity any article of food which may be placed in his mouth. Thirst is often
a constant and tormenting symptom. Deafness is even more frequent than
loss of, or disturbances in sight. There is always intolerance to noise, and
tinnitus aurium exists from the very commencement. Otorrhoea may be
extensive enough to result in tympanic perforation ; and the internal ear
may become the seat of an inflammatory process which sometimes ends in
suppuration. The semicircular canals would seem to be involved here, for
in many recorded cases "an uncertain gait" is mentioned as accompany-
ing the deafness. The respiratory tract, as a rule, is involved, the respira-
tions generally being accelerated out of proportion to the frequency of the
pulse, but when the exudation presses on the medulla and respiratory
centre, dyspnoea and slowed respiration occur, and in some few cases the
Cheyne-Stokes' breathing is noticed. Usually the violent headache and
the "wandering" are attended by great restlessness, tossing and jactita-
tion that frequently demand restraint. Insomnia is a common symptom.
There is often great tremulousness and subsultus tendinum ; in the ad-
vanced stage of the disease the pupils are dilated, the resjiiration markedly
sighing, deglutition diflBcult, the sphincters relaxed, or there is retention
of urine and faeces, the removal of which, by means of the catheter or
copious enemata, causes a slight return of consciousness.
The tongue, at first, is moist and covered with a whitish coating ; soon
it becomes dry and brown ; the joarotids may enlarge, and even suppurate ;
the abdomen is flattened. Eigidity, contraction and opisthotonus give way
to palsies. The skin becomes cyanotic as in the asphyxia stage of cholera.
In other cases tetanic spasms are the most prominent signs, the rigidity
and contraction of the muscles of the back and neck are excessive, and
the sufPerer dies with the grin of lock-jaw upon his face. In protracted
cases the patient becomes emaciated and loses strength in a degree out of
proportion to the duration of the disease.
The joints are usually tender, and often inflamed ; suppurative arthritis
occurs in a few instances.
The urine is but slightly altered. There is an increase in the urates
and phosphates, and albuminuria not infrequently occurs, especially late in
the disease. Polyuria is often present in children.
The bowels are constipated ; exceptions to this rule are seen only in
children. If the disease is prolonged, the symptoms assume a typhoid
character; and so "typhoid cerebro-spinal fever" is one of the many
varieties. The term intermittent cerebro-spinal meningitis has been ap-
plied to those cases where all the symptoms remit on the second or third
44
690 ACUTE GENEEAL DISEASES.
day from the onset of the attack, and soon reappear or exacerbate and the
patient rapidly passes into stupor and coma. As an epidemic advances the
cases grow milder, so that toward its end the patients may hardly be ill
enough to be confined to their beds.
In the form called " meni7igitis foudroyante " the patient is struck
down in full health, and death may occur within twenty-four hours from
the first symptom. The initial chill and headache are severe, there is
stasis in the capillary circulation of the surface, purpuric maculae soon
appear over the body, and active delirium is followed by profound coma
and death. The course is often so rapid that there are no tetanic exhibi-
tions. Exhaustion, paralysis, and anaesthesia are complete before the fatal
issue ; albuminuria is rarely absent in such cases. In fact all the prominent
severe symptoms of the disease are crowded into a few hours, and the pa-
tient rapidly passes into a state of collapse.
When recovery is to occur, the restlessness, jactitation, insomnia and
headache remit and finally disappear, or the patient emerges from a condi-
tion of coma into consciousness. The muscular paralysis continues, how-
ever, as well as the pains in the head and back of the neck, and in all
cases the convalescence is tedious. Stiffness of the muscles of the nape
of the neck is a persistent symptom during convalescence. Mental-
psychical disturbances are also common attendants of the convalescence.
Sometimes when the disease has pursued a mild course for a week or ten
days and convalescence seems about to be established, the patient gradu-
ally gets worse, and after weeks of suffering, death will occur from inani-
tion and general marasmus, the respirations becoming more and more
irregular, and deglutition often becoming impossible.
Differential Diagnosis. — Cerebro-spinal fever may, in children, be con-
founded with pneiiinonia, since convulsions and opisthotonus may occur
in either. It may be mistaken (at any age) for typhus, small-pox, tuber-
cular meningitis, the cerebral ioTm. ot pertiicious malarialieYer, and acute
myelitis.
When, from the ushering-in symptoms, doubt arises as to whether a child
lias thoracic or cerebral disease, a careful physical examination of the chest
will at once remove the doubt.
The differential diagnosis between cerebro-spinal fever and typhus and
pernicious malarial fever will be considered in the history of those fevers.
In small-pox the pain in the head is confined to the frontal region, while
in cerebro-spinal meningitis it has its seat in the occipital region. In men-
ingitis there is early stiffness and rigidity of the muscles at the back of the
neck. In small-pox this is a later symptom if it occurs at all. In small-
pox, on the fourth day of the fever, the characteristic eruption appears about
the roots of the hair, while in cerebro-spinal meningitis there is no peculiar
eruption, and no regularity in the date of its appearance. The tempera-
ture in small-pox is much higher than in cerebro-spinal meningitis. On
the second day of small-pox there are redness, swelling, and soreness of the
throat ; in spinal fever these are absent. Coma may occur early in cerebro-
spinal meningitis, but is a late symptom in small-pox. After the initial
EPIDEMIC CEREBRO-SPINAL MEN^INGITIS. 691
pains in the back and limbs, pain is not a prominent symptom of small-
pox ; while the severe and excruciating pains in the head, limbs, and
trunk increase in severity with the advance of cerebro-spinal menino-itis.
The diagnosis between tuhercular and cerebro-spinal meningitis is always
difficult and often impossible. A careful study of the previous history,
the insidious and characteristic slow advent of tubercular meningitis, the
slowed i3ulse at the beginning, the ''hydrocephalic cry," the absence of
eruptions, the very mild delirium, and the late appearance of muscular
rigidity, are the points on which we may differentiate the otherwise analo-
gous diseases.
The ushering-in symptoms of acute myelitis are very similar to those of
cerebro-spinal meningitis ; but when the myelitis is fully established there
are the peculiar "girdling" pains — the feeling as if an iron band were
around tlie waist — with paralysis of the lower limbs, which rapidly extends
upward. The temperature of the paralyzed limbs is first elevated, but
subsequently falls below the normal ; there is almost complete anaesthesia
of the surface, and impaired muscular contractibility ; later there is atrophy
of the muscles of the paralyzed parts ; — all of these, symptoms are in strong
contrast with the symptoms of cerebro-spinal fever. Again, pressure on
the spine in myelitis causes severe pain which is not increased by motion ;
while in meningitis motion rather than pressure causes pain. The recta''
and vesical sphincters are involved in myelitis, so that ammonaemia, pye-
litis, cystitis, and various urinary complications are early attendants on the
disease ; these are rarely present in cerebro-spinal fever. Trophic nerve de-
rangement is shown, in myelitis, by the extensive formation of acute bed-
sores, while this is a comparatively rare, and always a late, occurrence in
cerebro-spinal meningitis. Eefiex power is diminished or wholly absent in
myelitis, while it is exaggerated in spinal meningitis.
Prognosis. — Cerebro-spinal meningitis is always a grave form of disease,
and a guarded prognosis should be given. The death rate in severe epi-
demics is 80 per cent., and about 30 in mild ones. Toward the close of all
epidemics the death rate markedly diminishes. Hence, the period as well
as the severity of an epidemic will influence the prognosis. Its average
duration is about fourteen days, but cases are recorded where death has oc-
curred in five, twelve, fifteen, twenty-four, and thirty hours after the first
symptoms. In the majority of cases which prove fatal, patients die during
the second week ; if recovery takes place the disease is apt to last two or
three weeks. In quite mild cases the disease lasts about two weeks ; and
in the intermittent form, when the so-called relapses occur, the disease may
be protracted seven or eight weeks.
Age influences the prognosis. Statistics show that under fifteen, the
mortality-rate is much greater than between fifteen and thirty-five ; and
that after thirty-five, each year diminishes the chances of recovery. Every
day that is passed after the seventh renders recovery m.ore and more proba-
ble ; the symptoms that tend to render the prognosis unfavorable are a
rapid, and especially an irregular or intermitting pulse, an abundant erup-
tion, excessive hyperaesthesia and nervous excitement, absolute insensibility
692 ACUTE GEKEEAL DISEASES.
of the pupils, as well as symptoms of great mental depression and prostra-
tion early in tlie disease. Convulsions, a low temperature with attendant
collapse, paralysis of the muscles of deglutition, continued vomiting, shal-
low and irregular respirations and the occurrence of any of the complica-
tions, all render the prognosis unfavorable.
The co7npUcations of cerehro- spinal fever are bronchitis, broncho-pneu-
monia, croupous pneumonia, pulmonary oedema, pulmonary atelectasis aris-
ing from obstruction in one or more bronchi, and pleurisy. Endocarditis
or pericarditis and nephritis are frequent complications ; the lesions of the
eye, ear, joints, and subcutaneous areolar tissue can be regarded as belong-
ing to, and complicating the ordinary course of the disease.
The sequels of cerebro-spiual fever are numerous : even in the most
favorable cases basilar headaches and attacks of dizziness are liable to occur
for years after recovery. Deafness or blindness may result, and in chil-
dren deaf -mutism is a not uncommon sequence, especially if the disease
occur before the child has learned to talk. The eye lesions, already men-
tioned, may become permanent. The psychical disturbances may vary
from complete idiocy to .stupidity, impaired memory, and marked diminu-
tion in intelligence. General motor weakness is rather unusual ; but
paralysis of various muscles or groups of muscles is a frequent sequel.
Single nerves are sometimes paralyzed. Death may result from the pul-
monary complications, from paralysis of the muscles of deglutition and of
the thoracic groups, from heart failure, and consequent oedema of the
lungs, from intensity of poisoning at the onset, from asthenia, and from
coma.
Treatment. — The propliylactic measures to be observed during an epi-
demic of cerebro-spinal meningitis may be summed up in careful attention
to the surroundings : — remove all anti-hygienic influences, and when possi-
ble isolate the sick. Indeed the general principles of prophylaxis are the
same as in all miasmatic-contagious diseases.
A patient with cerebro-spinal meningitis should be immediately put to
bed, in a dark, cool, well- ventilated room, removed from noise and con-
fusion. During the entire course of the disease the diet should be of
the most nutritious kind, easy of digestion ; milk is to be preferred. The
exhaustion and emaciation that render convalescence so tedious must be
combated from the onset by a nutritious and generous diet. The thirst
which is so tormenting may be relieved by allowing the patient to drink as
much ice or seltzer water as he desires. If constipation exist it must be
overcome by promptly acting cathartics, — a calomel purge is to be pre-
ferred. It is well to administer a turpentine enema to aid the action of
the calomel. A free catharsis must be early obtained. The condition of
the bladder must be carefully attended to throughout the disease. If the
patient does not evacuate it at the proper intervals, recourse must be had
to the catheter. Sometimes cystitis has resulted from neglect of this.
As with all severe forms of disease, various plans of treatment have
been adopted. The plan of general blood-letting and depletion has no
doubt raised the death rate. In no case is blood-letting indicated or al-
EPIDEMIC CEREBRO-SPIXAL MENINGITIS. 693
]owal)le in this disease any more than in typhoid fever or diphtheria. The
internal and external use of calomel in its treatment, although it has been
extensively employed, is not sustained by the result of experience. Kor has
iodide of potassium the reputation which it once had for promoting the
absorption of inflammatory products. Quinine, if useful at all, is only so
at the very onset, and if used then it should be administered in large doses.
It has no antipyretic joower in this disease.
The medicinal agents which are generally accepted as most useful in
the treatment of this disease are the narcotics : among these opium stands
first in the list ; administered hypodermically, it not only j)romptly re-
licA^es the pain in the head, the restlessness, jactitation, insomnia, delirium
and convulsions, but it likewise increases the arterial tension. This drug
should be given until the desired effect is produced, namely, complete re-
lief ; there must be no hesitation in the administration of large doses if
required, for there is a remarkable tolerance of the drug in this disease.
It may be combined with atrojoia. Bromide of potassium is regarded by
some as especially indicated in this disease, and it has been given quite ex-
tensively with apparent benefit, esjDecially in children.
In my experience oj^ium, hypodermically, is superior to all other rem-
edies ; it should be administered early, in full doses, and the patient
should be kept in a semi-comatose state until the stage of effusion is reached,
after which it should be given in small doses. When cerebral symj^toms
are violent, cannabis indica ' may be cautiously administered. Chloral hy-
drate is contraindicated, and ether and chloroform inhalations should not
be resorted to unless neurotics have failed to relieve convulsions or pain.
Ergot is recommended by many on the ground that by its action on the
vaso-motor system it produces cerebral and sjiinal anemia. It is pro-
posed to give the ergot until dizziness is produced. Experience, however,
does not sustain the theory.
When symptoms of great exhaustion are present, stimulants are de-
manded ; decreasing restlessness and a continued fall of temperature are
some of the signs that indicate that stimulants are acting remedially.
The rules and methods of stimulation are the same as in typhoid fever. When
cerebro-spinal fever is long continued and there is reason to believe that
there is an abundant serous effusion, iodide of potassium in large doses
may be of service.
Cold applications to the head and spine, by means of evaporating lotions,
sprays, or ice-bags, are regarded by some as a most important adjuvant to
its treatment. In all cases their use demands great caution, and in this
country the profession favors the application of heat rather than cold to
the spine, in the form of hot-water douches or hot-water bags. Many are
in favor of first blistering the region over the spine from occiput to loins,
and then covering the parts with a poultice. Blisters at the nape of the
neck are of service in most cases after the acute stage is passed. In sthenic
cases leeches may be applied over the temples and mastoid processes ;
they diminish the headache at the beginning of the disease. The extremi-
■• Maniikopf.
694 ACUTE GBNEEAL DISEASES.
ties must never be allowed to get cold, and warm flannel is to be continu-
ally wrapped about the legs and body. Mustard foot-baths, stimulating
enemata, and the external use of turiDcntine are indicated when the simple
means fail to accomplish the desired result. Cold baths do harm. As soon
as convalescence shall have been established, a tonic plan is to be adopted.
The vegetable bitters, arsenic and iron are to be used. In some cases elec-
tricity may be employed with benefit.
SEPTICEMIA.
Septicaemia is a constitutional disease due to the absorption into the
blood of a septic material which has its origin in decomposing animal mat-
ter. This material is supposed to act on the blood as a ferment, and so
render it incapable of performing its physiological functions. As pyaemia is
called "purulent" infection, so septicaemia maybe denominated "putrid"
infection. The disease is closely allied to "surgical " or " traumatic fever."
Morbid Anatomy. — The changes in the blood in septicaemia are similar to
those which occur in fevers. It is darker than normal, coagulates less read-
ily, and tends to rapid decomposition. This loss of coagulating power
has been supposed to be due to the destruction, by the septic poison, of the
white blood corpuscles, which contain the main factors for producing
a clot. Bacteria and micrococci are said to abound in the blood in septi-
caemia ; other observers deny their presence.
The spleen is enlarged and often softened. The heart, kidney and liver
exhibit more or less cloudy swelling. The mucous membrane of the stom-
ach and intestines is congested and oedematous, and the agminated and sol-
itary glands are prominent. Enteritis is not frequent. In severe cases
ecchymotic spots are found in the intestinal tract.
The serous membranes may be inflamed, but generally they are only
ecchymotic. There is always more or less lymjahangitis present. It seems
evident that the septic poison is absorbed chiefly through the lymphatic
vessels.
. Etiology. — The nature of the septic poison that is the product of the
decomposing animal tissues is still a matter of dispute. Some claim that it
is a chemical substance, formed in a wounded part, which a'^ts as a ferment
in the blood and produces the septic symptoms. Others rej^ard the bacteria
which are present as themselves the sole cause of the septic infection.
Several pathologists have attempted to find the true poiscaous principle,
and have isolated — from decomposing fluids — what they call " sepsin," but
yet they are unable to prove that this alone is poisonous, for decomposing
fluids are still found to be noxious after the removal of the sepsin. It
has been observed that the blood of an animal with septicemia produces
greater disturbances and graver results when injected into a healthy animal
than decomposed fluid.
Dr. Sanderson, who says " that the agency of bacteria is essential to
the production of the septic poison," also says that '-'they are incapable
of producing the poison in a healthy organism." After considering the
SEPTICEMIA.
695
various theories wliich have been advanced, it seems most probable that
there is no one body which causes the septic infection, but the combina-
tion of a number of poisonous substances which produce changes analogous
to those caused by fermentation, and that the j)oison is absorbed chiefly by
the lymphatics, and only by the blood-vessels in exceptional cases, as when
their walls have undergone degenerative changes.
Decomposing tissues which cause septicsemia may be in the body, on the
surface of the body, or outside of the body.
L Thus, a decomposing placenta in utero, sloughing ulcers in typhoid
fever, necrotic processes in chronic phthisis, diphtheritic sloughs, ulcera-
tive endocarditis, abscess and gangrene of the lung, — these are some of the
internal conditions which may induce septicsemia.
II. Wounds, gangrene, decomposing membranes, or the suppuration and
necrosis in small-pox, any ill-conditioned wound, especially if lacerated and
contused, may cause septicaemia.
III. Dissecting wounds and post-mortem manipulation of those who
have died of infection, even without a surface abrasion, may induce sep-
ticaBmia. The respiratory and the gastro-intestinal tracts are sometimes
the mode of entrance of the infection.
Symptoms. — The symptoms of septicaemia will vary with the amount of
the septic material introduced into the system and the length of the in-
fection ; a slight infection will produce fewer and less grave symptoms
than one more extensive ; hence the symptoms will vary : — sometimes
urgent, sometimes so mild
as to be overlooked. In
a well-marked case, after a
rigor, or feeling of chilli-
ness, but rarely a distinct
chill, there is a rapid rise
in temperature ; 105"' or
107° F. may be reached
within the first twenty-
four hours. There is no
typical range to the tem-
perature. The pulse is
rapid (120 to 140), feeble
and thread-like. The
mouth, tongue, and sur-
face of the body become
hot and dry. If sweats
occur they are very slight,
and only present during ^ . t> ^ • ^^^'^^\ ,■ ■ .u ■
■J i- o Temperature Record m a cat^e of Septicaemia, followmn: an
the initial stage, and can Amputation.
hardly be confounded with the profuse sweats of pyaemia. Vomiting
is not infrequent. The nervous symptoms are always well marked.
The expression of countenance is dull and apathetic, the patient lying in a
listless condition, generally free from pain. There is restlessness and low.
696 ACUTE GENEKAL DISEASES.
muttering delirium. The respirations are feeble, labored, and hurried.
The skin may be slightly jaundiced. Diarrhoea is present in about 50 per
cent, of all cases, and in nearly all severe cases. The urine is scanty, high
colored, of high specific gravity, and contains urates and often albumen.
In mild cases the symptoms may remit, and complete recovery be
established within a couple of days. This happens when the septic cause
is discovered and removed. In severe cases death may occur within
twenty-four or seventy-two hours, the patient dying in comjalete collapse.
Typhoid symptoms, a dry tongue, rise in temperature, diarrhoea, and mut-
tering delirium, following an abortion or child-birth, should always excite
suspicion. Septicemia often gives rise to pysemia, or is combined with
it, which is shown by the initial chill being severe or often repeated, and
by the occurrence of profuse sweatings
Differential Diagnosis. — Septicaemia may be confounded with pycemia,
typhoid and typhus fever.
PycBinia is ushered in by a distinct chill ; septicaemia by slight shivering
or mild rigors only. In pysemia the chills recur ; in septicasmia there is
but one — the initiatory — chill. In pysemia there are profuse sweats which
recu7^ ; in septicaemia there are slight, if any, sweatings, and they are
never recurrent. In pygemia the temperature gradually rises to 102° to
104° F.; in septicaemia it is high at the onset, i. e., 105°' to 107° F. The
skin is of a dark, leaden yellow, jaundiced hue in pyaemia, while the dis-
coloration of the skin is never so marked in septicaemia. There is a sweet
" sickish " odor to the breath in pyaemia, absent in septicaemia. Pyaemia
develops slowly, septicaemia rapidly. In pyaemia the heart impulse is less
forceful than in septicaemia. Finally, itifarctions, thrombi and multiple
abscesses develop in pyaemia and are its distinguishing objective evidence,
while they never occur in simple septicsemia.
Prognosis. — This, in most instances, depends upon the extent of the
poisoning, " when the symptoms of the disease are well marked the prog-
nosis is bad." The possibility of the removal of the source of the infection,
and the length of time that the decomposing mass has been in contact with
the living tissues, influence the prognosis. Its duration is from two days
to two months. Death occurs from asthenia, exhaustion, or rapidly from
overwhelming of the system with the materies morbi. Collapse is nearly
always the precursor of dissolution.
Treatment. — The first thing to be accomplished in the treatment of this
condition is the discovery and, when possible, the removal of the cause.
Antiseptics should always be used at the seat of the infection. The bowels
must be freely acted upon by salines throughout the whole course of the
disease. The tonic, stimulant and antipyretic plan laid down for the treat-
ment of pyaemia should be employed here. Quinine, salicylic acid, and
brandy are the three drugs on which we place our reliance. Tanner
recommends quinine and nitric acid. The diet must be as nourishing as
possible.
Billroth's treatment is cooling drinks, a fever diet, morphine at night
to secure sleep, from six to ten grains of quinine during the afternoon ]
PYEMIA.
697
the induction of profuse perspiration when the skin is dry, by warm baths,
afterward wrapping the patient in blankets.
PYEMIA.
Pyaemia is an infectious disease caused by the introduction into the
blood of a miasm which arises from decomposing pus or its constituents,
attended by tlie formation of infarctions, metastatic abscesses and diffuse
local inflammation. Many authors make no distinction between septicaemia
and pyaemia.
Morbid Anatomy. — The blood in pyaemia is characterized by a tendency
to coagulate spontaneously wherever there is slowing of the blood-current.
Colonies of micrococci are very frequently found in the blood and on the
walls of the vessels ; ' venous thrombosis and embolism are essential feat-
ures-of this disease. The thrombi are usually near the seat of the pus ab-
sorption ; these emboli have a specific action on certain organs, stamped as
they are with the peculiar py^emic infection. When these emboli become
lodged in the small arteries of different organs they lead to the development
of infarctions which terminate in the formation of abscesses.
" Metastatic abscesses," the result of suppuration of a pyaemic in-
farction, caused by venous thrombosis and embolism, may form in the
lungs, liver, kidneys, spleen, muscles, heart and brain. '^ In the lungs
there is usually more or less
pneumonic inflammation about
the abscesses. Even patches of
gangrene may be found near
them. In the kidney the tu-
bules and vessels are found
crowded with micrococci.
The spleen is swollen and
shows more or less parenchyma-
tous degeneration, according to
the amount of fever. Gener-
ally will be found, scattered
through the organ, a few firm
wedge-shaped nodules with
their apices inward, or their
interior partly broken down
into pus. Metastatic abscesses
vary in size from a pea to a
large walnut. When multiple
abscesses are found scattered
through the various viscera,
softened puriform and decom-
posing thrombi are rarely found
in the veins ; but when the abscesses are few the reverse is the case.
Fig. 155.
Pyiemia.
Metastatic Pyaemic Abscesses of the Lung.
The
1 Weigi'rt states that rnnall thrombi are often formed, solely of bacteria.
* Recklinghausen says that these abscesses depend on " extra-vascular accretions offhnrji.^
698 ACUTE GENERAL DISEASES.
joints, the serous membranes of the body, and the connective-tissue of
various parts are often involved.
Pleurisy, pericarditis, and peritonitis of pyjemic origin are frequent and
always fibrino-purulent in character. I have known the pleural cavity to
fill with pus twenty-four hours after the first evidences of pysemic suppu-
rative pleurisy. Suppurative arthritis is a rare complication. Lymphangi-
tis is usually established in the neighborhood of the injury or source of in-
fection.
Ulcerative endocarditis with the presence of large quantities of bacteria is
not infrequent. Pyaemic pan-ophthalmia with sloughing of the cornea is of
rare occurrence. In some cases nearly all the tissues and serous and mucous
membranes exhibit deep post-mortem staining; the gastric and intestinal
mucous membrane being swollen and congested, the solitary glands and
Peyer's patches prominent. Ulcers may form at points along the intestine.
The skin always shows more or less jaundice. Suppurative cellulitis often
occurs. Occasionally there are cases of py83mia, or conditions closely re-
sembling pygemia, where there are no recognizable pathological lesions.
Etiology. — Eecent observations and experiments seem to show— ^rs^,
that pus with micrococci causes suppurative pyemic inflammation ; sec-
ond, that the micrococci alone can establish a similar inflammation ; and
third, that without micrococci pus is inert. Many regard the pysemic and
septicsemic poison as identical, and pyaemia as nothing but a metastatic
septicaemia, claiming that pyemia is invariably associated with more or
less septicaemia, and therefore have advised the use of the term septicc
pyaemia.'
The principal theories in regard to its nature are : 1st. That pus is ab-
sorbed and acts as a poison. 2d. That a chemical substance is evolved
from decomposing pus which enters the system and acts as a poison. 3d.
That microscopic organisms, finding their way into the blood and tissues,
there multiply and infect. Suppuration of bone is a very frequent cause
of a pJilehitis which leads to pyaemic infection. Thus a blow on the head
of one saturated with alcohol is followed by a phlebitis in some of the
diploic veins ; as a result, thrombi are formed, which break up into emboli
and thus lead to pyaemic infarction and abscess. Suppuration of the eye
or middle ear has led to the same results.
Cellulitis, carbuncle, erysipelas, '' malignant pustule," and dissecting
wounds often produce pyaemia. Endometritis or lacerations about the
genital tract are fruitful sources of pyaemia in the puerperal state. As
regards the question of pyaemic contagion, nothing definite can be stated.
From a surgical standpoint it has been proven that certain atmospheric
conditions and surroundings, such as want of cleanliness, will cause wounds
to take on an unhealthy action, and then pyemia will result ; but it has
'^Holmes' Sys. Surr/.,'Vol. v. Sanderson claims that "pysemic poison multiplies in the organism."
Whether the poison becomes more infective or virulent as time elapses or as it is developed from new
foci, is a mooted que^^tion. Panum chiimed that " there is, in putrefying fluids, a specific chemical sul>-
stance soluble in water and which, when introduced into the blood, causes the symptoms of putrid or
septic infection." Others claim that pytemia is due to a peculiar miasm which lias a specific action
similar to the exanthemata, and which may be introduced through the lungs, mucous membranes, and
through abraded surfaces.
PYEMIA.
699
never been shown that pyaemia can be contracted as small-pox or scarlatina
can.
Symptoms. — Pygemia is ushered in by well-marked symptoms. First,
there is a chill or decided rigor followed by a gradual rise of temperature
to 101° or 104° F., the rise of temperature being proportional to the phe-
nomena of the chill. The chills of pygemia occur irregularly, rarely at
night, and are followed, after the first two or three, by profuse and exhaust-
ing sweats, which only afford marked relief for a time, the skin soon be-
coming hot and dry. An irritability of the nervous system has been
noticed as preceding the occurrence of these chills. During the chill the
temperature will be higher than in the sweating stage, the thermometer
often showing a temperature of 103° or 105°
F., or 108° F., which often suddenly falls
below the normal, soon to rise again. ' The
heart power is notably and early diminished.
The pulse is frequent, 120 to 140, small and
often intermittent ; it does not vaiy with
the range of temperature. The conjunc-
tivaB and skin assume a sallow tinge ; later
they may become markedly jaundiced. The
breath has a peculiarly sweet, sickish odor.
The tongue is at first covered with a white
fur; later it becomes glazed, dry, brown,
and fissured. Sordes collect on the teeth.
Anorexia is marked from the onset. The
patient complains of great thirst. The
bowels are usually relaxed. The copious
diarrhoeal discharges, with the attendant
nausea and vomiting, soon bring about a
condition of asthenia. The mind remains
clear up to the time of great exhaustion
and the appearance of multiple abscesses in
some central organ or organs ; then the patient becomes dull, apathetic,
and often slightly delirious. The respirations are hurried and shallow,
and are always more accelerated just before a chill or sweat. As death ap-
proaches, delirium occurs, the pulse becoming more feeble and intermittent,
reaching at times 150 or 170, or 200 ; the face has a yellowish, leaden hue,
and finally the patient passes into a. comatose state and dies.
When the internal organs are involved the local signs of multiple abscesses
will be present. The physical signs of pyasmic pulmonic infarctions are at
first obscure, for the foci are so small and so scattered through the lung
that percussion fails to detect them. Usually the evidences of a severe
bronchial catarrh accompanied by a cough, with frothy, blood-stained,
watery expectoration, are followed by the physical signs of lobular pneu-
monia.
Fig. 156.
Temperature Record in a case of Pyaemia.
1 This intermittent type of fever is peculiar to tliia disease. Billroih says statistics favor the idea that
recurrent chills depend on new inflammations, having their chief source in repeated purulent infections
about the wound.
700 ACUTE GE]S"EEAL DISEASES.
The kidney changes are marked by albuminuria and hsematuria, together
with the i:)resence of epithelial and gelatinous casts. The amount of urea
is always increased. The changes in the liver and spleen cause abdominal
tenderness, accompanied by a marked increase in these organs as shown by
percussion. In pygemia there is generally more or less jaundice. The signs
of arthritis, pleuritis, peritonitis and cellulitis can be early recognized, and
should be looked for in severe cases after the second or third day.
Chronic pycBniia is met with among the robust, in whom the infection is
moderate, and not often repeated. The abscesses are confined to the cellu-
lar tissue and followed by suppuration in the Joints, marked debility and
muscular weakness. Weeks, or even months, may elapse before death or
recovery takes place in this class of cases.
Differential Diagnosis. — The diagnostic points of pyemia are, irregularly
Tecurring chills and sweats, great variations in temperature, with the signs
■of multiple abscess in the -internal organs. It may be mistaken for septi-
cceniia, iniermittent (malarial) /ever, acute yellow atropliy of the liver, acute
articular rheumatism, typhus and typhoid fever. The diagnosis between
pyaemia and septicaemia has already been considered under septicgemia.
The paroxysms in intermittent fever are regular in their development
and time of occurrence ; they are not so in pygemia. The temperature in
intermittent fever ranges higher than in pyaemia. There is slight, if any,
jaundice in malarial fever, while deep hematogenous jaundice is common
in pyaemia. The history of the case, together with the presence or absence
of small points of local infection, helps to differentiate between the two dis-
eases. The sweet, nauseating breath, marked muscular prostration, and
dull expression of the face, are noted in pyaemia and not in intermittent
fever.
The points of differential diagnosis between pyaemia, yellow atrophy of
the liver, rheumatism, and typhoid fever are found in the history of these
affections.
Prognosis. — In pyasmia the prognosis is always unfavorable. Some deny
the possibility of recovery in a well-marked case ; still recovery is possible
in cases that are mild at the onset and slow in their development, in which
the chills are not often repeated, the intermissions between the exacerba-
tions of fgver are long, loss of strength is not rapid, and the tongue re-
mains moist. Thus we see that the prognosis depends entirely on the course
of the disease. The duration of pyaemia varies : it is usually acute, lasting
from two to ten days, often subacute, lasting from two to four weeks, and
rarely chronic, when it may run on for months. The duration of puer-
peral pyasmi a is usually about one week. If death occurs in four or eight
days, it is due to the intensity of the pyaemic poison. If later, it depends
upon the exhaustion incident to the formation of abscesses and the occur-
rence of complications. The earlier the symptoms of multiple abscesses
appear the more hopeless the case.
It must be remembered that pyaemic patients differ in their power of
eliminating poison ; hence in some cases the system will be at once over-
whelmed, while in others the shock will be recovered from. Every day
ERYSIPELAS. 701
after the eighth that the patient survives increase-; his chance of recov-
ery.
Treatment. — The treatment of pyaemia may be divided into the prophy-
laxis, and the treatment of the developed disease. Its prophylactic treat-
ment is by far the most important : it consists in avoiding everything
that may favor the development of the disease, the details of Avhich are
included under the general management of surgical operations, and the
treatment of wounds. The history of these antiseptic methods comes
within the domain of surgery rather than medicine. Obstetricians cannot
be too careful in these matters.' Cleanliness, good ventilation, sunlight
and quiet are important prophylactic measures. There are undoubtedly
certain atmospheric conditions which influence the development of pysemic
marasmus and are always to be considered.
Pysemic poison, if eliminated at all, is eliminated by the intestinal
tract and not by the skin or kidneys, and treatment should be directed
to aid this elimination.^ With the idea of neutralizing the pysemic poison
after it has gained access into the body, or counteracting its effects, a long
list of antiseptics have been employed. The sulphites and hyposulphites
of sodium, calcium, and magnesium ; carbolic and salicylic acids, the oil
of turpentine, and many like agents, are still under trial. Quinine is the
drug which is most extensively employed, for its antiseptic and also for its
stimulant and antipyretic powers.
The most important thing in the treatment of pyaemia is to support the
patient ; and, with this end in view, the largest possible amount of nour-
ishment and stimulants should be administered. There is no disease in
which so large an amount of stimulants can be administered with benefit
as in pyaemia. The indications for their administration are the same as
in the essential fevers. If life can be prolonged, in mild cases, until the
violence of the infection is passed, recovery is possible.
ERYSIPELAS.
Erysipelas is an acute constitutional disease with local manifestations,
which are first developed in most cases about wounds, but may apjDcar
primarily in previously healthy parts.
Although it cannot be stated with certainty that erysipelas is*never idio-
pathic in its genesis, its unquestionably contagious nature when once de-
veloped, from whatever source it may have arisen, leads me to class it
under infectious diseaees, and to consider it a connecting link between the
general and local affections.
Morbid Anatomy. — The changes in internal organs and the blood are
in no way characteristic. Early in the disease the fibrin and white cells
are increased, but the blood rapidly assumes the condition found in other
acute febrile diseases, and becomes thm and fluid, or dark and pitchy, does
' An interesting proof of this is shown in the case I'elated by Dr. Teale : Three gentlemen who aided
him in dissecting a subject who died of hernia, attended the same day five midwifery cases in all. Four
of these cases died of puerperal fever, while no other cases of it occurred in their extensive practice.
2 Billroth says diarrhcea is a severe complication which quickly induces collapse.
702 ACUTE GEN"ERAL DISEASES.
not coagulate readily, and stains the heart and vessels. The local mani-
festations may affect any surface, as the mucous and serous membranes or
lining membrane of the blood-vessels and lymphatics, but are most charac-
teristically displayed in the skin.
They are essentially inflammatory. Early there is hypersemia, followed
by exudation of lymph and cells, which gives the part a bright red color and
causes some swelling and induration. This inflammation is peculiar in its
tendency to become diffuse, and in its antagonism to reparative processes.
When it attacks a wound already partly united the adhesions are speedily
resolved and the wound is reopened. On the unbroken skin it is not
limited by inflammatory products, but extends by continuity, and may
from a small primary focus, involve the head, an entire limb, or the whole
body. The intensity of the inflammation is very inconstant.
In most cases it involves only the skin, and is hardly more than a simple
erythema. In some, and generally where the skin is lax, there is well-
marked and more or less extensive oedema. In more severe cases there is
often suppuration, which is generally a diffuse infiltration, but may be cir-
cumscribed.
The inflammation may terminate in resolution, vesication, abscess, or
gangrene. The former is the usual ending. The hypersemia subsides, the
infiltration is absorbed, and the process terminates in desquamation.
When vesication occurs previous to resolution, the cuticle is raised by se-
rous effusion, and when thrown off leaves healthy skin or superficial ulcera-
tion. Abscess and gangrene present the same pathological changes as under
other conditions.
Erysipelas is not always limited to the skin, but often involves deeper
parts. It is somewhat doubtful, however, whether the inflammations of
the pleura, pericardium and peritoneum, which often complicate severe
attacks of the disease, are the result of direct extension of inflammation or
are due to the systemic poison.
When meningitis complicates erysipelas of the scalp, or laryngitis and
oedema giottidis accompany the inflammation of tlie neck, the relation is
probably one of continuity, but the peri- and endocarditis which are occa-
sionally present in a similar erysipelatous condition, together with the
implication of the veins and evidences of nephritic complications, point
to a more general etiological basis for such conditions.
The lymphatics are generally implicated, and their course can be traced
by red lines running from the inflamed area to the adjacent glands, which
are enlarged and indurated. Indeed, some authors believe that the primary
seat of the inflammation is often in this system. If the veins are in-
volved, a phlebitis may result in infarction, or more rarely in pyaemia.
Following an attack of erysipelas there remains some thickening and in-
duration of the skin, which may become permanent after repeated attacks. ^
The tissues in the inflamed area and the lymph-spaces and channels
connected with them are filled with bacteria, whose relation to the inflam
mation is not definitely determined.
^ Virchow.
ERYSIPELAS.
703
Etiology.— All the causes of general debility, as indulgence in drink and
anti-hygienic conditions, predisjDOse to erysipelas. In a large proportion of
cases it is preceded by some abrasion of the surface or a distinct wound,
and is then considered traumatic.
Some individuals show a constitutional predisposition to the disease, and
certain unknown atmospheric conditions favor its dissemination.
It is fully determined not only that erysipelas, once developed, is highly
contagious and spreads rapidly among surgical patients and puerperal
women, but that the disease is, in such cases, the result of a specific con-
tagion which may render buildings, clothing, and the persons of attendants
infectious centres. The nature of this contagion is entirely unknown.
Inoculation of the bacteria which fill the inflamed tissues produces ery-
sipelatous inflammation. It is not proven, however, that they are the sole
cause or vehicle of infection. Traumatic erysipelas is generally, if not
invariably, due to such a specific contagion. It is not equally certain that
idiopathic erysipelas is always primarily a constitutional disease, although
it is generally so considered. In its contagiousness, period of incubation,
and evidences of constitutional disturbance preceding the local inflamma-
tion, and in the fact that it can be propagated by inoculation, it is allied to
the purely contagious diseases.
On the other hand, contagious properties do not prove a specific origin.
The constitutional condition may be fully accounted for by the local
Fig. 157.
Temperature Record in a case of Facial Erysipelas.
affection, as in simple traumatic fever, and each attack renders the patient
more liable to another.
Therefore while erysipelas is more commonly the result of direct con-
704 ACUTE GEXEEAL DISEASES.
tagion, I believe that in some cases it may be primarily a local, non-specific
disease which becomes contagious in its development, in the same sense as
pneumonia is a local disease, and may be due to exposure or direct irrita-
tion under favoring constitutional conditions.
Symptoms. — The symptoms of erysipelas are constitutional and local.
Both traumatic and idiopathic erysipelas have a period of latency of from
two days to a week or more, during whj«n there will be some fever, pos-
sibly of a remitting type, with slight chills, headache and malaise. As the
local symptoms appear the fever increases, and is marked by decided even-
ing exacerbations. It seldom passes 106° F., and the morning remission
may be two or three degrees, and be attended by sweating. The fever is
accompanied by a rapid pulse, coated tongue, nausea, anorexia, and dis-
ordered bowels. In some sthenic cases the attack is sudden and attended
by severe chills and a rapid rise of temperature. The duration of the fever
is very varied.
When the inflammation is localized and recovery occurs, generally from
the fifth to the tenth day there is a rapid decline in the fever and dis-
appearance of all unfavorable symptoms. The temperature may even be-
come subnormal and continue so during early convalescence. When the
local condition is progressive, however, the fever continues at 104° or 105°
P. for two, three or more weeks. ^ In these cases the fall in temperature
is commonly more gradual and convalescence more prolonged.
In children and nervous patients a mild delirium may be present with-
out any meningeal complications, or in sthenic cases it may become perma-
nent and violent.
When the course of the disease is unfavorable it assumes a typhoid char-
acter, the temperature rises rapidly, the pulse is frequent and feeble or
irregular, the delirium becomes low and muttering, and passes into coma
which ends in death. Sudden extension of the inflammation, or relapses
when convalescence is apparently established, are frequent and are marked
by a rapid rise of temperature, corresponding with the extent of new tis-
sue involved. Final recovery may thus be delayed for weeks, during which
there will be periods of normal or subnormal temperature.
The urine is always scanty and high-colored. It contains an excess of
urea and often a small amount of albumen.
I'his course of the fever is often greatly modified by complications.
The local symptoms are equally variable. Traumatic erysipelas begins
as a diffuse rose or bright red blush about the point of injury, in which a
white line follows the finger as it is lightly drawn across the surface.
This is generally preceded for a day or two by some enlargement and ten-
derness of the adjacent lymphatic glands. In uncomplicated cases there
are no further changes, but the inflammation subsides and is followed by
flaky desquamation.
Idiopathic erysipelas is most commonly facial, starting from either the
nose, eyelid or ear. It may begin either in the skin or areolar tissue, and
1 In a case where the inflammation involved by degrees the entire surface from a wound on the head to
the toes, the temperature was between 103°-104° for over four weeks.
ERYSIPELAS. 705
is attended by more or less oedema. The part is first swollen and second-
arily the characteristic blush appears. The jmrt becomes enlarged, hot
and painful, and the swelling may extend so as to close the eyes and involve
the whole head and neck to such an extent as to greatly disfigure the
patient. In from six to twelve days the color becomes darker, the swell-
ing recedes and the cuticle peeling off leaves a slightly reddened surface
which slowly regains its normal color.
When the disease is " erratic " it extends more or less rajaidly from its
primary seat, where the inflammation slowly ceases as it advances else-
where, so that it may be present in all stages from the first faint blush to
desquamation.
When the disease assumes a phlegmonous or suppurative form, the pus,
if diffuse, gives a peculiar boggy sensation on palpation, but if circum-
scribed it has the usual appearance of an abscess.
Ap]3roaching gangrene is indicated by an intense burning j^ain, and the
parts become livid and finally black and crackling.
Erysipelas may be com|)licated by meningitis, which will be indicated by
its usual symptoms somewhat modified by the preexisting fever. Peri-
carditis and pleurisy are at times recognized by dyspnoea, or often only by
their physical signs.
Differential Diagnosis. — When erysipelas attacks n joint it may be mis-
taken for a short time for acute articular rheumatism, but the peculiar
deep rose color and the rapidity with which the inflammation extends will
speedily distinguish it. Similar symptoms with the oedema will also dif-
ferentiate the disease from simple erythema. High febrile movement
lasting twenty-four to forty-eight hours, and attended by pain, swelling and
tenderness of the lymphatics, has been considered diagnostic of develop-
ing erysipelas.
Other questions of differential diagnosis belong entirely to surgery.
Prognosis. — Traumatic erysipelas is a very unfortunate complication in
surgical injuries. It arrests all reiDarative action and adds largely to the
gravity of the previous condition.
Idiopathic erysipelas, when it attacks the face and head, is a dangerous
and uncertain disease under any circumstances, and is especially so in
aged people. Many patients suffer from a simple erysipelas of the face at
almost regular intervals without serious discomfort, but there is always
danger that the meninges will become involved and the disease at once
assume a most serious aspect.
Death may result from the overpowering effects of the poison, from the
complications, or from exhaustion due to suppuration, gangrene, or a pro-
longed course of the disease. CEdema of the glottis from extension of
inflammation may cause sudden death. The disease is especially fatal in
chronic alcoholism, Bright's and gout, and in patients over sixty. Eecur-
rent attacks indicate a debilitated condition and are apt to be of increasing
severity.
Treatment. — In common with other miasmatic-contagious diseases, great
care should be taken to avoid extension of the disease, and as we are unable to
45
706 ACUTE GESTEEAL DISEASES.
control the poisonous emanations, complete isolation of such patients
affords the only sure means of prophylaxis.
In mild cases local treatment is unnecessary, and it is doubtful if it ever
restricts the inflammation. Cold dressings with mildly astringent and
anodyne lotions are the most grateful to the patient and as efficacious as
any. More powerful astringents and distinct caustics, as iodine and a
saturated solution of nitrate of silver, or even the actual cautery have been
employed with a view to cut short the inflammation or to prevent its
spreading.
Erysipelatous inflammation often improves in five or six days under such
treatment, or halts at a line where iodine or silver has been employed ;
but it quite as frequently, when extending, is not perceptibly restricted by
such boundaries. A saturated solution of silver may be applied, however,
two or three times in twenty-four hours. Subcutaneous injections of
carbolic acid in surgical erysipelas have seemed to give more appreciable
and better results than any other local treatment. If oedematous swellings
are excessive, minute punctures will afford marked relief. Hot applications
and poultices are to be used only when suppuration or gangrene is present.
We have no means of neutralizing the poison of erysipelas, and internal
treatment is confined to general tonic measures. Concentrated nutriment
should be administered frequently in small quantities, and stimulants em-
ployed as in other acute febrile conditions. The bowels and kidneys should
be kept active by cathartics and simple diuretics. Various remedies have
been employed, but the tincture ferri chloridi seems to be generally ac-
cepted as the most useful drug, and is even considered to have specific effects
in erysipelas.
Quinine and other tonics may be employed with advantage.
The bromides and chloral are preferable as soporifics to opium or hyos-
cyamus.
ACUTE MILIARY TUBERCULOSIS.
Acute miliary tuberculosis is an acute general disease of an infectious
nature and non-inoculable. In nearly every instance it is secondary to,
and a part of, a more chronic tuberculous process, of which the symp-
toms, in some cases, are of so passive a nature as to escape notice, while
the manifestations of the more acute process alone attract attention. More
frequently the preceding chronic condition and the acute disease appear
as a part of a general tubercular process. It is only when it occurs with-
out previous tubercular infection that it can be considered a distinct dis-
ease. The question whether it is, strictly speaking, primary, awaits its
answer in an accepted definition of tubercle and a demonstration of its
etiology.
Morbid Anatomy. — While acute miliary tuberculosis is not a local affec-
tion and is to be carefully distinguished from acute phthisis, its pathologi-
cal changes are more abundant and far more frequently found in the lungs
than in any other organ. They are also generally present and may be
principally located in the pia mater (acute hydrocephalus) intestines,
ACUTE MILIARY TUBERCULOSIS. 707
lymph glands, serous membranes, and, rarely, liver, spleen and brain. The
characteristic lesion of acute miliary tuberculosis consists of an irrui^tion
of delicate, gray, translucent miliary granules, varying in size from a pin's
head to a poppy-seed. They are quite evenly distributed throughout the
affected organs and show little tendency to coalesce.
In the early stages affected lungs show little change from the normal,
aside from the presence of the tubercle granules. Later they become
slightly hypergemic and oedematous, with some infiltration about the
granules of an amorphous matter. Although the air cells may become
partially filled with epithelium, pus-cells and fibrin, hej)atization is of
rare occurrence. The pleura is studded with similar tubercular granula-
tions, and they are also present more or less abundantly in the peritoneum
and the various glands and organs throughout the body. They can be
recognized in some cases in the choroid. In the pia mater they occupy
the perivascular lymph spaces. Histologically a gray miliary tubercle con-
sists of-lymphoid and epithelioid elements enclosed in a fine reticulum re-
sembling coagulated fibrin. One or more masses of protoplasm containing
several nuclei with bright nucleoli and varying in size from 1-500 to 1-200
inch — the so-called ''giant cells" — are generally present in each tubercle,
but are not found in the tubercles of the pia mater, and cannot, therefore,
be regarded as essential elements of miliary tubercule.
All tubercle manifests a strong tendency to undergo caseous degeneration,
but in acute miliary tuberculosis the patient usually succumbs to the dis-
ease before any such change occurs. In the present unsettled state of the
pathology of tubercle it is impossible to formulate any accepted theory as
to the nature of the pathological processes or the origin of the histological
elements in acute miliary tuberculosis. The evident etiological relation of
caseous foci, plastic inflammations of serous membranes, and primary
tubercle to acute tuberculosis, and the fact that miliary tubercles are dis-
tributed by the lymphatics, lead me to the belief that the pathological
processes are essentially inflammatory in their nature, and result in a neo-
plastic growth.
Etiology. — The predisposing causes are very prominent in the etiology
of acute miliary tuberculosis, and it is very doubtful if it ever occurs
when they are not present. Most prominent of these is the undefined con-
dition so universally recognized as the strumous diathesis. However much
authorities may differ as to the ultimate cause of tubercle, the special
dangers to which persons of this diathesis are exposed are uniformly ad-
mitted. Caseous foci as found in chronic phthisis, inspissated abscess,
caries of bone, or caseous glands are to be placed in the class of predispos-
ing or exciting causes, according as we accept or deny the specific nature
of the ultimate cause of tubercle.
If the term tubercle is limited to that tissue in whose development the
tubercular bacillus, or any specific element is the primary etiological factor,
then caseous matter becomes simply a predisposing cause as furnishing a
favorable soil for the development of, and a means of transportation for
the bacillus. If, however, tubercle is defined upon an histological basis
708
ACUTE GENEKAL DISEASES.
and not from its etiology, I think I am justified in saying that while the
tubercular bacillus may be, and undoubtedly is, one cause of tubercle and
possibly of acute miliary tuberculosis, in whose development and distribu-
tion throughout the body caseous matter plays an important part, on the
other hand caseous deposits per se and other irritants may also become ex-
citing causes of the peculiar tuberculous inflammation and neoplastic
growth.
The process of infection appears to be one of metastasis in which the
irritating elements are distributed from infectious foci, especially of primary
tubercle, caseous matter, or the products of inflammation in serous mem-
branes. The channels through which this distribution occurs are probably
the lymphatics. The location of miliary tubercle in the perivascular
lyrnph spaces, however, does not preclude the possibility that the blood
may also transmit the infection. i
Symptoms. — When acute miliary tuberculosis complicates the last stage
of phthisis its symptoms are so modified that it is not easily recognized,
more especially as the tubercular deposit does not materially afl'ect the
physical signs. In such a case a sudden and decided increase in the fever,
and marked aggravation of the dyspnoea will be the most characteristic
symptoms, and, occurring in connection with unchanged iDhysical signs,
may lead to a corresponding diagnosis. When the disease attacks an indi-
vidual in apparent health the symptoms are well marked.
It is generally ushered in by repeated chills, a rather rapid rise in tem-
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Temperature Eecord in a case of Acute Miliary Tuberculosis.
perature and pulse rate, and the other symptoms of an acute general dis-
ease, accompanied by rapid respiration and a short, dry cough. The tem-
1 Ponflck found tubercle in the wall of the thoracic duct in a case of general miliary tuberculosis, and
this is adduced as a proof that the blood becomes an infective fluid.
ACUTE MILIARY TUBERCULOSIS. 709
perature ranges from 103° to 106° or 107° F., with irregular, but marked
remissions, and is more frequently high in the morning and low in the even-
ing than in any other acute affection. The pulse is soft, small, and com-
pressible, varying from 120 to 150 per minute, but in no constant or definite
ratio to the temperature. The respirations are from 50 to 60 per minute,
and later the dyspnosa becomes intense. The persistent sharp, hard cough
is rarely accompanied by expectoration ; when present, the expectoration
consists of viscid mucus, occasionally blood-streaked. The skin is pale and
cyanotic; there is anorexia, rapid emaciation, and diarrhoea, as a rule; the
lips and tongue become dry and covered with brown crusts ; the patient is
dull and semi-comatose, and at night delirious, presenting all the symjDtoms
of the typhoid state. The spleen is generally slightly enlarged.
The j)atient may survive for five or six weeks, but more frequently suc-
cumbs within two or three. As death approaches the pulse rapidly grows
weaker and more frequent, the cough ceases, the temperature falls, or, if
already low, suddenly rises, the cyanosis deepens and death occurs from
pulmonary oedema and asphyxia.
Physical Signs. — In most cases the physical signs are entirely negative.
Percussion may show points of slight dulness, surrounded by ex*"ra reso-
nant areas, and auscultation occasionally reveals moderate bronchial catarrh,
with fine moist rales, but they are not characteristic. A soft friction sound
may be produced by a roughened nodular pleura.
Differential Diagnosis. — The symptoms of acute miliary tuberculosis are
in many cases so exactly those of typhoid fever that a differential diagnosis
is impossible.
The fever curve of typlioid fever is regular and typical ; that of acute
miliary tuberculosis is irregular and not characteristic. Typhoid presents
a distinctive rasli not found in tuberculosis ; and the pea-soup discharges
with gurgling and tenderness in the right iliac fossa of typhoid are seldom
present in acute tuberculosis. In typhoid the bronchitis follows the dis-
tinct initiatory symptoms, and its physical signs are more prominent than
the cough and dyspnoea, while in acute tuberculosis the hard, persistent
cough and intense dyspnoea which precede or attend the development of
the fever are accompanied by few, if any, physical signs of bronchitis.
Large doses of quinine reduce the temperature of tyiDhoid from 2° to 3° F.,
but have little effect upon that of acute miliary tuberculosis, and, finally,
recovery is the rule in typhoid and would tend to invalidate a diagnosis of
acute miliary tuberculosis. Pneumonia and acute diffuse iroticliitis in
their early stages may simulate acute miliary tuberculosis, but the rapidly
developing physical signs and the absence of the constitutional symptoms
of an acute wasting disease render an early diagnosis possible.
Prognosis. — The prognosis must be almost absolutely unfavorable. The
duration of the disease is from a few days to six or seven weeks, with an
average of three weeks. The more general the infection, the more violent
the fever and the nervous symptoms, the sooner is a fatal termination to
be expected. When complicating phthisis, its course is very rapid. As-
phyxia from pulmonary oedema, asthenia, cerebral anaemia and collapse are
710 ACUTE GENERAL DISEASES.
the principal causes of death, but in about one-third of the cases it occurs
from implication of the meninges.
Treatment. — The only indications for treatment which afford any hope of
attaining favorable results are in the way of prophylaxis, and are largely
included in the treatment of the predisposing diathesis. In treating scrofu-
lous patients, acute miliary tuberculosis should be remembered as among
the impending dangers. Caseous matter, wherever situated, should be re-
moved when the attending danger is not great, and absorption of those
masses which cannot be reached, and of the products of inflammation in
serous membranes should be assisted by all the usual means. More defi-
nite knowledge of the etiological relation of the tubercle bacillus may afford
other indications for prophylaxis.
When the tubercular deposit has once taken place, treatment is confined
to the reduction of temperature and supporting the patient. For the first,
quinine is of little avail. It is sometimes used as long as recurring chills
are present, but is of doubtful value as the chills are probably due to new
deposits of tubercles. Cold will be found more useful in reducing tempera-
ture, and may be used in baths, packs, or by sj)onging. Stimulants and
highly nutritious food fulfil the second indication, and must be used as in
other wasting diseases. Morphia must be used for the relief of the cough,
and for the dyspnoea quebracho may afford temporary relief.
TYPHUS FEVEE.
Typhus fever is a contagious disease, which usually prevails epidem-
ically. Although it has many phenomena in common with miasmatic-con-
tagious fevers, and was at one time classed with typhoid fever, to-day it is
regarded as a distinct type of fever, dependent upon a specific poison with
certain pathological and etiological phenomena, which distinguish it from
all other forms of disease. It has received a great variety of names, such
as sJiip fever, hospital fever, jail fever, camp fever, petechial fever, putrid
fever, Irish ague, hrain fever, spotted fever , continued fever , typhus fever,
petechial and exanthematous typfius. '
Morbid Anatomy. — Those pathological lesions which are common to ty-
phus and typhoid fever will be first considered, and as the line of distinc-
tion between them is drawn it will be noticed that, in many respects, the
difference is one of degree, rather than of kind.
The changes in the blood are as follows : it is darker in color than nor-
mal, and when drawn from the body during life coagulates imperfectly or
not at all ; if a clot is formed it is of the consistency of putty. The fibrin-
factors are diminished, or the blood loses its coagulating power to a greater
or less extent. At first the red globules are increased in number, but as
the disease progresses they diminish ; the salts of the blood are also changed,
and urea and ammonia are present in excess ; by some the latter is sup-
1 The Germans describe an abdominal and cerebral typhus. Their abdominal typhus corresponds to
our typhoid fever and their cerebral typhus is our typhus fever.
TYPHUS FEVEK. 711
posed to be produced by the decomposition of the former. The blood of a
typhus fever patient, when drawn from the body, rapidly undergoes am-
moniacal decomposition. When the blood is examined microscopical!}^,
many of the red globules will be seen to have lost their normal outline,
and their edges to have become serrated and irregular. In some instances
they will be found to have undergone degeneration ; their coloring matter
will then ]oass through the walls of the blood-vessels and stain more or less
deeply the tissues and effusions which may have taken place in the serous
cavities. These blood-changes are very similar to those which take place
in the miasmatic-contagious fevers — they differ in degree only.
Parenchymatous Degenerations. — There is the same tendency to par-
enchymatous degenerations of the different organs and tissues of the body
in typhus as in typhoid. Usually the body is not very much emaciated ;
it undergoes decomposition rapidly after death. In severe cases decom-
position apparently commences before death. The muscles are usually of
a brownish color, dry, presenting an infiltration of fine granules in the
primitive fibres ; sometimes hemorrhages take place into them. The
liver and spleen undergo degenerative changes similar to those described
as occurring in typhoid, but they are not so extensive nor are they so con-
stant. One may make very many autopsies on persons dying of typhus
fever, without finding any softening, or only a very moderate softening, and
enlargement of the spleen, while blood extravasations are not uncommon.
In severe cases the cortical portion of the kidneys is swollen, opaque and
more or less fatty, according to the duration and severity of the disease.
The primary enlargement of the kidneys is mamly due to a cloudy swelling
of the epithelium of the renal tubes.
This tendency to cloudy swelling and granular fatty degeneration, the
so-called '^ vitreous degeneration of Zenker," which occurs in the vol-
untary muscles and the kidneys, also occurs in the muscular tissue of
the heart. If the fever is protracted, the cardiac walls become flaccid, of
a brownish color, and parenchymatous changes are found similar to those
which occur in typhoid fever, though less marked. There is often a con-
siderable amount of serum in the pericardium. Pultaceous clots are found
in the heart cavities, and thrombi are found firmly adherent to the walls
of the larger veins. There is the same tendency to ulceration of the
mucous membrane of the mouth and larynx as in typhoid fever. In ty-
phus fever the ulcers are deeper, involving more extensively the submucous
tissue. Splenization of the lungs also occurs, in typhus as in typhoid
fever. Hypostatic congestion of the lungs and pulmonary oedema are as
common as in typhoid ; some claim that they are found much oftener.
Thus far I have noticed only these lesions which occur both in typhus
and in typhoid fever. I now come to those which are found only in
typhus.
Brain. — Although there is nothing in the appearance of the brain which
is characteristic of this fever, yet it is very unlike that met with in ty-
phoid fever. In the latter disease it usually presents an anaemic appear-
ance. In all cases of typhus the cerebral vessels will be found more or less
712 ACUTE GE]!fEEAL DISEASES.
congested. In some epidemics all the sinuses and blood-vessels of the brain
will be found engorged with dark blood, so that when the calvarium is re-
moved the vessels will stand out upon its surface. In other epidemics, in-
stead of iinding intense congestion, there will be more or less extensive se-
rous effusion into the meshes of the pia mater : the quantity of the effusion
varies from one to eight or ten ounces, and it is most abundant upon the con-
vexity, although it takes place to a limited extent into the ventricles. When-
ever there is a large amount of fluid effusion there will be little cereDral
congestion. The fluid effusion is usually clear ; if it is turbid one may
be certain that the fever is complicated by meningitis. The arachnoid
loses its natural glistening appearance, and in many instances one will find
the membrane dotted over with yellow or yellowish-white spots. The
brain undergoes little or no change unless the fluid effusion is abundant,
when by its pressure the sulci are deepened and the convolutions are
sharpened.
Abdominal Lesions. — In typhus and typhoid fever, the lesions found in
the abdominal cavity widely differ. The real pathological distinction is
in the presence or absence of intestinal changes. These are present in ty-
phoid and absent in typhus. In tyijhus fever there are no changes which
show a tendency to ulceration of the intestinal glands, except those which
are produced by congestion, such as are frequently seen in scarlet fever and
measles, where the Peyerian patches present the shaven-beard appearance ;
while in typhoid fever, either ulceration of the intestinal glands will be pres-
ent, or the glands will present the apjDearance which just precedes ulceration.
At the post-mortem examination, if ulceration of the agrainated and sol-
itary glands is found, one may be certain the patient died of typhoid fever.
The presence or absence of intestinal changes settles the question as to
whether the fever is typhus or typhoid. '
Complications. — Although the complications which occur in the course
of typhus fever are in no way peculiar to it, yet they are of such frequent
occurrence, and are developed during its active progress, and modify its
phenomena to such a degree, that it is necessary that they should be taken
into account in the study of its pathological lesions. These complications
will vary according to the peculiar type of the epidemic which is prevail-
ing. In one epidemic the complications will be pulmonary, in an-
other they will be almost exclusively cerebral and spinal, in another nearly
all will be glandular in character. The pulmonary complications are bron-
chitis, pneumonia, pleurisy, pulmonary congestion, and oedema. In most
cases these pulmonary complications are developed during the primary
fever, before convalescence commences. Their advent is always insidious.
An extensive capillary bronchitis may develop with very few of the rational
symptoms of bronchitis until within a short time previous to the death of
the patient ; in fact, the bronchitis might pass unrecognized but for the
presence of its physical signs. All the rational symptoms of pneumonia
may also be absent and still a physical examination of the chest may reveal
1 Lebert states that rarely, in epidemics, small ulcers of Peyer's patches and of solitary glands and
swelling of the mesenteric glands have been seen. (Ziemssen's Encyc.)
TYPHUS FEVEE. 713
a whole lung in a state of pneumonic consolidation. The pneumonia which
complicates typhus is usually hjrpostatic. It sometimes leads to pulmonary
gangrene. At most of the autopsies there will be found pulmonary con-
gestion and oedema. In many cases when these are associated with capil-
lary bronchitis or pneumonia they are the immediate cause of death. Lar-
yngitis is often associated with more extensive bronchitis which occurs
during the active part of the fever.
The only cerebro-spinal complication which is met with in typhus fever
is meningeal inflammation. As has been stated, in a large majority of
autopsies of typhus fever serum is found in the meshes of the pia mater,
but that is not a certain sign that meningeal inflammation has existed prior
to death. In addition to the subarachnoid effusion, there must be an ex-
udation of plastic material into the meshes of the pia mater, causing it
to become thicker than normal. When such appearances are found it shows
that the case has been complicated by meningitis.
Glandular Enlargements. — The glandular enlargements and inflam-
mations which occur in the course of typhus fever are peculiar in their
character, and are rarely met with in typhoid, and then are not extensive ;
but in typhus fever the superficial glands — especially those about the neck,
the parotid and subling-ual— often become so much enlarged and inflamed
as to interfere with deglutition, and not infrequently these glandular en-
largements are apparently the immediate cause of death.' The inguinal
glands sometimes become so enlarged as to interfere with the return circu-
lation, and, as the consequence of this interference, swelling of the lower
extremities may be developed. The bronchial glands are nearly always en-
larged and softened. There is a swelling of the lower extremities which
depends upon a different cause. It may occur at the beginning of con-
valescence ; then the limbs will present very nearly the same appearance
as that noticeable in the condition called phlegmasia dolens. Under such
circumstances phlebitis might be suspected.
It has been stated that the voluntary muscles undergo a peculiar waxy or
vitreous degeneration, and that the same kind of degeneration occurs in
the muscular tissue of the heart. When this does occur the walls of the
heart become very flabby, and when this change has reached a certain point
there is developed a tendency to the formation of clots in the heart cavities,
and a slowing of the general circulation. The result of such retarding or
obstruction of the return circulation is the formation of thrombi in the
superficial veins, which interfere with the venous circulation, and a swell-
ing of the lower extremities follows ; this closely resembles that which is
seen in phlegmasia dolens. With this swelling of the lower extremities,
suppuration and cellular inflammation may occur, which often result in
the formation of quite extensive abscesses. '^
Diseases of the organs of special sense, which so frequently compli-
' Lebert regards enlargement and suppuration of the parotid as a very dangerous complication.
2 It is an established fact that whenever the return circulation is slowed from any cause in any disease
where there is great feebleness of heart power, thrombi are liable to form in the veins of the lower
extremities. This is often well illustrated in the later stages of phthisis, when swelling of one or both
lower extremities occurs as the result of the formation of venous thrombi in the superficial veins.
714 ACUTE GENERAL DISEASES.
cate typhoid, rarely occur in typhus fever, and there are no serious or
constant complications of the digestive organs ; the gastric mucous mem-
brane is sometimes softened, reddened and mammilated.
Etiology, — At the present day this fever is regarded as depending upon a
specific i)oison, of whose exact nature we are ignorant. AU observers agree
that in the majority, if not in all instances, it is the product of contagion,
and that the contagion only emanates from the bodies of those who are
affected with the fever. Careful clinical observation has established the
fact beyond a doubt that there exists a specific typhus poison which can be
communicated from the sick to the healthy, which some declare is never
of spontaneous origin, while others maintain that the poison may be
generated '^^e novo," Some have strenuously maintained that it can be
developed by overcrowding and filth ; others, who have seen the largest
number of typhus fever cases during the past ten years, maintain that it is
at least very doubtful whether typhus fever is ever of spontaneous origin.
It is possible to develop a fever from overcrowding, imperfect ventilation,
filth, and a combination of causes belonging to this category, but such a
fever is not typhus.
The results of my investigation of the origin of the epidemic of typhus
fever which prevailed in New York, from July, 1861 to 1864, have led me
to the belief that typhus poison is of endemic origin — in other words, that
there are certain endemic centres ; that Ireland, Italy, and Russia are the
great centres, and that, whenever it occurs in other localities, it has been
conveyed from these endemic centres to those localities. ' The histories of
those cases which were developed within the limits of the hospital, showed
that a residence in an atmosphere necessarily more or less tainted with
typhus poison, is not sufficient to develop the disease, but that it is neces-
sary for the subject of the contagion to have been brought in contact with
an infected person, or within the atmosphere immediately impregnated
with his exhalations. The fact that no employee in the hospital who was
only brought in contact with the clothing of fever patients contracted the
disease, as well as the absence of any evidence that the disease was propa-
gated by such clothing, goes far to show that typhus is not readily propa-
1 In the month of July, 1861, fourteen cases of typhus fever were admitted in one day to the fever wards
of Bellevue Hospital, of which wards I had the charge. Previous to this time, for several years (I think
for more than ten years), there had been no case of typhus fever in the wards of the hospital. limme-
mediately commenced investigations in order to ascertain the oris^iii of the fever in these cases. I found
that it had its origin in the upper story of a rear tenement-house in Mulberry Street, in the most filthy por-
tion of the city. The first case was that of a little girl, who had been brought into the house, ten days be-
fore she sickened, from a ship which had come from Ireland, and which had cases of t}'phus fever on
board. Two weeks after her illness commenced, her aunt, the only other occupant of the apartments (con-
sisting of a room and dark bed-room), sickened of fever and died. In gradual succession, nearly every
family residing in the building took the fever. Becoming frightened, some of these families moved into
other streets, formed the nucleus for the development of the disease in the different localities to which
they removed, and it soon became a wide-spread epidemic. There were two hundred tj'phus fever patients
at one time in the hospital. These families were as well nourished and lived in as well ventilated apart-
ments as thousands of their class in other parts of the city. The only difference was that typhus poison
was brought to them in the person of the little girl, and, on account of their badly ventilated apartments
and their utter disregard of all hygienic laws, they furnished a fit soil for the reproduction and spread of
that typhus poison, the constant and unrestrained intercourse between the healthy and the sick being the
means by which the fever was spread. I found unmistakable evidence that persons living in healthy locali-
ties, simply by visiting friends sick with the fever, contracted the disease.
TYPHUS FEVER. 715
gated by fomites alone,' although most authorities claim that it can be
thus propagated ; that it is thus that ships, barracks and jails become hot-
beds of it ; that the poison may be latent and held in garments, especially
those that are dark and woolen. The certainty with which every unpro-
tected person who was brought in personal contact with fever patients con-
tracted the disease, proves the contagious power of the poison.
The distance that typhus poison can be transmitted through the atmos-
phere (from the manner in which the disease was contracted by some of the
house physicians), would seem to be limited. It has been proved by actual
expei'iment that the contagious distance of small-pox, in the open air, does
not exceed two and one-half feet, and it would seem that the contagious
distance of typhus fever is even less.^ Typhus poison is undoubtedly
present in the body exhalations and the expired air of typhus fever patients;
but it requires a concentration of the poison to render it infectious. Slight
exposure is not sufficient ; it requires a concentrated j)oison and a prolonged
exposure. The more numerous the typhus fever patients are, the more power-
ful does the contagion become ; yet a single exposure even to such an atmos-
phere is rarely sufficient to develop the disease in an individual who is in
good health at the time of the exposure.
The length of the period of incubation varies. It usually requires about
two weeks of exposure such as comes to one who is around those sick with
the fever. Eepeatedly have I noticed this fact in my own case. I have
never had typhus fever, and have never taken special care to avoid infec-
tion. My immunity is probably due to some special constitutional idiosyn-
crasy. I have noticed that whenever I enter upon a typhus fever service I
do not experience any effects from the exposure to typhus poison until after
about two weeks ^ have elapsed, then I begin to suffer from a peculiar form
of headache which continues for about two weeks ; the period before the
commencement of the headache corresponds to the period of incubation,
and the period of headache to the average duration of the disease.
The established belief is that typhus fever attacks an individual but
once, and that those who have had typhoid fever are to a certain degree pro-
tected from typhus. Of all the typhus fever patients treated in Bellevue
Hospital, only three gave histories of having previously had the disease.
From these facts one may reach the following conclusions : —
First. — That typhus fever is due to a specific poison.
» In Quains Dictionary it is stated that It is " not carried by clothing or excreta, and free dilution with
fresh air destroys its virulence."
2 The question now arises :— can this poison be conveyed in the clothing ? During the epidemic to which
I have referred, when typhus fever patients were brought into the hospital, their clothing was removed in
the reception-room and afterward washed and packed away in a lower room of the building. Upon a most
thorough investigation made at that time, I found that not a single person contracted the disease whose
duty it was to wash or pack away the clothing; but every one whose duty it was to carry the fever patients
from the reception-room to the hospital ward took the fever. Every physician and nurse who had the care
of typhus fever patients 'contracted the disease ; those who were on the surgical service escaped. Every
clergyman who came to administer spiritual consolation to the patients in the fever ward fell a victim to
the disease. I have brought forward these facts to show that duiing this epidemic there was no evidence
that the disease was either of spontaneous origin, or that it was transmitted from the sick to the healthy,
except by direct personal contagion.
8 Lebert puts five to seven days, and Murchison says, " no longer than twelve days '" for the period of
incubation ; one week is the average ; some patients have the fever one-half to two hours after first and
second exposure (St. Thorn. IIos. Eep., vol. ii.).
716 ACUTE GENEEAL DISEASES.
Second. — That this poison is communicated from the sick to the healthy
mainly by personal contagion — that is, the recipient of the poison must be
brought in contact with the personal exhalations of the infected person.
Third. — That where there is free ventilation, personal contagion is con-
fined to narrow limits.
Fourth. — That the evidences of the spontaneous origin of typhus are not
conclusive, although there can be no question but that overcrowding and
bad ventilation favor its spread and increase its severity.
Fifth. — Typhus poison passes into the body mainly through the respired
air. Whether it can be taken into the system in the food and drink is still
an unsettled question.
Sixth. — Immunity from a second attack is enjoyed after the first in a
large majority of cases.'
Symptoms. — An outline of the phenomena which attend the development
of typhus will first be given and afterward some of its more prominent
symptoms will be considered in detail.
Its advent is usually sudden ; there are no constant premonitory symp-
toms. In some cases, for a few days, there may be a feeling of indisposi-
tion, perhaps of headache, restlessness at night, nausea, loss of appetite,
and vertigo ; but in a large majority of cases it is ushered in by a distinct
chill. This differs from the chill of pneumonia or that of malarial fever,
in that it is short, sharp, and sudden. It may amount to nothing more
than a chilly sensation. There may be several chilly sensations on the day
of attack with distinct intervals between them. Following the chill there
is a severe and steadily increasing headache ; it is frontal and increases in
intensity from hour to hour. This is accompanied by a more or less severe
pain in the back and limbs, especially in the thighs. The headache of
typhus is more constant and persistent than that which attends the devel-
opment of any other fever ; usually, after a few days it diminishes in inten-
sity. Headache is associated with dulness and confusion of mind, and in
the case of children with vomiting. A sense of extreme prostration very
soon follows the ushering-in chill.
In some cases the patient is compelled, within twenty-four hours from
the commencement of his sickness, to take to his bed from muscular weak,
ness. This loss of muscular power will sometimes show itself by the un
steady, tottering gait of the patient, and is more marked in the early stage
of typhus fever than it is in any other disease. At one time, while I was
making my visit in the fever ward, my house physician, who was sicken-
ing from typhus fever, staggered and fell by my side from loss of muscular
power. He died on the eighth day of the disease.
Within the first twenty-four hours after the chill the temperature may
rise as high as 105° or 106° F., although at the same time the patient
may complain of a chilly feeling, and will draw up to the fire or cover
himself with blankets. It is a peculiarity of this fever that, during the
1 Lebert say8 : " all agree that the disease is spread by a typhus germ. Some say it is microsphere ,
others that it is bacteria, spiral forms, fungus, eic, etc. It must either be organic poison or organized
TYPHUS FEVEK. 717
first two or three days the patient experiences a sensation of coldness,
while the thermometer shows the temperature to range at 105° F. or
higher. During tlie iirst week of the disease the temperature remains at
104° F. or 105° F. There will be morning and evening variations, most
marked at noon and midnight ; but these variations follow no regular
course, as in typhoid fever. From the eighth to the fourteenth day the
temperature is liable 'to sudden depression. Asa rule, the temperature
falls between the eighth and fourteenth days. There is, without doubt, a
day of crisis in this disease. Just before the critical fall in temperature
there may be an abrupt temporary rise of 3° or even 4° F. In typical cases,
before the fourteenth day there is a marked decline, and often a sudden fall
in temperature. By the beginning of the second week the temperature
ranges at its highest. If there is a sudden rise in temperature during the
second week, it is almost certain evidence that some complication exists.
At first the tongue is swollen and covered with a white coating. It pre-
sents very much such an appearance as is seen in many nervous affections.
As the disease progresses, after a day or two it assumes a yellowish-brown
color, and the coating becomes thicker ; later it becomes dry, dark and fis-
sured. Nausea is sometimes present, rarely vomiting. The abdomen is
free from pain, except over the liver ; the bowels are constipated. Some
enlargement of the spleen can usually be detected quite early.
The pulse is accelerated from the very beginning of the fever, ranging
from 100 in the morning to 110 or 130 in the evening ; the acceleration is
greater in children than in adults. At the onset of the fever the pulse is
full, but it soon becomes soft and compressible, and finally feeble. It is
rarely dicrotic. It is only in the severest cases, just pi-ecediug death, that
the pulse becomes irregular and intermitting. The face is flushed, the
conjunctivas injected, the expression of countenance is dull, heavy, and
weary, and as the fever progresses, the cheeks assume a mahogany color.
The sleep is disturbed, and when the patient is awake his mind is con-
fused ; in very severe cases delirium is very early present, and the patient
needs careful watching at night.
Between the fifth and eighth, usually on the fifth, day of the disease, an
eruption makes its appearance upon the surface. The skin is extremely
hot, and there is no tendency to perspiration. It appears first upon the
sides of the abdomen, and gradually extends over the whole anterior portion
of the body, except the face and palms of the hands. In a few cases it first
appears on the back of the hands and wrists. It is more marked upon the
trunk than on the extremities. At first the eruption consists of dirty pink-
colored spots, varying in size from a mere point to three or four lines in di-
ameter. These spots are slightly elevated above the surface, and temporarily
disappear on firm pressure. After a day or two the eruption becomes darker
in color, and assumes a purplish hue. It is no longer elevated above the sur-
face, does not entirely disappear on firm pressure, and the spots have no well-
defined margin. Thiserujotion is made up of irregular spots, varying from
a point to two or three lines in diameter, either isolated or grouped to-
gether in patches, presenting a very irregular outline ; in children it often
718 ACUTE GENEEAL DISEASES.
resembles the eruption of measles. When the eruption is abundant it im-
parts to the skin a mottled aspect, which has giyen rise to the term " mul-
berry rash " of typhus. Another distinctive peculiarity is, that each spot
or patch remains visible from its first appearance until convalescence is
established or death occurs, and it is often seen upon the bodies of those
who have died of typhus fever.
In some cases of typhus there are only a few spots of the eruption, while
in other cases they are very abundant, and the surface of the body -pve-
sents a v/ell-marked mottled appearance. In a certain proportion of
cases, after the eruption which I have just described has been visible for a
few days, there will appear, scattered over the surface, small dark spots,
due to minute subcutaneous hemorrhagic extravasation ; these are called
petechias. On this account the disease \\2i&\iQQn(i2i\\Qdi petechial typhus;
but these petechige are by no means distinctive of typhus, for they are also
met with in other diseases. The majority of cases of typhus which one
meets will have no eruption except the "mulberry rash." When the
petechial spots are present they indicate a severe form of the disease,
and more extensive blood-changes than usual. This mottling or marbling
of the skin begins as the mulberry rash fades ; it appears once for all — 7iot
in crops — and resembles slightly the rose-rash of typhoid fever. It is the
subcutaneous eruption, so-called.
In all severe cases, at the close of the first week the headache, which
has been the most troublesome symptom, disappears, and delirium comes
on. The delirium will vary in character and severity in different epidemics,
being much more violent and active in some than in others. Sometimes
at the very outset of the disease the delirium is very active, the patient
shouts and talks more or less incoherently, and is more or less violent. If
not restrained, he may throw himself out of the window. This period of
intense nervous excitement may last two or three days, during which the
countenance becomes livid, the conjunctivae injected, the hands tremulous,
and suddenly the patient may pass into a state of apparent coma. It is
not that of complete coma, for the patient can be easily aroused ; but he
lies upon his back, with a tendency to slip down in bed, picking at the bed-
clothes. The mental faculties, the special senses, are all blunted, and the
patient is in a condition of stupor for three or four days preceding the
delirious period, and sometimes, when the delirium is not active, this
stupor lasts till the end of the disease. It is not a state of unconscious-
ness, although one of apparent coma, for the mental processes are going
on with great activity, and the imagination will conjure up a great variety
of horrid fancies, and the visions which pass before the patient will be dis-
tinctly remembered after recovery has taken place.
This condition has been called "coma vigil." During this period the
experience of years may be crowded into a day or an hour, and the patient
may feel that he has lived a lifetime while in this state. Those who have
the greatest mental power and possess the highest culture have the most
distressing fancies during this somnolent period. If, in this condition,
there is a tendency toward a fatal issue, the patient will pass into a more
TYPHUS FEVER. 719
complete stupor and the coma will become more and more profound ; the
respiration hecomes less and less frequent ; the pulse, which has i-anged
about 1:30 per minute, rises to 140 or 150, and finally becomes imperceptible
at the wrist ; the tongue, rolled into a round mass, becomes brown and dry,
so that the patient is unable to protrude it from the mouth ; or, if he pro-
trude it, he does not withdraw it until asked to close his mouth ; sordes
collect upon the teeth ; the conjunctivae are red, and the eyes, when open,
present a leaden appearance. The face has a dusky pallor. The patient
has no longer power to move his body ; he lies on his back with his head
thrown back, perhaps is only able to make slight tremulous motions with
his hands. There may now be some intestinal catarrh, with diarrhceal dis-
charges. The urine collects in the bladder, and, if not removed with a
catheter, dribbles away. The extremities become cold, but the body tem-
perature remains at 105° F., or it may rise as high as 107° or 108° F. In
one case under my observation it rose to 110° F. just preceding death, while
the extremities were cold.
If the case is tending to a favorable termination, about the tenth to the
fourteenth day of the fever there is an amelioration of all the symptoms.
The patient falls into a quiet sleep, from which he awakes conscious and
convalescing. The pulse and temperature fall, the tongue becomes clean
and moist, the delirium subsides, and there is a desire for food. After two
or three days the pulse reaches its normal standard and strength gradually
returns. Critical sweats, diarrhoea, and large flows of urine are not infre-
quent occurrences.
This is an outline of the progress of the disease in a severe case of typhus
fever, terminating either in death or in recovery. In a mild case there will
be no delirium. The temijerature may not rise above 102° F. ; the tongue
is neither brown nor dry. There is no great acceleration of the pulse,
the rate never being over 120 per minute, and that only for a very short
period. During the entire course of a severe or mild case, there is no
gastric or intestinal disturbance, no diarrhoea, no distention of the abdo-
men, no pain in the right iliac fossa, no gurgling — in a word, no abdomi-
nal symptoms. In mild cases the erT-T^tion is never very abundant, but
it appears on the fifth day, and remains visible until convalescence is
established.
Those more important sym.ptoms which determine the character of the
fever will be considered in detail. As has been already stated, symptoms
indicating disturbance of the nervous system are among the earliest and
most prominent. Of these, headache is the most constant. For the first
week or ten days it is severe and persistent, after which time it gradually
abates and disappears towards the close of the second week ; it is confined
to the forehead and temples, rarely to the occiput.
Delirium comes on usually about the eighth day ; sometimes it is pres-
ent at the onset of the disease. At whatever period it may be developed,
it will continue until the termination of the disease. Delirium is preceded
by a dull, apathetic state, which follows the abatement of the headache.
At first it shows itself at intervals during the night, or lasts all night to
720 ACUTE GENEKAL DISEASES.
disappear during the day. Its character varies from a low, muttering form
to a very active and noisy delirium. Every possible variation is met with
during an epidemic of typhus fever.' Acute delirium is more liable to be
present with the intelligent and highly cultured, while the delirium is usu-
ally low and muttering in character in the case of the aged or uncultured :
other things being equal the intensity of the fever can be measured by the
kind and amount of delirium.
Stupor or somnoletice in some degree is seldom absent. It may develop
with or without previous delirium. Usually, as the case progresses toward
a fatal termination stupor comes on ; this becomes more and more profound
as the disease advances. The patient often lies for hours apparently un-
conscious, with his eyes open as though awake, but he is absolutely indif-
ferent to all that is going on around him. This is another condition to
which the term ^' coma vigil " has been applied. It is almost invariably fol-
lowed by a fatal termination. Sometimes coma comes on suddenly, without
any antecedent somnolence ; under such circumstances the urine will be
found loaded with albumen.
Loss of muscular strength is an early and striking symptom. In the
majority of cases it is present from the very first day of the fever. In many
cases, as the fever progresses, the loss of muscular power is so great that
the patient is unable to turn in bed ; the prostration always increases as
the disease advances. In some cases there is little loss of strength during
the first week, but the prostration comes on suddenly during the second
week.
In addition to the general loss of rauscular power, in certain cases there
is paralysis of some muscles, such as the sphincter ani and the muscles of
the bladder, so that the urine and faeces are discharged involuntarily. Dys-
phagia, partial or complete aphonia, and inability to protrude the tongue,
are common symptoms. Muscular tremor is an indication of very great
muscular prostration, and is usually met with in the aged and infirm and
in those who have been addicted to the use of intoxicating drinks. Muscu-
lar spasms and subsultus tendinum are present to a greater or less degree
in all severe cases ; the tendons of the wrist are most frequently affected.
One form of these spasmodic movements is manifested by the patient's pick-
ing or fumbling the bed-clothes ; another by obstinate hiccough. Trismus,
strabismus, and in rare cases opisthotonos, have occurred. All these symp-
toms must be regarded as grave. Emaciation is never a marked symptom.
It is rarely present to any great degree before the third week of the fever. '^
Temperature. — During the first week of typhus fever there are no such
marked typical variations in temperature as are met with in typhoid — none
that will enable one to make a diagnosis. Usually the temperature rises
rapidly from the very onset of the fever, and in cases of average severity
1 The incoherent, nonsensical muttering is beyond the control of the patient, who is himself aware of
its disjointed and erratic character.
2 The eyes at first are suffused ; later the conjunctiva becomes dry. The pupils are contracted and are
insensible to light in many cases. Vertigo, dizziness, noises in the head, partial and even complete deaf-
ness are observed. Coryza, epistaxis, slight hypersesthesia, and, finally, general anaesthesia, are infrequenr:
symptoms.
TYPHUS FEVER.
721
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attains its maximum from the third to the sixth day. At this period the
evening temperature will range
between 103° F. and 106° F. In
severe cases, the maximum tem-
perature is not reached until the
eighth or tenth day. Before the
temperature reaches its maximum,
the morning and evening varia-
tions are slight, about 1° or 1^° F.
After the temperature has reached
its maximum for several days there
will be little change, but at some
time, usually between the seventh
and tenth days, there will be a
slight remission until the twelfth p,g j^g
or fourteenth day, when it rapidly Temperature Kecord m a Case of Severe Typhus Fever,
„,,.,., L^ L X. ■ ending in Recovery.
tails, m typical cases that termi-
nate in recovery, to its normal standard. Any sudden rise or fall (except
in crisis) indicates a complication. Occasionally an elevation of two or
more degrees precedes the fall. This sudden fall about the fourteenth day
is peculiar to typhus. The fall may amount to 4° or 5° F.
A very high range of temperature during the first week is an indica-
tion that severe cerebral symptoms will be develoj)ed during the second
week of the fever. A case of typhus fever may terminate fatally, in which
the temperature at no time has exceeded 103° F. In all fatal cases, just
-preceding death there is usually a rise of from 2° to 5° in temperature.
During the first week of convalescence the temperature often remains below
the normal standard, especially in the morning.
Pulse. — The pulse in this fever is usually frequent, soft, easily com-
pressed, and often irregular. The heart may partake of the general muscular
weakness, so that the first sound may become inaudible. There is a soft sys-
tolic C fever") murmur heard over the heart. In the severe cases, during
the first week the pulse may reach 120 beats per minute, after which time
it increases in frequency and feebleness with the severity of the general
symptoms. By the third day it may reach 120 beats per minute ; usually in
the milder case it does not exceed on that day 100 beats per minute. If
during the first week it continues for three consecutive days so frequent as
120 beats per minute, it indicates danger. The rate may be 106 in the
morning and 120 in the evening. The higher the temperature, and the
more frequent the pulse during the first week, the more severe will be the
symptoms during the second week. If during the second week it becomes
small, feeble and frequent, perhaps beating 140 or 150 per minute, the case
may be regarded as unfavorable. Absence of pulsation in the radial artery
for several days has been observed, and is explained on the ground of embolic
obstruction of the medium-sized vessels.
During the first week, if the pulse increases in frequency the temperature
rises, and if the pulse diminishes in frequency the temperature falls ; but
46
72-i ACUTE GEKERAL DISEASES.
during the second week the pulse may increase in frequency, and the
temperature fall, or it may diminish in frequency and the temperature rise.
The pulse is not an infallible guide as to the condition of the heart, for
sometimes the pulse is full and distinct, while the heart power is yery feeble ;
on the other hand, the cardiac pulse may appear strong and the sounds
distinct, and yet the radial pulse may be im]3erce]otible. In most fatal cases,
after the first week the radial pulse becomes imperceptible for several days
prior to death. Although in most severe cases there is a rapid pulse, yet a
slow pulse does not necessarily indicate a mild attack. In some severe and
fatal cases the pulse may never be over 100.
Eruption. — The general character of the typhus eruption has already
been described. Its appearance is preceded and accompanied by a bright
redness of the whole surface, on which dark red spots are scattered, giving
the skin a mottled appearance '' sub-cuticular rash." These spots have
an irregular outline, and vary in size from a point to three or four
lines in diameter. Sometimes they are few in number, but more com-
monly they are numerous ; the large spots are formed by the coalescence of
the smaller ones. It is a macular, not a papular eruption. At first they
have a dusky pink hue, partially or wholly disappearing on pressure, and
as the finger passes over them they seem to be slightly elevated. After a
day or two they assume somewhat of a brick-dust color, and are but slightly
changed by pressure ; then the color of the spots becomes darker in hue,
and finally they are not affected by firm pressure. Another peculiarity is
that each patch or cluster remains visible from its first appearance until
the termination of the disease. The eruption may appear upon any por-
tion of the body. Usually, it first makes its appearance upon the trunk, soon
spreading to the extremities ; very rarely is it seen on the face. When the
eruption is scanty, it is limited to the chest and abdomen. In some pa-
tients the eruption, though well developed, is not prominently marked;
the spots are pale 'and undefined ; and though grouped in patches are so
irregular that they give to the entire surface a faint, dingy appearance.
Blood-extravasations into the centre of the typhus spots may occur at the
end of the second week.
Respiration. — Usually, during the first week the respirations do not ex-
ceed twenty or thirty per minute ; but during the second week they often
run up to forty or fifty per minute. In cases where there is great prostra-
tion accompanied by stupor, the respirations sometimes fall to eight or ten
per minute. Under such circumstances they are often irregular and pufiing
in character. Hypostatic congestion of the lungs, if extensive, is attended
by great frequency of respiration and evidences of cyanosis. The occur-
rence of these changes in respiration ought always to lead to careful exam-
ination of the chest.
The digestive system is very little disturbed in typhus fever. Nausea and
vomiting are rare, and an examination of the abdomen presents nothing
abnormal. There is no tympanitis or tenderness on pressure. Spontane-
ous diarrhoea is of exceedingly rare occurrence ; the bowels are generally
constipated. Intestinal hemorrhage is of rare occurrence, and wheu it is
TYPHUS FEVEE. 723
present depends either upon congestion of the mucous membrane of
the colon or on hemorrhoids, which accompany an engorged portal circu-
lation.
Urine. — The urine in typhus undergoes important changes. The quan-
tity varies somewhat with the amount of fluid taken into the stomach ;
usually, it is diminished during the first week to one-fourth or one-half the
normal quantity. In the advanced stage of severe cases there is sometimes
complete suppression of urine, but more frequently the quantity of urine
increases during the later stages of the fever. The reaction is first acid, later
neutral or alkaline. The quantity of urea excreted in twenty-four hours
during the first few days of the fever is increased, and the increase is in
proportion to the intensity of the fever. In the majority of cases it remains
abnormally increased until the period of crisis is reached, when it gradu-
ally, or in some instances rapidly falls below the normal standard. Uric
acid is similarly increased. The chlorides grow less and less till the second
week, when they disappear. In all severe cases, during the first week of the
disease, a small amount of albumen is found in the urine ; when the quan-
tity is large the case may be regarded as severe. In the severe cases the
urine will also be found to contain vesical and renal epithelium, and when
the quantity of albumen is large, epithelial and fatty casts of the urinifer-
ous tubes will be present with blood.
In this connection it is important to bear in mind the necessity of daily
inquiry into the expulsive power of the bladder. When there is little cer-
ebral disturbance, the urine is passed without difficulty ; but when stupor
and a tendency to coma exist, there is often retention or an involuntary
dribbling of urine, which might lead one to think that there was no ac-
cumulation of urine in the bladder. It is safe to inquire at least once a
day as to the state of this organ, and if involuntary discharges of urine
occur, the contents of the bladder should be evacuated by means of a
catheter. Copious sediments form in the urine on the day of crisis.
Differential Diagnosis. — Before the appearance of the eruption, the diag-
nosis of typhus fever is always difficult, and sometimes impossible. The
diseases with which it is most liable to be confounded are typhoid fever,
relapsing fever, measles, pneumonia, acute Brighfs disease, meningitis,
delirium tremens, and some of the other acute blood diseases, such as
erysipelas, pycemia, septiccemia, etc.
The early characteristic symptoms of typhus fever are chilliness, pain in
the back and limbs, and headache. During the first week the headache
increases in severity from hour to hour, and is accompanied by a rapid rise
in temperature. These symptoms occurring in one who has been exposed
to typhus poison are always sufficient for a diagnosis. The a23pearance of
the eruption settles the question. On account of the similarity in appear-
ance of the eruption of typhus fever and that of measles in children, the
one disease is sometimes mistaken for the other. In both diseases the erup-
tion may appear on the fifth day, but the eruption of measles is of a brighter
tint than that of typhus fever, and its appearance is preceded by a cough
and coryza, which are not present in typhus fever.
724 ACUTE GENERAL DISEASES.
Meningitis. — The differential diagnosis between typhus fever and cerebro-
spinal meningitis is often difficult. Not infrequently, days may elapse be-
fore one is able to decide whether a case is one of typhus fever or of cerebro-
spinal meningitis.^ The distinguishing points between the two diseases
are as follows : — the headache of meningitis, at the outset of the disease,
is much more distressing than that of typhus, and it alternates with delir-
ium. When delirium comes on in typhus fever, the pain in the head ceases.
Vomiting is prominent in meningitis, absent, as a rule, in ty|)lius. Photo-
phobia and contracted pupils are among the early symptoms of meningitis,
and the patient is greatly disturbed by noise, while in typhus fever he seems
indifferent to both. Dulling and blunting of all the senses are common
in typhus. All the senses are abnormally acute at the onset of meningitis.
Inequality of the pupils, strabismus, ptosis, and paralysis are common in
meningitis and rare in typhus. In meningitis the countenance is pale and
expressive of pain, wildness, and anxiety ; in typhus fever it is dusky,
blank, and stupid. Convulsions are an early symptom in meningitis and
rare in typhus. Again, in meningitis the pulse is hard and wiry, rapid
and irregular, and at the last intermitting ; while in typhus fever it is
rapid at the onset of the disease, easily compressed, full and bounding.
Lastly, the eruption of typhus fever is characteristic. If an eruption is
present in meningitis, it has no regularity in its development ; it may ap-
pear within twenty-four hours after the development of the first symptom
of the disease, or it may be postponed for several days. It does not appear
on the fifth or sixth day of the disease with the uniform regularity of the
typhus eruption. Petechias may be present in meningitis as well as in
typhus fever, but they are not characteristic of either disease. The tem-
perature rises rapidly in typhus, and reaches a higher range, e. g., 104° to
106° in twenty-four to forty-eight hours ; while in meningitis the average
temperature on the second and third days — indeed, during its entire course —
is 102°, often loioer. Eigidity of the muscles of the neck is not always
positive evidence of meningitis, for it sometimes occurs in typhus fever.
The ataxia, muscular prostration, aiid character of the tongue in typhus
are also points that greatly aid in distinguishing it from cerebro-spinal
fever.
Pneumonia. — Sometimes a latent pneumonia with typhoid symptoms is
mistaken for typhus fever ; especially is this the case when the latter is pre-
vailing. I frequently saw cases where such a mistake had been made, while
in charge of the typhus fever patients on Blackwell's Island, during the
epidemic to which reference has been made. In these cases there will be
active typhoid symptoms, e. g., dry tongue, delirium, high temperature, etc.
The countenance in this pneumonia, although the cheeks may have a pur-
plish hue, does not exhibit that dull, heavy expression so commonly seen
in typhus. Although there may be delirium in both instances, the delirium
1 To show how difficult is the diagnosis between these two affections, a circumstance ma}' be men-
tioned which occurred in Bellevue Hospital . A patient was brought into the hospital directly from a
ship, and the diagnosis of cerebro-spinal meningitis was made by several of the attending stafE ; but at
the autopsy there were found none of the lesions of meningitis ; all the changes corresponded to those
found at the autopsies of patients djdng of typhus fever.
TYPHUS FEVER. 725
in the former disease is of a milder type than the latter. The characteristic
pneumonic expectoration is not usually present in these cases ; so that in
making the differential diagnosis this symptom cannot be relied upon.
The physical signs of pulmonic consolidation will lead one to diagnosticate
pneumonia, and unless the typhus eruption is present, this will be sufficient
for a diagnosis. If pulmonary consolidation is a complication of typhus
fever, it will not be developed until after the sixth day of the fever, the
time when the eruption should have appeared. If no eruption is present,
the pneumonic consolidation may be regarded as the primary affection, and
the symptoms which simulated those of typhus fever may be regarded as
secondary.
Delirium Tremens. — The delirium of alcoholism may sometimes so
closely resemble that of typhus fever that the one may be mistaken for
the other. Typhus fever patients have been placed in the cells under the
supj)osition that they had delirium tremens. If the delirium tremens is
uncomplicated by pneumonia, the temperature will suffice for the differen-
tial diagnosis, for in delirium tremens the temperature is rarely above 100°
P. There may be a rapid pulse in delirium tremens, and often the joatient
has a brown, dry tongue, and other typhoid symptoms ; but there is only
a slight rise in temperature ; besides, there is no eruption. The attack is
not ushered in by headache, but by an inability to sleep ; and the circum-
stances which precede and give rise to such an attack will establish beyond
a doubt the true nature of the attack.
Acute Bright' s Disease.— It is not surprising that acute uraemia should
be mistaken for typhus fever. The brown, dry tongue, the tendency to
stupor, the contracted pupil, the low, muttering delirium, and all the phe-
nomena of the typhoid state, as well as the albuminous urine, belong to both
diseases ; but the temperature is not raised in uraemia as it is in typhus
fever, and the oedema which is always present in acute uraemia is absent in
typhus fever.
Erysipelas, pycemia, septiccemia, and all similar acute Mood diseases are
often attended by many of the symptoms which attend the development of
typhus fever. In pyaemia and septicaemia there are irregular chills, followed
by fever and profnse sweats, with evidences of septic and pygemic poison-
ing; in erysipelas, there are evidences of a localized phlegmon. It should
not be forgotten that erysipelas is sometimes ushered in by all the phe-
nomena that attend the ushering-in of typhus fever ; this is before the local
inflammation shows itself. In such cases it is impossible to make a differ-
ential diagnosis until the local phenomena which characterize erysipelas
show themselves, or until the typhus eruption appears. In many of the
acute infectious diseases one is compelled to wait until the time for the ap-
pearance of the eruption before typhus fever can be excluded. When ty-
phus fever is prevailing and the physician is watchful for its appearance,
there will usually be little difficulty in diagnosis. Sometimes typhoid, ty-
phus and relapsing fever prevail at the same time in the same locality.
The importance of early forming a correct differential diagnosis between
typhus and typhoid fever cannot be over-estimated ; and to accomplish
736 • ACUTE GENERAL DISEASES.
■ .A
this, the prominent symptoms of each will be reviewed and compared.
The first point to be considered in the differential diagnosis of these two
diseases is, that typhus fever is sudden in its advent, while typhoid fever
comes on insidiously, and is slowly developed. In the majority of cases of
the former disease there is a chill at the commencement, and severe pain
in the head, whereas in the latter there is only a chilliness, some aching in
the limbs, and a slight headache. Muscular prostration and progressive
muscular weakness appear earlier, and are much more marked in typhus
than in typhoid.
The ranges of temperature in the two forms of fever differ greatly.
Typhoid fever commences, on the first day, with a slight rise of tem-
perature, which continues, with morning remissions and evening exacer-
bations, until the end of the first week, when it has reached its highest
point ; during the second week it remains at about the same height,
with only slight variations ; during the third week there are more marked
morning remissions ; and by the end of the fourth week the temperature
has reached its normal standard, by intermittent periods. In typhus
fever, the temperature rises rapidly, and before tJie end of the second day
reaches 104° F. or 105° F. Whatever degree is reached on the third
day may be regarded as the maximum temperature ; after this time
there are slight, irregular variations until the tenth or twelfth day, when
the temperature begins to fall, and rapidly reaches the normal standard.
In typhoid there is great emaciation ; in typhus it is slight, but the
exhaustion and muscular prostration are far greater than in typhoid. The
eruptions of these two foi-ms of fever differ very markedly. In typhus it
makes its appearance upon the fifth or sixth day ; while the eruption of
typhoid fever makes its appearance between the seventh and ninth days.
The eruption of typhus fever appears upon the arms and chest, and more
or less over the entire body ; whereas the eruption of typhoid appears upon
the chest and abdomen, very rarely upon the extremities ; sometimes it
appears upon the loins when it cannot be found on any other part of the
body. As a rule, the spots in typhus are numerous, while in typhoid they
are not very abundant. In typhus fever, the spots at first are small,
slightly elevated, of a dark pinkish hue, and disappear only on firm press-
ure. As the disease advances they become darker, and finally are not
affected by firm pressure, and remain visible from the time of their appear-
ance until death occurs or convalescence is established. In typhoid fever
each spot is rose-colored, slightly elevated, and disappears on slight press-
ure. Each spot remains visible for three days and then disappears, to be
followed by another crop. Usually the eruption is visible about two
weeks, and when it disappears it leaves the skin unstained, whereas in ty-
phus the eruption leaves a stain upon the surface. There is a mottling of
the surface in typhus fever, the mulberry rash, which is not seen in
typhoid.
The brain symptoms in these two diseases also differ. In typhus
fever they appear early, and the headache and delirium are more intense
than in typhoid. Delirium in typhoid more commonly appears at the
TYPHUS FEVER. 737
end of tlie second or during the third week of the disease ; whereas in
typhus it appears early, and before the end of the second week has disap-
peared if recovery is to take place. As a rule, in typhus fever constipation
is present, and a mild cathartic must be given to move the bowels ; whereas
in typhoid fever the pea-soup diarrhoea is a prominent symptom. Tym-
panitic distention of the abdomen, gurgling and tenderness in the right
iliac fossa, and intestinal hemorrhage, are all phenomena of typhoid fever,
but are never present in typhus fever. Epistaxis is frequent in typhoid
and not in typhus fever. In typhus fever convalescence will usually be
established before the end of the second week ; it may occur at any time
between the eighth and fourteenth days. The average duration of typhus
fever is fourteen days, whereas the average duration of typhoid fever is
from twenty-one to thirty days. Typhus fever is contagious, typhoid fever
is non-contagious.' Typhus fever is generally epidemic ; typhoid fever is
always endemic. In regard to the protection which one attack of typhus
fever furnishes against a second attack, it very markedly differs from ty-
phoid fever. One may have typhoid fever whenever the system has been
exposed to the typhoid poison ; but one attack of typhus is almost a cer-
tain protection against a second attack.
Prognosis. — The prognosis in this disease is always grave, and no opinion,
as to its termination, can be given until every point in each case has
been considered, such as the age of the patient, the character of the epi-
demic, and the tendency to certain complications. In all eiDidemics the
majority of cases will recover. The ratio of mortality, as given by differ-
ent writers, varies from one death in five to one death in sixteen cases.* The
surroundings of each patient should be carefully noted, also the hygienic
influences which he is under, and his habits of life should be taken into
account. With the intemperate the disease is likely to prove fatal. Some
of the circumstances which increase the danger in any particular case are
a debilitated condition of the patient from advanced age, intemperate hab-
its, privation, and previous disease ; mental depression, presentiment of
death, overcrowding and bad ventilation ; a gouty diathesis is always dan-
gerous.
Death may occur in typhus fever from three general causes : first,
from coma, the result of overwhelming the system with typhus poison.
The patient does not die from the effect of a prolonged high temperature,
nor from any complication, but dies as patients die in acute ureemia, be-
cause the system is overwhelmed by the typhus poison, and the functions
of organic life are arrested by its action on the nerve-centres.
' When the pathological lesions are studied and the manner in which death occurs in these two forms
of fever is considered, it can readily be seen how widely they differ. The characteristic pathological
lesions of typhoid fever are the changes which take place in the intestinal glands, such as ulceration or
tendency to ulceration. In all cases these characteristic lesions are present. Suppose a case of what has
been called typhoid fever is followed to the dead-house, and ulceration or evidences of a tendency to ulcer-
ation of Peyer's patches are not discovered, then it is certain a mistake in diagnosis has been made. If,
on the other hand, in a case of supposed typhus fever is found ulceration of Peyer's patches, it is equally
certain that a mistake has been made, and that a case of typhoid, and not typhus fever has been treated.
The parenchymatous changes which are common to both diseases have already been sufficiently con
eidered.
* Griesinger and Murchison state " that in cariixm epidemics fhQ mortality runs as high as 40 to 50 per
cent." An average epidemic shows about 15 per cent, of deaths ; a mild one, about 6 to 8 per cent.
72S ACUTE GENERAL DISEASES.
Death may occur, secondly, from syncope, due to heart failure, whethej*
the heart failure is the result of the prolonged high temperature, or the
direct action of the typhus poison. A continued temperature of 105°
or 106° F. is very liable to be followed by fatal syncope from failure of
heart power, although the evidences of parenchymatous degeneration of
the heart may not be present. Death may occur, thirdly, from complica-
tions. Although they do not properly belong to the primary disease, yet
they so modify it that they enter very largely into its history. In a large
number of cases which terminate fatally, death is due to some one of
these complications. In some epidemics they are all pulmonary ; in others
they are all cerebral. The advent of pulmonary complications is always
insidious ; the cough and expectoration which usually attend pulmonary
diseases are either absent, or so slight as not to attract the attention of
the physician. Eapid breathing and lividity of the face are often the first
obvious indications of extensive disease of the lungs. When these symp-
toms are present, a careful physical examination of the chest should be
made.
Bronchitis may come on at any period during the fever, and it may
continue after the fever has subsided. So long as it is confined to the
larger tubes there is little danger, but som.etimes suddenly and insidiously
it extends into the smaller tubes, and is complicated with pulmonary con-
gestion and oedema. Under such circumstances it may be the direct cause
of death. The pneumonia which complicates typhus fever is lolular in
character, and is frequently preceded or accompanied by bronchitis. It
has a tendency to terminate in abscess or gangrene. During life it is not
always possible to distinguish it from hypostatic congestion. If, however,
the dulness on percussion is confined to one lung, if the respiration is
bronchial, the diagnosis of pneumonia is readily established. The seat of
pneumonia is generally at the upper portion of the lung. Pleurisy
(serous or purulent) may occur.
Laryngitis is sometimes a very serious complication of typhus. The
common form is that of acute oedema glottidis. Its occurrence is readily
recognized by the signs of laryngeal obstruction which attend its develop-
ment. "Whenever there is extensive swelling of the glands about the neck,
with great tumefaction of the mucous membrane of the pharynx, one
must be on his guard for the occurrence of this comjDlication.
On account of the extensive blood-changes whiqh sometimes occur in
severe cases of typhus fever, the blood readily escapes through the walls
of the vessels, giving rise to extensive hemorrhages from the mucous sur-
faces, nose, gums, bowels, the genito-urinary tract, vagina, etc., and into
the cellular tissue. The occurrence of the hemorrhages is peculiar to
certain epidemics, and when they occur it is during the first week of the
fever.
Meningitis is probably the only cerebral complication which will be met
with in this fever. This occurs more frequently in children than in adults,
and is not present in every epidemic. The cerebral symptoms which are
such constant attendants upon typhus fever do not depend upon menin-
TYPHUS FEVEK. 729
geal inflammation ; they belong to the natural history of the disease. If,
during the course of the fever, there is a deep-seated jiain in the head, with
restlessness, which shows itself by constant attempts to get out of bed, with
photophobia, contracted pupils, and flushing of the face and eyes, followed
by somnolence gradually lapsing into coma, it is almost certain that men-
ingitis is occurring as a complication. This is most liable to occur during
the second, week of the fever. The characteristic symptom which marks
its development is the constant attempt on the part of the patient to
get out of bed. He is so persistent in this that unless watched with the
greatest care he will be found upon the floor, vainly attempting to rise.
The patient has more muscular power than before the occurrence of the
meningeal complication, for he will perform acts which previously he was
wholly unable to execute. Usually the delirium lasts two days, then the
patient gradually passes into a state of coma from which he cannot be
aroused ; his respirations may not be more than eight or ten per minute.
Dilatation of the pupils, and an intermitting and almost imperceptible
pulse, immediately precede death.
I regard most of the Tcidney changes as a part of the history of the fever
rather than as complications, although in some few instances croupous
nephritis occurs, and must be included in the list of complications. Its
occurrence in the course of typhus fever is indicated by the almost entire
suppression of urine, and by the presence of albumen and exudative and
blood casts in the urine.
Glandular swellings are also occasional complications of typhus fever,
and sometimes may be of a very serious nature, for they may so interfere
with deglutition and respiration as to destroy life. The parotid, the sub-
maxillary, axillary and mammary glands may enlarge and suppurate. These
swellings usually appear immediately after ihe crisis of the primary fever.
They often enlarge with great rapidity, and in some instances terminate
in extensive suppuration.
Bed-sores are rather infrequent. Gangrene, necrosis, cancrum oris, sup-
purative cellulitis, purulent arteritis — all have occurred in various epidem-
ics, and render the prognosis unfavorable. If menstruation occur in a
female with typhus, the bleeding is commonly very profuse and may cause
death from acute anaemia.
Duration. — The average duration of the fever is thirteen or fourteen
days. Usually the day of crisis is between the tenth and sixteenth days.
It is of shorter duration in the young than in the old, in children
than in adults.' Relapses are extremely rare in this fever. I have met
with a second and third attack of the fever in the same individual, but I
have never met with a true relapse. Typhus fever varies very slightly in
its general character and different cases. A number of different varieties,
depending upon the mildness or severity of the disease, the prominence
of certain symptoms, the presence of comjDlications, and the circum-
stances under which fever appears, have been described, but the general
' In .'jOO cases ending in recovery, thirteen and a half days was tbe average ; and in 100 fatal cases, the
duration was fourteen and a half days.— Murchison.
730 ■ ACUTE GE]SfEEAL DISEASES.
description already given includes that of (so-called) " varieties " of
typhus/
The individual symptoms and signs which render the prognosis unfavor-
able are as follows :
A pulse continuing a number of days at more than 120 per minute,
becoming at times intermittent and irregular, bespeaks an unfavorable
prognosis. A hurried and difficult respiration, with turgidity of the face,
due either to cerebral or pulmonary oedema, renders the prognosis unfavor-
able.
Delirium which is very active and accompanied by great muscular pros-
tration, as indicated by subsultus, slipping down in bed, and accompanied
by that condition known as "coma vigil," lasting for a number of days, is
almost a certain indication of a fatal termination.
The " pin-hole pupil, ^' mentioned by old writers, is an unfavorable omen.
It does not necessarily indicate the presence of meningitis, as was once
supposed. Great muscular prostration at the very onset of the disease
renders the prognosis unfavorable.
Sudden fading of the eruption, and a widely expanded pupil may be
regarded as unfavorable signs. Marked impairment of the special senses,
accompanied by very great rapidity of the pulse, is an element of unfavor-
able prognosis.
The darker and more abundant the eruption, especially if accompanied
by petechial spots, the more unfavorable the prognosis. In children the
eruption is lighter in color than it is in adults, presenting an appearance
similar to the typhoid eruption. In adults where there is dark mottling of
the surface confined to the extremities, with evidences of blood extravasa-
tion, indicated by the presence of petechise, the prognosis is unfavorable,
but the case is by no means hopeless.
A dry, brown, retracted, tremulous tongue is seen only in severe cases.
A long-continued high temperature is always an unfavorable symptom.
Great diminution in the quantity of urine is an unfavorable symptom, as
also is the presence of casts and albumen in the urine. Eetention of urine
is a more unfavorable symptom than incontinence ; convulsions and coma
are liable to follow such retention. It is to be remembered that in typhus
fever, more than in any other disease, patients pass into an apparently
hopeless condition, and afterward rally and recover. A patient who seems
to be overwhelmed with the poison, who has "coma vigil," "pin-hole
pupils," rolling of the tongue, and a feeble, irregular, and intermitting
pulse, may recover, although these symptoms warrant an unfavorable
prognosis ; but "coma vigil " more than any single symptom indicates an
unfavorable prognosis.
The fii'st indication of recovery is a diminution in the frequency of the
pulse. The pulse may have been 130, but on the tenth, twelfth, or four-
teenth day it begins to diminish in frequency. The tongue has been
1 TVMw^'Sic^e^CfJW is that form where death occurs in three or four days, after the most intense febrile
movement and constitutional disturbance. Headaches and a feeling of malaise, etc., during an epidemic
give rise to what many call " abortive " typhus. Walking typhus is that form where the patient is not con-
fined to his bed until the second week.
TYPHUS FEVBE. 731
brown and dry, subsultusand delirium may iiave been present, even " coma
vigil " may have manifested itself; there has been great muscular pros-
tration ; the patient, attempting to rise from the bed, may have fallen ujDon
the floor ; now, the pulse begins to get slower, the patient falls into a re-
freshing sleep and awakes perfectly conscious ; his countenance is changed
from the dusky hue to an almost natural appearance, and he desires food.
In other words, within twenty-four hours an entire change comes over the
patient, and that change is first indicated by a diminution in the frequency
of the pulse, accompanied by a fall in temperature. The fall in tenxpeva.-
ture is not extreme ; j)erhaps a fall of two degrees is first noticed. In my
experience, there is an attempt at convalescence upon the eighth day of the
fever. Especially in those cases that recover, a slight fall in temperature
will be noticed on this (the eighth day), although the temperature may
again rise ; upon the twelfth or fourteenth day there is a distinct fall in
temperature and diminution in the frequency of the pulse that is indicative
of convalescence. The mode of recovery in typhus and typhoid is, perhaps,
the most distinguishing clinical feature. In typhus recovery is rapid, in
typhoid it is markedly slow.
Of all the conditions which influence the prognosis in typhus fever, age
and the habits of the patient have as great, if not greater, influence than
any other. I am convinced of this from an experience in the care of typhus
fever patients which dates back almost to the very commencement of my
study of medicine, for very early did I have the care of a typhus fever ward.
In children, typhus fever is a very simple form of disease. The rate of
mortality is very low. I remember having the care of sixty children with
typhus fever, and among these only one death occurred. This is as low a
rate of mortality as one can expect in measles. Under the fifteenth year
of life the rate is very low, viz., two or three per cent. From twenty to
thirty the rate is fifteen per cent., with advancing years the disease is more
fatal. When the patient has passed the middle period of life, there is great
danger from typhus fever. So with the intemperate, and those who have
livid amid unfavorable hygienic surroundings. The bright, educated and
cultured, those whose brains are active, are less likely to recover than the
stupid and uneducated.
Treatment. — The more prominent measures which have been and are now
employed in the management of typhus fever are in many respects similar
to those proposed for the management of typhoid fever patients, yet the
treatment of these two diseases differs in certain essential particulars.
When the symptoms are mild, very simple measures are all that is required.
Of these, confinement to bed, cooling drinks, mild aperients, a milk diet,
and free ventilation are the chief, and, indeed, the only means required.
It is also important to observe the same rules in regard to the arrangement
of the sick-room which are recommended in the case of typhoid fever
patients. The more perfect the ventilation, the greater the amount of
fresh air around the patient, the better his chances for recovery. The
majority of cases of typhus fever are ushered in by active and severe
symptoms, such as would tempt one to adopt a vigorous plan of treatment.
732 ACUTE GE]SrERAL DISEASES.
symptoms which at one time were thought to indicate the employment of
heroic antiphlogistic measures.
Writers usually consider its treatment under two heads — the preventive
and curative. I prefer to use the terms ^jrophylactic and remedial, for I
question our ability to cure this disease.
Much can be done to prevent its development, and this will constitute an
important part in its management. How, then, can the development of
typhus fever be prevented ? Medical skill cannot prevent the importa-
tion of the disease into localities where it is not indigenous, for this is con-
trolled by state and national authority. Consequently typhus fever will
probably continue to be imported into districts where it does not originate.
For examj)le, we shall occasionally see the disease in all our large cities ; it
may appear in any commercial seaport, and from there it may be carried
into the interior. Yet much can be done to prevent its spread after it is
imported, and to prevent its development as an epidemic when it is carried
into any locality in the interior.
It is important that the first cases of typhus fever which are developed
in any locality should be closely watched. They should be immediately
quarantined. The dwelling in which the fever has broken out should be
depopulated — that is, in a tenement-house in which the fever has made
its appearance, all the families should be removed, and the house should
be thoroughly disinfected. The disinfection must be thorough, not for a few
hours, but for one or two days, and afterward the house should remain
open for the free circulation of air for a considerable length of time before
persons should be allowed again to inhabit the rooms. If typhus fever
occur in the dwellings of the wealthy, their houses must be quarantined.
All persons must be prevented from visiting them, and all persons within
the dwelling must be prevented from going abroad. After the sick have
recovered, there mnst be the same thorough disinfection as in the tene-
ment-house. Usually, in epidemics of typhus fever there are certain foci
from which the disease spreads. Perhaps the points from which the con-
tagion more especially emanates are within an area of half a square mile,
and yet the disease may have been prevailing for two, three, or even four
months. Under such circumstances it is possible to prevent the spread of
the fever by the means Just indicated.
As far as its management in hospitals is concerned, I would say : never
undertake it within brick or stone enclosures. If possible, patients should
be placed in broad pavilions or tents, so that the largest possible amount of
fresh air shall be in circulation about them. It is not sufficient to have
free ventilation in the ordinary acceptation of that term. The opening of
a window will not accomplish the desired result. Eemove all the windows
in a room, regardless of the cold, and cover the patients with a sufficient
number of blankets to keep them warm. Allow fresh air to surround them.
When typhus fever manifests itself, it can readily be understood how im-
portant it is that the guardians of the poor should not only enforce cleanli-
ness, but that they should feed the poor better than at other times. If
cleanliness is observed, the dwellings thoroughly disinfected, and the poor
TYPHUS FEVEE. 733
well fed, the most virulent epidemic can soon be stayed. The effects pro-
duced by such measures are sometimes wonderful. In the year ISGl, at the
commencement of the epidemic (as has been stated), the first case occurred
in a tenement-house in a down-town street, in New York City ; it was six
weeks before it spread from that locality. The spread of the fever should
have been stopped at that point ; but veiy little attention was paid to it,
and it began to spread from one point to another, until some six or seven
thousand cases were developed. Many prominent citizens sickened with
the fever and died. This epidemic could have been prevented had measures
been taken early to prevent the spread of the disease. It seemed to me that
the authorities of New York City were responsible for a large proportion of
the deaths which occurred during the prevalence of that epidemic.
Medicinal treatment is powerless either to arrest the progress or shorten
the duration of this fever, but it can undoubtedly save lives that would
otherwise be lost, and hasten convalescence. The first point under this
head relates to neutralizing the poison. I have found no medicinal agent
which can neutralize or destroy typhus poison, or which has power to
arrest the progress or shorten the duration of this fever. Different agents
have been proposed for the accomplishment of this result, according
to the views held in regard to the nature of the typhus poison and its
effects upon the system. At one time the mineral acids were supposed to
possess this power, and were administered for that purpose, but have now
fallen into disuse.' The internal use of carbolic acid, chlorine water,
creasote, and, more recently, salicylic acid has been recommended for the
same purpose. The inhalation of oxygen gas has also been thought to be
of service in arresting the blood-changes, and thus preventing the poison
from having its customary effect upon the system. By the stimulation
which it produces, the patient may be brought out of an apparent state of
coma, and revive in a marked degree ; but the relief is only temporary.
For a time the patient may improve, his consciousness return, and his ap-
pearance indicate that convalescence is established ; but his unfavorable
symptoms will return, and it will become quite evident that the oxygen
has not neutralized the typhus poison.
Fresh air is the only thing which I have found to have power to neutral-
ize the poison of typhus fever. It certainly possesses this power when ex-
ternal to the body. For example : place a patient sick with typhus fever
in a well ventilated board pavilion, or in a tent, where an abundance of
fresh air can circulate about him, and it is almost impossible for him to
communicate the disease to a healthy person. Again, place a patient in
a closed room, perhaps twelve by fourteen feet square, let a healthy person
remain with him a single night — probably a much shorter time will be
sufficient — and the latter will be almost certain to contract the disease.
Why is the disease more readily communicated in the one case than in the
other ? Certainly the fresh air which circulated about the typhus fever
patient must have prevented contagion. Fresh air, when inhaled, produces
1 Though a very recent work (Wikon on Fevers) says nitro-miiriatic acid, alternating with turpentine is
preferred in the United States, and that mineral acids occupy the highest rank.
734 ACUTE GENERAL DISEASES.
to a greater or less extent the same effect. How do we know this ? As a
clinical fact, I have seen a typhus fever patient, who was apparently over-
whelmed by the poison — who within forty-eight hours from the commence-
ment of the attack was m a state of coma, with high temperature, a rapid
pulse, etc., and all symptoms indicating that he was fast succumbing to
the disease — when brought from a crowded tenement house and placed in
a tent where he could inhale plenty of fresh air, within four or five hours
from the time of admission begin to rally, and go on to recovery. Fresh
air was the only remedial agent employed.
If fresh air does not neutralize the poison, it certainly has some effect in
eliminating the poison, and thus mitigating the severity of the fever, and,
perhaps, shortening its duration. It may be regarded as a I'emedial agent,
for it certainly is of greater value than any so-called remedial agent at our
command. To accomplish the best results, place three or four patients in
a tent twenty feet square ; the fly of the tent should be thrown up, and if
the weather is cold, the patients should be well covered with blankets. By
this means all the advantages of free ventilation will be insured. The
question arises: what therapeutical agents can be employed with advantage
in order to accomplish the desired results ?
It is of the greatest importance to reduce temperature and to sustain
heart-power. The former is of as great importance in typhus as in typhoid
fever, and the same rules should govern one with regard to the agents to be
employed, and the mode of their employment. As in the management of
typhoid, so in this fever, we have two antipyretic agents, namely, the sul-
phate of quinine and the application of cold to the surface. These agents
may be employed separately or in conjunction. The temperature rise&
more quickly in typhus than in typhoid, after it has been reduced by tha.
cold bath, and all through the early part of the fever one will be obliged
to resort to the bath much more frequently than in typhoid.
The rules for the administration of the baths in typhus fever diffei
somewhat from those that obtain in typhoid. In typhus fever, as soon ah
the temperature of the patient rises to 104° F., he must be placed in a
bath the temperature of which is about ten degrees below that of the
patient ; gradually, by the addition of ice or ice-water, bring the tem-
perature of the bath down to 68° or 70° F. He must be kept in the bath
until his temperature falls to 101° or 102° F., then taken out, quickly
dried and placed in bed. For some time after the removal from the bath,
the axillary temperature will continue to fall, as the trunk parts with heat
to the extremities. As soon as the temperature rises again to 104° F., the
patient must receive another bath. If he suffers with intense pain in the
head, or is actively delirious during the bath, ice-bags may often be applied
to the head with benefit. If the cold baths do not readily reduce the pa-
tient's temperature, or if the fall is of short duration, antipyretic doses of
quinine must be administered, according to the rules given for its adminis-
tration in the treatment of typhoid fever. As soon as the first week of the
disease is past, having kept the patient's temperature below 103° F., it will
not usually be necessary or advisable to continue the baths. In most cases
TYPHUS FEVEE. 735
antipyretic doses of quinine will be found sufficient to keep down the tem-
perature.
Now, if not before, there will be evidence of heart failure, and the question
presents itself : shall alcoholic stimulants be administered ? The history
of alcoholic stimulants in the treatment of typhus fever dates back to the
teachings of Graves and Stokes, since which time until quite recently they
have constituted an important element in the treatment of this fever, re-
ceiving the approval of almost the entire profession. Even at the present
day the rule is to administer alcohol in large quantities in fever. Most
writers have regarded a frequent feeble pulse, with feeble cardiac impulse,
even though cerebral symptoms may be present, as certainly indicating the
administration of alcoholic stimulants. The directions were, to com-
mence their administration early, and in sufficient quantities to control
the pulse. It was thought that the earlier their administration was com-
menced, the better the chance for recovery, as the failure of heart-power,
which makes its appearance in the later stages of typhus, would be pre-
vented. No limit was given as to the quantity to be administered. The ob-
ject to be accomplished was to control the pulse. This could in most cases
be done for a time, but as the disease advanced, and the patient became
more and more overwhelmed by the typhus poison, alcohol lost the power
of giving force to the pulse. Under such circumstances, the rule was to
give it ad libitum, for alcohol was regarded as the only agent by which the
life of the patient could be saved. After carefully studying for two years
the action of alcohol on typhus fever patients, I became convinced that
in some patients, if not in all, those who were severely ill, especially
where there was interference with the function of the kidneys, its bene-
ficial effects were doubtful, if its action was not decidedly injurious.
That stimulants will control the pulse and sustain the heart's action for
a time, there can be no question ; but I found that in all severe cases
there came a time when alcohol, in however large doses it was given,
ceased to have power. Besides, it must be remembered that large quanti-
ties of alcohol thus administered disturb nutrition, lessen secretion, pre-
vent the elimination of urea, and tend to induce a state of coma, which
cannot readily be distinguished from that induced by the disease itself, all
of which must necessarily greatly increase the danger of a fatal termina-
tion. '
> During the prevalence of the epidemic of typhus fever in 1864, 1 took charge of the fever-tents on
Blackwell's Island, with the intention of testing the effect of the withdrawal of stimulants in the treatment
of typhus fever. In my earlier professional life I was thoroughly imbued with the idea (for I was almost
bom into the profession from a typhus fever ward) that alcohol was a necessity in the treatment of
typhus. My house physician, Dr. Engs, who took ihe immediate care of the fever-tents under my direction,
had had a large experience in the treatment of typhus fever in Bellevue Hospital, had there contracted the
disease, and believed that his life had been saved by the free use of stimulants. As we assumed the
charge of the tents I ordered that no stimulants or medicines should be administered to any patient.
The cases, as they were brought into the tents from the city, were of as severe a type as any we had
treated in Bellevue Hospital ; some were in a state of coma, with an imperceptible radial pulse, and
all the signs of speedy dissolution— conditions which I had been educated to regard as most cer-
tainly indicating the free administration of stimulants. The rule which I established was faithfully car-
ried out, with the following results : while the fever was in Bellevue the ratio of mortality was one death
in every five ; and in the tents one in sixteen. I do not claim that the great diminution in the ratio of
mortality in the tents, as compared with that of Bellevue Hospital, was due to the non-administration of
^736 ACUTE GEISTEEAL DISEASES.
Typhus fever patients under twenty-five years of age rarely require, or
are benefited by, alcohol, unless they were of intemperate habits prior to
the attack. To the old and feeble its occasional ad minis fcration may be of
great benefit, and at times be the means of saving life. A copious dark
eruption, with coldness of the extremities, especially indicates the use of
alcohol. As a rule, delirium, headache, scanty urine, and intense surface
heat contraindicate the use of alcohol. In any case when it is decided to
administer spirits, carefully watch the effect of the first few doses ; the
same rules govern here that were laid down for the administration of stimu-
lants in typhoid fever. It is impossible to give any positive rule as regards
the quantity of stimulants required in each case. It is very rarely neces-
sary at any time during the fever to give more than eight ounces of brandy
during twenty-four hours. If this amount will not sustain the heai't-
power, I am confident larger quantities will fail to do it, and also that such
administration has hastened the fatal issue. As soon as the symptoms on
account of which the alcohol may have been resorted to are relieved, the
quantity must be reduced, or its administration altogether stopped.
I do not altogether condemn the use of stimulants in typhus fever, but
I do so as regards stimulants as a " plan of treatment ;" and where the
patient can be freely exposed to fresh air, I doubt if their use is often re-
quired. To diminish the frequency of the pulse cardiac sedatives have been
employed, such as veratrum viride, aconite, and digitalis.
The rapid pulse in typhus fever, after the first onset of the disease, often
is not due to the high temperature, but to the failure of heart-power ;
when such is the case, digitalis should be employed. Digitalis diminishes
the frequency of the pulse, by increasing the power of the heart, and at the
same time it increases the secretion of urine, which frequently is scanty,
and thus, to a limited extent, it becomes an eliminative. From four to
six drachms of the infusion of digitalis may often be given with benefit,
during twenty-four hours. If the heart-power cannot be sustained by the
moderate use of stimulants and by digitalis (given as indicated), no more
can be done so far as remedial agents are concerned. The treatment of the
special symptoms of typhus fever require only a passing notice. The head-
ache, when intense, is best relieved by cold applications in the form of ice-
bags. If it is accompanied by intolerance of light, a blister to the back of
the neck will be found to give relief.
Sleeplessness in any stage of the disease, if it continues for two or three
days, must be relieved, for it is of itself sufiicient to cause a fatal termina-
tion. If sleep does not follow the application of cold to the head, opiates
may be administered in full doses. I have seen typhus fever patients that
had not slept for forty-eight hours drop into a quiet sleep within a few
hours after they had been exposed to free ventilation. Great care should
be exercised that their apartments are kept perfectly quiet and darkened.
stimulants in the one case, and their free administration in the other. I do, however, most certainly
affirm that my experiments in the tents convinced me that the beneficial effects which had been ascribed
to the use of alcohol in typhus fever were not fairly due to it. Although I would not entirely discard
the use of alcohol in the treatment of typhus, still I would greatly limit its use and give it only as an
occasional aid, to carry a patient over some time of peculiar danger from heart failure.
TYPHUS FEVER. 737
When delirium and cerebral symptoms are associated with sleeplessness,
hydrate of chloral may be carefully employed. Stupor is to be counter-
acted by promoting the action of all the excreting organs, applying exter-
nal stimulants, and administering diffusible stimulants, the most service-
able of which are black coffee, musk, and camphor. In the early stage of
the disease the cold douche may be employed.
Two remedies have been recommended for the coma of tyjahus, namely :
Talerian and phosphorus ; neither of these remedies has seemed to me to
be efficacious. When there are evidences of great prostration in connection
with any of these special symptoms to which reference has been made,
the moderate administration of stimulants may be resorted to, and if relief
follows the first few doses their use may be continued. In the treatment
of the complications which are liable to occur during the course of typhus
fever, one must be guided by general principles and by the symptoms
in each individual case, it being always remembered that the primary dis-
ease has a tendency to induce great nervous prostration and depi'ession, and
that the heart's action forbids the use of all depleting remedies, and indi-
cates a supporting plan of treatment. The pulmonary and laryngeal com-
plications, as well as erysipelas, bed-sores and gangrene are to be managed
in the same manner as was proposed when they occur as complications of
typhoid fever.
The diet is of primary importance. Though the patient refuse all nourish-
ment, if possible he must be required or even compelled to take it. As the
digestive powers are impaired, great care is required in selecting and admin-
istering the proper nourishment, and it must be given at stated intervals,
varying from one to two hours. Care must be taken not to overfeed —
much harm may be done in this way. When the patient clinches his teeth
and obstinately refuses all food, or is unable to swallow, his life may
sometimes be saved by pouring liquid nourishment into the stomach by
means of a long tube passed thi-ough the nose. Milk best serves the pur-
pose as an article of diet. It may be given ice-cold, if desired, and in such
quantities as the stomach can receive and digest. If more concentrated
nutrition is desirable, the yolk of eggs may be beaten up and added to the
milk.
The management of patients during convalescence from typhus fever is
a matter of very great importance. As soon as the fever ceases, most pa-
tients convalesce rapidly unless there is some complication, and the chief
duty of the physician is to prevent premature exertion and exposure tO'
cold, and to restrain the patient in the gratification of an inordinate appe-
tite. At this time porter or ale may be taken with benefit. The mineral
acids, Peruvian bark, and iron may also be given as tonics ; these are par-
ticularly called for when the pulse is slow and feeble. It is important,
to guard against any sudden physical effort during the early period of con-
valescence, as it may lead to coagulation of blood in the veins. An opiate
or hydrate of chloral is sometimes required to produce sleep during convales-
cence. In all cases great benefit will be derived from a temporary change
of residence and daily exercise in the open air.
47
738 ACUTE GEJSTEEAL DISEASES.
EELAPSING FEVER.
This has been called famine and seven-day fever, synocha, typhinia,
mild yelloiv fever, typhus recurrens, dynamic fever. The French call it
'^ Fievre a Eechute ; " and the G-ermans, " Hungerpest."
Relapsing fever is no new form of disease. It was described more than
a century ago by Dr. Kutty/ and since that time has prevailed as an epi-
demic disease in most of the countries in northern Europe." There is no
reliable history of its occurrence as an epidemic in this country until 1872-
3, when an epidemic prevailed in New York City. It has been reported that
in the year 1844 a vessel landed in Philadelphia passengers ill of relapsing
fever. At one time, while typhus fever was prevailing in Buffalo, some twelve
or fourteen cases of relapsing fever were reported ; but it is altogether prob-
able that they were cases of irregular typhus fever, for when relapsing fever
has been introduced into a locality it is not limited to one or two dozen
cases.
Morbid Anatomy. — In this disease there are no pathological lesions that
are characteristic. There are changes present in some of the organs which
very closely resemble those met with in typhus.
Spleen. — In the majority of autopsies, if death has occurred in the ac-
tive period of the disease, the spleen will be found increased in size, its
capsule thickened, smooth, tense and slightly clouded, the trabeculae of the
organ increased, and the Malpighian tufts more j)rominent than normal.
In some cases the spleen will be found enlarged, soft, flabby, and even dif-
fluent. There is no uniform change in its substance, although it is always
increased in size during the active period of the disease. After this period
has passed, it will be found diminished in size, and its surface will pre-
sent a shrivelled appearance, with the capsule rolled into folds. Infarc-
tions (not embolic in origin) are often found. In many cases a number of
Tounded or irregular miliary masses, of a dull yellow color, will be found,
containing granular detritus, cell-elements, and free nuclei.
Liver. — During the active period of the fever, the liver will also be found
enlarged. The gall-bladder is generally distended with dark yellow and
viscid bile.
Kidneys. — The kidneys are increased in size, the increase being due to
congestion of the cortical substance. There is a granular infiltration of
the epithelium of the uriniferous tubes, a change similar to that noticed in
other fevers. Small hemorrhages stud the whole organ in severe cases.
The urine often presents a cloudy appearance.
Intestines. — Usually enlargement of the glandular follicles of the intes-
tines will be found. The solitary glands are more commonly affected, but
even the Peyerian patches may present the ''shaven-beard" appearance.
The mesenteric glands are slightly enlarged in severe cases. Their appear-
ance is similar to that noticed in typhus.
1 John Rutty, " A Chronological History of, etc., etc., in Dublin, from 1725 to 1765." London, 1770.
2 Accounts in Hippocratic writings leave no doubt but that it prevailed 3,000 years ago in islands off
Thrace.
EELAPSIKG FEVEE. 739
Mucous Membranes. — In the majority of cases, small spots of blood-
extravasation will be found upon the mucous surfaces, especially the
membranes of the stomach and intestines, and they may be found on the
mucous membrane of the bronchial tubes. The stomach shows small
blood-extravasations when vomiting has been severe during life, or when
there has been black vomit. These spots of ecchymosis are perhaps as con-
stant as any pathological lesions of the disease.
Blood. — The blood coagulates imperfectly, as in typhus. Spirilli are
discoverable, oftentimes, provided death occurs in an active stage. The
heart presents no constant changes. In some cases fine granular infiltration
or vitreous degeneration of the muscular fibres has been observed. This
same granular infiltration is also sometimes seen in the voluntary muscles.
Coagula are rare. ^ Diffuse or circumscribed changes in the marrow of the
bones occur, according to Poufick. The lymphoid elements increase, and
large cells, filled with numerous oil globules, appear along the track of
vessels. Necrotic softening of the marrow has been seen in severe cases.
Etiology. — There have been differences of opinion and much discussion
in regard to the etiology of this disease. At the present time it seems to
be the unanimous opinion of those who have had the best opportunities for
study, that it is a contagious disease, and that it is a distinct type of fever.
Although it presents many phenomena which ally it to typhus, and many
other phenomena which ally it to malarial fever, it is neither typhus nor
malarial, but is a distinct type of fever having a distinct poison.
From observations which have been made upon the blood of patients
suffering from this fever, distinct organisms which have the power of de-
veloping the fever are thought to have been found. This parasitic organ-
ism [spirillum Ohermeieri) is a spiro-bacterium, unlike that sometimes found
in water and in mucus from the mouth. But Billroth and Manassein have
found them in fluid from noma and in a cyst of the antrum. Several
German observers, Cohnhein among them, have given drawings of these
organisms, which seem to be little spiral lines that are constantly under-
going a twisting, rotary, rapid motion, and these observers tell us that
they are distinctive of this form of disease, and are always present during
its active period.^ They are absent in the interval between the primary
attack and the relapse, but are to be seen as soon the relapse occurs. With
reference to these animal organisms, and others which are claimed to be
the cause of fevers and other infectious diseases, while it may be true that
distinct forms are found in different forms of fever, I question very much
if by the introduction of these organisms into the system the fever can be de-
veloped. In relapsing fever, more than in any other, have these organisms
been seen and studied, and yet all experimenters have failed to develop the
fever from them. This fact gives those who do not believe that living
organisms are the cause of infectious diseases a very strong argument ; yet,
' Ponfick, in Virchow's Archiv., B. 60, p. 153, 1874, states that the cardiac degeneration may be so
extensive as to cause death, resembling the heart of phosphorus poisoning.
2 Vide Centralblatt, 1873, and Virchow's Archiv., Bd. 47. Also Obermeier's article in Berliner Klin.
Wochen., No. 3.5, 1873. It is from two to si.^ times as long as a red blood disc, and no thicker than the
finest fibrin-fibril. It is readily destroyed by nearly every reagent.
740 ACUTE GENERAL DISEASES.
on the other hand, does nothing for those who hold the chemical theory ol
the disease.'
Clinical experience has shown that relapsing fever is a contagious disease,
and can be propagated by personal contagion. The disease is not neces-
sarily accompanied by starvation, for it is developed among those who
are well fed as well as among those who are badly nourished. As in typhus
fever, there is a connection between the development of an epidemic of this
fever and imperfect ventilation and bad hygiene.
I had never seen a case of relapsing fever until 1870, when the epidemic
prevailed in New York City. At that time patients were brought into my
wards in Bellevue Hospital with a fever differing from typhus fever by the
absence of an eruption ; from intermittent, in the order of its develop-
ment, and not closely resembling remittent fever. It seemed to me an
irregular form of malarial fever, differing from any with which I was
acquainted. Eight cases were brought in. From these my house phy-
sician contracted the fever, and during his illness I reached the diagnosis of
relapsing fever. Subsequently we had large numbers of relapsing fever
patients, and a hospital was established for their reception on Hart's
Island. In every case that occurred at that time, where the origin of the
fever could be traced, it was found that there had been direct exposure, and
it was established beyond doubt that the first cases were brought from Ire-
land. The contagious character of the affection was also established by
the fact that all the nurses and all the physicians who were in immediate
attendance upon the sick contracted the fever. If a patient was placed in
a bed previously occupied by a person sick with relapsing fever, before it
had been cleaned, he was almost certain to contract the disease. The closer
the contiguity the more certain is the individual to contract the fever.
At the time of this epidemic we found no evidence that the fever was
conveyed by clothing, although some British writers have claimed that it can
be done. When our patients were admitted into the hospital, their clothing,
as it was removed, was simply washed, not disinfected in any special manner,
then packed away, and not a single person who was thus brought in imme-
diate contact with the clothing contracted the disease. There is no immu-
nity from a second attack. The period of incubation ranges between five
and seven days, rarely nine.^
Symptoms. — The symptoms which usher in relapsing fever are usually
well marked. If there are any prodromes, they are the same as in typhoid
fever {q. v.).
It is sudden in its advent. This is marked by a severe rigor or by a dis-
tinct chill. Accompanying the chill there is frontal headache, vertigo, pain
in the limbs and joints, more or less pain in the back, nausea and not in-
1 Very recently spirilU have been found to develop in blood taken from relapsing fever patients,
when, on first withdrawal, none could be discovered. Small, rounded bodies, called spores, have been
found in the blood by Albrecht, and from these, it is supposed, that spirilli develop. Cent. f. d. Med.
Wissenschaften, May 22, 1880. Dr. Carter, of Bombay, has succeeded in reproducing the disease by in-
oculation in small monkeys. "Medico-Chir. Trans.," p. 125, 1880.
2 In some cases the fever begins a few hours after exposure. Lebert found 75 per cent, of cases to have
an incubatory period within seven days, and of these more than one-half sickened within three days after
exposure.
EELAPSING FEVER. 74l
frequently vomiting.' A rapid rise in temperature follows the chill, and
with the pyrexia the headache increases, as does also the pain in the limbs,
especially about the joints. Sweats may, at first, follow the rigors. There
is vomiting, at first only of the simple contents of the stomach, afterwards
of yellowish material. This may be followed by the ejection of a dark-
colored material, which very closely resembles the black vomit of yellow
fever. In this disease the rise in temperature is always rapid, and usually
attains its highest point within the first twenty-four hours; during this
time it may rise to 104° F., or even as high as 109° F. From this time,
for two or three days, there is usually very little variation. With tlie occur-
rence of the chill aiid fever there is also a rapid increase in the frequency
of the pulse. In uo disease does the pulse so quickly become rapid as in
relapsing fever. It is not uncommon for it to reach 140, 150, or even 160
beats per minute within the first twenty-four hours. It is usually small
and compressible, sometimes dicrotic. The mind is clear. There is nothing
peculiar about the countenance of the patient, but it presents the ordinary
appearance noticed in an active febrile excitement. Sleeplessness is often
present on account of the severe pains in the limbs. As the disease pro-
gresses the patient becomes more and more prostrated ; by the second day
he may be unable to turn in bed. The arthritic pains increase in severity
and often become the most distressing, symptoms of the fever.
As early as the second day, patients begin to complain of a feeling of
weight and uneasiness in the upper part of the abdomen, more severe in
the left than in the right hypochondrium. Profuse sweats are common
about the second day, but they afford no relief to the urgent symptoms.
Usually, there is considerable enlargement and tenderness of the liver. The
spleen, also, becomes rapidly enlarged, and its enlargement is attended with
quite severe pain and tenderness. Moderate meteorismus is not uncommon.
The muscles of the body are, however, the seat of the most severe pain,
which is increased by movement and by pressure ; the pain is piercing and
lancinating in character. On account of this pain, the patient usually lies
perfectly quiet ; he is not restless but sleepless. Delirium is not an infre-
quent symptom, and is sometimes very active ; yet in the majority of mod-
erately severe cases the mind remains undisturbed. There may also be
present irregularities of the pupils, photophobia, and other symptoms
which might lead one to the diagnosis of meningitis were it not for the
character of the pulse. The muscles of the eyes are often stiff and im-
movable ; the conjunctivae are reddened and the eyelids are swollen.
As the disease progresses, in a certain proportion of cases, jaundice is de-
veloped ; this is usually accomcanied by vomiting and severe diarrhoea;
and these symptoms seem to ally the disease to some forms of malarial
fever (''bilious typhoid"); not infrequently, especially in children, there
is epistaxis. The skin may be covered with herpes or sudamina. The
great prostration and rapid rise in temperature ally it to typhus fever, but
the rise is more rapid and reaches a higher point within the first twenty-
1 This headache persists till the remission ; it is unvarying'- and intense ; the vertigo is so severe that
the patient has to take to his bed as much from giddiness as pain.
742
ACUTE GENEKAL DISEASES.
four hours than it does in typhus fever. There is sometimes a slight rose-
colored eruption resembling roseola, but having none of the characteristics
of typhus erujjtion. The patient goes on from day to day gradually getting
worse; the fever becomes more and more intense; loss of strength and
emaciation are progressive, and the muscular pains are more severe. In
some cases the patient rejects everything taken into the stomach. The
pulse reaches 160 per minute, the tongue is brown and dry, extreme nausea
and bilious vomiting are present, and the severity of the symptoms indi-
cates that death may speedily occur ; when, on the seventh or eighth day
of the fever, a remission suddenly occurs, attended by a profuse perspiration,
by a critical diarrhoea, or, rarely, by bleedings from mucous surfaces.
With the occurrence of the profuse sweating the temperature falls; in a
few hours it may fall five, six, or even seven degrees ; the pulse becomes
less frequent ; the respirations, which have been hurried and diflBcult, be-
come regular ; the pains in the head and limbs pass away, the thirst disap-
pears, the tongue becomes moist ; the engorgement of the liver and spleen
rapidly diminishes, as is shown by the rapid diminution in the size of these
organs as determined by percussion. The bowels are constipated. Within
twelve hours from the commencement of the remission, the temperature
may fall to less than 100° F., perhaps below the normal standard, and the
pulse may fall to 80 or 90 beats per minute.
As soon as the remission occurs the patient feels perfectly well, except a
sense of weakness. He gets out of bed, and, if he is in a hospital, per-
haps insists upon his discharge ; his appetite begins to return, and he ap-
pears to be rapidly convalescing, but in many the pulse at this period is as
slow as 40 to 60 per minute, and the first sound of the heart is very faint,
the second being intensified.
His apparent convalescence is of short duration ; sometimes in three or
four days, usually at the end of a week, certainly by the twelfth or four-
teenth day of the disease, all the phenomena of the primary fever are
suddenly developed, or what is
termed the relapse occurs.' Some-
times the relapse occurs in the
morning, sometimes in the after-
noon, but more frequently it
comes on at night. The re-
lapse may be ushered in by a
chill, or it may occur without
a, chill. The pulse may begin
to increase in rapidity, and in
twelve hours reach 140 per min-
ute. With the rapid pulse, the
temperature rapidly rises to 306°
F. Usually the fever which at-
tends the relapse is more intense
than the primary fever, the liver
Fig. 160.
Temperature Record in a case of Eelapsing Fever.
Recovery.
I It is very rare for the disease to end in one single paroxysm.
EELAPSING FEVER. 743
and spleen becoming as enlarged as during the primary feyer. The relapse
usually lasts three or four days. In a few cases I have seen it last six or
seven days, and in some it does not continue more than forty-eight hours.
After it has continued a certain period, a second remission is developed ;
this, like the first remission, comes on suddenly, is accompanied by a pro-
fuse perspiration, and in twenty- four hours from its commencement the
pulse and temperature have reached their normal standard. From this
period, the patient usually goes on to complete recovery.
As many as three or four relapses may occur, but ordinarily the conva-
lescence becomes complete after the second remission. Convalescence from
relapsing fever is usually slow, the patient for a long time remains in a
weak condition, suffering more or less from arthritic and muscular pains.
The appetite returns slowly. An anaemic murmur, which is often very dis-
tinct during the active period of the fever, is heard for two or three weeks
after the commencement of convalescence. CEdema of the feet, due to gen-
eral anasmia, is often quite marked during convalescence. The period of
convalescence is usually as long as both the period of fever and remission ;
not infrequently six or eight weeks elapse before relapsing fever patients are
able to resume their accustomed avocations. At the commencement of con-
valescence, the decrease in the size of the spleen is rapid, but frequently it
is a long time before the organ reaches its normal size.
Complications. — Few complications have been noticed during the course
of relapsing fever. In some epidemics pneumonia has occurred quite fre-
quently ; at other times it has been exceedingly rare. When it does occur,
it is often double, and terminates in gangrene in a number of cases.
Sudden collapse may occur as a complication of relapsing fever> either
during the primary fever or during the relapse. The pulse suddenly be-
comes small, irregular, or intermittent, sometimes imperceptible. The
cardiac impulse is feeble, the heart sounds are lost, and the patient rapidly
passes into a condition of collapse and dies. The collapse may come on
suddenly in cases previously mild ; with fatty heart, death in relapsing fever
is nearly always from this cause.
Post-feirile ophthalmia is another very remarkable complication or
sequela of this fever. It has been observed in most epidemics. It presents
two distinct stages, the amaurotic and the inflammatory. During the first
stage the patient complains of impaired vision, with motes and luminous
circles floating before the eyes. The inflammatory stage is characterized
by intense circumorbital pains and lachrymation, without injected conjunc-
tivae or marked constitutional disturbance. Eecovery is tedious, and, unless
the case is carefully treated, may end in complete loss of sight. Both eyes
are rarely attacked ; the right eye is most frequently affected. Iritis,
choroiditis, and retinitis are not uncommon.
Diarrhoea and dysentery are common complications, and in some epi-
demics they are the chief cause of death. They are most likely to come on
during the relapse. In our epidemics the most frequent complication is
hemorrhage from the mucous surfaces, especially from the stomach and
intestines. In two cases that came iinder my observation hemorrhagic
744: ACUTE GENEEAL DISEASES.
pachymeningitis was the cause of death. In very rare instances, abscess of
the spleen, accompanied by pygemic symptoms, has occurred during the
relapse and convalescence. Pregnant females, no matter at what stage of
pregnancy, asually abort during an attack of relapsing fever.
Differential Diagnosis. — The diagnosis of relapsing fever is not difficult if
one has the entire history of the case ; but at the commencement of an
epidemic, during the primary fever the diagnosis will necessarily be doubt-
ful. The diseases with which it is possible to confound relapsing fever
are typhus, typhoid, remittent, yellow and dengue fever, small-pox (before
the eruption), and measles. It differs from all but typhus in the sudden-
ness of its invasion, in the short duration of the primary fever, in its termi-
nation in a crisis, and in the almost uniform occurrence of a relapse be-
tween the third and fifth days. Then the muscular and arthritic pains,
which are such constant attendants of relapsing fever, distinguish it from
the other forms of fever.
In typhus, the dusky face, contracted pupils, absence of all abdominal
pain, peculiar smell, stupor, apathy of mind, and pathognomonic eruption
on the fifth or seventh day will be sufficient to distinguish it from relaps-
ing.
In typhoid, the slow invasion, the ''step-ladder" rise in temperature,
the eruption, the characteristic diarrhoea, and the continuance without re-
mission or intermission, will enable a diagnosis to be reached.
A severe form of relapsing fever, attended by Jaundice, resembles very
closely, in its general appearance, yellow fever. In yellow fever the pulse
is rarely over 110, the spleen is normal ; but the high temperature and rapid
pulse which attend the development of the former readily distinguish it
from the latter ; besides, when the intermission comes on, there can no
longer be any question as regards diagnosis, for yellow fever is a disease
in which only a remission occurs, not an intermission.
Small-pox simulates relapsing fever only during the period of invasion.
One need make no doubtful diagnosis after the third day, when the red
epots appear along the edges of the hair. '
In measles the eruption following the symptoms of a common cold and a
bronchitis will suffice for a diagnosis.
Prognosis. — The prognosis in relapsing fever is always good. During our
epidemic about three per cent, of all the cases treated in hospitals termi-
nated fatally. This is a lower rate of mortality than we have with measles.
Usually deaths from relapsing fever occur, not from the disease, but from
some complication. During the epidemic in this city, syncope during re-
lapse was the most frequent cause of death. Eelapsing fever patients may
die of hemorrhage from some of the mucous surfaces. A fatal termination
may occur from bronchitis, pneumonia, or other pulmonary complications.
Diarrhoea and dysentery occurring during convalescence sometimes cause a
fatal termination ; purpura also. Sudden suppression of urine, dependent
> In dengue fever the pains in the joints are severe ; there are glandular swellings not found in relaps-
ing, the paroxysm is shorter (three days) than in relapsing (seven days) ; and there is an eruption (like
scarlatina's) on the palms and neck.
SMALL-POX. 745
upon renal congestion, may give rise to acute uraemia, and thus cause death.
My own experience leads me to the belief that the greatest danger in this
disease arises from sudden syncope. I remember one very marked case,
that of a young physician who seemed to be doing well in his second re-
lapse, when suddenly he passed into a state of syncope and died. At the
post-mortem examination no condition of the internal organs was found
which would account for his death.
Treatment. — Dr. Eutty stated more than a century ago that all those
cases of relapsing fever which were abandoned to whey and the good provi-
dence of God recovered. The experience of a century has furnished no ac-
cepted plan of treatment. The profession are still unsettled as to the best
course to be adopted in the management of this disease. When this fever
appeared in our midst, we thought we could control it by large doses of
quinine, but we soon found that quinine was of no service in its treatment.
Then arsenic, aconite and veratrum were employed in full doses as anti-
pyretics, but after a time these were abandoned as useless. Cold baths were
resorted to, as also was sponging of the surface in order to reduce the tem-
perature, but in their use we were disappointed. The temperature was re-
duced while the cold was being applied, but rose again very soon after the
patients were removed from the baths, and there was no evidence that it
diminished the severity or shortened the duration of the primary fever, or
prevented the occurrence of the relapse. Opium in full doses was then
tried, but with equally unsatisfactory results, although its free use was
found to give more comfort to the patients than did any other plan. In
some cases stimulants were administered quite freely, but without any ap-
parent beneficial results.
The conclusion arrived at was, that relapsing fever patients were as well
without as with medication. I would insist that relapsing fever patients
shoiild be kept quiet in bed during the primary fever, and should not be
allowed to leave their rooms until the period of relapse, shall have passed
and that the greatest care should be exercised to guard against the occur-
rence of syncope. If there is any evidence of heart-failure, digitalis and
stimulants should be administered according to indications. Beyond this
I have nothing to suggest. My experience leads me to place relapsing
fever patients under the best hygienic management, with free ventilation
and a milk diet, and then carefully watch lest some complication should
occur.
SMALL-POX.
{Yariola.)
There are three recognized types of variola, viz., — "variola discreta,"
" variola confluens," and '' variola hemorrhagica." '
Morbid Anatomy. — Besides those anatomical lesions which occur upon
the mucous membranes and skin, there is more or less intense congestion
' Small-pox is a very ancient disease. Before the Christian era a Goddess had been worshiped in India
as a protectress agninst it. The Arabians gave the first detailed account of variola. During the thirteenth,
fourteenth and fifteenth centuries it prevailed in Europe, and two centuries later it appeared on the
American coutinent. During the eighteenth century one-sixth to one-twelfth of the total mortality in
Europe was caused by small-pox.
746 ACUTE GENERAL DISEASES.
of the lungs, brain, liver, spleen and kidneys.' In the hemorrhagic form
of small-pox small hemorrhages occur in nearly all the viscera, with ecchy-
moses in the serous membranes and blood-stained fluid in the serous cavi-
ties. The mucous membrane of the stomach and rectum is oftenest the
seat of these extravasations.
The characteristic anatomical lesion of small-pox is to be found upon the
mucous membranes and upon the skin. This lesion is usually spoken of
as the eruption. It does not differ essentially in the different varieties ;
the modifications which are met with are due rather to its duration and
the order of its development. These surface lesions pass through regular
stages of development and decline.
The first step in the formation of a small-pox pustule is congestion of
the skin in discrete spots ; the vessels of the corium are dilated and tortu-
ous, and the connective-tissue of the papillae, in the centre of the congested
zone, shows more or less cedema. The non-elevated red spot (looking at
first like a flea-bite) is a macule. Next, the skin is elevated at these (macu-
lar) points and o. papule forms, from changes in the cells of the rete Mal-
pighii. Soon the papule becomes a vesicle ; in its centre the epidermis
becomes distended with serum and cells. As the effusion increases the
cells change ; the horny layer above is raised, and the summit of the papule
becomes the centre of the vesicle. The changed cell elements are pressed,
separated, and massed into groups from pressure of the effusion, and a
stringy mesh-work is formed in the vesicle. Meanwhile proliferation of
the adjoining cells forms a peripheral wall for the vesicle, the contents of
which soon become turbid.
Umhilication of the vesicles now occurs. Trabeculse slowly spread from
roof to floor of the vesicle, and hold down its centre, while marginal cell
proliferation and the accumulation of serum bulge out its periphery.'^
After the vesicles are fully formed, pus-cells appear in them, and as a re-
sult the vesicles change in color, and become pustules. At the same time
an inflammatory process, more or less extensive, is going on in the walls of
the pustule, and in the surrounding cellular tissue, which terminates in a
destruction of tissue at the point where the papillary congestion first oc-
curred. If only the superficial layer of the skin is involved, the infiltra-
tion of pus-cells into the vesicle and the formation of the pustule may take
place without extension of the inflammation into the cellular tissue beneath,
and necrosis or death of the part will not follow ; but if the inflammation
extends into the deeper tissues, a slough will be produced which necessarily
will be followed by a cicatrix and pitting. After the pustule is formed
1 Enlargement of the spleen is rather an infrequent event in small-pox. Weigert states that the blood-
vessels of the lymphatic glands and abdominal viscera are often filled vrith micrococci, that necrosis of the
cells about these colonies induces pus accumulation, the direct result of "coagulation necrosis" (see
Inflammation) : but that abscesses rarely form ; some find an analogy between these and the skin dis-
eases.
2 Some explain it by saying that each papule and subsequent vesicle holds imprisoned at its centre
either a hair-follicle or the duct of a sweat-gland, and that when this epidermidal layer of the papule is
elevated by the serous exudation or infiltration, the portion immediately about the hair-follicle or the
sweat-duct is held down, and a depression is produced by the exact point where the hair-follicle or duct of
the gland may be situated ; but since umhilication is present when neither structure is found, this view
cannot be accepted.
SMALL-POX. 747
the inflammatory products begin to dry down, and a crust is formed which
contracts in tlie central portion, and the same umbilicated appearance is
presented that is seen in the umbilicated vesicle. The incrustation begins
at the centre. The crusts are made up of dried pus-cells and detritus.
After a time these crusts are separated by the ordinary changes which
occur in the subsidence of an inflammatory process, and recovery is com-
plete, except that there is left behind a cicatrix which undergoes the same
changes as does a cicatrix formed under any other circumstances. These
pustules may be formed upon any mucous membrane. They occur often-
est in the nose, mouth, trachea, bronchial tubes and larynx.
There is nothing specific or essentially different in the development of
the pustules, in liemorrhagic small-pox, except that they contain blood in-
stead of serum or pus. In the hemorrhagic variety, larger or smaller
hemorrhages take place into the ceHular tissues and into the cutis ; in
the milder forms they take place only in the layer beneath the papillae ;
while in the severer forms they take place beneath all the cutaneous
layers ; even the subcutaneous fat may be infiltrated with blood. No
changes in the walls of the vessels have as yet been discovered which will
account for these hemorrhages. These extravasations more frequently oc-
cur in those cases in which death takes place before the period of pustula-
tion is reached- In hemorrhagic variola blood eitravasations occur into
the substance of all the organs, the marrow of the bones, and on mucous
and serous surfaces, and infarctions in the lungs are the rule. Hyper-
semia and cedema of the brain sometimes occur.
Etiology. — The disease is propagated only by contagion ; it is a disease
which can only be produced by its own specific poison, and is communica-
ble only to persons who are not protected from its influence. There has been
considerable question as to loliere the virus of small-pox Is located. Some
claim that it is exclusively in the pustule, and that it is not possible for a
person suffering from small-pox to give the disease to an unprotected in-
dividual unless some of the virus from the pustule is brought in con-
tact with a cutaneous or mucous surface. This is a mistake. That small-pox
can be conveyed by means of virus taken from a pustule there can be no
question, — "contagion by inoculation," — but the cutaneous surface of an
unprotected person may be rubbed with pus taken from a small-pox pus-
tule, and unless there is an abrasion of the surface the person will not be-
come inoculated with the disease ; but if the virus is brought in contact
with a mucous surface of an unprotected person he will almost certainly
contract the disease. It is equally certain that the disease can be com-
municated from one person to another by means of the breath and exhala-
tions from the skin.
There is no evidence that the disease can be conveyed by the discharges
from the bowels. Perhaps if a pustule should be developed somewhere
along the line of the intestine the discharges might become so contamina-
ted as to have the power of communicating the disease. Small-pox can
also be conveyed from one individual to another through the atmosphere.
In the open air the distance of contagion is about two and one-half feet.
748 ACUTE GENEEAL DISEASES.
In a small room the atmosphere may be so contaminated that an unpro-
tected person will contract the disease upon a single entrance into the
room. The disease can be conveyed in clothing, and the poison will re-
main for a long time in clothing unless it has been exposed for a consider-
able time to the air. In other words, there is no doubt but that it is a
portable disease. In order that the disease may be transferred by means
of the clothing or mercliandise, it is necessary that the clothing or mer-
chandise contain the pus or crusts from the small-pox pustules ; how long
a time may elapse before the virus loses its vitality is not known. There
are well-authenticated cases in which it has retained its virulence for
more than a year.
No period of life is exempt from the contagion of small-pox ; even intra-
uterine life is in danger from infection. Rarely does an individual have a
second attack, I remember one exception, that occurred in the person of
a young Swedish woman, who, under my observation, passed through three
well-developed attacks of the disease ; the last attack was the most severe.
Concerning the exact nature of the small-pox virus nothing definite is
known.' Some claim that the earliest period at which one suffering from
this disease can infect the unprotected, is the period of suppuration ; others,
that the infecting period is during the stage of desiccation. There are well-
authenticated cases, however, which prove that infection may take place
during any stage of the disease, even during the period of incubation.
There is little doubt but that the suppurative stage is the most infectious
period.
There are many views as to the manner in which the small-pox poison
gains entrance into the system ; the most probable of these views is, that
it is principally absorbed by the mucous membrane of the respiratory tract
during respiration, and it is also probable that exceedingly fine particles
detach from the pustules and crusts, which are suspended in great nurab3rs
in the air surrounding small-pox patients, and that these convey the con-
tagion. There are no facts to sustain the views as to the parasitic nature
of this contagion.
The length of time which elapses after exposure to, and reception of,
the variola contagion before the disease is developed varies from five to
thirty days, giving the extremes. This is called the period of incubation,
during which the recipient of the poison usually presents no abnormal
symptoms. If the poison is introduced into the system through inocula-
tion, only forty-eight hours elapse before the characteristic phenomena of
the variola are manifested. It is not known what change takes place in
the body of the infected person during this period of incubation. Usually,
twelve to fourteen days after exposure, one who has contracted small-pox
begins to feel chilly ; this feeling of chilliness increases until he has a dis-
tinct chill. This has been termed the initial stage, or the stage of initiatory
fever. Measles and small-pox poisons may be latent at the same time in
the same individual ; also scarlet fever and small-pox.
Symptoms.— The transition from the stage of incubation to that of the
1 Cohnheim and Weigert state that the micrococci in the vesicles are the contagious, specific elements.
SMALL-POX
749
initiatory fever is sometimes abrupt and sometimes gradual ; usually it
occupies two days, and is followed by the eruption. lu this stage there is
greater variation in the intensity than in the duration of the symj^toms.
The intensity of the symptoms bears no relation to the severity of the
attack. Not infrequently, the most violent symptoms in the initial stage
are followed by a mild attack of variola; while mild symptoms lu the
initial stage may be followed by the gravest form of small-pox. The head-
ache, which usually precedes the fever, grows more intense, only subsiding
as the eruption appears. With the chill, which may be more or less severe,
there is pain in the head and back, especially in the middle of the back
and loins,' with this pain there will be rapid rise in temperature. The
chill is more severe than in any other exanthem. During the first day the
temperature may rise to
104" F., during the sec-
ond day to 105° F., and
by the third day it may
reach 106° F. or 107° F. ;
in some cases it has been
said to have reached
109° F. Sweating be-
gins with the first rise in
temperature, and con-
tinues till the period of
eruption. With this rise
in temperature there will
be an acceleration of
pulse ; it may reach 100
or 120 beats per minute. fiq. lei.
In the stronff and robust Temperature Record in a case of Discrete Small-pox.
person, the pulse will be full and not easily compressed. In females, and
in the weak and feeble, the pulse has less volume and usually is more fre-
quent ; it may reach 140 beats per minute. In children, 160.
At the onset, there is usually more or less nausea and vomiting, and
soreness of the throat. This soreness of the throat may have preceded the
chill by twenty-four hours, but now in many cases it will be quite severe,
and the patient will complain of more or less dysphagia, and pain in the
pharynx. The extent of the throat symptoms will depend upon the sever-
ity of the attack. In the severer forms of the disease, by the third or even
before the end of the second day, there may be delirium. In all cases,
the face will be flushed, the conjunctivse congested, and there will be throb-
bing of the carotids. With these symptoms, there will be great restlessness,
and an anxious expression of countenance, with somnolence. The respira-
tions will be short, frequent, and labored, many complaining of dyspnoea
in whom there are no lung complications. Many suffer from extreme
vertigo, and in children convulsions are not infrequent. By the evening of
the second or morning of the third day swelling and diffuse redness of the
1 Incomplete paraplegia haa occurred, disappearing, however, with the appearance of the eruption.
750 ACUTE GENERAL DISEASES.
tonsils and soft palate are present ; not infrequently the swelling and red-
ness of the mucous membranes extend into the larynx, causing hoarseness
and huskiness of the voice and a stridulous cough.
During the fever of invasion patients are languid and weak in propor-
tion to the severity of the fever. " Frequently within twenty-four hours
after the ushering-in chill, the strongest and most vigorous will be unable
to get out of bed. Paralysis of the bladder may occur in this stage. The
tongue is coated. There is epigastric pain and tenderness. If vomiting
occurs it is present at the very beginning, and continues with great ob-
stinacy throughout its entire course. In the hemorrhagic variety the
matters vomited may contain blood. There is constipation, but diarrhoea
is not infrequent in children.
Stage of Eruption. — By the third day of the disease, at least after the
initial fever has continued three full days, an eruption will make its ap-
pearance upon the face, especially along the edges of the hair.^
The eruption, as it develops in a moderately severe case of discrete
variola, first appears in the form of slightly elevated maculae. These are
of a pale red color, varying in size from a millet-seed to a pin's head, or
even larger. These little red spots look very much like flea-bites. In most
cases the forehead, nose, and upper lip are first covered ; they gradually in-
crease in size, the increase being attended by a sensation of itching and burn-
ing of the surface. Usually, about twelve hours after their appearance
upon the face, similar small red points appear upon the neck and wrists,
then on the chest, arms, and legs. In children they may first appear on the
loins, nates, genitals, or about an excoriated or a blistered surface. They
are always less abundant on the body and extremities than on the face.
On the second day of the eruption, these spots assume a darker red color,
become elevated, and have a distinctly papular feel, like shot under the skin.
In a majority of instances, as they enlarge a depression is formed, which
gives them an umbilicated appearance. The appearance of the eruption
is attended by a subsidence of the febrile symptoms, the patient no longer
complains of pains in the head and back, the temperature falls two or three
degrees, and the pulse diminishes fifteen or twenty beats in frequency, some-
times to normal. Vesicles are also seen in the mouth, pharnyx, upper part
of the larynx, etc., etc.
Stage of Suppuration. — About the sixth day of the eruption the contents
of the vesicle, from the admixture of pus-corpuscles, gradually become
turbid, and by the eighth day the pustules . become fully formed, and the
disease enters on the stage of suppuration. The integument ia the im-
mediate vicinity of the pustule now becomes red, cedematous, and tumefied,
each pustule being surrounded by a broad red base, the " halo," and where
they are thickly set they become confluent. The face swells to a shapeless
1 Trousseau and many others state that the longer the skin manifestations are delayed, the more harm-
less the disease, and the more rapidly the eruption comes on the more dangerous is it.
^ Prior to the eruption a diffuse scarlatina-like redness sometimes covers all the body, and a few suda-
mina may appear in the erythema. At this point haste may lead to a diagnosis of scarlet fever or measles.
Petechise and ecchymoses are less frequently seen ; they are not necessarily followed by variola hemor-
ihagica.
SMALL-POX. 751
mass, and the patient becomes frightfully deformed. The eyes are closed,
and the hands and feet look like round balls. The itching now becomes
almost unbearable and causes the patient to scratch himself, thus causing
ultimate disfigurement. During this period a characteristic sickish odor
is emitted. The eruption passes through its stages two or three days later
on the extremities than it does on the face ; consequently, sujDpuration may
be complete on the face while it is incipient on the extremities, and the
eruption may be perfectly discrete on the trunk while it is confluent on the
face. About the eighth or ninth day of the eruption the pustule is fully
formed ; the stage of suppuration is complete. Then commence the retro-
grade changes. The pustule either ruptures, discharges its contents, dries
up and forms a yellowish crust, or it shrivels and dries up without ruptur-
ing ; this is the period of desiccation.
Stage of Desiccation. — Desiccation commences in those parts in which the
eruption first appeared, and commonly on the twelfth day of the disease.
As the drying down of the pustules takes place, the redness, tenderness and
oedema of the skin lessen, and the countenance begins to assume a more
natural appearance. At first the crust adheres quite firmly to the surface,
but about the fourteenth day of the eruption it becomes separated and
falls, leaving a stain of reddish-brown color, with elevated edges and de-
pressed centre, which remains visible for five or six weeks. These spots
gradually become lighter in color, until finally, if there has been destruc-
tion of the cutis, and if excoriation, ulceration and renewal of the scab
have occurred, a pit will be formed of greater or less depth, of a white
color, giving to the face a " pock-marked " appearance, which will remain
during the life of the individual. The febrile symptoms gradually increase
m severity until the third day of the disease, when the eruption appears
and the fever subsides. Then the vesicles form, the formation of which
is attended by only moderate fever.
On the eighth day the pustules are fully formed, and the " suppurative,''^
or secondary fever comes on. This secondary fever often commences with
a distinct chill. The fever is highest in the evening ; it is of a distinctly
remittent type, the pulse becomes frequent, the temperature rapidly rises,
perhaps reaches a higher elevation than it did during the initial fever,
sometimes rising as high as 108° or 109° F. ; it reaches its maximum when
suppuration is at its height. As desiccation commences, the temperature
begins to fall, and by the time the crusts are fully formed the temperature
reaches very nearly a normal standard. If the temperature rises again, its
rise is due to some complications such as erysipelas or some phlegmonous
process. With the fall of the crusts, the patient's appetite returns, and he
is able to sleep; convalescence is now fully established.' The dividing
lines between the different varieties of small-pox are not sharply defined ;
one variety gradually passes into another. It is unnecessary to consider all
the forms into which this disease has been divided by some writers ; fre-
quently the basis of the division is merely arbitrary. Our attention
' Thi; meiiBes appear in the initial stage in the large majoritj' of women with small-pox, even though it
be not the proper time. (Q,uinclce, Leo, Knecht, Curshmann, Bucli:, Obermeier, and others.')
753 ACUTE GENERAL DISEASES.
will therefore be confined to the more common and well-recognized
varieties.
Confluent Small-pox, or Variola Confluens. — This is a much more severe
form of the disease than variola discreta. It develops far more rapidly and
is much more fatal in its results. The fever of invasion is usually much
more severe, and of shorter duration, frequently not lasting more than forty-
eight hours.' The eruption spreads rapidly over the entire body, often
appearing simultaneously on the face and the other portions of the body.
The red dots which mark the first appearance of the eruption are very
numerous, especially on the face and hands ; on the first day of their ap-
pearance they are almost confluent. The conjunctivae are early involved
and suppurative keratitis is not uncommon in this variety ; — the whole eye
may be converted into an abscess. On the second day the skin is intensely
red and swollen, and so thickly studded with large flat vesicles that they
rapidly unite, suppuration speedily follows, and flattened, yellowish-colored
confluent patches are formed upon a dark, reddened, swollen skin. Gradu-
ally these patches run together over a still larger surface, and the epidermis
is elevated in the form of large, flat bullse, which are filled with a sero-
purulent fluid and are tense and elastic. In this way the entire skin of the
face is covered by an immense bulla, and the patient is as unrecognizable
as though he wore a mask. While the eruption may be completely con-
fluent on the face and hands, on other parts of the body it remains discrete,
and never becomes confluent except over limited spaces.
The period of desiccation is slowly reached. Large concentric crusts are
formed over the confluent patches ; these adhere firmly to the skin, while
beneath them suppuration of the papillary layer continues. The true skin
is more or less extensively destroyed, and when the crusts have fallen,
there is left extensive loss of substance in the cutis, giving rise to pits and
ugly scars, which have a tendency to contract, often producing permanent
and unsightly disfigurements. In this variety of small-pox, the eruption
is often confluent upon the mucous membrane of the mouth and throat ;
it may involve the mucous membrane of the posterior nares and extend
into the larynx. In some cases the attending pharyngitis is so severe as to
render deglutition impossible. The pharyngeal inflammation is submu-
cous, and is frequently accompanied by more or less enlargement of the pa-
rotid and sublingual glands. When this condition exists there is danger
of the sudden development of oedema glottidis, for the occurrence of which
one should be on the watch. ^
In confluent small-pox hemorrhage may occur in the pustules ; this is
not variola hemorrhagica, but a hemorrhagic pustular confluent small-pox.
In confluent variola the skin may exhibit erysipelas, phlegmon, gangrene
or multiple abscesses. In confluent small-pox the severity of the consti-
tutional symptoms corresponds to the severity of the local manifestations.
1 The thermometer not infrequently shows a fever of 106° to 110° F. for a short time, which sinks to
103° to 104° till suppuration, then rising even higher than before.
2 During the year thar, I had charge of the Small-pox Hospital, there were three cases in the hospital of
oedema glottidis : one case terminated fatally before I reached the patient ; life was saved in the other
two cases by the performance of laryngotomy.
SMALL-POX.
753
The temperature during the initial fever often reaches 106° V. or 107° F.,
and in very severe types of the disease it may rise as high as 110° F. The
Pig. 16-2.
Temperature Record in a case of Confluent Small-pox.
pulse is correspondingly frequent and feeble. After the appearance of
the eruption the temperature falls slowly to 103° F. or 104° F., where it
remains until the stage of suppuration is reached ; then it again rises, in
some cases even higher than during the period of invasion. Violent delirium
is very frequently present during the fever of invasion, as well as during the
period of secondary fever, and not infrequently patients pass quite sud-
denly into a state of coma. Uncontrollable vomiting and obstinate diar-
rhoea are not infrequent, coming on during the fever of invasion and con-
tinuing throughout the course of the disease.
In all severe cases typhoid symptoms manifest themselves soon after
the appearance of the eruption, and patients often lie for days in a semi-
conscious state, with dry, brown tongue, subsultus, a low muttering deli-
rium, and all the attendant phenomena of intense nervous depression. In
such cases albumen appears temporarily in the urine. Complications oc-
cur much more frequently in confluent than in discrete small-pox. Inflam-
mations of the serous membranes, especially pleurisy and pericarditis, are
the most common. Croupous and catarrhal pneumonia and acute laryn-
gitis frequently complicate the severe bronchial inflammation from which
so few patients with confluent small-pox escape. Permanent alopecia often
follows confluent small-pox.
Variola hemorrhagica ' is a form of small-pox which can hardly be
regarded as a distinct variety, but rather as a modification of other vari-
eties, called the black or malignant small-pox. It differs from the varie-
ties already described, not in the manner of its development as far as the
initial fever is concerned, but in the appearance of the eruption. This hem-
orrhagic tendency is often manifested as early as the first appearance of the
eruption, by the dark color which the eruption assumes. Sometimes the
> Zulzer found that in eighty-five to ninety per cent, of hijn cases of hemorrhagica, the period of incuba-
tion was only hIx to eight days, i. e., half as long as in simple small-pox.
48
754 ACUTE GENEEAL DISEASES.
papules become hemorrhagic from the very moment of their development)
at other times they first become vesicles, and then become hemorrhagic.
Again, at other times, the hemorrhage first shows itself after the vesicles be-
come pustules. In some cases the eruption over the whole body becomes
hemorrhagic ; in other cases, it is hemorrhagic in spots. In the majority of
cases, the eruption becomes hemorrhagic as soon as the papules have at-
tained the size of a lentil, and the hemorrhagic change comes on slowly,
generally commencing on the lower extremities. Petechise and ecchymoses
often appear between the points of eruption.
In connection with the hemorrhagic eruptions, hemorrhages from the
various mucous membranes of the body will simultaneously occur — from
the mucous membrane of the nose, perhaps from the bronchial mucous
membrane, and sometimes large ecchymotic spots may be seen upon the
mucous surfaces of the mouth and throat. Haematuria, conjunctival
hemorrhages, melsena, hsematemesis, haemoptysis, bleedings from the gums,
and particularly epistaxis are met with. It is rare for this form of
small-pox to reach the stage of suppuration, for before this sta.ge is reached
patients die. During the initial stage of this variety of small-pox, the
constitutional symptoms do not differ from those which attend the de-
velopment of the other forms of this disease. It is impossible, from their
character and intensity, to predict, with any degree of certainty, the subse-
quent development of hemorrhagic variola. It has been said that the pains
in the back and limbs are more severe ; but these are not characteristic.
Frequently the fever of invasion is exceedingly violent, while during the
eruptive period, and during the entire subsequent course of the disease, the
temperature is comparatively low. In cases in which extensive hemorrhages
have occurred, the temperature often falls below the normal, while the
pulse ranges from 140 to 160, and is exceedingly feeble in character. Only
when comparatively few of the vesicles become hemorrhagic does the case
terminate in recovery.
Differential Diagnosis. — The first question that arises is : how early can
>small-pox be recognized ? One who has seen very many cases of the disease
may be able to reach a diagnosis on the third day, that is, the first day of
:the eruption, although at that time there is nothing characteristic about
the eruption or the ushering-in symptoms. It is, however, better and safer
to wait until the second or third day of the erujDtion before making a posi-
tive diagnosis, for there is little to be feared from infection until the vesi-
cles are fully formed.
The eruption of measles, in its early stages, is liable to be taken for
small-pox. If one defers making the diagnosis until the vesicles are fully
developed, no such mistake will be made. In measles there is coryza, a
cough, sneezing, redness and suffusion of the eyes. These symptoms are
not present in small-pox. In small-pox, when the stage of eruption is
reached, the temperature falls ; while in measles, when the eruption ap-
pears, the temperature continues to rise. The range of temperature is two
to three degrees higher in small-pox than in measles. In these respects the
two diseases differ sufficiently to enable a differential diagnosis to be made.
SMALL-POX. 755
Again, if one waits until the vesicles become umbilicated, it will be impos-
sible that a mistake in diagnosis should be made.
During the period of initial fever it is possible to mistake small-pox for
typhus fever. In both diseases there may be delirium, pain in the head,
vertigo, high temperature, and evidence of great disturbance of the nervous
system. There is no system which will enable a positive diagnosis to be
made during the very early period of the disease. Of course, if typhus fe-
ver is prevailing, or if small-pox is prevailing, and the patient has been ex-
posed to either one of these contagions, one will be able to make a diag-
nosis without difficulty. Usually there is greater loss of muscular power
in typhus fever than in small-pox, but this symptom is not always well
marked. By the third day, the appearance of the eruption upon the face,
where it is first seen, settles the question of diagnosis. The eruption of ty-
phus fever is first seen upon the abdomen, and may extend over the whole
body without appearing on the face. It rarely appears before the fifth day
of the fever. Therefore, the differential diagnosis between small-pox and
typhus fever can be readily made as soon as an eruption appears. The
temperature falls as soon as the eruption occurs in small-pox, and does not
in typhus.
Meningitis is another disease which small-pox, in its initial stage, resem-
bles. There is always considerable cerebral disturbance and a full, hard,
bounding pulse in the initial stage of small-pox. Photophobia, intense
pain in the head, nausea and vomiting may be present in both diseases.
Unless it may be the expression of the face, there is often no distinguish-
ing mark between the two diseases in their early stages. In meningitis,
there is usually a pale, anxious expression of countenance, whereas early in
small-pox the face is flushed, and day by day the flush deepens until the
eruption appears. The fever in meningitis is lower than in small-pox by 2° to
3° F., the pulse is smaller, less compressible, and not as rapid as in variola ;
and the vomiting is projectile in meningitis, while it is retching in char-
acter in variola. On the appearance of the eruption, the differential diag-
nosis between these two diseases is readily made.
Prognosis. — The prognosis in any case of small-pox depends upon the
amount of the eruption ; the more abundant the eruption, the greater the
danger to life. The prognosis also depends upon the type of the disease. Un-
less some complication arises, most cases of discrete small-pox recover ; while
of confluent small-pox nearly one-half the cases prove fatal. ' The best record
obtained in the small-pox hospital on Blackwell's Island was one death in
every five cases. Only a very few cases of the hemorrhagic variety recov-
ered, and when recovery did take place it was only reached after the patient
1 In twenty years the "Loudon Small-pox Hospital " gives the following definite statistics :
No. Mortality.
Patients admitted with small-pox 4,8~9
A. With 1 vaccine scar 2,001 7 7-10 per cent.
B. " 2 *' scars 1,446 4 7-10 " "
C. " .3 " " 518 19-10 " "
D. " 4 or more scars 544 1-3 " "
E. Said to have been vaccinated, but no scar visible 370 2.3 1-2 " "
In the " London Small-pox Hospital " the mortality is: 4 per cent, of discrete, simple variola; 8per cent,
of semi-confluent variola ; and 50 per cent, of confluent variola.
756 ACUTE GENERAL DISEASES.
had passed through an apparently fatal condition of coma. The ratio of
mortality is always lower at the end than at the beginning of an epidemic.
The disease is more fatal in the summer than in the winter.
The age of the patient greatly influences the prognosis. In infancy and
old age the ratio of mortality reaches its maximum. Among adults the
prognosis is worse in females than in males. In the intemperate the prog-
nosis is always bad, for with this class of persons the disease is liable to
assume a hemorrhagic type. The intemperate die in discrete small-pox
when the temperate would almost certainly recover. In the overworked
and badly-nourished the prognosis is bad. The robust and healthy pass
through a severe type of the disease much more safely than those enfeebled
by chronic disease. The severity of the fever of invasion is not a safe guide
in prognosis. Sometimes a severe initial stage precedes a mild form of the
disesse ; sometimes patients with this disease pass into a state of complete
unconsciousness, remain in that condition for some time; then the erup-
tion begins to change in color, and finally recovery takes place. Such
cases, however, are exceptional. However well-developed the eruption
may be, or however well-filled the vesicles, it is to be remembered that the
eighth day is the commencement of the suppurative fever, which is the
period of the greatest danger. Upon this day the patient may pass into a
state of collapse, the result of the depressing influence upon the nervous
system produced by the large extent of surface involved in the suppurative
process. In most cases in which patients do not die until the second week
of the disease, the fatal result is due to exhaustion, although death may
occur from complications. Usually they pass into a typhoid condition, the
result of the excessive drain upon the system by the suppurative process.
Pregnancy is a bad complicating condition ; in the confluent, the ab-
sorption that is so liable to occur is likely to be attended by fatal hleecUng.
The most frequent complications which cause death are those which occur
in the throat and air-passages. In some instances swelling of the glands
of the neck and mucous membrane of the throat takes place to such an
extent as to seriously interfere with deglutition and respiration. When
this occurs it becomes an element of great danger, and materially affects
the prognosis. The tongue may become swollen to such an extent that the
patient will be unable to protrude it, or, being able to protrude it, will not
be able to retract it. Under such circumstances deglutition is almost im-
possible. There may be laryngeal ulcers, and ulcers occurring in the
trachea and in the bronchial tubes.' Whenever, in the course of the
disease, the urine becomes scanty and high-colored, but especially when it
becomes so at the commencement of the secondary fever, it is certain that
kidney complication exists. Under these circumstances the patient may
I Keratitis, choroiditis, iritis, conjunctivitis, inflammation of tlie middle ear, ulcers in the nose, acute
arthritis (of the large joints), pericarditis, ulcerative endocarditis, pycemia, and erysipelas— these are all
occasional complications. Diphtheria is a common complication of hemorrhagic variola. Cerebral hemor-
rhagei¬ an infrequent complication of small-pox; aphasia may also occur, and thrombosis of the
basiliar artery may induce a "dementia-like" condition. (Collie.) Boils, abscesses, and phlegmons of
the skin are frequent sequelae of small-pox. Blindness and deafness also not infrequently follow, as also
paralysis of the bladder and paraplegia, due (according to Westphal) to acute disseminated myelitis that
has complicated the fever.
SMALL-POX. 757
pass into a condition in which convulsions will be developed, and coma
and death ensue.
Treatment. — The first question that arises is : — have we any means by
which we can arrest small-pox after the initial fever has been established ?
In vaccination, properly performed, we undoubtedly possess a means by
which we may prevent one from contracting the disease when exposed to
its infection. But the question arises : have we any power to arrest the
development or mitigate the severity of the disease after the initial fever is
established ? No reliable affirmative answer has been given to this ques-
tion. It has been proposed to accomplish this by blood-letting, emetics,
diaphoretics, purgatives, cold baths, and more recently by the subcutane-
ous injection of the vaccine virus. All of these means have been tested,
and have failed to accomplish the desired result. The assertion that large
doses of quinine, given during the stage of invasion, will shorten the dura-
tion and modify the course of the disease is verified only by the experience
of its author (Stiemer). Quite recently, it has been claimed that carbolic
and salicylic acids destroy the septic poison of the variola, and thus shorten
and modify the course. My own experience as regards their use has not
been sufficient to decide the question, and I am unable to find any statistics
which sustain such an assertion.'
During the fever of invasion all that can be done is to treat special symp-
toms. Place the patient in bed in a large well- ventilated apartment ; if
possible, keep the temperature of the room below 60° F. I remember that,
in the Small-pox Hospital, those patients did best who were placed in bar-
racks, which were so open, that frequently, during the winter months,
when I made my morning visit, I would find little snow-drifts on the floor
between the beds. When the body temperature ranges as high as 107° F.
or 108° F., it is recommended to employ cold to the surface, and to give
antipyretic doses of quinine to rediice the temperature. If the headache
is severe and the face flushed, iced compresses and ice-bags to the head will
usually afford relief. If the vomiting is severe and constant, iced carbonic
acid water may be given, and if the vomiting is attended by great restless-
ness, hypodermic injections of morphine are indicated. Administer such
food as can be readily assimilated. I have found nothing better than iced
milk and seltzer water. If the bowels are constipated, it is well to relieve
them by enemata of cold water. In those cases in which the eruption is
tardy in making its appearance, and the temperature is higher, sometimes,
if the patient is kept in a warm bath for fifteen or twenty minutes, the de-
velopment of the eruption is hastened.
When the eruption has appeared, the measures to be employed will vary
with the character of the eruption. The milder forms of discrete variola
require no interference. In the severer forms the attendant symptoms
will decide the means to be employed. Sooner or later, sometimes very
early in the severer forms of the disease, the patient will be found sinking
from the depressing effects either of the small-pox poison or of the sup-
1 Zulzf.T Cone of the authors in Ziemsfen) states that xylol given internally coagulates the contents of
the pustules and cuts short their development.
758 ACUTE GEN"BRAL DISEASES.
purafcive process which is taking place upon the surface of the body.
Under such circumstances stimulants are indicated. There is no question
but that the free use of stimulants for a few days, just at the period of
suppuration, in very many cases does much to save life. At this time the
patient has a dry tongue, a frequent, feeble pulse, blue lips and finger ends,
giving evidence that he is rapidly passing into a state resembling that met
with in the later stages of typhoid fever. Active delirium is frequently
present ; the patient insists upon getting out of bed. Under these circum-
stances, life will often be saved by the judicious use of stimulants. If the
delirium is excessive, hypodermics of morphine may be combined with
the administration of stimulants.
During the stage of desiccation, warm baths employed every day or every
other day give great comfort, and assist in the removal of the crust. After
the baths the surface should be freely oiled. Complications will be treated
according to the general rules which govern their treatment. If abscesses oc-
cur in the subcutaneous tissue, they should be freely opened at once. We are
powerless when we come to deal with the hemorrhagic form of small-pox.
Although tonics and stimulants have been highly recommended, they do
little good. Transfusion has been proposed and practised with no definite
results. If the mouth and pharynx are very much involved, and there is
difficulty in deglutition, ice-cold carbonated water with a weak solution of
the muriated tincture of iron used as a gargle will often give great relief.
Sometimes the stronger antiseptic gargles, such as carbolic acid and the
permanganate of potash, will be of service.
There is still one point in the treatment of small-pox which is deserving
of attention, and that is, what means may be employed to prevent the
pitting, especially upon the face, which is so frequent a result. The erup-
tion first makes its appearance upon the face ; there it is usually most
abundant, and is most liable to be followed by pitting, and there it passes
more quickly through all its stages than upon any other part of the body.
In order to prevent pitting it has been proposed by some to exclude
light and air from the surface covered by the eruption. For this purpose
a great many substances have been employed, such as collodion, gutta-
percha, certain forms of. plaster, liquid paper, etc., etc. All these sub-
stances are to be so applied as to form a mask for the face, which completely
excludes light and air from the surface. ' The pitting is due to the forma-
tion of a slough, and the slough is seated in the areolar tissue ; if by any
means you can so interfere with the inflammatory process as to prevent the
formation of a slough, you will prevent the pitting. It was claimed by
those who advanced the theory that excluding light and air prevented the
pitting, and that it did this by preventing the occurrence of sloughing. °
1 Gold leaf, mild mercurial ointments, bismuth, chalk and sweet-oil, linseed meal poultices, collo-
dion, carbolic acid and white lead paint have all been extensively used.
» When I had charge of so many small-pox patients, I took pains to test all those applications which
at that time had been and are still recommended for the purpose, and I satisfied myself that about
the same results were obtained in the use of every remedy, and in no case was pitting prevented. Certain
patients were much more scarred than others, but that was the natural result of the disease. Some have
■nroposed to coagulate the serum in each vesicle by nitrate of silver, and to paint each papule with iodine,
and so arrest the inflammatory process and prevent pitting. But the use of tkese means has been
INOCULATION AND VACCINATION. i'59
ESrOCULATIOTiT AISTD VACCESTATION.
There are two recognized methods of protection against the infection of
small-pox : inoculation and vaccination. Inoculation was first introduced
into England by Lady Montague, who first practised it upon her own child.'
Subsequently it was quite generally practised throughout Great Britain.
Pus from a small-pox pustule was introduced beneath the epidermis of one
who had been prepared by diet and general hygienic measures for the safe
development of the disease. It was claimed that the disease resulting from
inoculation was a modified small-pox, differing from the original disease in
that it ran its course more rapidly, was attended by few pustules, perhaps
no more than twenty or thirty, and was said to rarely terminate fatally, the
ratio of mortality being about one in one hundred. Those who were inocu-
lated were as fully protected from small-pox as those who had the disease
in the ordinary manner. The disease developed by inoculation passed
through the regular stages of small-pox.
Early in 1776 Edward Jenner observed that in some of the northern coun-
ties of England persons employed in dairies, who suffered from a certain
form of ulcer upon their hands, did not contract small-pox when exposed
to it.' He also found that these ulcers upon the hands resembled pustules
found upon the udder of the cow, and seemed to have been caused by con-
tact with them. Jenner made a thorough investigation of the subject, and
arrived at conclusions sufficiently satisfactory to himself to warrant the ex-
periment of taking matter from one of these pustules found upon the udder
of the cow and introducing it into the arm of the individual who was sup-
posed to be unprotected from the contagion of small-pox. After the sore
upon the arm had run its course, he exposed the individual to the infec-
tion of small-pox, and in this way he established its protecting power. In
1796 he made his first vaccination on man. In 1798 he published his first
paper on the subject.^ Vaccination was introduced into this country in
the year 1799, by Waterhouse of Boston, and very soon became the practice
of the profession. In 1800 it was first practised in France. At the pres-
attended by the same unsatisfactory results. The only means which I found of certain value was a simple
cold-water dressing applied over the face, after having ruptured each vesicle before it became a pustule.
In this way, I was able to diminish the intensity and extent of the inflammation. This plan of treatment
I adopted in twenty cases of confluent small-pos, and it not only gave the patients very great comfort, re-
lieving them to a certain extent from the intense itching, thus avoiding rupture of the vesicles by scratch-
ing, but not in a single case that recovered was there bad pitting. In the treatment of smnll-pox, the pre-
vention of pitting is of greatest importance to certain patients, especially young unmarried females.
1 In 1717 Lady Montague, writing from Adrianople, in Turkey, where the practice of inoculation was in
vogue, says : " They take the small-pox here for diversion ; I have tried it on my dear little son ; I am
going to bring this useful invention into fashion in England." In 1718 it did become the fashion.
^ In 1771 a Holstein schoolmaster vaccinated three pupils, and in 1774 an English farmer vaccinated his
wife because of his belief in the power of bovine virus as seen in his dairymaids.
3 During six years no member of tlie profession ever received more anathemas or more scurrilous abuse
than Jenner. He was attacked by the leading physicians and surgeons of Great Britain, and persecution
and ridicule so followed him that placards with caricatures of Jenner were posted throughout the streets
of London and the principal towns of Great Britain ; Jenner kept steadily at work and repeated his ex-
periments, until he became fully convinced that by vaccination perfect protection could be obtained
against small-pox. Within the short space of six years Jenner compelled the profession to admit his state-
ments and adopt his practice, and within the five or six years following its first recognition, the pracUCCOS
vaccination became generally recognized and practised.
760 ACUTE GENERAL DISEASES.
ent time there is no question among the intelligent portion of the pro-
fession but that vaccination, properly performed, is a perfect protection
against the infection of small-pox ; if persons contract small-pox after they
have been vaccinated, then it has not been properly performed.
There are two methods of performing vaccination. One method is to
take the virus directly from the cow ; this is called hovine virus ; the other
method is to take the virus from a vesicle developed upon the human body, —
perhaps a vesicle removed from the original by several vaccinations, — this
is called humanized virus. To-day good humanized virus is warmly advo-
cated ; first, because it is more successful (98 per cent.) than bovine virus
(only 70 per cent. ) ; and secondly, because it is a surer safeguard. Jenner
found that there were several pustules developed on the udder of the cow
which closely resembled each other, but that only one contained the virus
which afforded protection from small-pox. In obtaining bovine virus it is
of the greatest importance that the genuine vesicle be selected. In order
to make the selection, it is necessary one should be familiar with the pe-
culiarities of each variety. If humanized virus is used, there is danger of
introducing into the system the infection of other diseases. I have in my
possession facts which prove beyond the possibility of a doubt that syphilis
can be conveyed from one person to another by vaccination. Cutaneous
eruptions may also be conveyed by humanized vaccine virus, which cause
the development of very extensive and serious cutaneous diseases. Again,
if any chronic or acute skin disease exist at the time the vaccine vesicle is
running its course the protective power of the vaccination will be altogether
destroyed or very greatly modified.' The vaccine virus is usually intro-
duced by scarifying the surface so as to redden it, scarcely drawing blood ;
then the surface of the quill containing the virus is applied to the scarified
part, or the lymph is conveyed from one to the other by direct transmis-
sion.
Any irregularity in the development of the vesicle destroys in a greater
or less degree its protecting power. When an individual has been once
vaccinated, a second vaccination is liable to run an irregular course.
A primary vaccination, such as the first vaccination of a child, sTiould
pass through the following regular stages, and if it does not it fails to give
protection : upon the third day after the introduction of the virus there
will be noticed at the point where it was introduced a little red spot, — a
papular elevation. By the fourth day this little red spot will be occupied
by a bluish- white vesicle, and at the commencement of the fifth day there
1 In obtaining vaccine virus for use, both the bovine and the humanized virus should be taken from the
vesicle on the eighth day. The lymph should be taken from the vesicle before the inflammatory process
has commenced which is to change it into a pustule. Jenner's " Golden Rule " was, any vesicle which
manifests an areola must be discarded in the matter of withdrawing lymph. A few years ago it was the com-
mon practice in this city to use the vaccine crusts, but this practice has fallen almost entirely into disuse
because of the great danger of thereby transmitting other diseases. I prefer bovine virus when It is possible
to obtain it. If compelled to use the humanized virus, use the lymt)h. The vesicles must be punctured in
such a manner that the Ij'mph cannot be contaminated by the blood ; this is best done by introducing the
instrument parallel with the arm. The vesicle must be tapped in several places. The lymph which spon-
taneously flows from such a puncture can be preserved upon the convex surface of a piece of quill, and
conveyed from one individual to another. Vaccine virus secured from the human arm in this maimer is
less liable than any other form of humanized virus to do permanent harm to the vaccinated individual.
INOCULATION AND VACCINATION. 761
will appear around the vesicle a little yellow margin. This vesicle goes
on increasing in size up to the eighth day, when it will become umbilicated
and there will appear around it a distinct areola ; about the seventh day
there has been a trifling areola present ; on the eighth or ninth day it be-
comes very distinct, Now a change is to take place in the vesicle, and by
the next day it will be noticed that the areola has extended, perhaps so as
to measure an inch in diameter ; this areola goes on extending itself
through the ninth, tenth and eleventh days, when it will have reached its
maximum extent, which may be one or two inches from the vesicle in all
directions. It is now a deep red color. The part over which the areola
has spread is more or less elevated, the arm is considerably swollen and
painful, and the adjacent glands more or less enlarged and tender to the
touch. The extent of the enlargement of the gland adjacent to the vac-
cine vesicle, — the axillary gland, if the vesicle is upon the arm, the inguinal,
if it is upon the thigh, — varies considerably in different persons.' In some
it is very great, in others it is scarcely noticeable. The maximum degree of
inflammation in the vesicle has now been attained, and there is a distinct
infiltration of the tissues about it.
On the twelfth or thirteenth day the pustule ruptures, and the contents
escape. The rupture belongs to the natural course of the vaccine vesicles,
and is independent of mechanical violence. From this time the inflamed
areola becomes less and less distinct, and by the fourteenth or fifteenth day
the crust has assumed a dark, brownish appearance, which goes on deep-
ening until on the seventeenth day a deep-brown crust is formed having a
central depression and no areola of inflammation. It may be attached
to the surface only in one or two places, and can be readily removed. If
permitted to remain, it usually falls off on the eighteenth to the twenty-
first day. This is the course pursued by a perfect vaccine vesicle. The
shape and size of the crust will correspond to the shape and size of the
vesicle. If the eighth day a pustule is formed instead of a vesicle, it is
evident that the regular development of the vesicle has been disturbed, and
that it will not afford complete protection.
The inflammatory process around the vesicle is usually more active when
the bovine virus is used, than when the humanized virus is introduced, and
there is more constitutional disturbance. Ordinarily, during the develop-
ment of the vaccine vesicle and pustule, there is but little constitutional
disturbance ; this is usually self -limiting, and not sufficiently severe to
require treatment. In children, eruptions, transitory in character, are
liable to occur about the eighth or tenth day. About the eighth or ninth
day the person vaccinated may feel a little chilly, and have severe headache ;
in most cases there is a slight rise in temperature.
The regular course of the vaccine vesicle may be interfered with by the
occurrence of an erysipelatous inflammation, and if such an inflammation
does occur during the course of its development, it entirely destroys the
protecting power of the vaccination. Again, if a large quantity of pus has
been discharged, and healing of the ulcei- does not take place for two or
' Tiie axillary swelling is sometimes so intense that abscess results.— §Mam's Diet
763
ACUTE GENEKAL DISEASES.
three months, it is probable that something besides genuine vaccine virus
has been introduced into the arm, and that the vaccination is not pro-
tective. As I have already stated, the presence of a vesicular eruption upon
the surface at the time vaccination is performed will interfere with its de-
velopment, therefore I would advise never to vaccinate one who has an ec-
zematous eruption upon any part of the body, unless he has been exposed
to the contagion of small-pox, for it is very probable that the vaccination
will not be a protective one. It is better never to vaccinate a person having
any form of skin disease, especially if the eruption is vesicular in character.
The best time for the first performance of vaccination is in infancy, between
the third and fifth months.
Eevaccination should be performed after puberty, and always after or
preceding a new exposure to the contagion of small-pox, for the period dur-
ing which revaccination will afford complete protection is not the same in
every individual. In some cases a single vaccination will afford complete
protection for a lifetime. In other cases it is necessary to frequently repeat
the vaccination, perhaps every two years, in order to secure the desired
protection.^
VAEIOLOID.
During every epidemic of small-pox there is a certain number of cS,ses
concerning which there will be doubt as to whether they are cases of variola
or varioloid. Certain persons who have never been vaccinated may, through
a naturally slight susceptibility to the infection of small-pox, have so mild a
form of variola that it is difficult to distinguish it from varioloid.
Varioloid differs from small-pox in the rapid development and decline of
the symptoms, in the small number of the pustules, and in the short time
required for the formation and separation of the crusts. The entire period
of the eruptive stage often does not
last more than a week. Earely are
cicatrices or pits left after the erup-
tion. In varioloid the period of in-
cubation is about one-half as long as
in variola, hence the onset of the
graver disease may be anticipated by
vaccinating one who is known to
have been exposed, and who, other-
wise, would go on and have the un-
modified disease.
In varioloid and variola the pus-
tules pass through similar stages. We
first have the small red spot, then
vesicles form, often within twelve
hours after the appearance of the erup-
iton. These vesicles rapidly increase
sometimes they are umbilicated ; by the end of the third day their
PiG.163.
Temperature Record in a case of Varioloid.
m size
The best plan is to vaccinate at intervals until the individual has four good scars.
CHICKEN-POX. 763
contents sometimes become purulent, without any tumefaction of the sur-
rounding skin. Many vesicles abort ; they do not become pustules. On
the fifth day desiccation commences, which is often complete by the seventh
day. The majority of the pustules simply dry up, without previously
bursting, and form brown crusts which are thinner and smaller than those
of variola. In varioloid there is no regular period of development as in
variola. In variola there is the period of eruption, during which the vesi-
cle is perfected ; this is succeeded by the period of suppuration, then by
desiccation, about fourteen days being required to complete the process ;
while in varioloid the course of the eruption is irregular, and is usually
completed within one week. Secondary fever is slight or absent. Again,
in varioloid there is but little constitutional disturbance after the appear-
ance of the eruption. By the end of the first or commencement of the sec
ond day the temperature is usually normal. It resembles variola in the
severity of the symptoms during the period of invasion, but as soon as the
eruption appears there is an entire cessation of all the active febrile symp-
toms. During the period of invasion varioloid may be said very closely to
resemble variola. When an unprotected individual is exposed to varioloid,
the most severe confluent small-pox may be the result. This fact proves
that varioloid is a modified form of small-pox. Varioloid is small-pox hav-
ing a shorter duration and a milder course than usual.'
Prognosis. — Usually the prognosis is good. The rapidity with which the
vesicles are developed, their shorter duration, the subsidence of the fever,
and the appearance of the eruption, together with the usual duration of an
attack, are sufficient to distinguish it from variola.
Treatment. — The treatment for varioloid is the same as for a mild or mod-
ified form of small-pox. The patient should be placed in a large, well-
ventilated room, and quarantined the same as though suffering from vari-
ola. If the form of invasion is severe, saline cathartics may be adminis-
tered. When delirium is present, and the pain in the back is very severe,
the moderate use of opium is admissible. As soon as the eruptive period
of varioloid is reached, no further treatment is required ; the patient passes
on to a rapid and complete convalescence.
CHICKE]Sr-POX.
(Varicella.)
Varicella is an acute contagious febrile disease accompanied by a vesicu-
lar eruption, which chiefly affects children. It has been called " spurious
variola," swine-pox, etc., etc.
Morbid Anatomy. — The only lesion of this disease is the eruption, which
consists of small slightly elevated rose-spots, varying in number from twenty-
five to two hundred, which in from ten to twenty-four hours become small
> It may be said that we modifj' small-pox by inoculation. We do not : we only modify its intensity.
There is the same regular development of the disease after inoculation that we have in the ordinary form
of small-pox ; while by vaccination we not only lessen the severity of the disease but we are able to so
modify the stages of its development as to shorten its duration.
7G4 ACUTE GENERAL DISEASES,
vesicles with, clear contents. They vary in size from a pin's head to a pea.
They are usually discrete, but may run together and form bullae three-
fourths to two inches in diameter. They rest on a hypersemic zone of skin.
In many cases the areola is absent. As the vesicles enlarge, they become
globular or ovoid in shape and their contents are translucent, glistening
and opalescent, never acid as in sudamina. Sometimes the vesicles are di-
vided into compartments. On the third day pustulation of a few vesicles
may occur. On the fourth day the vesicles commence to dry up ; on the
sixth crusts are formed. One crop occupies rarely more than six days, and
as a second crop appears or starts also on the second and third day of the
firsi crop, the whole number of days of the eruption is from seven to nine.
According to the shape of the vesicles, varicella is called lenticular, glob-
ular, conoidal,^ etc. Pitting rarely occurs ; should cicatrices remain, they
disappear in two years.
Etiology. — Opinions are still divided as to the identity of variola and vari-
cella. Hebra claims that there is one poison for the two diseases. Senator,
Thomas, and others regard it as a specific disease. It occurs sporadically
and epidemically. Inoculation has given negative results. The period of
incubation varies from eight to seventeen days.
Symptoms. — Twenty-four hours preceding the eruption there is usually
lassitude and a feeling of malaise. The eruption appears first on the back
or cheek, and then on the face or scalp. It spreads irregularly to the abdo-
men and extremities. About the second day vesicles may appear upon the
tongue, lips, cheeks, palate, and on the mucous membrane of the genitals.
On the second day after the first crop of the eruption a new crop appears,
and in many cases there is a third crop on the following day. The tem-
perature rarely rises over 100° or 101° F.
Diiferential Diagnosis. — The points of differential diagnosis between
varicella and variola are as follows : — varicella runs rapidly through its
stages ; small-pox has three distinct periods — the papular, the vesicular,
and the pustular. The eruption of varicella is complete by the third, while
the eruption of variola is never complete until the ninth day. In both
natural and modified small-pox prodromata occur before the eruption ap-
pears, and then the temperature falls ; in varicella there are no prodromata,
and a rise in temperature folloios the eruption. Varicella spreads irregu-
larly. Small-pox vesicles are umbilicated and multilocular ; those of
chicken-pox are globular or pointed, unicellular, and collapse on pressure.
Small-pox is inoculable, varicella is not.^ The stage of incubation is much
longer in chicken-pox than in small-pox, and vaccination does not protect
against it ; and during its progress a child can be successfully vaccinated.
It is very doubtful whether varicella ever attacks the same individual twice.
Prognosis. — The prognosis is always good.
Treatment. — The treatment is rest in bed, cleanliness, a non-stimulating
diet, and cooling drinks.
1 Conoidal is also called swine-pox.
2 Small-pox and vaccinia are often early followed in tlie same individual, say within two or three
years, by chicken-pox, or vice versa. Chicken-pox, vaccinia, and small-pox have been known to follow
in immediate succession in the same individual.
SCARLET FEVER. 765
SCARLET FEVER.
Scarlet fever or scarlatina is an inflammation of the tegumentary invest-
ment of the entire body, both cutaneous and mucous, accompanied by a
fever of an infectious or contagious character. This name has been given
on account of the bright red appearance of its eruptions. It is a disease of
childhood, but may occur at any age.
Its development and course are divided into three periods : first, the
period of invasion, which lasts from twenty-four to forty-eight hours ;
second, the period of eruption, which lasts from five to seven days ; third,
W\Q, period of desquamation, during which the entire epithelial surface is
removed. Some classify the disease according to its severity ; others ac-
cording to the prominent organs of the body which are involved ; others
according to the prominent phenomena which attend its development.
The more common classification, and certainly the simplest, is that which
divides it into scarlatina simplex, scarlatina anginosa, and scarlatina
maligna. I shall adopt this classification.
Morbid Anatomy. — It has no characteristic anatomical lesions, except
those which occur in the skin and mucous membranes. The eruption is
its distinguishing lesion ; it makes its appearance on the second or third
day after the commencement of the febrile symptoms. At that time it con-
sists of very numerous and closely aggregated points about the size of a
pin's head ; between these the skin is of its natural color. In typical cases,
these points are equally distributed over the entire body, except the face.
These red spots are usually circular in shape, slightly elevated, ahove the
surrounding skin, and so close to each other that they give a confluent red-
ness to the entire surface. In mild cases the red points remain isolated,
and do not become confluent ; as the eruption develops, these red points
unite. In severe cases the skin becomes turgid and swollen, and presents
a uniformly red and glistening appearance. In malignant cases the hyper-
aemia of the skin is often accompanied by more or less extensive hemor-
rhages, causing petechise and extensive ecchymosis. The redness of the
eruption gradually increases up to a certain point, which is not the same
in all cases, then remains unchanged for twelve or twenty-four hours, after
which time the redness slowly joasses away. During the course of the dis-
ease, the color often changes with the exacerbations and remissions of the
fever. As a rule, the degree of redness depends upon the intensity of the
fever, and may vary from a pale red to a deep scarlet. If the respiration
becomes impeded, the eruption assumes a bluish-red hue. During the first
forty-eight hours after the appearance of the eruption, when the respiration
is unimpeded, the redness completely disappears under firm pressure, and
reappears as soon as the pressure is removed. After this period, the pressed
point does not entirely lose its red color. In a certain proportion of cases,
the eruption only appears in spots on the surface of the body, on the trunk,
or face, or about the flexor surfaces of the joints. When it only appears on
the face, the diagnosis is difficult.
766 ACUTE GENEEAL DISEASES.
In addition to the cutaneous hypersemia which gives the redness to the
surface, there is more or less serous and lymphoid, exudation into the " rete
Malpighii," which is followed, on the decline of the redness of the surface,
by an abundant epidermic exfoliation. Blood extravasations into the sweat-
glands often occur. The exfoliation marks the period of desquamation,
which may immediately follow the decline of the redness or may be delayed
a few days. This is due to an excessive production of newly-formed epi-
dermis, and the process may last only a few days, or if the eruption is abun-
dant it may continue for several weeks, and may recur a second time on the
same surface. After the desquamation has ceased, it does not reappear, ex-
cept in cases of relapse ; these are followed by renewed and sometimes by a
very complete desquamation. Desquamation has not infrequently occurred
on skin that has 7iever been the seat of the eruption.
In connection with these cutaneous changes the scarlatina poison causes
changes in the mucous membrane of the mouth and throat, the most fre-
quent of which is catarrhal pharyngitis, which at first gives to the mucous
surface of the tonsils and pharynx a red, swollen, and dry appearance. After
a little time, these mucous surfaces become covered with a tenacious mucus.
Upon the reddened mucous membrane small elevations arise, like the smaller
follicles in an ordinary catarrh. In mild cases, all these changes disappear
in a few days ; in the severer cases, the mucous surface assumes a dark,
livid color, the parts become more or less cedematous, and are covered by
an abundant secretion. Follicular ulcers also form. The oedema may be
so extensive as to render deglutition difficult ; the tonsils are often so
swollen that they touch each other.
Besides the redness and oedema of the mucous membrane of the mouth
and throat, there is often inflammation of the parotid and sublingual
glands as well as of the connective-tissue of the neck. This glandular in-
flammation may end in resolution, but often it terminates in suppurative
or diffused necrosis. It may give rise to extensive gangrene of the tonsils
and adjacent soft parts ; sometimes it is followed by extensive abscesses
and destruction of the cellular tissue about the neck ; the skin in the region
may slough, and not infrequently fatal hemorrhage results from the de-
struction of small vessels ; or the whole region may lie open as if dissected
out.
Diphtheria is so often a complication of scarlatina anginosa, that it has
been assumed that there is some necessary relation between the two dis-
eases.' Yet diphtheria is as frequently met with in the mild as in the
severe types of scarlatina, and occurs in every stage of the disease ; it is
often present during the period of incubation, so that the symptoms of the
two diseases appear simultaneously. Again, it is met with during the
period of convalescence. In some instances, scarlatina seems to complicate
diphtheria.
In a mild form of scarlet fever, when the disease runs a regular course,
the nasal mucous membrane is usually pale, and its secretion is not in-
1 Hubner states that the pseudo membranes are much thinner in scarlatinal than in ordinary diphtheria,
and that in the former, fibrin is found between the epithelia and in the mucous and submucous connective-
tissue.
SCARLET FEVER. 767
creased. "When the disease is severe, the nasal mucous membrane becomes
secondarily, never primarily, involved. This is the result of a catarrhal
affection of the throat. It is a purulent catarrh of the posterior nares,
which gradually extends to the anterior nares, and gives rise to a very
troublesome form of coryza. During the eruptive period of scarlatina,
affections of the ear frequently occur in connection with those of the throat.
Usually these have their seat in the middle ear, pus being the product.
They are always tedious and may become chronic. The eye maybe involved;
keratitis and ulcers are not uncommon.
Next to the skin and mucous surfaces, the kidneys are the organs most
frequently affected in this disease. There is no question but that, in a cer-
tain proportion of cases, recovery takes place without any kidney lesions ;
but these are the exceptions and not the rule. In some ej^idemics the
scarlatina poison induces a so-called " croupous" inflammation of the urin-
iferous tubules. The tubules of the cortical substance of the kidneys are
most extensively affected ; the morbid processes commencing at the Mal-
pighian tufts ' follow the course of the convoluted tubules. If the tubules
are only slightly affected there will be no symptoms except a slight albu-
minuria. The kidney changes are rarely well marked before the second or
third week of the disease, and usually terminate in complete recovery. The
character and extent of these kidney changes vary in different epidemics.
During some epidemics, the kidney changes are slight ; during other
epidemics almost every case, whether mild or severe, will be attended by
extensive kidney lesions.
At the post-mortem examination of one who has died of scarlet fever,
there will be found more or less extensive congestion of the internal organs,
the brain, liver, spleen, etc., but these congestions do not differ from those
met with in other acute infectious diseases. The changes in the con-
stituents of the blood ^ are such as to diminish its coagulating power.
The Peyerian patches will often be found presenting the '^shaven-beard
appearance." There may be parenchymatous degeneration of the gastric
tubules.
Etiology. — The cause of scarlet fever is a contagion, which is transferable
from the sick to the healthy. It has been claimed that sporadic cases do
occasionally occur ; but there is little doubt that if the history of every
case of supposed spontaneous scarlet fever could be carefully taken, it would
be found that at no place and at no time had the disease ever been of spon-
taneous origin. It may be conveyed directly from the affected to the
healthy by contact, through the atmosphere and by clothing which has been
thoroughly saturated with the scarlet fever poison ; therefore it may be
considered a portable disease. Animals that have been around those sick
with scarlet fever may convey it. I recall an instance in which the scar-
let fever poison was conveyed in this way : — For a number of days a little
dog had been around children sick with scarlet fever, and by a single visit
1 There is proliferation of epithelial nuclei in the glomeruli, distending them to twice their size,
and thus comprc«sing the vascular tuft. There is hyaline degeneration of the capillaries (Klein).
'^ Micrococci are found in the blood.
768 ACUTE GENERAL DISEASES.
of the dog to the children of another family the disease was conveyed.
There has been considerable discussion as to whether the disease Can or
cannot be conveyed in milk. This is possible.'
The infection of scarlatina is not so certain as that of measles or small-
pox. When one member of a family is sick with measles, usually every
other member of that family who has not had measles will contract the dis-
ease ; whereas one member of a family may be sick with scarlet fever and
every other member may escape. Some seem to have a certain idiosyn-
crasy, so that when they are brought in contact with the poison of scarlet
fever they do not contract the disease. The poison which they receive into
the system has power to produce some of the symptoms but has not power
to fully develop the disease.
Scarlet fever can be communicated from one individual to another by in-
oculation. If some of the watery material or serum that can be obtained
from the minute vesicles occasionally seen upon the surface of the body in
connection with the scarlet fever eruption, be taken and introduced into
the body of an individual who has not had scarlet fever, it will develop the
disease. It has been proposed to inoculate those who have not had scarlet
fever in the same manner as one would inoculate those who have not had
small-pox, and, by so doing, produce a modification of the disease. But it
has been found by experiment that those who have been inoculated for
scarlet fever have suffered more severely than those who contracted the dis-
ease by any of the common methods of contagion. There is no question
but that the scarlet fever poison can also be introduced into the system
through the respired air, but whether it can be taken into the system
through the medium of food or fluids is still an unsettled question.
A question of great practical importance is : if the disease can be con-
veyed by clothing, is it safe for a physician to visit patients sick with scar-
let fever, and go from them directly to those who have not had the disease ?
Unquestionably it is possible to so convey the disease, but in my own ex-
perience I know of no case where it has been so conveyed. The clothing
in order to be sufficiently impregnated with the poison to render it a means
of contagion must be longer exposed than is the case when a physician
makes a visit of ordinary length. Unquestionably, nurses who have been
with a scarlet fever patient for a number of days, and whose clothing has
become filled with the poison, may carry the disease. These should change
their clothing before they go from the sick to the healthy. The real nature
of the scarlatina poison is undetermined. The period at which this disease
is most infectious is probably the desquamative period, although some main-
tain that it is most infectious during the eruptive period.
An individual is almost certain never to have a second attack.
The period of incubation varies from two to ten days, the average dura-
tion being from three to five. It may be only three hours. Age has a
great influence on individual predisposition. The greatest susceptibility
to the influence of the poison exists between the second and seventh years ;
' Quain says : "Milk is a great medium for carrying scarlet fever, and cream, even more than mUk,
often carries it from sick to well."
SCARLET FEVER. 769
it rapidly diminishes after the ninth year, so that adults, and especially the
aged, have only a slight predisposition to the infection. Those who have just
undergone surgical operations seem to be especially prone to contract the
disease. Scarlet fever may be endemic or epidemic. No reason can be as-
signed for its variations in type or severity. For years the type of fever
•vfhich appears in a given locality will be exceedingly mild in character,
when suddenly, without any assignable cause, a most malignant epidemic
will prevail. Usually epidemics of scarlatina prevail in the autumn and
spring.'
Symptoms. — The symptoms of scarlet fever vary with the type and with
the severity of the fever. In moderately severe eases, before the appear-
ance of the eruption, the patient will have a more or less severe headache,
pain in the back and limbs, and at first coldness of the surface. Epistaxis
is not rare. In some cases I'igors will occur, and perhaps distinct chills.
In children convulsions and coma often occur. These ushering-in symp-
toms are immediately followed by a sensation of intense heat, with great
acceleration of the joulse, which at this time often beats 120 or 130 per
minute. There will also be nausea and vomiting, frequently most jaer-
sistent and distressing. Besides, there will be a rapid rise in temperature.
It may reach 103° F. or l04° F., within a few hours.
Within a period lasting from twelve to forty-eight hours, the average
being thirty-six hours, the eruption makes its apj^earance, and the fever
increases. The elevation in temperature is accompanied by restlessness, a
burning sensation, perhaps delirium ; the nausea and vomiting become
more urgent, and now the papillge of the tongue become swollen, and the
organ presents the appearance of a strawberry : — (the " strawberry tongue"
of scarlet fever) . This appearance is not commonly seen in the milder cases,
but, as a rule, is present in all the severer cases. With the appearance
of the eruption, all the symjDtoms, perhaps exce23ting the pain in the head,
increase in severity. The urine, if it has been scanty, will now become
more so, and may be nearly suppressed ; if it has been sufficiently abun-
dant, not infrequently, as the eruption makes its appearance, it becomes
scanty and high-colored. In some cases the disease is so mild that there
is but little disturbance, except that caused by the eruption, the tempera-
ture being not over 102° F. In other cases the disease is ushered m by
violent nervous symptoms, such as delirium and coma, accompanied by
extreme exhaustion, and the patient dies before the eruption makes its ap-
pearance. In other words, the patient dies during the period of invasion,
from the overwhelming of the nervous system with the scarlet fever poison.
During the earlier stages of the disease the throat symptoms are quite
characteristic. Adults and older children complain of a pricking sensation
in the throat, and difficulty in deglutition ; the tonsils, uvula, and posterior
Avail of the pharynx are red and CBdematous, and from their aj)pearance,
with the attendant symptoms, in most instances, one is able to very early
' Trojanowsky and Thomas describe a variety called " recurrent," where two series of eruptions over-
lap, as it were, and finally merge into one attack. But the latter's cases all occurring in marshy districts,
hf; inclines to the view that the poisons of malaria and scarlatina were combined and perhaps modified by
each an unicii.
49
770 ACUTE GENERAL DISEASES.
decide that the ease is one of commencing scarlatina. There are cases
in which the throat symptoms are altogether absent at first, and do not
come on until later in the disease. The symptoms which mark the de-
velopment of this disease remain to be studied in detail.
As already stated, the whole course of scarlet fever may conveniently be
divided into three stages. First, the stage of invasion, or the febrile
stage. Second, the stage of eruption. Third, the stage of desquamation.
The duration of the stage of invasion varies with the type of the dis-
ease. In most cases, it is from twelve to twenty-four hours ; it may be
four or five days. Usually the onset is marked by chilliness and slight
rigors, followed by a rapid rise in temperature. The skin becomes dry, the
face flushed, and the pulse accelerated. At the same time there is slight
soreness of the throat, the face appears red and dry, the neck is stiff, the
eyes suffused, and there is some tenderness about the joints. Vomiting
and thirst are prominent symptoms. The tongue is red at its tip and
edges, the papillae are enlarged, and it presents the so-called strawberry
appearance. Lassitude, pain in the head, aching of the limbs, and rest-
lessness are generally present. There may be some delirium at night.
Twenty-four hours after commencement of the fever of invasion, the
eruption may make its appearance. The period which elapses between the
exposure and the appearance of the eruption varies. In some cases the
eruption is said to have appeared as early as twenty-four hours after ex-
posure, while in others one or two weeks have elapsed after the exposure
before the disease was developed. No definite statement in regard to the
duration of the period between the exposure and the appearance of the
eruption can be made. The eruption first makes its appearance upon the
neck and upper portion of the chest, and is first seen as little red dots,
varying in size from a line to a line and a half in diameter. These gradu-
ally coalesce and the eruption extends over the entire surface of the body,
perhaps on the face, and lastly it appears on the lower extremities. It
presents its brightest appearance upon the evening of the fourth day.
After the second day of the eruption, if not before, the entire surface
will present a uniform redness, the color varying with the severity of the
disease.
In the milder cases one will have a bright rose-red eruption or rash, while
in the severer types the eruption will assume an appearance resembling the
deep-red color of the boiled lobster. The darker the eruption, the more se-
vere the form of the disease and the greater the danger. When the erup-
tion is fully developed, it will be noticed that the surface is somewhat ele-
vated, the parts present a swollen appearance, the vessels of the skin seem
to be congested, and there will be soreness of the throat more marked thar
in the febrile stage. Miliaria appear when the rash is most intense, anQ
sudamina are common.
Usually, vomiting is present at the commencement of the disease, but
becomes more severe and a more marked symptom as the stage of eruption
is ushered in ; if not present at the commencement, it is certain to make
its appearance with the appearance of the eruption. The vomiting is pe-
SCAELET FEVEE.
771
culiar, not on account of the matters ejected, but the ad of vomiting is
projectile in character.
In scarlatina the condition of the throat depends upon the severity of the
disease. In some cases there is simply a blush of redness over the posterior
portion of the pharynx and uvula and anterior pillars of the soft palate. In
other cases a general tumefaction and oedema of all the soft parts of the
throat will be seen, and the tonsils will be the seat of a more or less intense
parenchymatous inflammation, which gives rise to a swelling that encroaches
more or less upon the pharynx. Again, ulcerative pharyngitis will occur,
or upon the surface of the enlarged tonsils and swollen mucous membrane
of the pharynx there may be an exudation, which will be more fully de-
scribed hereafter.
In this, the ordinary form of scarlatina, when it runs its ordinary course,
there will not be much swelling of the glands about the neck, nor very much
tumefaction of the soft tissues in the pharynx. On the morning of th,e fourth
day, if the finger-end is drawn across the surface, a clear, well-defined line
will be made, which will remain for some time. This distinct white line
is a point of some importance in distinguishing scarlatina from roseola.
Usually the eruption begins to fade upon the fourth day, and by the sixth
day it has entirely disappeared, and desquamation has commenced. During
the time the eruption is developing, the temperature continues to rise until
perhaps it has reached 106° F. or 107° P. In the meantime the pulse may
increase to 120 or even 140, or perhaps 150 beats per minute, and not in-
frequently there is some delirium during this stage ; there may be also more
or less stupor. There is an intense itching and burning upon the surface,
and a great restlessness.
Between the fifth and eighth days of the eruption, the temperature be-
gins to decline, and at the same time
the eruption fades. This fading of
the eruption goes on rapidly, so that
by the end of the eighth, certainly
early on the ninth day, sometimes as
early as the sixth day, it is no longer
visible. With the disappearance of
the rash, desquamation commences,
and with this there will be a still
more marked fall in temperature, and
diminished frequency of the pulse.
All the febrile symptoms disappear, all
the throat symptoms subside, there is
no longer any difficulty in deglutition,
there is no more pain in the throat,
no more swelling of the external
glands, if previously it had existed.
The period of desquamation lasts Fro. i64.
about two weeks, during which time Temperature Kecord in a case of Scarlatina.
there is the greatest danger of communicating the disease. At the end
Da
ly.
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98'
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772 ACUTE GENERAL DISEASES.
Of that period, if no complication occur, the patient is well. The fine
scales which are so abundantly thrown off contain the specific poison, and
they are so delicate that they are blown about with every breath, and car-
ried in every current of air, and are in the most favorable condition to be
taken into the system in the respired air. Some have maintained that the
contagious period in this disease does not occur until the period of des-
quamation. This statement is not sustained by clinical facts. The
amount of the desquamation depends upon the intensity of the eruption.
The skin has a dry feel before desquamation commences. Where the skin
is thin the epidermis comes off in thin scales, '' branny" desquamation.
Where the skin is thick, as on the palms of the hands and the soles of the
feet, it peels off in extensive patches, " scaly " desquamation. With the
desquamation, the fever subsides more or less rapidly. The entire period
occupied by a case of scarlet fever, when it runs its regular course, is from
two to three weeks.
Scarlet fever is liable to irregularities which it is important to consider.
It is claimed by some that these irregularities depend upon the organ or
set of organs primarily affected by the scarlet fever poison. They are
rather due to some peculiarity in the type of the disease, to the degree of
poisoning, and in some instances to the particular set of organs that are
involved in the different epidemics. In some epidemics even milder forms
of the disease than have been described are seen. The attack may be so mild,
and there may be so little fever that if the eruption was not present one
would not be able to recognize the scarlet fever ; and even that may be so
light that the stage of eruption and the stage of desquamation may pass
unnoticed, and one may be scarcely able to decide whether the patient has
or has not had an attack of scarlet fever.
The most frequent irregularity in the manifestation of the disease is
noticed in that class of cases where we have complications resulting from
the overwhelming of the cerebro-spinal system with the scarlatina poison.
This is due to some peculiarity of the poison, and is characteristic of cer-
tain epidemics. In a large number of cases in the febrile stage, especially
in young children, convulsions may occur, but they do not depend upon
the peculiarity referred to. In the class of cases to which reference has.
been made, where complications arise from the overwhelming of the cerebro-
spinal system with the scarlatina poison, from the very onset of the disease
there seems to be a tendency to stupor and delirium, a peculiar restlessness,
an apparent wandering, a picking at the bed-clothes, accompanied by a
peculiarity in the appearance of the eruption, which may caujse it to assume
the boiled-lobster appearance, or even a darker hue. The eruption is slow
in its development, and there is not that uniform redness over the entire
body that is seen in ordinary cases ; it appears in patches, and with it there
is exhibited a tendency to blueness of the finger-ends, indicating that there
is acting upon the nervous system a poison which possesses the power of
very greatly lowering the vitality of the patient. These symptoms pre-
dominate in some epidemics.
There is a class of cases in which there is not much swelling of the
SCAELET FEVER. 773
throat, nor is the pulse more frequent than 130 or 140 per minute, but
during the second day of the eruption the temperature ranges very high,
reaching 107*^ or 108° F., and then the pulse becomes intermittent. Under
such circumstances the disturbance of the nervous system is due to the
high temperature which may have been present for two or three days ;
these disturbances may be j)revented if the temperature is not allowed to
rise above 103° or 104° F.
Again, in cases where there is marked swelling of the throat, and a
general infiltration of the tissues and glands of the neck, the develojjment
of the nervous phenomena is due to an interference with the return circu-
lation. The condition which gives rise to the cerebral symptoms is one of
mechanical cerebral congestion.
There is still another class of cases in which the marked nervous j)he-
nomena appear still later in the course of the disease. Under such cir-
cumstances they often indicate a typhoid condition. This typhoid condi-
tion is not induced, nor are the nervous phenomena developed, on account
of the peculiar effect produced upon the nerve centres by the scarlet fever
poison, nor are they due to the effects produced by a high temperature,
nor by an interference with the return circulation, but they are due to
septic poisoning, a poisoning entirely different from scarlet fever poisoning.
The nervous phenomena develop after the eruption. During the develop-
ing period, there may be noticed a peculiar ichorous discharge from the
nostrils, and frequently it is said that the patient has become repoisoned
by scarlet fever poison — but this is not the case ; he has become repoisoned
by the septic element of these discharges. During the period of desqua-
mation the nervous system may be involved in consequence of the presence
of urgemic poisoning.
The mere terms, scarlatina simplex, scarlatina anginosa, and scarlatina
maligna, do not indicate all that may be embraced under each of the divi-
sions.
Scarlatina maligna is that form of the disease in which tl>e cerebro-
spinal system becomes early involved. What the changes are that produce
these nervous phenomena, when high temperature is present, is still an un-
settled question.
Again, scarlet fever may run an irregular course in those cases in which
there is present an extensive infiltration of the tissue of the neck, with
inflammatory products, swelling of the glands, and extensive suppuration.
Not infrequently these cases terminate fatally ; doubtless in some cases the
extensive suppuration in the areolar tissue about the neck produces this
result, and in other cases it is produced by the interference with respira-
tion caused by enlargement of the glands and swelling of the tissues of the
neck. Exhaustion from sloughing is a cause of death. In these cases
there is danger from oedema glottidis, the consequence of extension of the
inflammation from the adjacent tissues.
There are cases in which the eruption is not very well marked ; the pa-
tient passes safely through the stage of eruption, and the stage of desqua-
mation is fully established ; but, instead of making a good recovery from
774 ACUTE GENERAL DISEASES.
this point, immense abscesses are rapidly developed in the cervical region,
blood-changes begin to manifest themselves — changes that favor hemor-
rhages. Hemorrhages are then petechial in character and occur on the
mucous surfaces, and the patient passes into a typhoid condition, with hem-
orrhages occurring from the nose, mouth, intestines, etc., and death en-
sues. Such a result is produced by the peculiar action of the septic poison
developed during the suppurative process, and perhaps from outside influ-
ences (as bad hygiene).
I regard scarlatinal coryza, in which the discharge contains elements
capable of producing septic poisoning, as an unfavorable symptom. The
clear serum which runs over the lip never causes death ; but the fact that
it sometimes produces excoriation and ulceration of the tissues with which
it comes in contact, indicates that there are nasal and pharyngeal changes
which may destroy life ; especially is this the case in young children.
Sloughing ulcers sometimes develop in the mouth and throat ; and when
they do occur, the patient is said to have ulcerative stomatitis ; but these
ulcerations are really due to a peculiarity of the scarlatina poison. Under
such circumstances the patient may go on through the period of eruption,
enter the stage of desquamation, and then rapidly sink and die, with symp-
toms similar to those which attend diphtheria. Although the odor of the
breath may very closely resemble that noticed in some cases of diphtheria,
there is no diphtheritic exudation present.
Scarlatina may also, run an irregular course by the development of in-
flammation of the internal ear. This inflammation extends from the
throat up the Eustachian tube, involves the middle ear, and gives rise to a
train of symptoms, such as intense pain, delirium, and rolling of the head,
all of which suggest the presence of acute meningitis. I recall several in-
stances in which the diagnosis of acute meningitis was made, where from
the after-history of the case there was no question but that the symptoms
were due to such an inflammation of the middle and internal ear.
Complications and Sequelce. — The most common sequela is anasarca.
The anasarca of scarlatina usually appears at the time the patient is conva-
lescing, during the period of desquamation, or just as desquamation is being
completed. It has been thought that anasarca is due to some exposure to
the influence of cold during this period. It is possible that the changes in
the kidney which give rise to the anasarca may sometimes be produced by
the influence of cold, and undoubtedly anasarca is occasionally developed in
this manner; but in the majority of cases it is due to some peculiarity in
the scarlet fever poison, or to some peculiar atmospherical condition. Dur-
ing some years anasarca is a very common sequela of scarlet fever ; while
during other years in equally severe cases, scarcely a case of anasarca occurs.
While we recognize the fact that it is possible for kidney lesions to be de-
veloped which shall give rise to anasarca in consequence of exposure to
cold, it is also of importance that we recognize the fact that the lesions and
the anasarca may be developed independent of such exposure. The ana-
sarca first shows itself on the face, and from the face it extends over the
entire body, and if it becomes general more or less ascites is developed.
SCARLET FEVER. 775
In most cases, at the time of, or previous to, the occurrence of the anasarca,
certain premonitory symptoms occur, and it is of great importance to be
familiar with these symptoms, and be on the watcli for their appearance.
For two or three days previous to their development a certain restlessness
will he noticed, with nausea and vomiting. Tliese symptoms are almost
universally present. The nausea and vomiting so commonly present dur-
ing the early periods of the disease have subsided, and now, during the
period of desquamation, or perhaps after it has been completed, the vomit-
ing returns. The patient has some pain in the head, has loss of appetite,
is annoyed by the light, does not sleep well, and the temperature is raised
perhaps two or three degrees. But the pulse now grows remarkably slow : —
50 to 60 in children. When a patient complains in'this manner during the
desquamative stage of scarlet fever, our suspicions should be aroused, and
if the urine has not yet been examined, an examination should be made
at once.
The urine may be entirely suppressed for a day, and then it will usually
be found scanty and high-colored, will contain albumen and casts. Haema-
turia and hsemoglobinuria both occur quite frequently. If previous exam-
inations of the urine have been made before the development of these symp-
toms, a cloudiness will have been noticed (non-albuminous) due to epi-
thelia and hyaline material, but now there are present casts which indicate
the existence of scarlatinal nephritis. After the anasarca has been present
two or three days, and the abdomen has become tense, swollen and painful,
if the case is to have a favorable termination it will begin to decline, will
be less and less marked about the face and feet, the tendency to stupor
which has accompanied it will begin to disappear ; and as the dropsy sub-
sides, and the patient is not so lethargic, the appetite begins to return, the
urine increases in quantity, the albumen diminishes, the casts disappear,
and convalescence is fully established. Anasarca may have been developed,
all the symptoms have disappeared, and the patient have recovered within
two weeks from the commencement of the attack. If, however, after the
anasarca is developed, the case is to go on to an unfavorable termination,
the anasarca instead of diminishing will increase ; the face will become
more and more pufFy, the legs more and more cedematous, the abdomen
more and more distended, the pulse more and more frequent and feeble,
the temperature more and more elevated, until a condition of coma is
finally reached, which condition is sometimes preceded by convulsions, and
followed by death.
Another sequela of scarlatina is inflammation of the serous memhranes.
The serous membrane most liable to be involved is the endocardium, and
this inflammation may pass unrecognized unless its occurrence is closely
watched, and there may be no rational symptoms present. Endocarditis,
when it does occur, is liable to be ulcerative in character. Inflammation
of the pericardium may occur as a complication of scarlet fever, but it does
so much less frequently than inflammation of the endocardium. Inflam-
mation of the pleura, and occasionally inflammation of the peritoneum, is
met with as a sequela of this disease. If peritonitis does occur it is usually
776 ACUTE GENEEAL DISEASES.
subacute in character. It is possible to have peritonitis developed as a
sequela to scarlet fever and to be entirely recovered from. Rheumatism
may be developed during the desquamative period of scarlet fever. Under
such circumstances it assumes the ordinary appearances of inflammatory
rheumatism. It is not a serious sequela, and a complete recovery usually
occurs within ten or fourteen days from the commencement of the attack.
Suppurative inflammation of the joints is sometimes a sequela of scarlet
fever.
Another serious complication of scarlet fever is diphtheria. It may
occur at any period of the fever ; usually it occurs during the period of
desquamation. There is developed the characteristic exudation of the dis-
ease, with the attendant depression noticed in a case of diphtheria devel-
oped independently of scarlet fever. It differs in no respect from primary
diphtheria, except in the rapidity of its development and in its fatality.
In scarlet fever there is no more serious complication. Usually it appears
quite suddenly, and perhaps does not occur more frequently in those who
have a severe form of the disease than in those who have a mild scarlet
fever. The lympliatic glands may be enlarged and swollen, i. e., a lym-
phadenitis may be a sequel of scarlatina. Keratitis, retinitis, and total
blindness are rare sequelae of scarlet fever. Anaemia, paralysis of single
nerves, spinal disease, chronic Bright's, deafness, chorea, epilepsy (melan-
cholia and mania in adults), valvular diseases, stone in the bladder, etc.,
etc., are also named as sequelae.
Differential Diagnosis, — The diagnosis of scarlet fever is usually not diflB-
cult after the eruption has made its appearance, for, in well-marked cases,
that alone will readily distinguish it from the other eruptive fevers. At
the very onset of the eruption, and sometimes in irregular cases, the differ-
ential diagnosis is difficult. The eruptive diseases which are most liable to
be mistaken for scarlet fever are measles, small-pox, roseola, and an erythema
which sometimes appears in surgical cases. In all doubtful cases a careful
study of the history of the patient is necessary before making a diag-
nosis.
In measles the appearance of the eruption is preceded by a cough and
coryza. These symptoms are never present in the ushering-in stage of
scarlatina, but maj folloiv the eruption. Besides, the eruption of measles
first appears on the face, whereas the eruption of scarlet fever first makes
its appearance upon the neck and chest. The fever in scarlatina persists
after the eruption, while in measles (and in small-pox too) it falls when
ihe eruption appears. The incubation period is shorter in scarlet fever and
the early pyrexia is higher than in measles. After these diseases are once
fully developed, the course of the one so differs from that of the other that
there will rarely be any chance for doubt after the first week of the disease.
The minute punctate appearance of the scarlatina eruption before it be-
comes confluent is an important element in its diagnosis.
Although the eruption of confluent variola, for the first twenty-four hours,
may sometimes resemble that of scarlatina, yet the development of the first
Tesicle settles the question.
8CAELET FEVER. 777
The appearance of erythema bears a close resemblance to a perfectly de-
Yeloped scarlatina eruption ; it is not, however, present on the extremities,
neck, and portions of the trunk, and it spreads in a very irregular manner,
whereas in scarlatina such is not the case. But if, on account of the scanti-
ness of the scarlatina eruption, any doubt arises as to the nature of tlie erup-
tion, the fact that in scarlatina the throat symptoms are rarely absent, that
the tongue presents the strawberry appearance, and that at an early period
there is usually some swelling of the cervical glands, will decide the case.
In those cases in which, during the early part of the disease, it is impossible
to make a diiierential diagnosis, the diagnosis will be readily made when the
period of desquamation is reached.
The differential diagnosis between roseola and a very mild form of scar-
latina is sometimes attended with great difficulty. If scarlatina is prevail-
ing, and a child has an eruption which lasts for two or three days, then
disappears, and is not followed by desquamation, it may be thought that the
case is one of scarlatina ; and yet the sequel proves that the case was one of
roseola. Such a form of roseola sometimes prevails epidemically, and
attacks children in a certain locality, whether they have or have not had
scarlatina. Under such circumstances, adults and children are said to have
had a second attack of scarlet fever. In making a differential diagnosis
between this form of roseola and scarlatina, the duration of the eruption
and the character of the throat symptoms must decide. In scarlatina the
posterior part of the pharynx is affected, while in roseola the redness is con-
fined to the anterior portion ; besides, the throat affection in roseola is
much milder than in scarlatina. In roseola the white line that the finger
leaves disappears immediately ; while in scarlatina it remains — indeed, a
letter may be traced on the skin in well-marked cases.
One can hardly mistake erysipelas for scarlatina, for erysipelas com-
mences at one point and gradually extends from it ; there is also marked
oedema of the connective-tissue, and there is a very marked difference in
the constitutional symptoms of the two diseases.
Malignant cases of scarlet fever, in which no eruption appears, prove
rapidly fatal. In such cases, the fact that an epidemic of scarlet fever is
prevailing (which is usually the case), the rapid development of the disease,
the very high range of temperature, and the very grave nervous phenomena,
will aid in the diagnosis, and these can only be accounted for on the ground
that the patient is overwhelmed by some very active blood-poison. In this
class of cases the entire surface of the body should frequently be examined,
for the eruption is sometimes very transient, perhaps appearing only for a
few hours on the neck or extremities.
It is sometimes difficult to draw the line of distinction between scarlatina
without an eruption, but with swelling of the cervical glands and ulcera-
tion of the throat, and diplitheria. If a patient has swelling of the
cervical glands and well-marked febrile symptoms, which have come on
gradually — ^that is, have been two or three days developing — and yet no
scarlatina eruption has appeared, but a gangrenous ulceration has developed,
involving the tonsils, the posterior wall of the pharynx, and the anterior
778 " ACUTE GEN"EEAL DISEASES.
pillar of the soft palate, and if scarlet fever is prevailing in the locality, it is
very difficult to decide between it and diphtheria. There can be no doubt
but that scarlatina poison may excite a tubular nephritis without an erup-
tion appearing on the surface of the body, or without any of the other
ordinary symptoms of scarlatina.
Prognosis. — The prognosis in scarlet fever is always uncertain. It will
be influenced more by the character of the prevailing epidemic than by any
other circumstance. According to statistics, the rate of mortality ranges
from one death in five to one in twenty. Some epidemics are very mild.
During one epidemic, in one month, I treated fifty cases of scarlet fever,
with only two deaths. During the same month of the following year,
I treated twenty cases, with seven deaths. In giving a prognosis one must
always take into account the type of the prevailing disease. Even when
the disease is mild in character, and is running a perfectly regular course,
dangerous symptoms may suddenly arise without any assignable cause.
The conditions of a favorable prognosis are as follows : when the erup-
tion appears within forty-eight hours from the commencement of the
attack, and rapidly completes its course, reaching its maximum on the
second day ; when the throat symptoms are mild, little difficulty being ex-
perienced in swallowing ; when the cervical glands are but slightly enlarged;
when the temperature does not rise higher than 104° F., and the pulse beats
only 120 per minute ; when the cerebral symptoms are not severe, and are
of short duration ; and when the disappearance of the eruption is attended
by a steady decline in temperature. Even if there is a slight affection of
the Joints and a moderately severe nephritis during the period of desquama-
tion, a favorable termination may be predicted. The nephritic symptoms
will almost always entirely disappear during the third or fourth week.
The conditions for an unfavorable prognosis are an irregular course ; a
temperature rising above 105° F.,' with dyspnoea and extreme frequency of
the pulse ; symptoms of collapse attended by a cold surface and a small
pulse, an eruption of a livid hue, and abundant hemorrhages in the skin ;
ulcerative pharyngitis, especially when it extends to the nasal passages, ac-
companied by copious coryza and infiltration of the glands and tissues of
the neck ; severe nervous symptoms, with typhoid symptoms and long con-
tinued vomiting with diarrhoea coming on at the commencement of the
attack ; early nephritic symptoms and general dropsy, excessive hsema-
turia, or almost complete suppression of urine, with high temperature.
The occurrence of any of the more serious complications, such as pneu-
monia, diplitheria, pericarditis, oedema glottidis, etc., always renders the
prognosis bad.
Before making a prognosis, decide whether the scarlet fever is regular or
irregular in its course, and if irregular, what are the causes of the irregu-
larity. It is also important to determine the patient's power of resisting
disease. Autumn is the most unfavorable season. Favorable hygienic sur-
I A temperature of 110" has been reached and yet followed by recovery ; it rose to 115° F. in a fatal case.
Scarlet fever is an intensely febrile disease ; hence the temperature is not such a very important element
in the prognosis.
SCARLET FEVER. 779
roundings, good nursing, and well-directed medical treatment will greatly
lessen the death rate in scarlet fever epidemics, and these should he con-
sidered elements of the prognosis. Patients with scarlet fever do better
when left to themselves than when badly nursed, even if under the care of
skilful medical attendants.
Age is an important element of prognosis. The period of greatest mor-
tality is from infancy to five years of age. Beyond this period until adult
life, the prognosis is decidedly better. Five per cent, of the whole mortality
falls in the first year, fifteen per cent, in the second, twenty per cent, in
each of the next two years, and then decreases progressively. In adults,
the mortality is greatest in pregnant women, and those who are suffering
from some organic disease, especially some disease of the heart or kidneys.
Treatment. — In connection with the treatment of this affection, the first
question that presents itself relates to prophylaxis ot preventmi.
ThQ prophylaxis of scarlet fever is a system of the strictest quarantine.
The sick must be removed from the healthy. All useless articles of furni-
ture must be removed from the sick-room. Fresh air renders the contagion
of scarlet fever less powerful ; therefore, free .ventilation is of the utmost
importance. All the clothes and excretions of the patient should be dis-
infected in the same manner as in typhoid fever. To prevent the dissemina-
tion of the dusty particles of the desquamating epidermis, during the period
of desquamation the surface of the body should be frequently sponged, and
after each sponging the surface should be rubbed with olive oil. Those con-
valescing from this disease should not be allowed to leave their apartment
until desquamation is completed, which usually requires at least three
weeks after the commencement of the jjeriod of desquamation. The
sick-room and everything which has been used about the patient should
be thoroughly disinfected, and the windows and doors of the apartment
should be allowed to remain open for a long time before it is again
occupied.
To prevent the spread of the disease, nurses and attendants upon the
sick should not be allowed to have any intercourse with the healthy until
the period of desquamation is passed, and after that time not until there
has been thorough cleaning and disinfecting. The funeral of those dying
of scarlet fever should not be public. There is no known prophylactic
treatment, except isolation, and a thorough disinfectioij of everything con-
taminated by the contagion.
A theory has been advanced that belladonna has power to prevent the
development of this disease in those who have been exposed to its con-
tagious influence. This drug has been very extensively administered in
order to test its effects as a preventative in scarlet fever. After having
carefully examined the subject, both in its literature and clinically, I am
convinced that belladonna has no power to prevent the development, or
mitigate the severity, of the fever in those who have been exposed to its
infection. Fresh air is the only agent which can render the contagious in-
fluence of this fever less powerful.
Medicinal Treatment. — The medicinal treatment of scarlet fever is al-
780 , ACUTE GEI^ERAL DISEASES.
most entirely expectant. It is a disease which cannot be aborted, and if
left to its natural course tends to recovery if the fever and the local symp-
toms remain within certain bounds. It has certain stages to pass through,
and one cannot safely interfere with its regular course. To stand by and
watch, and, as far as possible, to guard against complications are the physi-
cian's chief duties. There are certain details which it is important to attend
to. The bed and body linen should be frequently changed. As soon as
the period of desquamation has been reached the patient should have a
warm bath once or twice during the day, the surface of the body being
well washed with carbolized soap. The baths hasten the process of des-
quamation and aid in bringing the skin into a healthy condition as rapidly
as possible ; the kidneys will also be relieved, and serious lesions of these
organs may thus be prevented. Such general means as are applicable in
the treatment of all fevers may be employed.
If the temperature of the patient rises above 104°, certainly if it rises
above 105^ F., it is important that some measures be resorted to for its re-
duction. The temperature should never be allowed to remain at 105° F.
longer than twenty-four hov.rs. The means which are to be employed to
accomplish this reduction are the antipyretic measures already referred to,
such as the application of cold to the surface by means of sponging and
baths, and the administration of large doses of quinine. There is a strong
prejudice against the application of cold to the surface of the body in
scarlet fever. I am by no means certain that cold baths are al ways safe,
or that in all cases the application of cold to the surface is Judicious treat-
ment. It is said that the kidneys will be most readily relieved of the scar-
let fever poison when cold is used for the purpose of reducing the temper-
ature. It is claimed that when the temperature of a patient is kept below
103° F., scarlatinal nephritis rarely occurs. This statement is not sustained
by facts ; it has been found that kidney complications are as extensive in
the cases where cold is employed as in those cases where the temperature
ranges higher and cold to the surface is not employed. We should be gov-
erned by the same rules in the application of cold to the surface in scarlet
fever as govern us in the treatment of typhoid fever.
With regard to the use of quinine as an antipyretic, I need add nothing
to what has already been said in connection with its antipyretic power in
the treatment of other fevers. Unless the temperature in a case of scarlet
fever ranges above 105° F., do not apply cold to the surface, or give quin-
ine in antipyretic doses. With such a temperature there will be probably be
delirium, but it must be regarded as one of the phenomena of the disease,
requiring no special treatment. If the temperature rises above 105° F. ,
perhaps reaching 106° or 107° F., and the patient manifests the nervous
phenomena which have been referred to, such as restlessness, tossing, blue-
ness of the surface, tendency to coma, etc., the temperature is to be re-
duced either by the application of cold to the surface or by the administra-
tion of one or two antipyretic doses of quinine.
In all cases the patient is to be sponged frequently with tepid water, and
if there is intense burning of the surface, a saline is to be added to the
SCARLET PEVER. 781
water. Sponging in this manner will give the patient very great comfort.
Some advise that the surface be anointed with oil for the relief of the
burning. My own experience has led me to rely upon simple tepid saline
water. I have found that it gives patients greater relief, is more easily
applied, and is every way more agreeable than any of the substances which
have been used for this purpose. I have not found that the application of
oil to the surface has any effect in controlling the temperature, nor does it
seem to have any effect on the process of desquamation. As soon as
desquamation commences the process should be assisted by frequent wash-
ings with soap and water.
For the throat complications, which will give more or less trouble in all
severe cases, especially when there is much enlargement of the glands at
the angle of the jaw, causing difficulty in swallowing, leeches were for-
merly employed, but their use has now been almost entirely abandoned.
Of all the remedies which I have employed for the relief of throat comj)li-
cations, cold carbonic acid water proved best. Whether it does more than
afford relief, I am not able to say, but I am certain that cold carbonic acid
water or pieces of ice held in the mouth, and brought as much as possible
in contact with the swollen mucous membrane of the throat, if used early,
afford most marked relief.
In the advanced stages of the disease, where there is great infiltration
of the glands and tissues of the neck, cold applications do not afford the
same relief as when they are used in the early stage ; then cloths wrung out
in tepid water and applied to the surface seem to be of service. During
this stage, hot applications are generally much more agreeable to the pa-
tient, and the hot cloths may be covered with oil -silk. These applications
will not hasten the suppurative process, unless suppuration is already estab-
lished. While using hot applications externally, warm water gargles and
steam inhalations may be used internally. Of these methods of treating
throat affections, the one which seems to be the most rational plan of treat-
ment should be chosen. In scarlet fever I favor the use of hot water rather
than cold applications. The superficial and deep ulcers which are some-
times seen in the throat of scarlet fever patients can best be treated by
spraying them with carbolic acid, muriated tincture of iron, chlorate of
potash, tannic acid, or any of that class of remedies. Whatever remedy
maybe chosen, it can be much more successfully applied by means of spray
than by a camel's-hair brush or a probang. Such local remedies thus ap-
plied afford great relief. The pain from these ulcerations is sometimes
very severe, and bromide of potassium, ether, or other anodyne applications
in the form of spray may be used with satisfactory results.
In a certain class of cases, where there is marked disturbance of the
nervous system accompanied by great depression of the vital forces and
feeble heart action, stimulants will be demanded early. It is not necessary
to wait until a certain stage of the eruption or of the disease is reached
before commencing their administration. It may be necessary to resort to
their use within twelve hours, or even within a less time, from the com-
mencement of the attack. In some cases the beneficial effect that may be
782 ACUTE GENEEAL DISEASES.
produced by the free and early administration of stimulants will be the
physician's sole reliance.
The approach of kidney implication in scarlet fever will be indicated by
the development of those premonitory symptoms which precede the ana-
sarca ; and whenever such symptoms are developed, dry or wet cups, accord-
ing to the condition of the patient, should be applied over the region of the
kidneys, upon either side of the spine ; three or four cups are to be applied
on each side, and their application followed with hot fomentations over the
kidneys. At the same time the temperature of the sick-room is to be raised
to 73° or 74° F.,the body of the patient covered with flannel, hot-air or
warm baths are to be administered, and the administration of diuretics is
to be commenced early. Of these, digitalis will act most favorably. If the
anasarca does not disappear under the influence of the digitalis and the
other means employed, calomel may be combined with the digitalis and
its use continued for a few days. Pilocarpin is recommended by some ;
my experience with it has not been satisfactory. The action of diuretics
is increased by having a mercurial combined with them. In certain
cases, when the patient is going from bad to worse, when the anasarca is in-
creasing, the tendency to coma is becoming more and more marked, indi-
cating an unfavorable termination to the case, cups have been applied, and
hot baths and diuretics employed with no satisfactory result — if then small
doses of calomel are combined with the diuretics, and their use continued
for two or three days, the entire phase of the case may be changed. When
toxic symptoms are marked, some advise carbolic acid, the sulpho-carbo-
lates, the hypophosphites, inhalation of ozone, etc., etc. In conjunction
with the measures recommended, the patient may drink as freely as possi-
ble of water. If convulsions occur, or threatening symptoms indicating
the approach of convulsions are developed, opium, either hypodermically
or by the mouth, may be given. Under such circumstances, the effect of
opium is often most satisfactory. It not only arrests the convulsive tenden-
cies, but produces the most profuse diaphoresis and aids in restoring the
renal functions.
MEASLES.
Measles, or ruheola, is a disease from which few persons escape. It is
essentially a disease of childhood, but it may occur at any age ; it is, how-
ever, less liable to occur in young infants than in children after the period
of dentition. A second attack is of rare occurrence. It is characterized bj
an eruj)tion of red spots, accompanied by a catarrh of the mucous mem-
brane of the air passages, and a more or less severe fever. It is infectious
and contagious. It may prevail as an epidemic or endemic disease, and not
infrequently there are sporadic cases of measles.
Morbid Anatomy. — Its anatomical lesions, with the exception of the erup-
tion, are similar to those of small-pox and scarlatina. There are similar
changes in the blood, and the same tendency to congestion of the internal
organs. The spleen and liver are moderately enlarged. The mucous mem-
branes of the nose, pharynx, larynx and larger bronchi, and the conjunc-
MEASLES. 783
tivse, are more or less intensely congested and present all the lesions of acute
catarrh. In the majority of instances this catarrh is most severe just be-
fore and during the early period of the eruption ; generally, it begins to
disappear when the eruption has reached its height, and within two or
three days entirely disappears. Where death has resulted from measles,
in the majority of autopsies, evidence of capillary bronchitis is found, and
not infrequently of catarrhal pneumonia also.
Strictly these are not anatomical lesions of measles, but complications ;
they are, however, such frequent attendants of this disease, that they are
almost a part of its history.
The eruption is papular ; the papules first show themselves upon the
face, especially upon the chin ; gradually they extend to all parts of the
body, and lastly appear upon the back of the hands. When the eruption
is well developed the spots are slightly elevated, and have a diameter vary-
ing from two-fifths to one-twentieth of an inch ; in form they are crescent-
shaped, their margins are sharply defined, usually their color is bright-
red, sometimes shading off into blue, in most cases the spots are distinct
and separated from each other by pale tracts of skin ; they may become
confluent, and thus give to the surface a uniform redness. When this
occurs the surface presents an appearance similar to that seen in scarlatina.
The earlier papule in each spot usually occupies the place of a hair-follicle ;
hence some regard inflammation of a sebaceous follicle of the skin as the
first event. The spots disappear on pressure, but immediately return when
the pressure is removed. Sometimes each spot contains several papules.
The diversity in form and appearance of measle-spots in different cases
depends upon variations in size, elevation, and grouping of the papules.
When the spots assume a dark-red color, and do not disappear on pressure,
capillary hemorrhages have taken place into the papules, and the eruption
is called hemorrhagic. When the eruption is very abundant, little vesicles
sometimes appear upon the papules, especially upon the trunk when there
has been profuse perspiration, called by some vesicular or miliary measles.
As soon as the spots have reached their maximum of development, their
color begins to fade ; the fading is progressive, the centres of the spots
retain their redness longest ; the elevations subside with loss of color. In
a varying time, from one to five days, the spots entirely disappear, leaving
a yellowish or brownish stain. This staining is due to pigmentation of the
skin, and is sometimes visible for two weeks.
Exfoliation of the epidermis or desquamation takes place only upon the
sides of the measle-spots ; it is never so extensive as in scarlet fever. The
skin does not desquamate in layers, but in fine brown scales, i. e., is fur-
furaceous, not squamous, hence it is called the hran-like desquamation. It
may commence before the redness of the eruption disappears, but it does
not usually occur until the eruption has entirely faded. In most cases the
period of desquamation is short, rarely lasting a week.
Etiology. — It is essentially a contagious disease. So far as has yet been
determined, it is only propagated by contagion. There are places, extensive
districts, and countries thickly inhabited, where this disease has never pre-
784 ACUTE GENEEAL DISEASES.
vailed. There is no authentic evidence that it ever originated spontane-
ously. The poison of measles is located either in the mucous secretion, or
in the exhalations from the body of the infected so contaminating the air
about fche sick that when persons who have not had the disease are brought
within its influence measles will be developed. It has been proved that the
blood, the mucous secretions, especially the nasal, and even the tears have
the power of conveying the disease by inoculation. ' There is little question
but that the disease can be conveyed in clothing, or, in other words, that
it is a portable disease. One not protected when exj)Osed to measles is
much more certain to contract the disease than is an unprotected person to
contract small-pox or scarlet fever. It is possible for the infection to be
conveyed from one place to another in clothing and in fluids. The exact
nature of this poison is still unknown.
The average period of incubation is eight days. During this period the
poison remains latent, giving its possessor no knowledge of its presence.
In most cases a slight exposure is sufficient to induce the disease ; in some
cases it is contracted only after prolonged exposure. Susceptibility to this
contagion is almost universal. All classes are equally subject to the in-
fection. Second attacks are exceedingly rare. The exact time in the
course of the disease when measles is most infectious is not definitely deter-
mined. Statistics furnish almost absolute proof that it may infect through-
out its entire course.
Symptoms. — Measles, like the other exanthematous fevers, if uncompli-
cated, runs a definite course.
Premonitory or precursory Stage. — At the end of the stage of incubation
or latent period of the disease, which is without fever, and free from local
symptoms, or from eight to ten days after exposure, the patient begins to
suffer from coryza, is languid, chilly and exceedingly irritable. Sometimes
a subnormal temperature precedes the first symptoms. Occasionally, in
young children, convulsions occur. The coryza and other catarrhal symp-
toms, at first, may or may not be accompanied by fever, or the sudden
initial fever may be very intense. Very soon, in either case, occurs a
marked febrile movement. The eyes will be injected and watery, there
will be a burning sensation and an aversion to light, and the eyelids will be
red and tumefied. There is a constant, irritating, watery discharge from
the nose, with frequent sneezing and pain over the frontal sinuses. Sore
throat is complained of, and the voice is a little husky. Bronchial catarrh
is indicated by uneasiness and constriction over the chest, with a frequent
dry, hoarse cough, hurried respiration, etc. The suffused, red appearance
of the eyes is peculiar, and distinguishes measles from scarlet fever and
other forms of eruptive fever.
After the early symptoms have continued perhaps for twenty-four hours
an initial fever will be developed which, with the catarrhal symptoms, con-
1 An organized ferment, bacterium or tarnea (which develops to a certain point in a proper medium and
then suddenly ceases its career), has been found in blood and breath and in gl}'cerine on which children
with measles have breathed. They have been found in the true skin. lymph-spaces and sweat-glands ; in
shape they are rod, spindle and canoe shaped, also spherical and ovoid. They are also found in the lungs.
MEASLES. 785
tmues from forty-eight hours to four days ; then the eruption makes its ap-
pearance.
Eruptive Stage. — The eruption is first seen upon the face (about the
chin, forehead, mouth, and side of the nose), then upon the neck, then
upon the chest and over the body, afterwards upon the legs and arms, and
lastly upon the back of the hand. The eruption on the face feels like
small shot early in the disease. The eru23tion may appear first on a part
of the skin that has been the seat of injury. Usually it is about four days
from the time of the appearance of the eruption upon the face before it has
passed over the entire body, and it begins to fade from one part about thirty-
six hours after its appearance upon that part ; first, it begins to fade from
the face, then the neck and chest, and finally from the back of the hands.
If closely examined, the eruption will be found composed of little, fine, red,
crescentic dots, which, after a little time, will be seen crowded together in
patches of irregular shape. Between these patches the skin usually has its
natural appearance. The odor is peculiar during this period. The erup-
tion of measles presents more of a papillary appearance upon the face than
upon any other part of the body. With the appearance of the eruption there
is more or less swelling of the surface, with itching and burning, and the
color of the eruption will vary from a bright rose-red to a dark mahogany
hue. The difference in color depends upon the condition of the individual
and the peculiarity of the type of the disease, rather than upon any change
in the skin itself. The respirations are hurried, and convulsions may, in
children, prove fatal. Epistaxis is common, and the lymphatic glands
are enlarged. As the eruption disappears it loses its bright red color and
becomes a yellowish red, until finally nothing but a staining of the sur-
face is left; then desquamation commences. Increase in fever and rise
in pulse and nocturnal delirium often follow the first outburst of the
eruption.
Desquamative Stage. — The desquamation which follows the eruption is
not like the desquamation of scarlet fever — scaly or " peely," — but it occurs
in very fine dust-like flakes, which may pass unobserved. The eruption
reaches its height by the third day from the time of its appearance, and
generally has disappeared by the end of the sixth day. As a rule, during
the development of the eruption the catan-hal symptoms and fever are in-
creased in intensity ; the patient will sneeze and cough, and frequently
with such severity and with such a coarse, grating tone, that it has re-
ceived the name of "iron cough.'' It is not the cough of croup (though a
true croupy cough is sometimes present) ; there is no stridulous breathing
accompanying it, but it is the result of an ordinary catarrhal laryngitis,
which causes the patient to cough perhaps for two or three days without
expectoration, or any attempt at expectoration. During this period the
pulse will range from 100 to 120 beats per minute, and in young chil-
dren it may reach IGO. In the majority of cases the temperature does
not rise above 103° F., but it may rise as high as 106° or 107° F. As
soon as, or eve^i lefore the eruption begins to decline the temperature often
falls two or tfiree degrees. As the decline in the eruption goes on, the
50
78G
ACUTE GENEEAL DISEASES.
Fig. 165.
Temperature Record in a Case of Measles.
temperature gradually falls, until by the time the eruption has entirely
disappeared the patient will be
Y!^ fully convalescent.
Measles, like scarlet fever, is lia-
ble to irregularities in its develop-
ment. When it is prevailing in a
locality, cases occur in which all
the catarrhal symptoms of the dis-
ease are present without an erup-
tion : again, there is an eruption
closely resembling that of measles,
with no catarrhal symptoms ; from
the appearance of the eruption one
will not be able to say whether the
patient has or has not measles ; if
the subject has been exposed to the
contagion of the disease, the case
will probably be regarded as one of
measles, and yet if there are no
catarrhal symptoms, but simply an
eruption, such a diagnosis would be
made with a question.
There is a form of roseola which very closely resembles measles in every
aspect of the disease, except the catarrhal symptoms. There is an irregu-
lar form of measles which prevails epidemically, which is characterized by
a tendency to ulceration of mucous surfaces. This form shows its peculiar
tendency by the development of ulcers at the angle of the mouth, within
the nose, around the vulva, anus, etc. Sometimes these ulcers spread and
so interfere with deglutition and respiration as to endanger life. The ul-
cerations are accompanied by great prostration of the vital powers and a
tendency to gangrene of the above-named parts and also of the lungs. This
irregular variety only occurs in those who are poorly nourished, live in badly
ventilated houses, and are surrounded by unfavorable hygienic influences.
Again, there is a form of measles in which, at the very onset of the
disease, there is a very high range of temperature. There will be no
more severe catarrhal symptoms than in the ordinary forms — no more
bronchitis ; but there will be a higher range of temperature, perhaps rang-
ing as high as 106° or 107° F. Associated with this pyrexia there will
be restlessness, a dry tongue, and, very soon after the appearance of
the dry tongue, a change in the color of the eruption, which will assume
a dusky purplish hue. The eruption may present this ]3eculiar appear-
ance at the very commencement of its development. This type of measles
is called " Mack measles." The color of the eruption simply shows that
there have been extensive blood-changes. In most cases, these changes
have taken place prior to the development of the eruption. By some it
has been claimed that there is at work a peculiar epidemic or endemic in-
fluence that gives rise to the peculiar type of the disease : but as I have
MEASLES. 787
been brought in contact with it, it has seemed to me that it differed from
the ordinary type only in the intensity of the fever. It is the high range
of temperature which stamps it as a peculiar type of the disease ; but as
soon as the eruption has made its appearance, although at first it may be
of a bright red color, within a day or two it assumes the peculiar dusky
black appearance which has given rise to its name.
There is another irregular form of measles in which the eruption is
largely made up of petechial spots scattered over the surface of the
body, due to a hemorrhagic diathesis. It is really a hemorrhagic form
of measles, and is a very unfavorable type of the disease. At first the
eruption presents the same appearance as the ordinary eruption of measles;
but, after the fever has continued a few days, it assumes a dark color, the
patient becomes restless, the tongue dry, there may be vomiting and
diarrhoea, and, if death occur, at the post-mortem examination lesions
very closely resembling those of typhoid fever, such as changes in the
spleen and elevation of Peyer's patches, will be found. These cases are
also known by the term ''black measles." Hemorrhages also occur from
nose, mouth, urethra, intestinal and other mucous tracts.
There are thus two forms of black measles — one in which the eruption
consists of petechial spots scattered over the surface, and dej)endent upon
a hemorrhagic tendency ; in the other form the eruj)tion assumes a dark
appearance on account of changes which have occurred in the blood, the
result of a very high temperature at an early period of the attack. There
is always more or less danger connected with any of the more severe forms
of irregular development. Although measles is usually not a disease of
much severity, yet, however mild the type may be, it is liable to complica-
6ion, and the most frequent complications are to be found in the respira-
tory organs.
Complications. — Of these the most imjDortant is capillary bronchitis.
Rarely is there a case of measles without more or less bronchial catarrh ;
but the bronchial catarrh which ordinarily attends it is not of much con-
sequence. When, however, the bronchitis becomes capillary, the patient
is in great danger. Upon auscultation, if instead of loud, sonorous rdles,
which indicate that the catarrh is confined to the larger bronchial tubes,
there are fine crackling sounds, accompanied by an entire loss of, or an
extremely feeble, vesicular murmur, the catarrhal inflammation has ex-
tended into the finer bronchial tubes, and there is always danger of lobular
pneumonia (g. v.). A lobular pneumonia which complicates measles is
always attended with danger, and when depression of temperature fol-
lows decline of the eruption, all the pulmonary signs may grow very in-
tense. With serious lung complications, the eruption may recede. As
a rule, it attacks both lower lobes at the same time, especially their dor-
sal aspect, while in the upper lobes only a few tubes are involved. This
complication may occur at any time during the course of measles, but it
is more liable to occur Just after the eruptive stage. Its development is
attended by a rise in temperature, in proportion to the extent of lung in-
volved. The urine is always scanty and may be suppressed.
788 ACUTE G ENTERAL DISEASES.
Secondary meningitis not infrequently occurs as a complication of measles.
When it does occur, it is deyeloped during the period in which the eruption
is disappearing. It is more likely to occur in this disease than in scarlet
fever.
A sequela of measles is a mild form of ophthalmia. This ophthalmia
may considerably inconvenience the patient, and lead to permanent injury
of the eyes. It is especially important to remember that it appears during
the convalescing period, that it is a conjunctivitis, and usually entirely
disappears if the eyes are frequently bathed with warm water and properly
protected from the light.
OtorrhcEa, or inflammation of the external ear, is another sequela of
measles. It most commonly appears in those patients who have what is
called a strumous diathesis, have phthisical parents, are themselves badly
nourished, or who have suffered from a severe form of measles. This
otorrhoea is sometimes very obstinate, and if it yields to treatment does so
very tardily ; it may be followed by permanent deafness.
In adults acute miliary tuberculosis not infrequently occurs as a sequela
of measles. Within the past three years I have seen two cases of what,
previous to death, seemed to be acute tuberculosis, and when the autopsy
was made, throughout the lung substance, here and there, were little points
or nodules which presented the usual appearance of miliary tubercles, but,
when microscopically examined, they were found to be points of vesicular
pneumonia. These patients really died from pneumonia, and not from
acute tuberculosis, although the lungs presented the gross appearance of
acute tuberculosis. The mucous membrane of the intestinal canal may
also become the seat of important complications in measles. A mild form
of gastric catarrh is of quite frequent occurrence, but is rarely serious in
character. Severe intestinal catarrhs, giving rise to troublesome diarrhoea
and dysentery, are sometimes very serious complications, especially in very
young and feeble children. Occasionally malignant epidemics of measles
prevail, during which the fatal results are chiefly due to intestinal catarrhs.
Diplitheria does not so frequently complicate measles as it does scarlet
fever. It generally makes its appearance when the eruption is at its height,
and when severe its occurrence is marked by a rapid rise in temperature.
The symptoms of the diphtheria are the same as when it occurs as a
primary disease. It must always be regarded as a serious complication.
Not infrequently measles leaves the patient in a state of general ill-health.
Especially is this the case in scrofulous and rachitic children.
Differential Diagnosis. — Ordinarily, when the eruption is well defined,
the diagnosis of measles is not difficult. In some cases, however, the
eruption presents an appearance which closely resembles that of scarlet
fever and roseola. In nearly every case of measles the catarrhal symptoms
accompany the precursory stage, and increase in severity during the period
of eruption. The presence or absence of these catarrhal symptoms will
enable one in the majority of cases to make a differential diagnosis.
In children, the eruption of typhus fever very frequently closely resem-
bles that of measles, but it does not appear upon the face, and is not
MEASLES. 789
accompanied by catarrhal symptoms. In typhus feyer, nervous symptoms
are quite frequently present, such as delirium, prostration, and tendency
to coma. Such symptoms are only met with in the hemorrhagic or typhoid
variety of measles. Before the appearance of the eruption a careful ex-
amination of the mucous membrane of the pharynx will settle the question
of diagnosis. In measles the mucous surface will be more or less intensely
injected; in typhus fever it will not be so injected.
The differential diagnosis between measles and small-pox has been con-
sidered.
The eruption of measles differs from that of roseola. In measles it is
partially confluent, in roseola it is non-confluent. In roseola the mucous
membrane of the fauces is not intensely injected, and the fever does not
run a characteristic course, the reverse of which occurs in measles. If the
temperature is normal, if the eruption on the trunk is of a bright color,
if the surface is smooth, and if catarrhal symptoms are absent, measles
may be excluded.
It is hardly possible to mistake syphilitic exanthemata for measles, for
there are certain glandular changes which attend the development of
syphilitic eruptions which establish the diagnosis. In the early period of
the disease, when coryza is a prominent symptom, before the appearance
of the eruption, measles may be mistaken for an ordinary influenza.
Prognosis. — The prognosis in uncomplicated measles is always good.
Any irregularity in its development, and dentition in children, may render
the prognosis unfavorable. In the hemorrhagic, ulcerative, and in the ty-
phoid varieties the prognosis is grave. Measles occurring in pregnancy does
not prove fatal to the extent that scarlet fever does ; but abortion is very
common. Intra-uterine measles may be recovered from, and the child is
then proof against a second attack. In severe cases, the deviations from
the typical course of the disease which render the prognosis unfavorable
are a temperature of 105° or 106° F. during the period of initiatory
fever, a retardation or an irregularity in the appearance of the eruption at
the beginning of the eruptive stage, and the occurrence of complications,
especially broncho-pneumonia, croupous laryngitis and diphtheria. Pro-
fuse hemorrhages from the mucous surfaces, during any period of the fever,
render the prognosis unfavorable. Eecession of the rash is very unfavor-
able when there are any pulmonary symptoms. The hygienic surroundings
of the patient greatly influence the prognosis.'
The prognosis also depends upon the age of the patient ; the rate
of mortality is much greater among adults than children, and in very
young children than in older children. The character of the prevailing
epidemic determines to a very great degree the prognosis. When measles
is developed in one who is suffering from a severe chronic disease, especially
some organic disease of the lungs, the prognosis is unfavorable. The
patient will not probably die during the active period of the measles, but
the chronic pulmonary disease may terminate fatally from the effects of
the measles. For instance, a patient has evidences of consolidation about
1 The presence of sewer-gas renders nearly every case fatal.— Quain.
790 ACUTE GENEEAL DISEASES.
the apex of the lung, a condition which justifies a favorable prognosis ; let
measles be developed in such a case and capillary bronchitis, terminating
in more or less extensive pneumonia, will probably occur, from which
acute phthisis may be developed.
In measles, death rarely occurs during the first week of the disease ; it
usually takes place during the second week ; if serious complications occur,
it may take place later in the disease. The rate of mortality is estimated at
from one to four per cent.
Treatment. — The prophylactic treatment of measles consists in isolating
the affected person. When measles run a regular course, the principal duty
of the physician is to watch for, and guard against the occurrence of pul-
monary and other complications. All that is necessary is to place the
patient in a large, well- ventilated, darkened room, with the temperature
of 63° or 65° F., so that the congested conjunctivae may not be exposed to
light.
The chief article of diet should be milk. If the patient complains of
itching and burning of the surface, he may be frequently sponged with
tepid water ; this causes an alleviation of the itching and burning, and re-
duces the temperature. In an ordinary case this is all that will be re-
quired. Hot drinks or stimulants have no power to hasten the appearance
of the eruption ; the administration of the latter may be followed by very
injurious results ; convulsions and death may occur. In an ordinary case,
stimulants should never be administered during the initiatory period of
the fever, unless there is some special indication for their use, such as great
prostration or bronchial complication ; then they may sometimes be used
with benefit. Covering the patient with heavy clothing does not hasten
the appearance of the eruption. The' greatest cleanliness should be ob-
served ; besides, there should be free ventilation, avoiding all draughts,
in the sick-room. If there is thirst, cold water may be freely taken in
small quantities at a time.
If the case is severe, and the temperature rises to 103 or 104 degrees
F., it may be reduced by frequently sponging the surface with tepid
water. '
Post-pharyngeal catarrh is liable to extend into the larynx and bronchial
tubes and give rise to bronchitis. One of the most important duties of the
physician is to watch for the occurrence of this complication ; he should
frequently examine the chest, and when the bronchitis is found to have
reached the capillary tubes, should immediately commence treatment for
its relief. I have found the inhalation of steam to afford the greatest re-
lief, and to best control the bronchial inflammation. As soon as the larynx
has become so involved as to interfere Avith the respiration of the patient,
and there is danger of croupous laryngitis, immediately order vapor inhala-
tions, and insist upon their continuance until the laryngeal symptoms shall
have subsided. Sometimes this subsidence will take place within two or
1 German writers recommend the cold bath in the treatment of measles. I should hesitate ro place a
patient with measles in a cold bath, on account of the great tendency in this disease to pulmonary com.
plications.
GERMAN MEASLES. 791
three hours, and, again, not until after two or three days. The value of
vapor inhalations in the treatment of the laryngeal and bronchial complica-
tions of measles, I regard as very great. When catarrhal pneumonia is de-
veloped, it is to be treated in the same manner as catarrhal pneumonia
developed under any other circumstances ; the patient should be sustained
by the free use of stimulants.
Pulmonary complications in measles are often the result of exposure to
sudden changes in temperature ; the severity of catarrhal symptoms will al-
ways be increased by such exposure, therefore it is of great importance in
the management of every case of measles that the patient should be pro-
tected against sach changes. When there is great restlessness during the
fever of invasion, or during the early jseriod of the eruptive stage, small
doses of opium, in the form of Dover's powder, may be administered with
marked benefit.
The management of the different varieties of measles will be indicated by
the general condition of the patient. In the ulcerative, hemorrhagic, and
typhoid varieties, the free administration of stimulants should be commenced
early. Usually in these varieties there is great prostration, and the main
indication is the support of the patient. Diarrhoea at the close of measles
may take the place of lung complications, and should not be too suddenly
checked.
GEEMAlSr MEASLES.
(Rotheln.)
German measles, or epidemic roseola, has been regarded by some as a
modified form of measles ; by others as a modified form of scarlet fever ;
again, it has been thought to be a combination of the two diseases — a hy-
brid disease. Some maintain that it is not an independent and specific dis-
ease, but that it may embrace any blotchy exanthem.' I am disposed to
regard it as a different type of measles from that which ordinarily pre-
vails, and by way of distinction would call it German measles, or epidemic
roseola.
Morbid Anatomy. — It is one of the mildest of the eruptive fevers. It
prevails epidemically and endemically. The study of its morbid anatomy
has been almost exclusively restricted to the eruption. This consists of ir-
regular spots, or hypersemic blotches, varying in size from a pin's head to
a large pea, usually slightly elevated, so that when the hand jDasses over
the surface of the skin it feels somewhat rough. Sometimes these spots oc-
casion intense itching ; they are quite distinctly separated by healthy skin,
and disappear under pressure. As a rule, even at the acme of the develop-
ment of the eruption, their color is a pale rose-red, paler than the intense
red of the eruption of scarlet fever, or the peculiar bluish hue of the erup
tion in severe cases of measles. It appears upon all parts of the body, but
' Later German writers regard it as an independent affection, a specific, acute, and contagious eruptive
fever, and have given to it tlie name of rubeola.
792 ACUTE GENERAL DISEASES.
is most abundant upon the face and trunk. The spots are usually discrete,
are round (not crescentic), they often lie crowded closely together, but they
are not confluent.
Mild roseola is a punctate rash. The throat is red and the glands in
the neck may be enlarged. The rash rarely lasts more than two days, and
it is attended by itching. In some cases there is slight desquamation ;
it disappears and leaves no trace, except in occasional instances, when there
is a transient, yellowish discoloration of the skin.
Some affirm that the rash may disappear and reappear alternately
for several days, and when it has finally disappeared the disease has ter-
minated, and there is nothing to fear from complications or sequelee. In
certain rare cases vesicles resembling miliaria may be developed upon the
hyperaemic spots, especially upon the back ; these are chiefly due to external
conditions.
Etiology, — Doubtless this disease is contagious. Nothing is known con-
cerning the nature of its contagion. It is essentially a disease of child-
hood. In those over forty years of age its development is of very rare
occurrence. It is conveyed from one person to another in the same man-
ner as measles. It has been stated that women are more susceptible to it
than men.
Symptoms. — Epidemic roseola is so mild an affection, that it is question-
able whether it has an invasive stage. The duration of the stage of incuba-
tion has not been determined. Generally, the symptoms which manifest
themselves two or three days before the appearance of the eruption are
much less marked than they are in any other eruptive fever. Perhaps in
many cases they escape notice. The period of invasion is seldom more than
twenty-four hours. Quite frequently the eruption is the first symptom of
the disease.
In most cases there may be nothing more than a feeling of discomfort.
In other cases the disease may be ushered in by vomiting, diarrhoea, and
convulsions. In many cases, immediately preceding the eruption, and ac-
companying its appearance, there is well-marked fever, headache, loss of
appetite, and sometimes noticeable prostration. When the eruption is
regular in its appearance it affects first the neck and chest, then the face
and scalp, and then gradually extends downward over the trunk and ex-
tremities. Usually, the development and spread of the eruption are rapid,
perhaps no more than two or three days being occupied in its passage over
the entire body. Its duration upon any one part of the body before it be-
gins to disappear is not more than twelve or twenty-four hours. In the ma-
jority of cases the temperature does not rise more than 1° or 3° F. It may
rise to 103° F, or 104° F. During the second day, the temperature begins
to fall. Sometimes it reaches the normal within twelve hours, occasion-
ally not until the third day. Sometimes it reaches it by crisis, at others
by lysis. The pulse increases and diminishes in frequency according to
the rise and fall of temperature. The tongue is usually covered with a
whitish coating, and is dotted here and there with red and swollen papillae.
The mucous membrane of the fauces is generally congested and the tonsils
GERMAN MEASLES.
793
Day.
1.
3.
4.
5.
6'.
7.
,n
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,n
r.
f/t
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104'-
jm"-
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Fig. 166.
Temperature Record in ^ case of German
Measles.
moderately swollen ; there may be some soreness of the throat. The
mucous membrane of the air-passages is
usually in a condition of mild catarrh,
consequently, at the onset of the disease,
sneezing and coughing are frequently
present, but they are less marked and are
of shorter duration than in measles. Suf-
fusion of the eyes with congestion of the
conjunctival vessels is rarely present ; there
may be a slight degree of photophobia.
The face and eyelids are usually slightly
swollen at the time the eruption makes its
appearance, but this swelling rapidly dis-
appears.
In most cases, there is moderate swell-
ing of the lymphatic glands of the neck,
and enlargement of the glands at the nape
of the neck. Moderate enlargement of the
occipital glands may continue for a num-
ber of days The disease is so mild in char-
acter that children are with difficulty kept
in bed.
Differential Diagnosis. — One of the promi-
nent features of this disease is the close resemblance which its eruption
bears to that of measles. In certain cases it may be impossible by the erup-
tion alone to make a differential diagnosis. When the eruption of measles
is not typically developed, a complete history of the case must be taken
into consideration. When this has been done, there is usually no great
difficulty in arriving at a correct diagnosis. Perhaps that which will best
aid in making a differential diagnosis between roseola and measles is the
fact that an attack of one does not protect against the other, any more than
does an attack of varicella protect an individual from an attack of variola.
This fact certainly establishes the non-identity of the two diseases. The
short period of invasion, the eruption appearing first on the chest and neck,
the very mild nose and throat symptoms, and the low temperature are in
contrast with the symptoms of measles.
It has been questioned whether a person may not have a second attack
of epidemic roseola. The latest observations go to prove that a second attack
is of as rare occurrence as a second attack of measles or scarlet fever.
Again, one attack does not protect an individual against the contagion of
scarlet fever ; nor does an attack of scarlet fever protect one against the
contagion of roseola. An individual may have an attack of epidemic
roseola very soon after he has been ill with measles or scarlet fever.
Prognosis. — The prognosis is always good. Complications rarely occur ,
when they do, they are usually pulmonary.
Treatment. — The treatment of this affection consists in protection against
exposure. Tepid sponging will relieve troublesome itching, and reduce
794 ACUTE GENERAL DISEASES.
fever. Regulate the diet, and carefully watch the catarrh of the air-pas
sages. As a rule, convalescence is rapid.
MILIARY FEVEK.
This form of fever cannot strictly be regarded as a contagious disease,
but it so frequently prevails in connection with measles and scarlet fever,
and has apparently so many elements of contagion, that it is included in
the list of contagious fevers. Some deny its existence as a distinct fever.
Writers have described it under the names of sudamina, sudoral exanthema,
and miliaria alba, etc. Several diseases which are accompanied by sweat-
ing, and which exhibit a tendency to the formation of miliary vesicles, have
been called miliary fever.
Until the occurrence of the severe epidemic of the disease known as the
''English Sweating Sickness," its specific type was not recognized. It has
prevailed epidemically over limited areas, in Belgium, France, England,
Germany, Italy, and Austria. In some of these epidemics eleven to twenty
per cent, of the whole population of the invaded district has been attacked.
The average duration of the epidemics has been from three to four weeks •
occasionally they have lasted from three to four months.
Morbid Anatomy. — Few post-mortem examinations have been made, and
those few have failed to reveal any characteristic lesion. The miliary
vesicles which are seen upon the surface of the body, and the cutaneous
eruption, are developed because the secretion of the sudoriferous glands
cannot escape. The escape of the contents of these glands may be pre-
vented by two causes : (1) the gland-ducts may become obstructed ; or, (2)
the secretion may be so abundant that it cannot be transmitted by the
gland-duct. In either case, the secretion emerges under the epidermis
around the sweat-duct, and as the scales are lifted up, a small clear vesicle
is formed. The liquid contained in the vesicle at first is transparent, has
an acid reaction, and is said to contain free nuclei and cells which have
three or more nuclei ; these nuclei remain visible after the cell membrane
has been destroyed by the addition of acetic acid. The contents of the
vesicle becomes milky and yellowish from pus (m. alba). It has been
claimed that the virus of the disease is contained in these polynucleated
cells. After death, the skin becomes oedematous, and very soon the odor
of decomposition is perceptible.
Etiology. — It has been supposed that miliary fever was indirectly induced
by scarlatina, the puerperal condition, variola, vaccinia, typhus fever and
like diseases, and that it was not a distinct disease arising from some con-
stitutional cause. The prevalence of this fever in connection with these
diseases gave rise to this supposition. Epidemics of this disease have
generally prevailed during the spring and summer months ; from this fact
one would be led to think that there is some atmospheric condition pecul-
iar to these months. Again, the disease has most frequently appeared in
ivarm, moist weather, and from this fact it has been supposed that some
peculiar condition of the soil is necessary to its development. Certain
MILIARY PEVER. 795
epidemics have shown a close connection with contaminations of the soil,
such as arise from neglect of drainage, collections of refuse, etc. Doubt-
less, such conditions of the soil may increase its severity, and cause it to
prevail more extensively, but facts do not prove that, directly or indirectly,
they cause its development.
The disease usually attacks healthy adults, and occurs more frequently
among females than males. It attacks all classes, and its spread does not
seem to be affected by crowding. '
Symptoms. — The average duration of the disease is from five to eight
days. It has three stages: (1) tlie stage of invasion ; (2) the stage of
sweating ; and, (3) the stage of erupiion and desquamation.
The Stage of Invasion. — The average duration of this stage is from
forty-eight to seventy-two hours. It is characterized by an excessive irri-
tation of the skin, thirst, general lassitude and headache. There is also
more or less febrile movement. Some writers mention a feelinsr of suf-
focation, which is usually preceded by a sense of oppression at the epigas-
trium. These are the characteristic symptoms of the stage of invasion.
The Stage of Swezting. — This stage is usually ushered in by rigors ;
rarely, by a well-marked chill. The characteristic symptom of this stage
is profuse and persistent sweating. The sweating is accompanied by a
prickling sensation of the skin, distress, and a sense of compression at the
epigastrium, and by more or less violent palpitation of the heart, with pre-
cordial pain. Usually the sweat appears on all parts of the body at the
same time. Sometimes it appears first upon the head and breast, then
gradually descends, and soon becomes so abundant that every article of
clothing, bed-clothes and bedding, becomes saturated. The pulse some-
times reaches 140 beats per minute, the temperature rises to 103° F., 104°
F., or even 105° F., and the skin, notwithstanding the profuse perspiration,
feels extremely hot. During this stage the headache and the sense of
suffocation increase ; the epigastric and precordial pain and the palpita-
tion increase in severity, and sometimes become alarming, although the
most careful physical examination fails to discover any lesion in the
heart or lungs to account for them. The respiration becomes rapid, often
irregular and intermittent.
Irregular exacerbations, or even intermissions, in these symptoms may oc-
cur, but, as a rule, they continue without abatement until the vesicle ap-
pears, on the third or fourth day of the disease.
The Stage of Eruption. — This stage is characterized by the appearance of
a rash. It is first seen upon the neck and breast, then upon the back and
' It can hardly be regarded as a contagious disease, in the sense that it can be communicated directly
from the sick to the well. It does not seem to be well established that the disease can be developed by
inoculation with the contents of the vesicle, notwithstanding it has been supposed that certain cells in
the fluid hold the contagion of the disease. The infrequency of the simultaneous occurrence of miliary
fever with epidemics of measles or scarlet fever, is unfavorable to the theory that there is a specific rela-
tionship between the poisons of these diseases. The view that there is an intimate relationship between
cholera and miliary fever has been accepted by some writers, and the accession of the latter during
the course of the former has been supposed to exert a favorable influence over the course of the disease ;
the opposite, however, docs not appear to hold good, but on the contrary, favors a fatal termination.
Much remains to be learned in regard to the relationship existing between miliary fever and the other
diseases whicli 've have mentioned.
796 ACUTE ge:n"eeal diseases.
extremities, sometimes upon the mucous membrane of the mouth, nose, and
conjunctiva, sometimes upon the abdomen and scalp. This eruption con-
sists of irregularly shaped spots, 1-8 to 1-16 in. in diameter. In some
cases they stud the skin so thickly that it appears like an uniform sheet of
vivid redness. After the lapse of a few hours, vesicles can be seen in the
centre of these spots ; perhaps at first they are so small as to necessitate
the aid of a lens to discover them. These vesicles rapidly increase in size,
and may reach the size of a millet-seed or a small pea. The contents of
these vesicles have already been described. Occasionally, as the eruption
appears, all the constitutional symptoms are increased in severity, but usu-
ally they are modified and disappear either suddenly or gradually after its
development. In the milder cases the vesicles only, without the efflores-
cence, are seen. Vomiting is rarely present, although nausea is a common
symptom, as is also constipation.
The urine is usually scanty and high colored ; in some cases there is sup-
pression of urine. Occasionally, during the stage of eruption, profuse
secretion of urine takes place. This has been regarded as a favorable
symptom. The vesicles, clear at first, soon become opaque and yellowish,
remain for two or three days, then burst and begin to fall off in scales.
Desquamation is usually completed within forty-eight hours, but convales-
cence is often quite protracted on account of the debility and emaciation.
Such is a brief description of miliary fever, when it runs a regular course,
but there are certain variations in the development of the symptoms which
should be noticed. In the severest form of the disease, the temperature may
rise to 107° or 108° F., and there may be delirium and a sense of suffocation.
Again, even in fatal cases, the eruption, sweating and convulsions may
be absent. Occasionally sudden and fatal collapse follows the sweating
sta^e. The typhoid condition may be developed in the sweating stage,
and may be attended by black sordes upon the teeth and tongue, epistaxis
and uterine hemorrhage, and may terminate fatally, without any consid-
erable anatomical changes recognizable after death.
Complications are not of frequent occurrence. Occasionally there is
bronchitis, pneumonia, and diarrhoea.
Relapses are of common occurrence, but recovery generally takes place
after a short relapse.
DiflFerential Diagnosis. — Miliary fever may be confounded with measles,
with malarial fever, and with typhoid fever.
The profuse sweating, the prickling of the skin, the intense oppression
at the epigastrium, the sense of suffocation, with precordial pain, and the
peculiarity of the eruption, are sufficient to distinguish it from measles,
from intermittent fever (although a decidedly intermittent type of the dis-
ease sometimes prevails), and from typhoid fever. When the disease pre-
vails epidemically, the diagnosis cannot be difficult.
Prognosis. — When the disease runs a regular course, with only a moderate
degree of severity, the prognosis is good ; whereas great severity of the fe-
brile symptoms, exceptionally profuse sweating, and increasing sense of
constriction of the chest, with suffocation, render the prognosis unfavora-
INFLUENZA. 797
ble. The accession of profuse hemorrhages, coma, convulsions, active de-
lirium, or symptoms of collapse, render the prognosis unfavorable. The
severity of the symptoms is usually mitigated when the eruption makes its
appearance, and death rarely occurs after that stage is reached. If a fatal
termination is reached, it usually takes place during an exacerbation, prior
to the appearance of the eruption. In some epidemics, the mortality has
been very great ; in other epidemics the disease has been mild in character ;
eight or nine per cent, is the average death-rate. The character of the
epidemic affects the prognosis.
Treatment. — At one time diaphoretics were employed in the treatment of
this disease, on the supposition that the sweating and eruption were criti-
cal manifestations, and must be aided by all possible means. The sense of
suffocation, with that of constriction of the chest, was thought to indicate
blood-letting ; but it was soon decided that loss of blood aggravated rather
than improved the patient's condition. Antispasmodics, nervines, quin-
ine, emetics and counter-irritants at different times have formed the basis
of various plans of treatment. Of late, subcutaneous injections of mor-
phine have been used with advantage. Sinapisms and blisters have been
employed for the relief of the sense of constriction in the chest, and for the
ej)igastric and precordial distress, with benefit to the patient. It is now
acknowledged that the administration of purgatives in large doses should
be carefully avoided, as well as blood-letting, general or local.
At present the expectant plan of treatment is regarded with most favor.
It chiefly consists in the use of cooling drinks, aromatic teas, acidulated
water, sponging with warm water, or the employment of warm baths. It
has been thought that the addition of alum or vinegar to the water used for
sponging or bathing is beneficial. In the treatment of this affection, quin-
ine seems to be regarded with almost universal favor. If restlessness is
persistent, opium, ether, valerian, and antispasmodics may be employed in
moderate doses, carefully watching the effect produced. The patient should
be surrounded by proper hygienic influences, the diet should be moderately
nutritive, and in those cases in which convalescence is tedious a steady and
continued tonic treatment is indicated. In the severest form of the disease
stimulants may be employed with benefit.
INFLUENZA.
{Epidemic Cata/rrJl.)
Influenza is a specific continued fever, generally widely epidemic, and at-
tended by catarrh of the respiratory and digestive tracts. It has received a
great variety of names. In 1830 and '31 a severe influenza epidemic swept
over the whole civilized world.
Morbid Anatomy. — There are no special pathological lesions of influenza.
There is generally more or less extensive inflammation of the respiratory
organs ; the lungs are usually inflated so that when the chest is opened they
protrude from the cavity instead of collapsing. Sometimes they are very
dry, at others oedematous. Spots of lobular consolidation appear as de-
798
ACUTE GEKEEAL DISEASES.
pressions between the inflated portions. The mucous membrane of the
trachea and larger bronchi is red and covered with frothy or viscid muco-
pns. The injection is usually most marked in the smaller tubes. The
bronchial glands are enlarged and softened. Pale, firm clots are found in
the right heart. The gastric and intestinal mucous membrane is congested ;
the stomach is usually more congested than the intestines. Hence the name
gastric influenza.
Etiology. — All conditions and ages suffer alike; but children are some-
times remarkably exempt. The disease travels very rapidly ; it has passed
over the whole of Europe in six weeks. It passes quickly from one country
to another, visiting whole continents in a short time. It rarely continues
in one locality more than two months. There is no doubt that influenza
is due to some powerful special morbific agent, which is given off by the
mouth of the infected, and which acts specifically upon the respiratory
mucous membrane and also upon the nervous system.'
Symptoms. — Influenza comes on suddenly, A feeling of chilliness,
sometimes distinct rigors, flashes of heat, and a feeling of lassitude are fol-
lowed by symptoms of a severe naso-pharyngeal catarrh, with frontal
headache, pains in the limbs and back, soreness of the throat, hoarseness,
and a frequent racking cough, difficult breathing and constriction across
the chest. The sputa are first mucous and then scanty, later copious and
muco-purulent. The respirations are accelerated ; there is great prostra-
tion, lassitude, apathy, muscular
weakness, and precordial oppres-
sion. The fever assumes a remittent
type, attended by profuse perspira-
tion. Sudamina appear on the sur-
face and herpes on the lips. The
pulse is rarely over 90 ; yet a tem-
perature of 104° has been observed,
and the pulse has been feeble, ir-
regular, and 130 per minute. The
tongue is moist and covered with a
white fur ; it may be dry and brown.
There is anorexia. Nausea and
vomiting may be early symptoms
and continue throughout the whole
course of the disease. The bowels
at first are constipated, later there
is diarrhcea. There may be hepatic tenderness and slight jaundice. As
the disease advances the face gets congested and livid, the frontal head-
ache becomes more severe, the pulse increases in frequency and becomes
feeble, the tongue becomes brown and dry. There are muscular tremors
and subsultus, the patient becomes dull and listless, and delirium is often
present.
J)a^.
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Fig. 167.
Temperature Record in a case of Influenza.
1 Brimer (in Virchow's Handbnch) thinks it is a miasmatic disease, caused by a living miasm capable of
being transmitted by the air and having an independent existence. It is probably contagious.
INFLUENZA. 799
On auscultation sibilant and sonorous rales are heard over some portions
of the chest, while at others the inspiratory sounds are dry and harsh. The
Tesicular murmur is always indistinct. Measle-like spots are often seen on
the palatal mucous membrane. In mild cases the disease is at its height
on the third day and then gradually declines. In the severe cases where the
pulmonary symptoms are prominent, convalescence does not commence until
the tenth or twelfth day ; convalescence is protracted and relapses are fre-
quent. The urine is less in quantity than normal ; sometimes there is
complete suppression. It is high-colored and deposits a sediment on stand-
ing. The different " varieties" of influenza as described by writers are due
to the different complications.
Differential Diagnosis. — The large number of persons attacked, the nerv-
ous debility which accompanies it, and its short uniform course are gener-
ally sufficient for its diagnosis.
The Prognosis is good except in the very old, very young, and in those al-
ready subjects of pulmonary or renal disease. Whenever there is a high
mortality-rate, the fatality is due to complications which have been en-
grafted on the influenza. Its complications are chiefly of the respiratory
tract, the more frequent of which are laryngitis, bronchitis, pulmonary
congestion and oedema, pneumonia,' which is usually lobular, and pleurisy ;
these complications have given to the disease the name of epidemic catarrhal
fever. Pharyngitis, parotitis, salivation, hypersemia of the liver, and sub-
acute gastritis are rare complications of the digestive apparatus. Herpes
labialis occurs often. The duration of influenza varies from four to twelve
days ; and an epidemic rarely continues more than from four to six weeks
in one locality.
Treatment. — When influenza is prevailing all exposure to cold must be
carefully avoided, and in its treatment the general hygienic measures of
the acute infectious fevers are to be employed ; medicinal treatment is not
very efficacious. Quinine sometimes aborts it, if given in large doses at its
very onset. In the early stages liquor ammonii acetatis and pulvis ipe-
cacuanhse (one grain of the latter in one-half ounce of the former) every
two or three hours is all that is required. The bowels should be kept
freely open with salines ; milk combined with alkaline waters is the only
food w^hich should be allowed for the first forty-eight hours. If patients
are restless, Dover's powders may be given in small doses. Steam inhala-
tions will relieve the laryngeal and bronchial symptoms, and may be con-
stantly employed during the acute stage. The prostration which occurs
in the old, young, or feeble must be combated early with stimulants.
All revulsives, blood-letting and depressing remedies are contraindi-
cated. Colchicum, carbonate of potash, and opiates are of service in those
cases of influenza where pain and rheumatic symptoms are predominant.
When convalescence commences the patient should begin to take quinine
and iron in small doses with a nourishing diet ; a change of air is often of
great service, especially if there have been pulmonary complications. It
' In one hundred and eighty-three patients at H6tel Dieu over twenty per cent, had lobar pneumonia.
—Copland.
800 ACUTE GE]S"ERAL DISEASES.
must be remembered that influenza is often the exciting cause of a phthi-
sical development m subjects who are so predisposed.
PEETUSSIS.
( Whooping -Cough. )
Whooping-cough is an acute contagious disease, attended by a peculiar
spasmodic cough. It should be classed among the diseases of children,
although it may occur at any age.
Morbid Anatomy. — The principal, if not the only, morbid changes in
this affection are those of catarrhal bronchitis. Those who regard the
disease as of nervous origin claim that there are evidences of inflammation
of the vagus nerve, or congestion of the medulla oblongata. I am dis-
posed to regard it as a specific catarrh of the respiratory mucous membrane,
which differs from other forms of catarrh in being contagious and attended
by peculiar laryngeal and bronchial spasms. Its complications are cerebral
oedema and congestion, lobular collapse, lobular emphysema, bronchial
dilatation, or capillary bronchitis and catarrhal pneumonia.
The specific catarrh is located chiefly in the bronchi, although some re-
gard it as at first limited to the pharyngeal mucous crypts, and still
others regard it as confined to the larynx. The bronchial and mediastinal
glands may undergo softening, the pleurae and pericardium may be ecchy-
motic. The mucous membrane of the stomach is congested and sometimes
studded with petechial extravasations. Follicular enteritis is not uncom-
mon. The liver and the spleen are often enlarged and fatty. Letzreich
claims to have found a fungoid vegetation in the epithelium of the air
tubes. Buhl, Oertel, and Hiiter also found them.
Etiology. — Whooping-cough depends upon a specific poison which is
given off in the breath of the affected, and conveyed through the air to
the healthy. A second attack is rare. The period of incubation varies
from five days to two weeks ; micrococci are sometimes found in the sputum.
Teething and measles predispose to the reception of the infection. It may
be carried in clothes. It may prevail epidemically, attacking nearly all
the children of a neighborhood or township.
Symptoms. — There are three recognized stages in whooping-cough, a
catarrhal, a spasmodic, and a stage of decline.
The catarrhal stage is marked by the ordinary symptoms of a severe naso-
pharyngeal and bronchial catarrh. It rarely commences with a chill, but
fever, restlessness, and languor are marked. The fever in the early stage
is intermittent. It commences with coryza, and a severe dry paroxysmal
cough, which is soon attended by an abundant, tenacious, viscid, transparent
mucus. The respirations are shallow and the pulse is rapid. The dura-
tion of this stage is from two days to three weeks ; nine to ten days is the
average.
The spasmodic stage is attended by a characteristic spasmodic cough.
This cough is very severe and distressing ; the face grows red, and then
begins a long, clear, piping sound, followed by a series of rapid, convulsive
PERTUSSIS. 801
and forcible expiratory puffs, which are succeeded by a prolonged, shrill
inspiratory sound or whoop. If the fit lasts any length of time, the cough
becomes inaudible, and a considerable quantity of clear, yiscid mucus is
expectorated or vomited with the contents of the stomach. During the
paroxysm the patient grows red or purplish in the face, the eyes pro-
trude, the tongue assumes a dark appearance, and he seems on the verge
of suffocation. Bleeding from the mouth, nose, ears, and lungs often
occurs during a violent paroxysm. The face becomes puffy, and ulcers
form on the tongue, and hemorrhages occur into the conjunctivae. The
subsidence of the paroxysm is usually followed by a sense of exhaustion,
with soreness about the muscles of the chest, and expectoration of whitish,
viscid mucus.
A physical examination of the chest during a paroxysm of whooping
cough shows a feeble or absent respiratory murmur over the whole chest,
with sibilant and sonorous rales ; during the interval mr.cous rales are
usually heard. The frequency and duration of the paroxysm vary greatly
in different cases. There may be one hundred in twenty-four hours. They
are most frequent, or occur only at night. As a rule the more violent the
paroxysm the sooner it is followed by another. The disease usually attains
its height by the end of the fourth or fifth week. In mild cases the pa-
tient is well in the interval between the paroxysms, but m severe cases
there may be languor and debility, loss of appetite, headache, and more or
less fever. Moist or dry crepitations and a weak inspiratory sound are often
heard during the interval.
The stage of decline is marked not by any sudden transition, but by a
gradual diminution in the frequency and severity of the paroxysms. The
j)eculiar whoop ceases, the expectoration is less difficult and becomes more
purulent in character, and finally, after a period of about nine weeks, the
characteristic cough ceases altogether, and the patient passes into a rapid
convalescence. Whenever the coughing fits lose their characteristic feat-
ures and become dry and hacking, and the dyspnoea is greatly increased
and continues through the intervals with a marked rise in the temperature,
it indicates some pulmonary complication. Another complication which
is particularly to be feared in this disease is cerebral congestion. When,
during a paroxysm, the countenance becomes flushed and swollen, the
jugular veins turgid, with a gush of blood from the nose, there is danger
of such an occurrence. When the face is continually flushed, the head
hot, the patient' drowsy or restless in his sleep, moaning and grinding his
teeth, there is danger of convulsions and coma, and the disease often termi-
nates fatally.
Differential Diagnosis. — In its earlier stages, it is not possible to diagnos-
ticate whooping-cough with certainty ; but its existence may be suspected
if the cough is of a violent spasmodic character, and if the disease is prev-
alent. When the disease is fully established, the peculiar cough and ex-
pectoration distinguish it from all other catarrlis.
Prognosis. — Whooping-cough is always a serious disease, although it is
rarely directly fatal ; yet indirectly it frequently causes death. It is dan-
51
803 ACUTE GENEKAL DISEASES.
gerous in proportion to the number and severity of the paroxysms, the in^
tensity of the fever, and the character and severity of the complications.
Cerebral or pulmonary complications are always dangerous. Teething
children are liable to convulsions during paroxysms of the coughing.
Death may result from laryngeal spasm independent of complications. A
condition of general debility, rickets, poverty and destitution, a residence
in a city in badly ventilated apartments, and epidemic influences, tend to
render the prognosis unfavorable.
Treatment. — The chief indications in the treatment of whooping-cough
are, first, to diminish the severity of the paroxysms ; secojid, to prevent
and treat as far as possible the complications ; third, to attend to the gen-
eral health of the patient. There are no known means by which this affec-
tion may be averted. The paroxysms cannot be altogether prevented, but
their severity may be lessened.
All of the internal and external specifics for the prevention of the parox-
ysms of whooping-cough, which have been proposed, and in some instances
strongly advocated, are of very doubtful benefit. The most important and
reliable remedies for relieving the paroxysms of coughing are the sedatives
and antispasmodics, the most efficient of which are belladonna, hydrocyanic
acid, hydrate of chloral, hyoscyamus, cannabis indica, the bromides, chloro-
form and musk ; all of these remedies must be given in minute doses, and
their effects closely watched. The dilute mineral acids, arsenic, nux vomica,
cochineal, bromide of potassium, and repeated emetics — emetics are no
longer given — have each in turn been highly recommended as specifics for
the control of the paroxysms in whooping cough. Alum is recommended
by Golding Bird (gr. i-v every four hours) and Meigs ^ says it is the best
remedy. No form of opium or belladonna is to be used till after the
catarrhal stage is past. Infusion of chestnut leaves is regarded highly.
Inhalation of coal gas is recommended by the French Academy of Medi-
oine. Ergot, the carioUc acid spray, asafoetida, arsenic and quinine are
iighly efficacious,^ the second and last especially. The nitrite of amyl and
jaborandi are drugs that I would not give to very young children. Local
;applications to the larynx, such as solution of nitrate of silver, etc., ac-
.cording to my experience, do more harm than good ; and the same is true
of counter-irritants, such as liniments and plasters.
I desire to impress this fact, that whooping-cough is a self -limiting dis-
ease, and, like all other diseases of that class, must be treated expectantly.
The patient, by warm clothing, should guard against undue exposure. In
bad weather, he should be confined to the house in a room of uniform
temperature ; but there is no reason, if the weather is favorable, why he
should not go out into the open air. The diet should be simple, and the
state of the alimentary canal carefully looked after. Adults and older
children should be taught to suppress the cough as much as possible.
Complications must be watched for, and treated as soon as they occur.
Bronchitis is the most frequent complication ; when it occurs it should re-
ceive prompt attention, according to the rules already given for the man-
1 Dis. of Children. * Binz and Squire.
HYDROPHOBIA. 803
agement of bronchitis, great care being taken tliat it does not become a
broncho-pneumonia. If the symptoms of congestion of the brain or of
pneumonia are developed, they should be met by the most prompt and effi-
cient remedies adapted to these conditions, and their earliest appearance
should be watched for. It is important to remember that in any or all of
the complications of whooping-cough, the treatment should be supporting
in character.
During convalescence, tonics, such as iron, quinine and cod-liver oil, are
indicated ; in fact, in a large proportion of cases these remedies are service-
able throughout the whole course of the disease. Astringents and restora-
tives are called for in the third stage and at the commencement of conva-
lescence. Sometimes this affection assumes a chronic form, continuing after
several relapses much beyond the usual period. In these cases, the great
remedy is change of air. In all stages of whooping-cough, benefit is de-
rived from a short sea-voyage and a temporary residence in a warm climate.
It has been recently stated by some very judicious observers, that large
doses of the sulphate of quinine have the power of aborting this disease.
My experience in this direction is not sufficient to deny or sustain the state-
ment ; but my impression is that this, like many other so-called specifics,
after a more extended trial, will be found unavailing.
HYDEOPHOBIA.
Hydrophobia, or rabies, is a specific contagious disease special to animals
of the canine and feline species, which may be communicated to man and
to all warm-blooded animals.
Morbid Anatomy. — There are no constant pathological changes. The
mucous membranes of the alimentary and respiratory tracts, especially of
the fauces and pharynx, are congested, (Edematous, and possibly show points
of hemorrhage. The tongue, tonsils, and the salivary glands are enlarged
and softened, and the lungs and other internal organs are congested.
Eecent investigations have shown ' congestion of the nervous centres, most
marked about the basal ganglia, the medulla and the gray matter of the
cervical cord. This is accompanied by a diffuse cellular infiltration of the
adventitia of the veins, with venous injection and thrombosis. Miliary an-
eurisms and minute hemorrhages have also been noted in the medulla, cer-
vical and dorsal regions of the cord.^
The blood is dark, forming soft clots, and putrefactive changes appear
early after death.
Etiology. — The cause of the disease is unquestionably a specific virus
which is most abundant and concentrated in the saliva and secretions of
the mouth and pharynx.
The poison retains its vitality for some time after the death of the
affected animal. Although not proven, it is probable that the disease is
never of spontaneous origin, but spreads among animals by contagion. It
1 Fitz and Shattuck.
2 Benedict considers the essential pathological change in the nerve centres to be "an acute exudative
inflammation attended by hyaloid degeneration."
804 ACUTE GENERAL DISEASES.
certainly is communicated to man solely by inoculation, which can take
place only through some break in the surface. Applied to the skin or swal-
lowed the virus is inert.'
Symptoms. — As in other infectious diseases, there is a period of latency
following the inoculation, during which the wound heals readily and pre-
sents no peculiarities. This period of incubation varies from a few days to
several months, and in some cases even to years. It is seldom, however,
that the disease appears after five months, and usually within two to six
weeks the stage of invasion begins.
This may or may not have been preceded by slight reddening about the
seat of the inoculation, with pain which radiates from the wound along the
nerve trunks. In a few cases the inflammation causes suppuration and re-
opening of the wound.
The period of invasion, or melancliolic stage, is attended by marked de-
pression of spirits and change in the disposition. The patient is feverish
and shivering alternately, is restless, uneasy and sleepless, and speaks in
a sharp, quick manner. The pupils are dilated and the eyes bright, and
the countenance has a look of anxious anticipation of some unknown
danger. The pulse is increased in frequency, the skin dry, and there is
constipation, with perhaps nausea and vomiting. In this stage the respi-
ration is oppressed, and shows evidences of the approaching spasms. There
is epigastric heaviness, and with inspiration the shoulders are elevated and
the epigastrium protuberant.
There may be also slight constriction of the throat and hesitancy in
swallowing, with general hypera^sthesia and sexual excitement.
These symptoms increase in severity for two or three days, when the
patient passes into the C07ivulsive stage.
The restlessness and undefined dread are more marked, the eyes have a
wild look, are bright, staring, and constantly moving ; the brows are con-
tracted, the surface pale, and the patient not only often appears like one
with acute mania, but the fear and horror may pass on to halluciations and
delirium.
The mouth and fauces are dry, congested, and covered with thick,
tenacious saliva, which gathers about the lips in frothy masses. Thirst is
intense, but every effort the patient makes to drink, and later the sight
of water or thought of drinking is followed by increase of the pharyngeal
constriction at first, and later by violent spasms of the muscles of deglu-
tition and respiration, attended by general tremors and most terrific mental
distress.
At first the convulsions only follow attempts at drinking, but the general
hypersesthesia increases rapidly and becomes so intense that the weight of
the clothes, loud harsh sounds, bright lights, or a draught of cold air will
excite general convulsions that leave the patient utterly exhausted and with
the most agonizing horror of their repetition.
In some cases death occurs early in the disease from asphyxia during a
1 Pasteur's experiments show that inoculation with a diluted virus affords protection from the actual
disease. Not over seventy per cent, of tliose bitten by rabid animals become hydrophobic, owing, doubt-
less, in many cases to the cleansing which the fangs receive as they pass through the clothing.
HYDROPHOBIA. 805
spasm, but more commonly as the symptoms increase in severity the patient
is rapidly exhausted ; the pulse becomes feeble, frequent, and irregular,
and as the spasms are more prolonged, he may die from gradual asphyxia
or exhaustion.
In rare cases a, paraplegic stage is said to occur, in which the paralysis is
most marked in the under jaw and lower limbs.
The '* hydrophobia " which is so characteristic of the disease as to give
it a name, is due entirely to fear of the distressing spasm which every effort
at swallowing produces, and is generally absent in dogs and other animals.
For the same reason the patient is continually hawking and spitting out
the thick, ropy mucus which is so abundantly secreted.
The peculiar characteristics of the dis-^ase are the intense hyperaesthesia
of the skin and organs of special sense ; the exalted reflex irritability of
the nervous centres, which results in the peculiar spasms ; and the parox-
ysmal rabid impulses that lead the patient to injure, it may be, his dearest
friends, even when he is conscious of the nature of his frenzy and is strug-
gling against it.
Differential Diagnosis. — Hydrophobia may be confounded with tetanus,
but in tetanus the mind is clear throughout, there is no fear of liquids,
the spasms are tonic and the hyperaesthesia is not so acute, nor does it in-
volve the special senses.
In hysteria the difficulty in swallowing is the only symptom of hydro-
phobia, and the expressions of fear are out of all proportion to the other
symptoms. A spurious rabies may be developed by the imagination in
patients, who suppose they have been bitten by a rabid animal, but the
course of the disease, its milder symptoms and favorable termination, will
readily distinguish it.
Prognosis. — Most authors regard the disease as absolutely fatal, and in
tables of cases which record a small per cent, of recoveries the possible
hysterical nature of these cases must be considered. I have never known
a case to recover.
The duration of the disease is from two to ten days, but in rare cases may
be extended to two or three weeks. Death usually occurs from asphyxia,
rarely from exhaustion or inanition.
Treatment. — When it can be done immediately, if the injury is upon a
limb, a tight ligature should be applied above the wound, which is then to
be widely excised and the part cupped. Venous hemorrhage should be
encouraged.
Of the many remedies proposed, curare offers the most encouragement.
It should be given hypodermically, in doses of one-third grain every fifteen
minutes, increasing until the spasms are controlled. Recovery has been
reported in one case where it was used.
806 ACUTE GEIfTERAL DISEASES.
MALABIAL FEVEE.
Introduction.
The different varieties of malarial fever are like different branches of
the same tree ; they have many things in common, yet differ from each
other so widely in the phenomena which attend their development,
that they may be regarded as distinct diseases. They have a common
origin in a poison which has received the name of miasm. ' All varie-
ties of malarial fever depend upon one and the same poison, which is-
subject to certain variations in quantity. The concentration of this poison
determines the severity and, to a certain extent, the type of the fever. It
is possible to arrange the different types in a progressive scale, from the
mildest to the most severe, beginning with simple intermittent and passing
on to pernicious fever. The extent of the morbid processes and the rapid-
ity with which they are developed depend npon the intensity of the malarial,
poison, the length of time the individual has been under its influence,
and, to some extent, upon individual idiosyncrasies.
Many theories have been advanced as to the nature of this miasm
or malarial poison. By some it is regarded as gaseous in its nature ; others
believe it to be a living vegetable organism ; and again, others think it a.
specific poison, having no tangible, chemical or microscopical constituents.
No one of these theories, nor any of the many others which at different
times have been advanced, has been sustained either by fact or by reliable
chemical or microscopical analysis. Thus far we have no pof^Uive knowledge
in regard to its true nature, but we do know something of the circum-
stances which are necessary for its production and the laws which regulate
its development.
First. — There must be a certain amount of vegetable matter, either on
the surface or in the substance of the soil where the malarial poison is gen-
erated. It is not necessary that the quantity be large, but a certain amount
is a necessity.
Second. — A certain amount of moisture must be on the surface or in the
substance of the soil ; it need not be excessive ; but some is indispensable.
Third. — A certain average degree of temperature is necessary for its pro-
duction. It cannot be developed below an average temperature of 58° F.
for the twenty-four hours, and will not prevail as an epidemic unless the
average temperature ranges as high as 65° P. for the twenty-four hours.
In regions where these fevers prevail, their type, form and intensity, to
a great degree, depend upon the height of the temperature. As a rule,
malarial fevers are endemic, rarely extending over large sections of coun-
try in the form of an epidemic. We also have some knowledge concerning
the regions in which malarial fevers are most likely to prevail, and which
seem most favorable to the development of malarial poison.
First.— Marshes are especially favorable to the development of this poi-
son, and may generate it for an indefinite period. The Pontine marshes
I " Telluric poison " is a term which has recently come into vogue.
MALARIAL FEVEE. 80?
have been malarial for more than two thousand years. Yet all marshes
are not malarial ; their power to generate the malarial poison varies with
the amount of water they contain. Where there is an abundance of water,
malarial fevers are rare ; when they are covered only with a thin sheet of
water, and are exposed to the direct rays of the sun, malarial poison will
abound. Marshes that have dried up are especially favorable to the de-
velopment of this poison, yet as soon as heavy rains submerge the previously
parched surface, the power to generate the poison is for a time diminished
or entirely arrested. Scattered here and there over our own continent are
districts which have been malarial ever since the white man has held pos-
session of them ; whether such was the case in earlier times, history is too
uncertain to determine.
As a rule, salt-water marshes are especially free from malaria, but when
salt and fresh water are mixed in the marsh, the most favorable conditions
for the abundant development of malaria occur. Marshes that rest on a
substratum of sand are far less malarial than those resting on limestone,
clay, or mud. There are marshes in the higher latitude of New York and
other States which often, during the heat of summer, become dry, yet no
malarial poison is generated (although during the day the thermometer
may reach 90° F.), since during the night the temperature falls below 50°
F. There are some quite extensive marshes in which, apparently, every con-
dition of development of malaria exists, and yet none is generated. We
cannot account for this fact unless we accept the theory that the ozone
which is claimed to be present in such marshes arrests or prevents its gene-
ration. Damp " bottom lands " that are exposed to an annual overflow,
such as are found along the southern shores of the Mississippi River, are as
fruitful as swampy regions in the generation of this poison.
Second. — Another condition which seems to favor the development of
malaria is the upheaval of new alluvial soils, such as obtains when new
lands are first brought under cultivation. This same state of things also
occurs throughout the middle and southern portions of this State, and in
the New England States. Where railroad excavations are made, malarial
fever is very frequently developed. In New York City, while the Fourth
Avenue improvements were being made, the entire region along the
avenue was rendered highly malarious by the excavations. Such excava-
tions bring decomposing vegetable matters to the surface ; these, under
the influence of heat and moisture, generate miasm,
The fact that fevers of this type appear in regions previously free from
them, as soon as the conditions favorable to their development exist, is
confirmed by the testimony of many careful observers.
Third. — Eegions otherwise non -malarial may have malarial poison
brought to them by the waters of rivers which have their source in, or
flow through, malarial districts. Examples of this kind are found along
the banks of our Western rivers, where some of the most pernicious types
of this fever are developed; while in places only a short distance from
these rivers it is unknown.
Fourth. — Non-malarial regions may be rendered malarial from poison
808 ACUTE GEITERAL DISEASES.
transmitted by the wind. There has been considerable discussion as to
whether this poison can be transmitted in such a manner, and if it can be,
to what distance; there is no reliable account of its transmission over a
greater distance than four and three-quarter miles. ' The wind may also
carry malarial poison up along the sides of mountains, to an elevation of
one thousand feet ; some writers say no higher than six hundred feet.
American writers give an account of its being carried higher than six hun-
dred feet, while some German writers give well authenticated cases, which
show that it must have been carried to the height of one or two thousand
feet. *
The circumstances which are inimical to its production are:
First. — Hig}i latitude. In this country malarial poison is not generated
in higher latitude than that of Quebec. The limit of its development is
63° north and 57° south latitude. Between these two parallels of latitude,
both on the eastern and western hemispheres, malarial fevers may be
developed ; the nearer the approach to the equator, the more severe the
type. They do not prevail over the entire region embraced between these
parallels of latitude, but it is possible for them to be developed at any
point where the altitude is not too great.
Second. — Higli elevation is another condition inimical to its development.
As a rule it is not generated above an elevation of one thousand feet above
the sea. There are, however, some remarkable exceptions to this rule.
We find recorded cases of malarial fever which have been developed upon
plateaus among the Pyrenees, at an altitude of five thousand feet, and in
South America at ten and eleven thousand feet above the sea-level.
Among the Pyrenees, there is a marsh which has a clay bottom, and there
malarial poison is developed which is very persistent.
Third. — Drainage is another means which diminishes, and in certain
conformations of soil entirely destroys, malarial generation. In the ma-
jority of marshes, this generation can be arrested or prevented by free
drainage. Yet there are marshes upon which millions have been expended
in drainage and which still remain pestiferous. Perhaps it is possible to
drain the Jei'sey flats so as to render them non-malarial in their character,
out it is hardly probable that this change can be effected, for they have a
clay bottom, and contain both salt and fresh water, conditions which are
most favorable to malarial generation. Years of labor and large expend-
itures of money have been bestowed upon the Pontine marshes to render
them non-malarial, yet they are as pestiferous as they were twenty cen-
turies ago.
Fourth. — Cold is a powerful agent in arresting malarial generation. If,
in a pestiferous region, the temperature should fall below the freezing
point, only for one night, nothing more need be feared in that region from
1 Malarial fever broke out in the crew of a ship, which was anchored just four and three-quarter miles
from shore where this fever was prevailing. No cases were on board when the anchor was cast, nor did
any of the crew go on shore. So long as the wind blevi^ from the ship towards shore, the crew remained
well, but when the wind changed its direction and blew from the shore towards the ship, within six days
from the time of change, cases of well developed malarial fever appeared on board. This seemed to prove
conclusively that the fever was brought to the ship by the wind.
MALARIAL FEVER. 809
malaria, until the average temperature shall have again reached 60" F.
This law holds in all malarial districts^. In these districts, after the
temperature has fallen below the freezing point, persons may have the
fever, but it is the result of previous poisoning. Again, the generation
is less rapid and the poison is less virulent during the day than at night.
This is the uniform testimony of those who have seen most of, and written
most on malarial diseases. It is also almost universally conceded that mala-
rial districts are most j)estif erous during months when the atmosphere is hot
and dry, with little or no wind, especially when this state of atmosphere
has been preceded by long, heavy rains, and that the virulence of the
poison is greatly diminished as soon as fresh, strong winds clear the atmos-
phere.
The question arises : How does malarial poison gain entrance into the hu-
man body ? The most reasonable view is that this is effected through the
respired air. Certain facts seem to show that it maybe introduced through
the intestinal tract with the food and water. There seems to be scarcely
a doubt but that it may be taken into the stomach with foul drinking-
water. When this poison has once been introduced into the circulation, it
undoubtedly has the power of reproducing itself. From this fact, which
must be regarded as well established, these who regard this jjoison as a liv-
ing organism, claim that these organisms may reproduce themselves in-
definitely, but this has never yet been demonstrated.'
It has also been claimed that certain races are more exempt than others
from malarial fever, also that there are idiosyncrasies of constitution which
render certain individuals exempt from diseases of this type, for in dis-
tricts where these fevers prevail there are persons who never have the
fever. This exception, both in races and individuals, is due to the greater
physical power of the individual, which enables him to resist these noxious
atmospheric influences. In a district where malarial influences prevail,
the weak and anaemic are the most liable to be attacked, and aU those in-
fluences which tend to lower vitality, and to render feeble the powers of
resistance, must be regarded as special predisposing causes. A strong man
may resist for a long time, while the old and children very quickly suc-
cumb to the influence of the poison. Women are more susceptible than
men. We can no more account for the fact that one person can take in
large doses of malarial poison without being affected by it, while another
is affected by a very small quantity, than we can account for the fact
that one person can take large quantities of alcoholic stimulants without
showing any signs of intoxication, while a very small quantity will intox-
icate another, supposing, in both instances, the individuals to have ap-
parently an equally vigorous constitution. Some claim that when a jjerson
' 1880. Recently Crudeli (of Romel and Klebs of Prague) examined the lower strata of air, the soil, and
the stagnant water, and in the two former they found a " microscopic fungus," consisting of numerous
movable shining spores, long and oval, nine micro-millimeters in diameter. This fungus was cultivated
and when inoculated into animals they all had a regular typical chills and fever with an enlarged spleen-
They call this the hacillm malaria. Roman physicians now claim that they have found this in the human
subject. It is said to be always in the blood during the period of invasion. The spleen and the marrow of
the bones are its favorite seats.
810 ACUTE GENERAL DISEASES.
has been poisoned witli malaria, complete recovery never takes place ; others
that even in the worst cases recovery is possible. My own experience leads
me to believe that when an individual has once suffered from malarial
poisoning, he is much more susceptible to the poison than one who has
never been so poisoned. Some unknown physical change has taken place
which renders him a fit subject for malarial manifestations upon the
slightest exposure.
The doctrine of latency of malarial poison in the human body is an in-
teresting and at the same time a very obscure subject. That there is a
period of incubation, or rather that a certain time elapses between the ex-
posure and the development of malarial fever, seems to be settled. For a
certain period, often a long one, always elapses before new-comers in a
malarial district have their first attack of the fever ; sometimes the poison
remains latent until after they have removed from the district. It is on the
basis of the latency of the malarial poison that the relapses can be ac-
counted for which occur in those who, having lived in a malarial district,
remove and remain in a non-malarial one. This reawakening of the mala-
rial poison may depend upon a variety of causes, such as taking cold, over-
fatigue, sudden changes of temperature, etc. From my own observation, I
am convinced that it is impossible to bring one wholly from under the
infiuence of the poison while remaining in a malarial district, though he
may become exempt from its influence if he remains beyond the malarial
belt. Undoubtedly, an individual may become so acclimated as to resist
malarial influences, and live for a long time in a malarial district without
suffering any evil effects from it. There can be no question but that those
living in such districts suffer less from the acute manifestations of the
poisoning than new-comers. But those changes which are called chronic
malarial manifestations are constantly going on in those who are supposed
to be acclimated.
Malaria acts like any other poison : after a time the system reaches a cer-
tain degree of tolerance. This tolerance; or immunity from its manifesta-
tions, amounts to nothing more than the accommodation of the system to
its influence. Let the acclimated person, as he is called, be taken sick
with any active form of disease, such as diphtheria or pneumonia, and it
usually proves fatal, not that there is anything unusually severe in the
diphtheria or pneumonia, but death is due to the fact that the system is
"depressed by the malarial poison, and its power of resistance to disease is
lessened.
rN^TEKMITTENT FEVEE.
Like typhoid fever, intermittent fever is met with in all parts of the
world, although the region of its development may be said to be limited
by 63° north and 57° south latitude. Within these parallels it is the
more prevalent nearer the equator.
Morbid Anatomy. — Its anatomical changes are few. None of those
changes in the blood which are present in the more severe forms of in-
fectious diseases are found, nor those which are present in the pernicious
IlsTERMITTENT FEVER.
811
type of malarial fever, such as ijigmentation and marked diminution in
the red globules. But the blood clots imperfectly, and is of an abnormally
dark color, and if the fever has continued for a long time there may be
slight diminution in the number of the red globules and a decrease in the
fibrin-factors ; but these changes, to a great extent, are due to the high
temperature which attends its paroxysms.
The only constant pathological lesion of intermittent fever is congestion
of the internal organs. The spleen and liver are always more or less en-
larged, but the enlargement is due to simple hyperasmia; no structural
changes occur in these organs until the intermittent paroxysms have been
often repeated, and the malarial poisoning has been of long duration.
There is also more or less hyperaemia of the kidneys and the mucous mem-
brane of the intestines, but it is not attended by any signs of gastric or
intestinal catarrh. As yet no one has been able to prove that any structural
change takes place either in the nerve tissue or in any other tissue of the
body ; nor from the structural or functional disturbances that occur during
the fever has any one been able to find satisfactory answer to the question:
why is it a paroxysmal and not a continued fever? During a paroxysm of
the fever the white blood-globules are very rapidly increased in number.
Etiology. — This subject has just been considered. All agree that simple
intermittent fever is due to malarial poisoning, and that the poison is in-
troduced into the body either through the lungs or through the intestinal
tract. Whatever tends to depress the mental or physical powers of an in-
dividual renders him more susceptible to malarial influences, and con-
sequently these depressing influences must be regarded as predisposing
causes. Among these may be included
intemperance, exposure to night air, exces-
sive fatigue, bad hygiene, and a long list
of like debilitating causes.
Symptoms. — This fever is paroxysmal,
and differs in its types according to the
period of time which intervenes between
the paroxysms. The first, and most com-
mon, is the quotidian type, in which the
paroxysm occurs every day, and there is
an interval of twenty-four hours between
the paroxysms.
The second is the tertian type, in which
the paroxysm occurs every third day, with
an interval of forty-eight hours between the
paroxysms.
The third is the quartan^ type, in which
the paroxysm occurs every fourtli day,
with an interval of three days or seventy-
two hours between the paroxysms. These
are the regular and more common types.
Vacf. 1.
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4.
5.
6.
7.
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Fig. 168.
Fever Curve in Quotidian Intermittent.
1 III 98,237 cases iu tlie U. S. army, only 1,757 were quartan.
812
AOFTE GElsTERAL DISEASES.
Pig. 169.
Fever Curve in Tertian Intermittent.
Other types exist, which, altliough irregular, are unquestionably modi-
fications of those already mentioned. Among these is the double quotidian,
in which two paroxysms occur daily. Usu-
ally one paroxysm is scYere, the other mild ;
the severer one generally occurs in the
morning, the milder in the afternoon or
evening. There is also double tertian, in
which a paroxysm occurs daily, but it
differs from the quotidian as the paroxysms
that resemble each other occur at intervals
of forty-eight hours. For instance, the
paroxysm of to-day is characterized by the
occurrence of a severe chill and mild fever ;
to-morrow it is characterized by a short
chill and severe fever ; the following day
there occurs the severe chill and mild fever,
as on the first day.
A form of intermittent fever is met with
in which the paroxysm occurs on the
seventh, fourteenth, twenty-first day, etc.,
with an interval of seven days between the
paroxysms. The types most frequently met
with are the quotidian, tertian and quar-
tan. In the quotidian variety the paroxysm occurs in the morning, in
the tertian it occurs about noon, while in the quartan it occurs in the
afternoon or evening. The duration of the
paroxysm varies with the type of the fever.
In the quotidian it lasts from eight to ten
hours, in the tertian it lasts from six to
eight hours, in the quartan from four to six
hours. There are many exceptions to these
rules, but it is a question whether there
would be any if the disease was permitted
to run its course without treatment.
Paroxysms. — A paroxysm of intermit-
tent fever has three stages —the cold stage,
the hot stage, and the stage of sweating.
In most cases these are readily distinguished
from one another. In the true type of
intermittent fever regular intervals between
the paroxysms of fever occur. The phenom-
ena which usually precede the cold stage
are pain in the head, a sense of languor,
and some nausea.
Cold Stage. — Passage into this stage is
first marked by a sensation of coldness
along the back, which soon extends to the extremities, and an uncom-
Bay. /.
2.
3.
4-.
5.
6.
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Pig. 170.
Fever Curve in Quartan Intermittent.
IISTTEKMITTENT FEVEK. 813
fortable sensation of coldness gradually creeps over the entire body. The
skin becomes shrivelled, the finger ends and lips become blue, the face
is pale, the eyes are sunken, chills rapidly follow each other, the teeth
begin to chatter, any voluntary motion is attended by trembling, until
finally, as one chill after another in quick succession jiasses over the body,
the teeth chatter so that the noise can be heard some distance from
the patient, and there is a shaking of the entire body. The surface of
the body becomes rough, the blood seems to recede from it, and it as-
sumes the appearance of goose-shin or cutis anserina. The temperature
of the surface of the body is lower than normal, but if the thermometer
be placed in the axilla or under the tongue the tcmiierature marks 104°
or 105° F. The voice of the patient is weak and husky ; the respirations
are rapid, short and sighing, but the mind remains clear. The urine is
increased in quantity and paler than normal, and there is frequent desire
to empty the bladder. Usually these symptoms last from half an hour to
two or three hours ; the length of time depends upon the severity of the
case. Children do not have a regular chill ; they merely grow cold, blue
and livid.
After the cold stage has continued for a longer or a shorter period, the
patient begins to have flashes of heat alternating with the chilly sensa-
tions. Usually these are first felt at the extremities, but they rapidly ex-
tend over the whole body, and the hot stage is established.
Hot Stage. — The skin is now no longer shrivelled, but becomes red,
swollen and turgid, and there is a recession of the blood from the central
organs to the surface of the body. That the temperature is elevated can-
not be ascertained simply by laying the hand upon the surface. If,
however, the thermometer is placed in the axilla, in most cases the tem-
perature marks 106° or 107° F. Thirst is intense. The uncomfortable sen-
sation which the patient experienced while passing from the cold to the
hot stage, has given place to great restlessness, the patient tossing from
side to side, with face flushed and eyes red and fiery. Sometimes her-
petic vesicles appear about the mouth. The tongue becomes dry, the caro-
tids pulsate, the radial pulse becomes firmer and more rapid than in the
cold stage, and nausea is marked. It may have been present in the cold
stage, but in the hot stage nausea and vomiting become the prominent
symptoms. As a rule these symptoms last from half an hour to two hours.
In exceptional cases they may continue for a much longer time, the ordi-
nary duration of a paroxysm of a quotidian intermittent being from eight
to ten hours ; that of a tertian, from six to eight hours ; and that of a
quartan, from four to six hours. It is possible, especially in those forms
of malarial fever in which the poisoning is intense, for the hot stage of
a quotidian to continue twelve hours.
There is no condition in which, for the time, there is more intense fever
than in the hot stage of intermittent fever. The urine, which during the
cold stage was abundant and of a pale color, now becomes highly colored
and scanty. Not infrequently it is almost suppressed during the hot stage.
Complete suppression of urine occurs only in the pernicious type of the dis-
814 ACUTE GENEEAL DISEASES.
ease. When the fever has continued for a longer or shorter time, a slight
moisture appears upon the forehead, which gradually spreads over the en-
tire body, and the patient becomes bathed in a profuse perspiration. He
is now in the sweating stage. In children, just before the sweat, coma or
convulsions may occur.
Sioeating Stage. — As this stage comes on, restlessness and uneasiness de-
cline, and a feeling of comfort is experienced as the perspiration makes its
appearance. The temperature rapidly falls ; the pulse rapidly diminishes
in frequency and force ; the pulsation of the carotids ceases ; the face as-
sumes its normal appearance ; the congestion of the conjunctivaB disap-
pears ; and the patient rapidly passes from a high state of fever into
one in which he falls asleep, and awakens after a period ranging from one
to three hours, with a sense of exhaustion.
Interval. — During the interval between the paroxysms at first the
patient may feel perfectly well, but if there is a frequent repetition of
the paroxysms, there will very soon be a marked loss of vitality ; he be-
comes pale and feeble, and all the symptoms of malarial cachexia are pres-
ent. There will be more or less of a Jaundiced hue to the skin, enlarge-
ment of the spleen and liver, and pigmentation of the tissues. It is
true that many paroxysms of simple intermittent may occur before any
such general disturbance of the health of the patient manifests itself ;
yet, in the interval between the paroxysms, we cannot call the patient's
condition one of perfect health. Usually, in the quotidian type, the day
previous to the development of the first paroxysm, unnoticed by the pa-
tient, there is a slight rise in temperature, perhaps to 101° F. At the
same time he experiences a sense of lassitude, and is disinclined to make
any exertion, either mental or physical. The temperature commences to
rise in the morning, and by noon it has reached its maximum ; then it be-
gins to fall, and by evening it may have fallen to nearly its normal stand-
ard. Thus the course of the temperature is quite characteristic, and may
be summed up as a rapid ascent, a short and intense stationary period,
and a critical defervescence constituting the paroxysm, with a perfectly
normal temperature in the interval. The following day another rise in
temperature will be noticed ; now the rise does not occur in the morning,
but after midday, perhaps as late as in the evening. IJsually in the quo-
tidian type of intermittent fever the highest temperature is reached a little
earlier each day ; if it is reached a little later, the fever is being modified
or controlled by treatment.
When the paroxysm comes on a little earlier each day, it is called antici-
pating, and indicates that the fever is not being controlled ; when it comes
on later each day it then indicates that the fever is being controlled, and is
called a postponing intermittent . The types of intermittent fever which
occur most frequently in temperate climates are the quotidian and the
tertian. In those whio have suffered repeatedly from intermittent fever,
the disease is liable to run an irregular course, the paroxysms occurring on
irregular days, and with irregular intervals. In children this fever shows
certain deviations from the ordinary course. The paroxysms may be
INTEEMITTENT FEVER. 815
Tisliered in by convulsions, or by a period of stupor. Children rarely have
the distinct chill ; after a period varying from ten minues to half an hour,
we have the hot stage of regular intermittent fever coming on, with all its
attendant phenomena. The intermissions are rarely complete. The child
loses his appetite and flesh, becomes irritable, and has a pale, waxen look,
suffers from gastric and intestinal disturbances, and the intermittent very
soon lapses into the remittent form.
Differential Diagnosis. — The differential diagnosis of simple intermittent
fever is never very difficult. There are only tAvo diseases which are liable
to be mistaken for it, namely, remittent fever , and pymmia.
It is readily distinguished from remittent fever, for in remittent fever
there is never a complete intermission, whereas in intermittent there is
always a period in which there is no fever. A careful thermometrical ob-
servation for twenty-four hours settles all questions in regard to it. There
is also a regular development of the paroxysm in intermittent, which does
not occur in remittent. In remittent, there is usually but one chill, while
in intermittent a chill precedes each paroxysm of fever. When the chill
and sweat are absent, but a sense of heat, malaise, headache and lassitude
come on at pretty regular periods in a malarial district, the thermometer
showing a pyrexia of 102° to 104° F., the patient is said to have '^dumb-
ague."
Prognosis. — The prognosis in simple intermittent fever is good. The
possibility of the development of malarial cachexia must enter into the
prognosis. When this occurs the case is more than one of simple inter-
mittent fever ; there is enlarged spleen and liver, with pigmentation of
the tissues.
Treatment. — The treatment of intermittent fever is divided into that for
the paroxysm and that for the interval.
The treatment for the paroxysm, in most cases, is simply to render the
patient as comfortable as possible while passing through its various stages.
At one time it was proposed to tourniquet the limbs, so as to prevent con-
gestion of internal organs, and thus arrest the paroxysms. Again, it has
been proposed to apply cold to the surface for the purpose of giving a
shock to the nervous system, and in that manner to arrest the paroxysm.
Some propose to cover the surface of the body with sinapisms, in order to
irritate the cutaneous surface. Some have claimed that if an individual is
brought fully under the influence of alcohol the regular development of a
paroxysm can be prevented. It has also been claimed that opium, given
in full doses at the usual time for the recurrence of the paroxysm, has
power to prevent it. Experience does not lead me to accept any of these
statements. It is true that, in some instances, a sudden shock to the
neiwous system may prevent the development of an intermittent paroxysm
when the paroxysms have become a habit.
If there is anything in the entire list of means (either remedial or
hygienic) which has power to prevent the full development of a paroxysm,
it is opium. When this is administered hypodermically, early in the cold
stage, it will diminish the severity of the cold and hot stages. Whether,
816 ACUTE GESTEEAL DISEASES.
in the treatment of the milder forms of intermittent fever the combination
of opium with quinine is advisable, is still an unanswered question, though
it seems to me that in such cases much comfort can be afforded, and the
patient be much less injuriously affected by the paroxysm if opium be ad-
ministered in moderate doses. Patients with intermittent fever should be
kept in bed during the entire paroxysm, however mild it may bo.
During the cold stage, cover them with blankets, surround them with
bottles of hot water, and let them drink freely of hot water. All these
means will hasten the hot stage of the disease.
During the hot stage, the extra clothing and external heat should be
gradually removed and cold instead of hot drinks should be administered.
If nausea and vomiting are present in this stage, opium, administered hypo-
dermically, affords great relief. When the patient reaches the sweating
stage, let him alone ; within a few hours he will be entirely relieved and
in a state of convalescence.
The treatment of the interval is to prevent the occurrence of another
paroxysm. A patient should never be allowed to have a second intermit-
tent paroxysm ; for if the system once becomes accustomed to these parox-
ysms, they will be repeated upon the slightest provocation. This will be
found to be the case with those who for a long time have not been sub-
jected to malarial influence, and yet upon the least nervous excitement or
fatigue will have a paroxysm. The great remedy at this time is the sul-
phate of quinine. Skilfully used, it is all-powerful to accomplish this re-
sult. How and why it arrests the development of these paroxysms is still
unknown. Our knowledge of its antiperiodic power is purely empirical.
There is much difference of opinion as to the mode in which it should be
administered. In commencing the treatment of a case of intermittent
fever, after the occurrence of the first paroxysm it is always safe to assume
that the fever is of the quotidian type. At least thirty grains of quinine
should be administered between the termination of one paroxysm and the
hour when another is to be expected. The first dose of ten grains should
be given toward the close of the sweating stage, and twenty grains about
two hours before the time of the expected paroxysm. If possible, give the
quinine in solution. If irritability of the stomach causes rejection of the
quinine, it may be administered hypodermically, or by enema. Three
grains administered hypodermically has about the same antiperiodic power
as ten grains administered by the stomach. If one succeeds in preventing
the occurrence of a second paroxysm much has been accomplished. Hav-
ing prevented the occurrence of a second paroxysm, it is important that a
moderate degree of cinchonism should be maintained for a number of days,
by the daily administration of quinine in moderate doses. About two
hours before the time of day at which the first paroxysm occurred, from
ten to fifteen grains of quinine should be daily administered.
A patient should visit his physician one month from the date of the first
paroxysm, for although he may not have had a fresh malarial exposure,
there will be a strong tendency at this time to a repetition of the paroxysm,
and it is important that at that time he should be again brought fully
INTERMITTENT FEVEE. 817
under the influence of quinine. If it is possible for him to remove from a
malarial district a second paroxysm will almost certainly be prevented. If,
however, the patient is not seen in his first paroxysm, and if he lives in a
malarial district, sulphate of quinine, administered in the manner I have
just recommended, may only prevent for a time the return of the parox-
ysm, and even complete cinchonism may fail to control it. The case
should now be carefully examined in order to ascertain if there is not some
condition present which interferes with the antiperiodic action of the qui-
nine, such as hepatic or splenic hypersemia. When careful percussion shows
that the liver and spleen are increased in size, even after the administra-
tion of full doses of quinine, the administration of full doses of calomel
with the quinine will increase the antiperiodic power of the latter, and
diminish the percussion areas of these organs.
Occasionally, when full doses of quinine combined with calomel have
failed to prevent a recurrence of a paroxysm, I have noticed an unusual
excitement attending its development, and believing from this circumstance
that owing to individual idiosyncrasies the malarial poison had a more
than usual irritating effect upon the nervous system, I have accomplished
the desired result by administering full doses of opium with the quinine.
In fact, if the patient is of a highly sensitive, nervous organization, I
never allow a second paroxysm to pass without administering a full dose of
opium before the time when its return is to be expected. In all those cases
which are called obstinate, we must ascertain why we fail to control the dis-
ease by the use of quinine. I rarely have administered arsenic in simple
intermittent fever. If I fail to control the fever with quinine, after I have
reduced splenic and hepatic congestion, controlled nervous irritability, and
increased nutrition by the administration of iron and the moderate use of
stimulants, I never succeed with arsenic. In some of the chronic forms of
malarial manifestation, I have found arsenic of great service, but never in
simple intermittent fever. Salicin, strychnia, piperine, eucalyptus, and
hydrastia sometimes act antiperiodically when quinine fails.
Mashed Intermittent. — In this connection should be mentioned a
form of intermittent fever which has been designated as masked inter-
mittent fever. For example, to-day a patient has a regular intermittent
paroxysm, but to-morrow, instead of its recurrence, perhaps he suffers
from the most intense neuralgia. This neuralgia may have its seat in
an intercostal or in the sciatic nerve, or, perhaps, more frequently in the
frontal branch of the ophthalmic division of the trigeminus. Some one
nerve becomes involved and no other seems to be affected. In some cases,
an intense hemicrania takes the place of the paroxysm. As a rule, these
neuralgise have distinct intermissions, and so come to be regarded as masked
forms of intermittent fever. Instead of a neuralgia, the patient may have
an attack of asthma, or an attack of indigestion. Diarrhoea, dysentery,
and sometimes hgematuria and apparent suppression of the urine may take
the place of a distinct intermittent fever paroxysm. Again, a patient may
have a single well-defined chill, or even two chills, followed by most intense
hemicrania, and then have no more for a long time ; but sooner or later he'
52
818
ACUTE GENERAL DISEASES.
will have a well-defined intermittent paroxysm which will reveal the real
nature of the disease.
EEMITTEJSTT FEVEE.
This is a continued fever, with diurnal exacerbations. It is known by
different names, such as Southern, Western, African, continued, bilious,
acclimative, and remittent fever. The term remittent fever is the one
more generally accepted.
Morbid Anatomy. — The anatomical lesions of remittent fever resemble
those of intermittent fever ; and the differences are in degree rather than
in kind.
Unquestionably, both these types of fever are the result of malarial
poisoning, and the same diminution of the red globules and the same
changes in the fibrin factors occur in remittent as in intermittent. Yet
there are other changes in the blood which are usually present in the
former, and quite rare in the latter, namely, the presence of free pigment-
granules. These pigment-granules are met with in some of the pernicious
forms of intermittent fever ; but in all cases of well-develojjed remittent
fever they are present at some time during the progress of the disease.
This pigmentation is due to haemoglobin which has been liberated from the
blood-corpuscles within the blood-vessels, and the coloring matter may re-
main either within the blood-corpuscles, which, after a time, become trans-
formed into pigment-granules, or remain free in the fluid portion of the
blood, or infiltrate the adjacent
cells and tissues. It may be
transformed into granular or
crystalline hsematoidin.
The spleen is not so much
enlarged in remittent as in
intermittent fever, and the
increase in size seems to be of
a different nature. The enlarge-
ment is evidently the result of
congestion, and the organ some
times presents very nearly the
same appearance as it presents
in typhoid fever, except that
there is more pigmentation.
There are also structural lesions
^^ j^ found in the liver, in the
Section of the Liver from a case of Remittent Fever, showing stomach and in the intcstinCS,
. „ , , . P^rt"f a Lobule. which are uot present in inter-
A - Central vein of the lobule. -"^
5, B. Intralohvlar capillarief! densely pi(/mented.
C. Hepatic cells, also containing pigmeni.
mittent fever. The liver is
not very much increased in
size, and is of a hronze hue. The principal change is in color, which
is uniform throughout its entire substance. This varies in degree in
•different types of the disease, and in different cases of the same type.
REMITTENT FEVEE. 819
The peculiar color is due to pigmentation of the liver-tissue, and varies
according to the amount of pigment deposited. Pigmentation may occur
in other tissues of the body, but not to the same extent as in the liver. On
a microscopical examination of the liver, pigment is found throughout its
entire structure — not only in the hepatic cells, but in the nuclei of these
cells, and in the walls of the blood-vessels. This discoloration is of such
uniform occurrence that it has been recognized as the characteristic path-
ological lesion of remittent fever. Consequently, the " h'0)ized liver" is
spoken of as the characteristic lesion of this fever. Occasionally this lesion
occurs in intermittent and pernicious fever, but this is so seldom, and its
presence is so constant in remittent fever, that if met with at an autopsy
remittent fever may be suspected.
The mucous membrane of the stomach is more or less congested, thick,-
ened, and softened. Changes similar to those in typhoid are found in the
mucous membrane of the intestines ; it is more or less congested, and pre-
sents very much the appearance seen when a moderately severe catarrhal
inflammation is present. The Peyerian patches are usually enlarged, and
quite frequently present the shaven beard appearance. In some cases
there are ulcerations, not, however, as extensive or of the same nature as
the ulcerative processes of typhoid fever. The mesenteric glands are not
enlarged, and there is none of that granular infiltration so noticeable in ty-
phoid fever.
Etiology. — The great predisposing and exciting cause of this fever is ma-
larial poisoning. There can be no question but that the same malarial poi-
son which gives rise to intermittent fever can produce a remittent fever. In
other words, a remittent can pass into an intermittent fever, and an inter-
mittent into a remittent fever. While it is possible for this to occur, the
two diseases do not, as a rule, prevail in the same locality at the same time.
Endemics of one form may occur and be followed by endemics or sporadic
cases of the other form. In some localities remittent fever is almost the
only form of malarial disease, intermittent fever only occasionally occur-
ring.
There is probably no form of endemic disease the geographical bounda-
ries of which are more extensive than those of remittent and intermittent
fever. In general terms they may be said to encircle the earth parallel with
the equator, circumscribing a broad belt, limited by GS"" north and by 57°
south latitude. The boundaries of this belt are quite irregular, now ap-
proaching the line of the tropics, now receding from it. The remittent
fever which occurs within the temperate portions of this belt is much less
severe than that which occurs in the tropical regions. From the localities
in which this fever prevails, it would seem that a higher average tempera-
ture is required for its development than is required for the development of
intermittent fever. As already stated, a remittent fever during its con-
valescence may become an intermittent, and, conversely, an intermittent,
either from new exposure to malarial influences or to the influence of high
temperature, may become a remittent. Prom this fact, the conviction is
forced upon us that both types of fever are developed from a common poi-
820 ACUTE GENERAL DISEASES.
son. Usually certain atmospheric changes will have taken place to change
the type of the fever. Intermittent fever may prevail early in the season,
but as the season advances, and the temperature ranges higher, the fever
which prevails will assume the remittent type. Those who go from a non-
malarial district into one where remittent fever is prevailing are likely to
have it, while the old inhabitants only suffer from the milder form of inter-
mittent.
Sjrmptoms. — Its ushering-in symptoms are usually well marked. The
most constant as well as the most urgent of the premonitory symptoms is
oppression in the epigastrium. This may be present for forty-eight hours,
or even a longer time, prior to the development of the fever. There is
also a certain lassitude, nausea, and loss of appetite ; and with these feel-
ings uneasiness and perhaps pain in the head and limbs. It does not come
on gradually, like typhoid fever, but abruptly, usually with a chill. It is
not difficult to determine when the patient began to be sick. The chill is
neither so complete nor so long continued as in intermittent fever or pneu-
monia. During the chill the thermometer will indicate a temperature two
or three degrees above the normal. With the chill there is a most intense
headache, and pain in the back and limbs. As a rule the chill is not of so
long duration as the chill of intermittent, neither does it begin like it, by
creeping down the back and gradually extending over the body, but there
is general coldness over the entire surface at the very commencement of
the chilly sensation. Again, there is not that tremulousness and shaking
of the body, nor that chattering of the teeth, which are so frequently ex-
perienced in intermittent fever. Following the chill there is fever, during
which the temperature rises very rapidly. The fever increases in severity,
and, within twelve hours from the time of its commencement the tempera-
ture may reach 105° or 106° F. As soon as the temperature commences to
rise, the pulse is increased in frequency, and perhaps beats 100 or 120 a
minute. The face becomes flushed, the eyes are usually suffused, and the
conjunctivse are somewhat congested. The patient is restless, tossing in
bed, in the vain search of an easy posture. As the hot stage advances,
nausea and vomiting are always present, and the sense of oppression in the
epigastrium increases, and is not relieved by vomiting, which is persistent
and distressing.
In the febrile stage of remittent fever the patient suffers from pain in
the epigastrium, to such an extent that quite commonly it is the only thing
of which he complains. The epigastric distress is often accompanied by
the most extreme tenderness upon pressure. The material first vomited
simply consists of the contents of the stomach, next follows the vomit-
ing of a greenish matter, and finally, in severe cases, there may be a
slight amount of black vomit. The quantity of fluid vomited is greater
than the quantity taken into the stomach. Vomiting of stringy mucus
tinged with green is always present. Sometimes the patient's stomach
rejects everything taken into it, and the vomiting is accompanied by intense
pain in the head. Usually at the commencement of the fever, the bowels
are constipated.
KEMITTEKT FEVER.
821
The febrile symptoms increase in severity for ten or twelve hours,
when a slight perspiration appears upon the forehead. In a short time, it
extends over the entire body, not profuse, but a slight moisture upon the
surface. With the perspiration there will be a fall of one or two degrees
Fig. 172.
Temperature Kecord in a case of Remittent Fever ending in recovery.
in temperature, and a fall in the pulse of ten or twenty beats in the minute.
The thirst will diminish, the vomiting grow less, there may now be ability
to retain fluids in the stomach, and the patient falls into a quiet, refresh-
ing sleep, and is relieved from all the severer symptoms of the paroxysm.
If, however, the thermometer is placed in the axilla, it will indicate fever,
and although the temperature may show a marked decline, it is still above
the normal standard. At no time is there a complete interruption ; the
fever is continuous. This is termed the period of remission. At the same
hour on the following day all the active febrile symptoms return, the range
of temperature is higher, the gastric disturbance is more marked, the
countenance assumes an anxious expression, and all the symptoms are more
severe.
This return of the severe febrile symptoms constitutes what is called the
exacerbation, and the period between the time when the fever abates and
the development of the exacerbations is called the j)eriod of remission.
Remissions and exacerbations are the characteristic symptoms of a remit-
tent fever when it is fully developed, at which time a morning remission
is the rule, though the time of the first paroxysm varies. The morning
remission is so invariable that it is regarded by many as a diagnostic sign.
If the exacerbation begins at noon it will usually decline about midnight,
and the remission will last until about noon the next day. In very severe
cases there may be a double exacerbation, one at noon, the other at mid-
night, the remissions being in the evening and morning. The second
exacerbation is similar to the primary in its attendant phenomena, except
that it is more severe and of longer duration, ends in a less profuse per-
spiration, and the remission is not so well marked as the first. On the
third day at about the same hour, or a little earlier, there is another
822 ACUTE GE2^ERAL DISEASES.
exacerbation, which has a sfill longer duration, is of greater severity, and
is followed by a more incomplete remission.
If the disease continues, the remission from day to day becomes less and
less distinct. By the end of the first week the remission can no longer be
detected, and the fever becomes continuous, without any marked daily va-
riation in temperature or pulse. As the remissions become less and less
distinct, with each returning exacerbation, the tongue becomes more and
more parched, sordes collect upon the teeth, the countenance becomes dull
and heavy, distress and pain in the epigastrium continue, and are accom-
panied by tenderness, although the senses of the patient are so dulled that
he may scarcely complain of it ; and the Vomiting is not so constant, and
is of a less distressing character ; constipation, which was present at the com-
mencement of the fever, has now given way to diarrhoea, the discharges usu-
ally being of a brownish color. With tlie diarrhoea there is some fulness of
the abdomen, and some local tympanitis. Hiccough is often obstinate and
distressing. The pulse is increased in frequency, and will reach 120 or 130 ;
it is small, thready, and feeble— at the onset of the disease it was full and
compressible. The patient slips down in bed, picks at the bed-clothes ;
there is subsultus and difficulty in deglutition, and the tongue is protruded
with difficulty, as in the severer forms of typhoid fever. The urine is
scanty, acid, dark colored, but very rarely is it albuminous. It may be
bloodj. The patient passes into a condition closely resembling that of one
in the third week of typhoid fever, with the exception that there is no erup-
tion.
The diarrhoea, abdominal disturbance, and tympanitis, and often the
tenderness over the ileo-caecal region, the typhoid tongue, and the low mut-
tering delirium, closely ally this stage of remittent fever to typhoid fever.
After these symptoms have continued a week or ten days, if the case is to
terminate in recovery, remissions occur and become more and more dis-
tinct, until finally there is no exacerbation, and the patient passes into a
state of convalescence. If, however, a fatal termination is to take place,
the remissions will not recur, but- the typhoid symptoms become more
marked, and the patient finally dies from exhaustion or from complica-
tions. Of all the symptoms which attend remittent fever, nausea and
vomiting are the most constant and the most distressing. I have seen pa-
tients, after the temperature has fallen to its normal standard, suffer for
weeks from gastric disturbance, attended by more or less jaundice.
If, in the progress of a remittent fever, the exacerbation occurs a little
earlier each day, then treatment is not controlling it ; the fever is then said
to be anticipating, and the disease is almost certainly passing from a dis-
tinct remittent to a continued remittent. If, on the other hand, the ex-
acerbation occurs a little later each day, the fever is said to be postponing,
and it is under control, the remissions become longer, the exacerbations be-
come shorter and less severe, until the patient reaches complete convales-
cence. The thermometer will indicate to what extent the disease is being
controlled.
Bilious Remittent Fever. — In a certain proportion of cases in all endem-
REMITTEKT FEVEE. S'i'd
ics of remittent fever, vomiting of " bilious " material, and jaundice are
prominent symptoms, the skin often becoming so yellow that the patients
present an appearance similar to that of those suffering from yellow fever ;
with this yellow discoloration of the skin there is an unusual tenderness on
pressure over the hepatic region. Under such circumstances this fever
has been named " bilious remittent." By some of the older writers it has
been described as an idiopathic fever, distinct from remittent or any other
form of malarial fever. Medical literature, however, contains no facts in
support of such a view. The pathology and symptomatology of the fever
described by writers under the head of bilious remittent fever differ in no
respect from those of simple remittent, except that the fever is accompa-
nied by symptoms of more than usual hepatic and gastric disturbance. My
own experience leads me to regard it as a form of simple remittent, accom-
panied by a more than usually severe gastro-hepatic catarrh, and that it
is not entitled to a separate place in the nosology of fevers.
Infantile Remittent Fever. — It is a matter of every-day experience that
children are subject to certain gastric and intestinal derangements, which
are attended by more or less fever, which is very apt to assume a remittent
type. Such fevers cannot, however, be regarded as specific diseases, for
they are developed independent of any specific fever poison, and are only
symptomatic of some local irritation. There is a form of mild typhoid fe-
ver which is often met with in children, especially in the autumn, which
has also incorrectly received the name of infantile remittent fever. In
this class of cases, the usual symptoms of typhoid fever are so modified by
age that the fever assumes a remittent type. The presence of rose-colored
spots, and the characteristic typhoid lesion of the intestines, will determine
the true nature of these fevers. Simple malarial remittent in children does
not differ from the remittent of adults. Remittent fever in children is more
liable to be followed by malarial cachexia than in the adult.
Differential Diagnosis. — The rules by which a remittent is distinguished
from an intermittent fever have already been given.
The differential diagnosis between remittent and typhoid fever is often
attended with difficulty, if the patient is not seen until the second week of
the disease, but if he is seen at the very onset of the fever, it is hardly pos-
sible to confound these two forms of fever. The sudden advent of a remit-
tent is in marked contrast to the slow development of a typhoid fever. Be-
sides, they widely diff'er in the range of temperature during the first week
of their development. In remittent there is a distinct remission, and there
can be no doubt as to the type of fever after the first, certainly not after the
second remission has occurred. Gastric symptoms are much more severe in
remittent than in typhoid. By these symptoms alone a differential diag-
nosis can be made. If, however, the fever has been protracted to the third
week, and the remissions are slight or altogether absent, although many of
the symptoms of typhoid fever are present, the absence of the rose-colored
spots, taken in connection with the previous history of the patient, is suf-
ficient to establish the diagnosis.
Remittent fever may be distinguished from yellow fever by its high range
834 ACUTE GENERAL DISEASES.
of temperature, by its daily exacerbation and remission, by the presence o:
pigment in the blood, and by the absence of albumen in the urine, which
is present in yellow fever. In remittent fever, hemorrhage from the mu-
cous surfaces, especially from the mucous membrane of the stomach, indeed
from any source, is of rare occurrence, while in yellow fever it frequently
occurs from mouth, nose, eyes, ears, bowels, and urinary passages. Death
often occurs on the third day in yellow fever, but in the severest cases of
remittent fever not before the seventh day. Yellow fever is portable and
contagious ; remittent is neither. Eemittent fever may be confounded with
pygemia and septicaemia, but their differential diagnosis has already been
sufficiently considered.
Prognosis. — The prognosis in simple remittent fever is good. Even cases
of the severe types of this fever should terminate in recovery, if skilfully
managed, especially if they are seen in the early stages. Its type varies very
much according to locality. The remittent fever in New York City is of a
mild type. In that form which prevails in our Western and Southern
States a fatal termination is of frequent occurrence. There is a type which
soon loses its remission, and becomes a pernicious malarial fever, the prog-
nosis of which is unfavorable. The complications which may render the
prognosis unfavorable are meningitis, pneumonia, gastritis, enteritis, diar-
rhoea, dysentery, and splenitis. The prognosis will also be modified by the
condition of the patient at the time of the attack, and by the character of
the endemic which is prevailing.
The symptoms which indicate that recovery is to take place are the fact
that the exacerbation is delayed or rendered less severe, the early subsidence
of gastric symptoms and headache, and a decrease in the frequency of the
pulse, and the appearance of vesicles about the lips. Distinct remissions,
accompanied by moderately free perspiration, indicate an approaching fa-
vorable change. On the other hand, if the fever is more continuons than
paroxysmal, with a pulse becoming daily more feeble and more frequent, if
there is a tendency to collapse at the close of the exacerbations, and sup-
pression of urine, with signs of extreme exhaustion, danger is indicated.
The average duration of this fever is two weeks.
As this fever varies so greatly in severity at different times and in dif-
ferent localities, it is impossible to accurately determine its average rate of
mortality.
Treatment. — In this disease, we have means at our command by which,
in the majority of cases, it can be controlled, and by which, in most in-
stances, its duration may be much shortened. It is hardly necessary to
refer to such remedial agents as blood-letting, emetics, cathartics and
diaphoretics, which have all been employed in the treatment of this fever,
for they have all been supplanted by a single remedy. Experience has
proved that the poison which causes the fever cannot be removed from the
system by any of the so-called eliminative methods of treatment. If this
class of patients are depleted to any extent, the development of those
typhoid symptoms which are especially to be avoided will be hastened.
Those living in malarial districts are never up to the normal standard of
EEMITTENT FEVER. 835
vigor, and, consequently, are in a condition to be affected unfavorably oy
any plan of treatment or by any remedial agents which shall enfeeble the
vital powers.
The first thing to be done in the successful management of this fever is
to place the patient under the best possible hygienic surroundings. The
same care should be exercised in the arrangment of the sick-room as has
already been proposed in the management of tyjjhoid fever. Those who
have seen most of remittent fever in its severer form recommend that the
treatment of each case be commenced by administering a mercurial purge.
They claim that there is always more or less engorgement of the liver,
spleen, and mucous membrane of the stomach and intestines, and that,
so long as these organs remain in this condition, no plan of treatment
will be successful. However great may be the differences of opinion
in regard to this, all agree that the sulphate of quinine should be used
in its treatment. Practitioners differ as to the mode of its administra-
tion, but all advocate its use. Some maintain that it has greater power
over the disease when administered in small doses, rejoeated at short in-
tervals ; others, that it should be given in one or two large doses during
the remission, an hour or two before the commencement of the expected
exacerbations. Others, again, claim that the quinine has its greatest
power over the fever when administered during the activity of the febrile
excitement.'
From these reports, and from my own experience, I do not hesitate to
administer quinine at any time during the period of the exacerbation or
remission. My rule is to give ten or twenty grains at a dose, according
to the severity of the fever, and repeat it every two hours until cinchonism
is produced. When cinchonism is reached, although the fever may not
be controlled, it is well to stop its administration until twenty-four hours
have elapsed ; by doing this one can better determine the antiperiodic
power of the drug. If the exacerbations do not disappear, but are de-
layed and are less severe, the fever is being controlled. If, notwithstand-
ing this free use of quinine, the exacerbations are more severe and longer
in duration, and the remissions less frequent, and typhoid symptoms are
manifesting themselves, stimulants may be demanded. Even large doses
of stimulants may be required to sustain the patient while he is passing
through this period of the disease.'*
Remittent fever is not, like typhoid fever, a disease of days or weeks.
1 This subject was carefully studied by those engaged in the English Medical Service in India. Under
the direction of the Surgeon-General in that department quinine was administered at different periods in
the course of the fever, one surgeon giving quinine at the commencement of the exacerbation, another
immediately after the exacerbation had passed its height and as the sweating stage was coming on, an-
other immediately preceding the exacerbation, and still others giving it during the remission. This plan
was adopted to determine with positiveness when the smallest amount of quinine would have the greatest
controlling eflfecl over the fever. Prom the various branches of the department reports were made,
whence the conclusion was arrived at that quinine, administered during the time of the exacerbation,
had not only a greater influence in diminishing the severity of the disease, but it also more completely con-
trolled the fever, and more markedly shortened its duration than when it was administered during the re-
mission.
"Livingstone and other African travellers advise bitter ale as about the best stimulant, and the one best
borne by the irritable stomach in this fever.
826 ACUTE GENERAL DISEASES.
In its severer forms no time should be lost while waiting for the action of
cathartics or other remedial agents which are supposed to be of importance,
but the administration of quinine should be at once commenced. When
the disease has reached its second or third week, and there is no evi-
dence that the patient is passing on toward recovery, administer a sec-
ond time large doses of quinine ; in this way the progress of the
fever may be arrested. If, after a second cinchonism is produced,
the fever is not arrested, omit again for a few days the administration,
of quinine ; then repeat the large doses a third time. Ifc is much better
to proceed in this way than to keep the patient in a continued state
of cinchonism. It is not necessai:y to enumerate the long list of drugs
which at different times have been proposed as specifics in this fever, all
of which, by common consent, are now regarded as far less reliable than,
quinine. The important thing is to know how and when to administer
quinine.
There are certain palliative measures which it is sometimes important
to employ. If the exacerbations are very intense, the headache very
severe, and the restlessness or other febrile symptoms are not relieved by
full doses of quinine, cold may be employed for its antipyretic effect, as
in typhoid fever. Full doses of the bromide of potassium promote sleep.
Frequently, in mild cases, sponging the surface with tepid water is not
only grateful to the patient, but it has a controlling influence over the
fever. If vomiting is constant, severe, and exhausting, hypodermics of
morphine will be found of service. Some advise Fowler's solution to check
the distressing vomiting. The treatment of this fever is expectant, save
in the use of quinine.
CONTIIS^UED MALAEIAL FEVER.
I have included this fever in the list of the malarial fevers, although it
is not altogether malarial in its origin ; malarial poison, however, is es-
sential to its development. As i'*: has many elements in common with
typhoid, and many which ally it to remittent fever, it has been called
"typho-malarial." ' During the late civil war it was called camp and
Chickahominy fever.
In its etiological aspect it partakes more of the character of typhus than
of typhoid. The name typho-malarial fever has been employed by one
class of observers to indicate the presence of malaria, and the specific poison
of typhoid fever. By another class the term has been employed to indi-
cate the presence of malaria and a septic poison. Many doubt the exist-
ence of such a form of fever, and regard the so-called typhoid element as
nothing more than a typhoid condition, liable to be developed in con-
nection with remittent fever, as well as with many other diseases. The
term typho-malarial is a convenient one for the first class of observers, and
is one which can be employed by them without confusion ; whereas to the
1 Wood (Prac. of Med.) calls it entero-miasmatic, and Drake (Dis. of Mississippi Valley) gives it the
name Remitto-Typtius.
CONTINUED MALARIAL FEVER. 827
second class of observers it is exceedingly objectionable, and gives rise to
confusion.
This fever is produced by the combined action of a septic and a malarial
poison. In some the septic element predominates, and in others the
malarial. The preponderance of the one or the other will determine with
a good degree of certainty the course, prognosis, and treatment of each
individual case. The distinguishing lines, however, between these two
elements are not always sharply drawn ; both may be modified in their
manner of development and in their morbid anatomy, by the development
of intercurrent complications, such as scurvy, pneumonia, etc.
Morbid Anatomy. — The changes which take place in the constituents of
the blood are a decrease in the albumen and fibrin-factors, and an increase
in white blood-globules. In connection with these blood changes there are
more or less extensive parenchymatous changes in the internal organs simi-
lar to those met with in other forms of acute infectious diseases.
The liver is increased in size, and its cut surface presents an appearance
which closely resembles that known as nutmeg liver. Sometimes it presents
the peculiar bronzed color of the liver in remittent fever ; at other times it
very closely resembles the liver of yellow fever. A microscopical examina-
tion shows free fat and pigment granules, as well as lymphoid, fusiform
and stellate cells — which are perhaps derived in great measure from the
spleen ; no pigment is found in the hepatic cells, but they are stained with
bile, as is also the inter-lobular tissue.
In most cases the spleen is enlarged, softened, and of an almost black
color. The Malpighian bodies are prominent, and present the appearance
on the torn surface of the spleen of little tumors, varying in size from a
pin's head to that of a pea. The organ is rarely as much enlarged or 'soft-
ened as in typhoid or remittent fevers. It is always the seat of more or less
pigmentation. The pigment is in the lymphoid cells of the spleen chiefly,
but it also accumulates about the veins.
No uniform change will be noticed in the kidneys, except hyperaemia,
which will be most marked in their cortical substance.
The lungs are the seat of more or less extensive hypostatic congestion.
Splenization of the lungs is not frequent.
The lieart is pale and flabby. Its muscular fibres are the seat of granular
or vitreous degeneration similar to that which takes place in the heart in
typhoid fever. Exsanguinated clots more or less firm may be found in its
cavities, but they have nothing peculiar about them. They closely re-
semble those found in persons who have died from failure of heart power.
They are rarely, if ever, the direct cause of death.
The intestinal changes resemble those of typhoid fever ; by some they
have been regarded as identical, but if carefully observed some very marked
differences can be recognized, especially when attempts are made to divide
the stages of their development into periods so as to correspond to the days
■In 1847, Wood stated that "remittent or bilious fever, as it was then popularly called, was some-
times of a low adynamic character, from co-operation of a typhoid epidemic influence with miasmata."
Forty years ago the term gastric fever was given to that variety of marsh fever where the stomach was
deranged and irritable from the onset.
828 ACUTE GENEEAL DISEASES.
and weeks of the fever. The closed follicles of the intestinal tract are enlarged
and more or less pigmented.' At the post-mortem examination of one who
has died of this fever these glands will usually be found in all stages of
this pathological process, from slight enlargement and softening to ulcera-
tion of the entire follicle. The summit of the enlarged follicle is the first
seat of the ulcer. These ulcers may involve a single follicle, or they may
invade the adjacent mucous membrane and produce ulcers from one-half
an inch to an inch in diameter. The largest and most extensive ulcerations
are to be found in the ileum, involving the Peyerian patches. The edges
of these ulcers are irregular and everted ; their base is usually of a grayish
color, often mottled with black points. There is little to distinguish these
intestinal changes from similar ones which develop in typhoid fever, ex-
cept, perhaps, the tendency to the deposit of black pigment in the enlarged
follicles. The mucous membrane between the follicles presents the ordinary
appearance of catarrhal inflammation.'^
The minute anatomical changes which attend the development of these
intestinal lesions do not essentially differ from those already described as
occurring in typhoid fever, except that they have no regular stage of de-
velopment, the processes are slower and the presence of pigment in the
enlarged and ulcerating follicles stamps it as depending upon an essentially
different exciting cause. Intestinal perforation and consequent peritonitis,
the result of the intestinal ulceration, may occur, but such accidents are
rare. Usually, the mesenteric glands are more or less enlarged. They are
of a livid color, and more or less pigmented. The principal changes in the
glands are similar to those which occur in a purely inflammatory process.
Occasionally the mucous membrane of the stomach and large intestine, if
there have been any manifestations of scurvy during the progress of the
fever, will be thickened and softened, perhaps extensively ulcerated, pre-
senting an appearance, in some instances, closely resembling that found
after death in malarial dysentery.^
While, therefore, no pathological lesions which can be regarded as char-
acteristic of this type of fever are found, and while the lesions very closely
resemble those of typhoid fever on the one hand, and remittent fever on
the other, still there are differences which are sufficient to distinguish it
from both and to stamp it as a distinct type of fever.
Etiology. — It is difficult to determine the true etiology of this fever.
That malarial poison is necessary for its development there can be no
question. It is equally certain that some other poison besides malaria is
in operation whenever it prevails. This poison is not the specific poison of
1 Maclean, in Quain's Die, p. 1334, says that the adynamic form of remittent is called typho -malarial
by many English physicians resident in India ; but that Italian and French physicians prefer the term
" pernicious." At the jiosi-mortem, ulceration of the Peyerian patches is found.
2 Wood mentions certain cases of bilious remittent, with ulceration of the intestines ; evidently writers
before 1860-1870 found lesions that struck them as peculiar in malarial fever, for we find them saying
that "some cases of typhoid were during life wrongly called remittent, as ulcers were found in the intes-
tines at the autopsy.''^ — (1847, Wood's Prac. Med.)
3 In 1821 there occurred in Philadelphia a f e\'er among the negroes, where symptoms of a septic or
typhus fever were united with those of marsh poisoning. Dissection revealed inflammation of stomach
and intestines and almost complete disorganization of the blood. — Account of an Epidem., by Dr. Emer-
son, Phil. Jour, of Med. and Phys. Sci. , iii , 1831.
COKTINUED MALARIAL FEVER, 829
typhoid fever ; nor are its development and spread in any way connected
with the excrements of one suffering from tlie fever. There are a few
facts connected with its development which are now well established :
First. It is met with only in malarial districts.
Second. In the majority of instances, when this fever has prevailed, its
development has been preceded or attended by marked and easily recognized
anti-hygienic conditions, such as overcrowding, bad sewerage, and other
conditions favorable to the development of septic poison.
Third. That it is a 7ion-contagious disease, and is never propagated from
the affected to the healthy, either directly by personal contagion, or indi-
rectly by morbid excretions.
Fourth. In its morbid anatomy and symptomatology it is a combination
of malarial and septic fever. The special symptoms and lesions of one or
the other of these fevers stamp its character. In large cities in which
malarial diseases are prevalent, seiuer gases seem to furnish the septic element
which is so essential for its development. The history of disease in New
York City during the past few years furnishes striking examples of the
combination of these two poisons in develoj)ing a type of fever which must
be classed under the head of non-specific continued fever, attended by
typhoid symptoms and intestinal ulceration.'
Symptoms. — It is difficult to present a typical picture of this fever. To
give even an outline of its symptoms which shall be approximately true of
all, or even the majority of cases, is impossible. Its clinical history varies
as the malarial or septic element predominates. Besides, there is a large
number of cases in which neither of these elements predominates, for the
patient almost insensibly passes from a malarial into a typhoid condi-
tion. There are also certain anti-hygienic conditions which may be pres-
ent, which give to the fever an unusual and peculiar type. For examjole,
when those conditions exist which favor the development of scurvy, as the
patient enters upon the second week of the fever the scorbutic phenomena
will become prominent. At times the dysenteric element may be engrafted
on this fever, and greatly modify its course, and lead to a train of symp-
toms and morbid changes which closely ally it to epidemic dysentery. The
course of this fever may also be greatly modified by certain local complica-
tions which are especially liable to occur during the second or third week.
The presence of any of these conditions will greatly change its clinical his-
tory, bub the phenomena which attend its early development will always be
sufficient to determine its true character.
In considering the symptoms in detail, that class of cases in which the
malarial element is predominant will first be described. This type of fever
is usually ushered in by a distinct chill." In some instances no premonitory
^ When Dr. Drake (Dis. of Inter. Valley of N. A.) called this disease remitto-typhus. he came nearer
than any other observer in giving it a name corresponding to its etiology. That it partakes of re-
mittent characteristics, no one can deny; that it has a septic, a "crowd-poison," a ''sewer-gas," a
"typhus " character, seems to me to be incontestable, hence " remitto-tjrphus " would be unobjectionable,
were not the word typhus now restricted to the specific, contagious fever of that name, whose poison can
only cause one disease, and cannot mingle with, or be modified by any other.
2 In Gibb's account of a malignant epidemic in Nicaragua, Central America, none of the cases began
with a chill.
830
ACUTE GENERAL DISEASES.
symptoms are present ; in others the chill is preceded by wandering pains
in the limbs and back, headache, loss of appetite, and a feeling of great
exhaustion. In a large proportion of cases m the early stage, the counte-
nance has a peculiar waxy, clay-colored or yellowish tinge. The chill yaries
in duration from half an hour to an hour, and in character closely resem-
bles the chill of simple remittent fever. It is immediately followed by
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Fig. 174.
Temperature Record in a case of Continued Malarial Fever. Septic variety.
third weeks it is small and compressible, and in severe cases ranges from
110 to 130 per minute.
The appearance of the tongue varies with the period of the fever. At
first it is swollen, with red projecting papillae, and has a light white coat-
ing. As the typhoid condition becomes more marked its appearance
changes ; it becomes dry and brown, and frequently the brown coating
cracks and fissures are formed in the mucous membrane underneath.
Should the tongue become moist and begin to clean, it is an indication
that convalescence is being established. The coating is removed in two
ways, either gradually from the edges to the centre, or it is thrown off in
flakes. In the latter case, after the removal of the coating, the tongue as-
sumes a beefy red appearance, and after a short time may again become
brown and dry. Under such circumstances there will be a renewal of the
fever-symptoms. After the fever has continued a few days the surface be-
comes dry and harsh, and the skin assumes a dingy hue, which is quite char-
acteristic ; sometimes there is a well-marked jaundice. The urine gradually
diminishes in quantity and deepens in color until convalescence com-
mences, when it increases in quantity. It is rarely albuminous.
Diarrhma may occur at any period. It is not usually excessive until the
second or third week. There is nothing characteristic about the discharges.
They are usually of an exceedingly fetid odor, watery and dark-colored ; in
the later stages of the disease they sometimes contain blood. In some in-
stances the character of the stools is termed bilious and an excessive he-
patic secretion is then indicated ; at other times they are of dark clay
color, showing a deficiency of the biliary secretion. With the diarrhoea
there is usually more or less abdominal tenderness, especially in the right
CONTINUED MALARIAL FEVER. 833
iliac region ; but tympanitis is rarely well-marked. In many cases there
is retraction of the abdomen.
As already stated, headache is very constant in the early period of the
fever. It often precedes the ushering-in chill. As the fever progresses it
gives place to a delirium, which is never violent, but which is muttering
in character, and is attended by restlessness and insomnia, or by drowsi-
ness, subsultus, picking at the bed-clothes, and great nervous prostration.
If delirium is not present, or after it has disappeared during convales-
cence, there is great lack of mental vigor and a tendency to apathy.
The other nervous phenomena, which are usually present in any con-
dition when marked typhoid symptoms exist, are not prominent in this
fever.
The subsequent phenomena which may attend its development will vary
with the intensity of the fever and the resisting power of the patient.
Epistaxis is not uncommon ; bl-onchitis is a frequent complication. In
fatal cases, at the close of the second or during the third week, symptoms
of extreme prostration come on, the patient gradually passes into a state of
stupor, which lapses into one of coma, and death ensues. In cases that are
to recover, usually by the end of the second week the tongue begins to
clean, the gastric and intestinal symptoms, with the exception of the diar-
rha3a, begin to subside, the pulse becomes slower, the nervous disturbances
disappear, the appetite returns, and the patient enters on a convalescence
which is usually protracted. Its phenomena may be modified by certain
anti-hygienic surroundings, to which those suffering with this fever may
have been subjected prior to, and during, its development. Thus, when it
prevails among those who have suffered privations, been badly fed, badly
clothed, overcrowded in badly ventilated apartments, or surrounded by de-
composing animal and vegetable substances, although the fever is attended
by the same general phenomena, there are certain variations which ally
it to relapsing fever. Prominent among these are neuralgic and arthritic
pains in various parts of the body, especially in the back and limbs ; hem-
orrhagic tendencies marked by bleedings from the gums and mucous sur-
faces ; and not infrequently large ecchymoses occur in various parts of the
body.
In this class of cases the fever is of a low type from the commencement,
with quotidian exacerbations and remissions. Diarrhoea usually precedes
the development of the febrile symptoms. Frequently during the second
week a muttering delirium comes on, accompanied by drowsiness and a
tendency to stupor. Despondency, indisposition to make any exertion,
and a state of utter indifference as to the future are frequently met with
during the entire period of the fever ; in fact, mental and bodily prostra-
tion is more marked here than in any other fever. In fatal cases death may
be the result of hemorrhage from the mucous surfaces, or from exhaustion.
In cases that recover, convalescence comes on late, and is slow and tedious.
Diarrhoea frequently follows the subsidence of the fever, and leads to a
fatal result.
Differential Diagnosis. — The affections with which continued malarial
53
834 ACUTE GEISTERAL DISEASES.
fever is likely to be confounded, are typJioid, remittent, relapsing, typhus,
and yellow fever .
The septic type, in many of its phenomena, so closely resembles typhoid
fever that frequently it is difficult to make a differential diagnosis. The
advent of continued malarial fever is usually marked by a distinct chill,
while typhoid comes on insidiously and is attended not by a distinct chill,
but by a chilly sensation. The rise of temperature in continued fever is
sudden and follows no typical range, while in typhoid the typical range of
temperature during the first week is diagnostic of the fever. In typhoid
fever, on the sixth or eighth day, rose-colored spots appear ; in the other,
although an eruption may be present it has none of the characteristics of
the typhoid eruption, is not rose-colored, does not disappear on pressure,
and remains visible throughout the whole course of the fever. Besides the
absence of these characteristic symptoms of typhoid fever, there is, in con-
tinued malarial fever, a distinct periodicity in the febrile action, a certain
icteroid hue of the skin, hepatic tenderness, and great gastric disturbance,
conjoined with which the appearance of the tongue, the character of the
diarrhoea, and the non-infectious character of the stools will serve as im-
portant aids in the differential diagnosis of these two forms of fever. If
upon microscopical examination of the blood, free pigment is found, the
■diagnosis of continued malarial fever is established.
The malarial type resembles remittent fever in its ushering-in symptoms.
In both cases there is a chill followed by fever, attended by one or more
distinct exacerbations and remissions. The early appearance of the enteric
symptoms, attended by other well-marked typhoid phenomena by the end
of the second week, establishes the diagnosis, and as the fever progresses
the typhoid condition becomes more and more apparent. Besides, remit-
tent fever yields more promptly to quinine.
Severe cases which are complicated by scorbutic tendencies marked by
petechiae and great prostration of the vital powers may be confounded with
iyphus fever ; yet the severity of the attack, the higher range of tempera-
ture, the greater frequency of the pulse, the dusky countenance, the ab-
sence of diarrhoea and all other abdominal symptoms in typhus fever, ren-
der it easy to make the differential diagnosis between the two types of
fever. Besides, typhus fever has a characteristic eruption, is only propa-
gated by contagion, and, if it prevails, does so epidemically.
Occasionally yelloio fever has been confounded with continued malarial
fever. The range of temperature is lower in yellow fever, and on the third
or fourth day it falls suddenly, and there is a more or less complete remis-
sion. The circumorbital pain, the appearance of the eye, the pulse rarely
ranging over 110, the peculiar color of the skin, the character of the mat-
ter vomited, the absence of diarrhoea, and the shorter duration of the dis-
ease, will enable one to make the diagnosis of yellow fever. The urine is
rarely albuminous in continued fever ; nearly always so in yellow. Again,
yellow fever usually prevails epidemically, and is confined to certain locali-
ties and certain seasons of the year. It is a portable disease, and the
yellow fever poison may be conveyed from an infected to a non-infected"
CONTINUED MALAEIAL FEVER. 835
district by means of clothing or merchandise, while the poison of contin-
ued fever is of endemic origin, and cannot be carried beyond the infected
district. '
Prognosis. — The ratio of mortality in continued malarial fever varies
greatly in the diiferent regions in which it occurs, and as the malarial or
septic element predominates. The hygienic surroundings of the patient
and the range of atmosphei'ic temperature will also very greatly influence
the prognosis. Statistics of this fever in different localities and in diiferent
years give the ratio of mortality from eight to ten per cent. The septic
type is more fatal than the malarial. Great caution should be exercised
in prognosticating the result of any case, for the mildest cases sometimes
suddenly assume a severe type and terminate fatally, while very severe and
apparently hopeless cases unexpectedly improve, and recovery takes place.
The average duration of those cases which terminate in recovery is from
three to four weeks. The duration varies with the different types of the
fever: in the malarial variety it is always shorter than in the septic. The
period of convalescence is prolonged; three or four weeks often elapse
before the patient is completely restored to health. A fatal relapse may
occur at any period during convalescence. In those cases that terminate
fatally, death most frequently occurs during the second or third week ; it
may occur as late as the close of the sixth week.
Its most frequent complication is inflammation of the respiratory organs,
the development of which is marked by those symptoms which usually
attend the development of the different acute pulmonary affections. In
the majority of instances the signs of bronchitis are not present until the
fever is well established. The bronchitis resists treatment, and does not
disappear until convalescence is fully established. When pneumonia occurs
it is catarrhal in character, and few of the strongly marked rational symp-
toms of ordinary pneumonia are present. The physical signs, however,
will always enable one to determine the presence of pulmonary complica-
tions, and any great irregularity in temperatui-e during the course of the
fever should be an indication for a careful physical examination of the
chest.
It is sometimes difficult to distinguish between the cerebral symptoms of
this fever and those symptoms which attend meningeal complications, but
the meningeal complications are of so very rare occurrence that it is safe
to assume they are not present until some of the diagnostic symptoms of
meningitis occur. Serious abdominal complications, such as intestinal
perforation, peritonitis, and hemorrhage are rare, but when they do occur
their advent is marked by such urgent symptoms that one loses sight of the
ordinary symptoms of the fever. It is hardly necessary to refer to those
modifications in the clinical history of this fever which follow the develop-
ment of abscesses, bed-sores, gangrene, etc. The occurrence of any of
these complications will very materially influence the prognosis in any
given case. Capillary bronchitis and pneumonia are especially dangerous
1 The points of difEerential diagnosis between this disease and relapsing fever, are considered under
the head of relapsing fever.
836 ACUTE GEIfEEAL DISEASES.
when they develop during the third week of the fever. Anti-hygienic sur-
roundings, such as over-crowding and improper food, materially affect the
prognosis. If continued malarial fever prevail among those who are
crowded into badly- ventilated apartments, who from filth and improper
nutrition have septic and scorbutic tendencies, the ratio of mortality is
much greater than among those who are free from such complicating in-
fluences.
The symptoms which may be regarded as indicating an unfavorable ter-
mination are a continued high temperature, showing little or no tendency
to remission ; a very frequent, feeble, fluttering joulse ; continued hiccough ;
profuse diarrhoea, the discharges at times being involuntary and con-
taining mucus, pus, and blood ; a dry, red, cracked, and fissured tongue ;
great drowsiness, with a tendency to stupor and coma ; and the appearance
of petechial spots on the surface of the body, attended by frequent hemor-
rhages from the lips, gums, and tongue. In a severe case, the occurrence
of any of these phenomena renders the prognosis more unfavorable.
The character of the prevailing fever will also greatly influence the prog-
nosis in any given case. If the type of the prevailing fever is mild, or if
comparatively few deaths have occurred, though the symptoms in a given
case may appear unfavorable, yet recovery is probable. If, on the other
hand, the type is severe, and many deaths have occurred, cases apparently
mild will suddenly become severe, and the prognosis becomes unfavorable.
As already stated, the hygienic surroundings and the previous habits of the
patient very greatly influence the prognosis. With drunkards, and those en-
ervated by vicious habits, a mild type of this fever will probably prove
fatal.
Treatment. — The treatment varies with its type. No plan can be pre-
sented which will be applicable to all cases.
The first question which meets us is : cannot the development of this fe-
ver be prevented ? It has been stated that its development was principally
due to three causes — namely, malarial poison, overcrowding, and improper
diet. In a large proportion of instances it is possible to do away with the
last two causes. The overcrowding and the faulty diet may be prevented,
and thus the septic poison which gives to this fever its " typhoid " type
may be destroyed or its development prevented. The strict observance of
hygienic laws in the localities where this fever prevails has in some instances
entirely changed the type of the disease. Even after the fever symptoms
have been well developed, the removal of patients from anti-hygienic sur-
roundings has frequently been attended by the most satisfactory results.
When isolated cases of this fever are met with in localities apparently free
from such sources of infection, a careful search should be instituted in or-
der to find the source of the infection. Defective sewerage and faulty drain-
age have been found to be fruitful sources of infection.
The therapeutic measures which may be employed in its treatment vary
with its type and the peculiarities of each individual case. There are no
specifics. In those cases in which the malarial element predominates, the
administration of quinine will in many instances arrest its progress or
CONTINUED MALARIAL FEVER. 837
sliorten its duration ; but in those cases in which the septic element pre-
dominates, while quinine may act as an antipyretic, it has little power to
arrest its progress or to shorten its duration, but it will, in many instances,
render the course of the fever milder. In those cases in which the malarial
element predominates, which are ushered in by distinct chills, followed by
one or two distinct remissions and exacerbations, during the first remission
twenty or thirty grains of quinine should be administered, in houi'ly doses
of ten grains each. If it is promptly and freely administered, it seldom
fails to produce a beneficial effect ; the febrile exacerbations will not return,
or if they do they are less severe, and in a few days entirely disappear. In
those cases which begin more insidiously and are developed more gradually,
if there is a distinct periodicity to the febrile phenomena, without distinct
remission, the administration of quinine may cause the fever to run a milder
course. If the first full doses of quinine fail to produce any effect in this
class of cases, its administration in moderate doses, perhaps ten grains
twice a day, must be continued for several days before it will markedly
modify the severity of the fever. In no type of the fever does the quinine
exert any specific influence except over the malarial element ; the enteric
phenomena are either not at all, or only indirectly, modified by the anti-
pyretic power of the drug. Hence, it is apparent that in those cases in
which the malarial element is slight, -and in which the septic element is
prominent, while quinine fails to exercise any controlling influence over the
progress of the fever, it will mitigate its severity, and act more powerfully
as an antipyretic than it will in any other form of continued fever. War-
burg's tincture in many cases will have a controlling jDower over the fever
when quinine fails.
It has been claimed by some that arsenic has a specific influence over the
fever, and that it exercises a peculiar and most beneficial effect upon the in-
testinal lesions. There is little doubt but that arsenic, like quinine, acts
beneficially in many cases of the malarial type of this fever ; but unques-
tionably this beneficial effect is due to its acknowledged power over malarial
affections, and not to any specific influence which it has over the fever. As
an antiperiodic it is inferior to quinine. Eucalyj)tus does not act as bene-
ficially in continued malarial fever as in the simpler forms of malarial
fever.
It is of importance to remember that this class of patients do not bear
well the prolonged application of cold to the surface, either by means of
the cold bath or the cold pack, and that, unless the antipyretic power of
quinine is added to the application of cold, very little benefit will be ob-
tained from the use of the latter. The danger resulting from the in-
judicious use of cold baths is greater in this than in any other infectious
disease.
The rules for the administration of stimulants are the same as those
given for their administration in typhoid fever. The effects of the first
few doses should be carefully watched. They should never be given in-
discriminately, for there is greater danger of over-stimulating in this than
in any other fever. Their use is indicated whenever signs of heart-failure
838 ACUTE GENERAL DISEASES.
are present, such as a feeble pulse and an indistinct first sound of the heart.
No fixed rule can be laid down as regards the quantity to be administered
in any given case ; it will vary with the type of the fever and the previous
habits of the patient ; it should always be administered at stated intervals.
The period of the fever at which stimulants should be commenced will
also vary. In some cases stimulants are never required, while in other
cases, from the very outset of the fever, they are demanded. In the
majority of cases their use is not indicated before the end of the second
week. It must be borne in mind that alcohol is not a specific, curative
agent in this fever, but that the object of its administration is to sustain
the heart and prevent the vital powers from falling below the point at
which reparative processes are possible. The use of stimulants is not
necessarily contraindicated when delirium is present. Frequently after
their administration the delirium will pass away, and only when it is de-
cidedly increased by their use should they be abandoned.
The state of the bowels, skin and kidneys demands the closest attention.
If, early in the disease, the bowels are constipated, a calomel purge com-
bined with ten or fifteen grains of quinine will often be followed by marked
benefit. In any stage of fche disease brisk purgation should be avoided.
If diarrhoea is present, it should not be interfered with unless it becomes
exhausting ; then it should be checked by small doses of opium combined
with astringents. Symptoms referable to disturbance of the nervous system
sometime require special treatment. If there is extreme restlessness, mus-
cular twitchings, or active delirium, opium may be administered in full
doses. The effect of the first dose must be carefully watched. If sleep
soon follows its administration, and the delirium gradually subsides with-
out any aggravation of the other symptoms, its use may be continued ; if,
instead of producing sleep, the patient becomes more wakeful, and the de-
lirium is increased and more active, and the other symptoms are greatly
aggravated, its use must be immediately abandoned. Under these circum-
stances chloral may be tried with great care.' Quain advises gr. xv.-xx. of
bromide of potassium under similar conditions.
Some claim that spirits of turpentine in the treatment of this form of
fever has almost a specific power, while others regard it useful only as a
stimulant. My own experience leads me to employ it only as a stimulant
during the second and third week of the disease, when there is great pros-
tration and marked typhoid symptoms. It may be given as an emulsion in
doses of twenty drops every two hours. The diet best suited to patients
with this fever is milk administered in the same way as was proposed in
the case of typhoid fever patients. Special complications occurring during
the non-septic variety must be met with such remedies as the condition of
the patient and the peculiar complications may require.
J Wood recommends Hoffman's anodyne and spts. seth. nitrosi for restlessness ; and musk, asafoetidaa
camphor, and similar drugs for the hiccough.
BERKICIOUS MALARIAL FEVER. 839
PERmCIOUS MALAEIAL FEVEE.
This form of fever has received other names, at different times and in
different localities. It has been called congestive fever, ardent fever, tropical
typhoid fever, and pernicious fever. The latter name seems most appro-
priate, and at the present time is generally adopted.
It is true that in the majority of cases there is more or less congestion of
the internal organs, and sometimes the patient is overwhelmed by these con-
gestions, but in a large number of cases no such congestions exist, and under
such circumstances the designation pernicious is to be preferred. In its
severe and dangerous form it may be remittent or intermittent in character,
and may assume any of the types of periodical fever, but the quotidian and
tertian types are the most common. Sometimes its pernicious character is
clearly marked at the onset of the fever, during the first paroxysm ; at
other times it comes on insidiously, and its pernicious character is not
suspected until after the occurrence of two or three paroxysms.
There are several well-marked and distinct varieties of pernicious fever —
the most common and most important of which are the comatose, the delir-
ious, the algid, and the gastro-enteric. It is the locality in which perni-
cious fever prevails that gives the fever its distinctive peculiarity. Perni-
cious fever not infrequently appears as an epidemic ; sporadic cases are met
with in those regions where simple intermittent and remittent fevers
prevail.
Morbid Anatomy. — Its anatomical lesions are similar in kind to those of
intermittent and remittent fevers, but they differ very much in degree. For
instance, the pigmentation is more abundant. The abundance of the pig-
ment, and the extent of the pigmentation will vary with the severity of
the fever. The other changes in the different organs and tissues of the body
are very similar in character to those described in connection with inter-
mittent and remittent fever. The post-mortem appearances in pernicious
fever vary with the intensity of the malarial infection and the peculiar
atmospheric conditions under which the fever is developed. In some in-
stances there will be evidences of intense engorgement of the blood-vessels of
the brain, and the entire brain substance will be more or less thoroughly
pigmented. In others, minute blood-extravasations will be found scattered
here and there throughout the substance of organs. Small blood-extravasa-
tions into the spinal cord, accompanied by more or less pigmentation, are
very apt during life to be attended by tetanic spasms. In persons dying
of pernicious fever after the third attack, I have found all the organs of the
body pigmented. Sometimes there is intense engorgement of the liver, that
is, the most marked post-mortem changes will be found in that organ, and
the amount of pigmentation present will correspond with the intensity of
the congestion. With intense engorgement of the organ there are usually
blood-extravasations.
Occasionally, infarctions occur in the spleen, and around each there will
be a mass of pulpy material. The spleen is more invariably found softened
840 ACUTE GENEEAL DISEASES.
than in any other fever. In connection with this softening, which is very
extensive and similar to that found in typhoid fever, the organ rapidly be-
coming a soft, pulpy, bloody mass, it is also enlarged even beyond what it is
in typhoid fever and is darker in color than normal. It is unnecessary to
describe in detail the enlargement of the capillary vessels which occurs as a
necessary result of this intense engorgement. Sometimes the kidneys and
the lungs are the seat of intense hyperae.mia, as the result of which the
functions of these organs are more or less extensively interfered with.
Hemorrhagic infarctions in the lungs are not infrequent. A low form of
pneumonia is sometimes present. The heart is pale and flabby.
Etiology. — The exciting and predisposing causes of pernicious fever differ
from those of the simpler forms of malarial fever only in degree, not in
kind, but a higher range of temperature is requisite for the development of
pernicious fever. It prevails only in those localities where the average
range of temperature, for a time, reaches 65° F.
Symptoms. — Pernicious fever may commence abruptly ; generally the pre-
monitory symptoms which mark its development do not differ from those
which mark the development of intermittent and remittent fever. In most
varieties the attack commences with a chill, which is usually severe and
prolonged. The attack may commence with distinct intermittent parox-
ysms of the quotidian type, but rarely more than two of these intermittent
paroxysms will occur before it assumes the pernicious type ; or a remittent
fever with a distinct exacerbation and remission may go on for four or five
days before its pernicious character will be developed. The milder form
either gradually passes from a simple intermittent into a pernicious fever
by a progressive increase in the severity of the paroxysm, or a single parox-
ysm of not unusual severity is suddenly, followed by a pernicious one ; a
fatal result rarely occurs until the third paroxysm is passed. Again, a dis-
tinct chill may be followed by a condition that will at once be recognized as
one of the varieties of pernicious fever. The ushering-in symptoms will
always vary with the type of disease which is about to be developed. I shall
not describe the phenomena that attend all these different varieties, but
only those most commonly met with.
As the varieties in type of this fever are as numerous as the localities in
which they occur, and as the type in any locality may change with every
succeeding year — that is, the type of one year may be very unlike that of
the preceding or following year — it is very difficult even to classify its dif-
ferent forms. The slight variations which are met with in the pathologi-
cal lesions of the different varieties are still more difficult of description
and classification. For instance, there is one variety which is character-
ized by a tendency to coma, called the comatose variety ; another is charac-
terized by a tendency to a peculiar form of delirium, termed the delirious
'Variety ; still another is characterized by a marble-like coldness of the sur-
face, called the algid variety ; again, we have one which is characterized
by vomiting and purging, or choleraic symptoms, termed the gastro-enteric
iiariety ; then one in which there is acute jaundice, termed the icteric
■i^ariety ; then one in which there are profuse hemorrhages, termed the
PERNICIOUS MALARIAL FEVER.
841
hemorrhagic variety ; and still another in which there is profuse diaph-
oresis, termed the cnlUquative variety.
Comatose Variety. — A patient has a distinct paroxysm of one of the sim-
pler forms of malarial fever (intermittent or remittent), with no s^Decial
phenomena attending it, except that he has had a more than usually severe
headache ; with this there has been perhaps vertigo, stammering and in-
distinctness in the speech, an inability to talk with freedom, and a more
than usual tremulousness during the hot stage. From this condition he
passes as usual into the hot stage of an intermittent, or rapidly into an ex-
acerbation of remittent, then into a state of stupor and unconsciousness,
and finally lies upon his back, with a flushed face, congested conjunctivae,
dilated pupils, slow, deep, stertorous respiration, and perhaps a very slow
pulse, or, if slow at first, it may soon become frequent. The axillary tem-
peratures range from 105" to 107° F. The
patient is now partially unconscious ; he is
apparently paralyzed ; the urine is retained
in the bladder, and the bowels move invol-
untarily. If the pulse is slow, it is full
and hard. The respiration becomes more
and more stertorous, and unconsciousness
more and more complete. Usually a moist-
ure makes its appearance within twelve
hours from the commencement of the first
paroxysm, and the patient awakes to con-
sciousness perspiring profusely. The head-
ache and giddiness pass off, and if the fever
which preceded it was remittent, there may
be a well-marked remission ; if it was an
intermittent, there may be a distinct inter-
mission. With the next remittent exacer-
bation or during the hot stage of an inter-
mittent, the pain in the head, giddiness,
unconsciousness, and all the symptoms al-
ready described will return with greater in-
tensity than before. With the second at-
tack the patient may pass into a fatal coma. Temperature Record^in^a case of Pemi-
In this variety patients sometimes pass {Comatose variety.)
into a condition of apparent death,
which may last for hours. Some are, nevertheless, perfectly conscious, see-
ing and hearing everything which occurs around them, although unable to
move or utter a sound ; others are unconscious. Even though the strong-
est counter-irritants are applied to the surface, there is no sign of life,
until, at the beginning of the sweating stage, the patient comes to con-
sciousness. If a patient sitrvives the second paroxysm, quite probably he
will die during the third. With each successive paroxysm the prognosis
becomes more and more unfavorable ; patients sometimes lie in a comatose
condition for days, and finally die apparently from cerebral congestion.
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Fig. 175.
842 ACUTE GENEEAL DISEASES.
Delirious Variety. — In this variety, the patient, after passing into the
hot stage of an intermittent or into the exacerbation of a remittent, becomes
delirious. Mild delirium is not uncommon during the progress of an inter-
mittent or a remittent fever, but the delirium now referred to is of a more
active character. If delirium is developed during the exacerbation of a re-
mittent or during the hot stage of an intermittent, which has been preceded
by severe headache, dizziness, ringing in the ears, and great restlessness,
one may be quite certain that he has to deal with a case of pernicious fever,
especially if it is prevailing in the locality. In this variety of pernicious
fever there will also be more or less headache during the interval, and per-
haps other peculiar cerebral phenomena. The delirium which appears is
always violent in character ; perhaps the patient will require restraint ; he
may be disposed to jump out of the window, or in some way to do injury
to himself or those around him. During the paroxysm of delirium the
face becomes flushed, the eyes brilliant, the conjunctivae injected, the
pupils dilated, and the patient is constantly crying, singing, and trying to
escape. In those who are extremely anaemic the countenance assumes a
pale, sunken aspect. The pulse is full and hard, and the carotids beat
violently, the temperature often reaches 107° or 108° F. This delirious
state may continue for hours. Suddenly the patient passes from it into a
condition of collapse, or gradually sinks into a coma from which he never
wakens. During the whole period the axillary temperature rarely falls be-
low 105° F.
In favorable cases the delirium gradually becomes milder, a profuse per-
spiration comes on, and the patient falls into a prolonged sleep, from which
he awakens conscious, though weak and exhausted, with headache and
vertigo, but without the slightest recollection of what has passed. These
attacks of delirium may be repeated three or four times before a fatal ter-
mination is reached, but so much danger attends them, that a second attack
should never be allowed to occur if it can be prevented.
In this variety of pernicious fever, other nervous phenomena may accom-
pany or take the place of the delirium, such as epileptiform convulsions,
tetantic spasms, etc. The tetanic spasms sometimes resemble the phe-
nomena of hydrophobia. That form of tetanus which occurs in various
malarial districts, and is sometimes called sporadic tetanus, I believe
will be found to have many things in common with this type of pernicious
fever.
Oastro-Enteric Variety. — In this variety the patient, after he has passed
into the hot stage of an intermittent, or the exacerbation of a remittent,
is seized with almost incessant vomiting and purging. The vomiting and
purging are peculiar, altogether unlike that w'hich is sometimes present in
the simpler forms of malarial fever. There is blood-stained material, both
in the matter vomited and in that discharged from the bowels. In some
instances, the discharges may be so reddened as to look like beef-brine or
the washings of raw meat; sometimes the proportion of blood is so great
as to cause the discharges to have the appearance of clear blood. In some
endemics the discharges assume the appearance of rice-water, having no
PERNICIOUS MALARIAL FEVER.
843
odor, and similar in appearance to those of Asiatic cholera. The patient
has no abdominal pain or tenderness, but has a'sense of weight and burning
in the stomach, accompanied with cramps in the calves of the legs, cold-
ness and blueness of the surface, with a small, almost imj^erceptible pulse,
sunken eyes, and the "facies" of cholera. So closely do these patients
resemble in appearance those of Asiatic cholera that this disease has fre-
quently been mistaken for it. During the attack the thirst is most in-
tense. The respiration is peculiar ; it consists of a double inspiration,
followed by a double sighing expiration. The restlessness is yery great,
the patient is constantly tossing from one side to the other ; sometimes, an
hour or two before death, he suddenly springs up and walks across the room.
The usual length of the fatal paroxysm is from three to six hours.
Patients die in a state of collapse. After the vomiting and diarrhoea have
assumed the characteristic appearances already described, very few patients
recover. As death approaches, the pulse becomes more frequent, feeble,
irregular, and fluttering in character. The respiration is more and more
prolonged and sighing, the skin cold and shrivelled, and covered with a
cold, clammy perspiration. It frequently happens when all these symp-
toms are present that the patient cannot be convinced that he is seriously
ill, and wishes to get out of bed and go out of doors.
Algid Variety. — This variety is characterized by coldness of the surface
of the body, while the rectal temperature may range from 104° to 107° F.
The attack begins with a chill of not un-
usual severity or duration, but soon after
the patient enters into the hot stage of the
paroxysm, or, during the exacerbation of a
remittent, the surface of the body begins
to grow cold, while at the same time he
complains of a sensation of burning and
intense thirst. A cold perspiration soon
covers the surface. The pulse becomes
slower and slower, falters, and disappears at
the wrist. Alternately the extremities and
face become cold ; only the abdomen re-
tains its normal temperature. The surface
has a cold, marble-like feel, and the tem-
perature in the axilla may fall to 88° or
84° F. In the comatose and delirious
varieties the temperature rises higher than
normal, and may reach 106° or 107° F,, but
in this variety it sometimes falls two or
three degrees below the normal. The
tongue becomes white, moist, and cold; the
breath is cold, and the voice feeble and in-
distinct. The action of the heart is feeble,
often perceptible only on auscultation. The
mouth is clean, and the patient seems to himself to be in a comfortable
Day:
J.
Z.
3.
4.
s.
6.
z
JOS-
IH-
JOS-
J02''
JO/'-
JOO-
99'
9S°-
9f-
m.
e, 7
n e-
m. a.
me.^
..
e^.
m,
e.
m\a.
.
V
J
j
^•^
_^
Ml
^
Fig. 176.
Temperature Record in a case of Per-
nicious Fever.
{Algid varietT/.)
844 ACUTE GENERAL DISEASES.
condition, except that he feels exhausted and is sensible of great internal
heat. The mind is clear. The expression of the countenance is that of
death.
This variety is very insidious in its progress. To one not familiar with
it, the calm which follows the febrile excitement will be mistaken for relief,
perhaps attributed to some plan of treatment pursued, or to some remedial
agent which has been employed. If a patient in one of these paroxysms is
to pass on to recovery, the pulse gradually returns in the wrist, and the sur-
face regains its normal feel and temperature. As the warmth returns to the
surface, the patient passes on to convalescence in the same manner as pa-
tients recover from a comatose or delirious paroxysm. An algid pernicious
paroxysm is rarely preceded by a distinct intermission, and it rarely has any
appreciable remission. Once established, it marches steadily on to a fatal
issue, unless arrested by treatment.
There is another variety which will occasionally be met with, in which a
profuse perspiration, called a "■ colliquative sweat," comes on at the end of
the fever stage and continues through the succeeding intermission, accom-
panied by great prostration, feeble heart action, and labored respiration.
Upon the second or third return of this sweat the patient sinks and dies,
apparently from exhaustion. Again, severe hemorrhages from the stomach,
bowels, or kidneys may occur during the sweating stage of a pernicious par-
oxysm and endanger the life of the patient from sudden syncope.
A mild form of hsematuria sometimes occurs independent of a pernicious
paroxysm in chronic malarial poisoning.
Icteric Variety. — This is always endemic, confined to certain localities,
and occurring in them whenever any form of pernicious fever prevails. It
begins with a violent, long-continued chill, during which jaundice shows
itself. The jaundice gradually deepens, and extends over the whole body.
Intense nausea accompanies its development, with a copious vomiting of
bile, and a bilious diarrhoea. The patient suffers with a most intense head-
ache, pain in the region of the spleen and over the kidneys, and a feeling of
numbness in the limbs. The pulse is small, frequent, and hard. The urine
is dark colored. As the hot stage comes on, the pulse becomes fuller and
more frequent, the respiration is labored, the skin very hot, the tempera-
ture reaching 106° or 107° F., and the thirst is most intense. This stage
lasts three or four hours, and often terminates in death. If the patient
passes into the sweating stage, recovery usually takes place. During the
intermission the mind is clear, but the jaundice continues. Unless the
disease is controlled by treatment, each succeeding paroxysm becomes
more and more severe.
This variety is incorrectly called pernicious bilious remittent fever. If
the attack is mild, there is only a slight staining of the skin, but in that
form in which there is an apparent arrest of the functions of the liver, the
patient may die deeply jaundiced within two or three days after the first
discoloration appears. The mild form of so-called bilious remittent fever,
in which the febrile movement is constant, is very different from the form
under discussion, and is better classed under the head of simple remit-
PERNICIOUS MALAEIAL FEVER. 845
tent. All these different varieties depend on the same blood-iooisoning,
differing in its manifestations according to its intensity and the predispos-
ing atmospheric or septic conditions which may exist in the localities where
they are developed.
Differential Diagnosis. — The diagnosis of pernicious fever is sometimes
very difficult. In determining whether a given case is, or is not, one of
pernicious fever, the first inquiry will be in regard to the character of the
prevailing fever. If pernicious fever is prevailing in the locality, a diagno-
sis will easily be made ; if, however, the first case in the locality falls under
observation, probably great difficulty will be experienced in making a diag-
nosis, and this difficulty, to a certain extent, will vary with the type of the
fever. If, for example, a case belongs to that class in which there is a
tendency to coma, delirium, etc., it may be confounded with some form of
cerebral disease. This form of pernicious fever has been mistaken for cere-
bral apoplexy, meningitis, and acute urcemia.
As a rule, it is not difficult to draw the line between apoplexy and perni-
cious fever of the comatose or delirious variety. The constant and promi-
nent symptom of apoplexy is hemiplegia, which is of rare occurrence in per-
nicious fever. It may occur, but if it does, it is developed slowly. Nei-
ther coma nor hemiplegia is ever reached suddenly in pernicious fever. Eise
in temperature, rapid pulse, and all the phenomena of intense febrile ex-
citement are present before the occurrence of either. On the other hand,
in apoplexy the hemiplegia is of sudden development, attended by a slow
pulse, irregular contracted pupils ; or, perhaps, one j)upil is dilated and
the other contracted, and its occurrence is preceded by a sudden loss of con-
sciousness, and not attended or preceded by high febrile excitement.
As regards . pernicious fever and meningitis, although in both diseases
the patient reaches a condition of coma, yet in meningitis days elapse be-
fore the coma is reached, and during those days there has been pain in
the head, photophobia, and delirium, extending over a considerable period
of time ; whereas, in pernicious fever the patient reaches his condition of
coma within twelve hours. Besides, in pernicious fever there will be a
history, not only of the prevailing type of malarial disease, which will in-
dicate its character, but the attack of coma or delirium will be preceded
by a distinct malarial paroxysm — perhaps two of these paroxysms ; then
the patient will pass rapidly into a state of coma. In meningitis the fever
rarely ranges above 102° or 103°, the face is pale, the abdomen retracted,
and the pulse is tense and wiry — all markedly contrasting with delirious
pernicious fever.
The gastro-enteric and cold or algid varieties of pernicious fever closely
resemble cholera. They may be distinguished from it by the character of
the primary discharges. There may be a time in this type of pernicious
fever when the discharges will very closely resemble those of cholera ; but
they will always have been preceded by one or two bloody discharges. In
cholera there is albumen in the urine, the occurrence of which is com-
paratively rare in pernicious fever. In cholera there are the peculiar sur-
roundings of the patient, the prevalence of cholera in the locality, etc.
846 ACUTE GE^JTERAL DISEASES.
When the endemic is at its height it is almost impossible to make a differ-
ential diagnosis between the two diseases from the clinical history of the
cases ; but, when we take the early history of the endemic, at which time
the cases at their commencenient were marked by distinct intermittent or
remittent paroxysms, the true character of the disease is very readily de-
termined. If in any given case there is still a question whether it is or is
not one of pernicious fever, it may be determind with positiveness by a
microscopical examination of the blood, which will be found to contain
free pigment.
The icteric variety of pernicious fever which often, in many of its phe-
nomena, so closely resembles yellow fever, maybe distinguished from it
not only by the history of its development, but by the fact that when it
prevails as an endemic, those are seized with the fever who have been long-
est under the influence of malarial poison, whereas new-comers are not
usually attacked ; in yellow fever districts new-comers are almost certain
to contract the disease. The symptoms in icteroid pernicious fever tend
to become typhoid and adynamic, while in yellow fever the symptoms are
active and there is little tendency to a typhoid condition. Then the jaun-
dice of yellow fever appears late in the disease, while the jaundice of this
form of pernicious fever comes on early, even before the chill passes away.
Again, bloody urine is frequently present in this type of pernicious fever,
while in yellow fever hsematuria rarely occurs without the accompanying
evidences of nephritic inflammation. The presence of free pigment in the
blood will aid in settling the question of diagnosis in difficult cases.
Prognosis. — In all varieties of pernicious fever the prognosis is unfavor-
able, unless it can be controlled before the occurrence of the second parox-
ysm. The prognosis will depend in a great degree upon the character of
the prevailing endemic or epidemic, as also upon the stage of the epidemic,
for the ratio of mortality is always greater during the earlier period of an
epidemic than during its decline. All agree that the prognosis is better in
every variety of pernicious fever if there are distinct intermissions, however
short may be their duration. If the paroxysm does not last more than
twelve hours, and terminates in a distinct remission, the prognosis is far
better than when one paroxysm follows another without any distinct re-
mission. Unquestionably the most favorable cases are those of the tertian
type. Those varieties in which the cases most frequently terminate fatally
are the gastro-enteric and the algid ; those in which recovery is most
likely to occur are the comatose and delirious.
The prognosis is also much influenced by the age and condition of the
patient and by the presence or absence of complications. The mortality
is greatest among the very young and very old, and among the intemperate.
Patients with pernicious fever may die suddenly during a paroxysm, or the
paroxysms may be prolonged and run into each other, and the patient may
finally pass into a typhoid or collapsed condition. * If the second or third
paroxysm is not attended by signs of intense visceral congestion, if it de-
clines with profuse warm sweats, if it has been preceded by distinct inter-
vals, if the urine is free, and the appetite early returns, a speedy recovery
PERKiCIOUS MALAEIAL FEVEB. 847
is at hand. On the other hand, if the second or third paroxysm is pro-
tracted and accompanied by great anxiety and restlessness, with active de-
lirium and a tendency to coma, with coldness of the surface ; if there is
intense pain in the epigastrium, with tingling of the surface, and scanty
and high-colored urine; if there is profuse vomiting and purging, bleeding
at the nose, and cold, colliquative sweats.; if the pulse becomes small and
feeble, or the radial pulse is imperceptible, the danger is very great, and a
fatal issue is almost certain. Sometimes severe and fatal dysentery comes
on at the end of a paroxysm ; at other times, as the paroxysm subsides,
the fever assumes a typhoid type, and, after a period of continued fever
ranging from ten to twelve days, it terminates fatally.
Treatment. — The expectant plan of treatment cannot be practised in the
treatment of pernicious fevers. The alarming symptoms crowd upon one
another with great rapidity, and it is only by prompt and vigorous measures
that in the severe forms of the disease the patient can be rescued from im-
pending death. The issue of life or death often hangs upon a single hour.
Some have proposed, before administering the only specific which we
possess capable of controlling this disease, to produce free purgation by the
administration of cathartics ; others to bleed and freely vomit the patients.
If the case is one of the gastro-enteric variety, emetics and purgatives are
certainly very plainly contraindicated. It is now a well established fact
that in no variety of pernicious fever do patients bear depletion. In India,
where the most severe types of this fever prevail, the English surgeons are
very positive in their testimony upon this point. All forms of depletion
have been abandoned by them. Although stimulating enemata and friction
to the surface may act as aids in the management of the algid and delirious
varieties, they must not be relied upon as having any controlling influence
over the disease.
Those who have bad the most extended opportunities for testing the dif-
ferent remedies and plans of treatment which have been employed in the
management of this fever are united in the opinion that quinine and opium
are the only agents which can be relied upon for controlling its different
varieties. In fact, the hypodermic use of these drugs has inaugurated a
new era in its treatment, for in a large proportion of the severer forms it is
impossible to get the full effect of either of these remedies by the ordinary
methods of their administration, the usual avenues for their introduction
being closed.'
Whatever solution may be used, administer from five to seven grains of
» The solntion of quinine commonly employed by the English surgeons for this purpose is made by
adding one hundred and fifty grains of quinine and fifty drops of dilute hydrochloric acid to four ounces
of water, and then evaporating the solution to two ounces. Of this, thirty drops may be administered at
CHch injection. Some add carbolic acid to a solution of quinine in dilute sulphuric acid ; the carbolic
acid is added to prevent abscess at the point where the injection is introduced.
The formula for this solution is as follows :
Quiniffi disulphatip gr- !•
Acidi sulphuric, dil t^'V.
Acidi carbolici tH, ij-
Aquse destillat 5 i-
M.
Thirty minims is the quantity usually administered at each hypodermic injection.
. 848 ACUTE GEiq-BRAL DISEASES.
quinine every hour until the paroxysm has passed away, then continue its
use in the three-grain doses every four hours. With the first hypodermic
of quinine administer one-fourth of a grain of morphia. The morphine
should be administered with each dose of quinine until the patient is
brought fully under its influence, without regard to the stage of the
paroxysm. "
During the past few years a remedy known as " Warburg's Tincture "
has been quite extensively employed in the treatment of pernicious and
other forms of malarial fever.^ Each half ounce of this tincture contains
seven and a half grains of quinine. It is recommended to give half an
ounce of this tincture at the onset of the paroxysm ; if this does not con-
trol it, the same quantity must be repeated in four hours. If it cannot be
retained by the stomach, it may be administered in capsules, §i every
1 1 have recently used the following :
QuiniEB sulphatis 3 i.
Acidi hydrobrom 3 ij.
Aquae destillat 3 vl.
M.
Thirty minims may be administered at each injection.
The bimuriate of quinine with urea, made by Messrs. McKesson and Eobbins, Phila., is highly recom.
mended for hypodermic injection, as it is very soluble, and abscesses seldom or never follow its use.
Formula :
Bimuriate Quiiiia and Urea 3i,
Aq. Destillatae, ad f 3 ij.
M. f. soi.
Two minims contain one grain of the salt.
» Formula, Warburg's Tincture:
Ead. Rhei
P. Aloe Soc.
Ead. Angelica Officinalis, 35 sjy^
Ead. Helenii
Crocus Hispan.
Sem. Foeniculi
Cretse Preparat., 5a , sm
Ead. Gentian
Ead. Zedoar
P. Cubeb
G. Myrrhse
G. Camphor
Boletus Laricis, 55 z:
Confect. Damocratis* "" zjy
Quiniae Sulph i... .".'!!!!.'!.'."!.".*!'.!!'.'.."!!.'.'!!.* Slx'xxy.
Sp. Vini Kect O xx
A qu 83 P u r a3 !!!!!!!'./.*.*.'.!! O xi j
Macerate, in a water bath, twelve hours, express and filter.
* Confeotio Damocratis :
Cinnamon
MjTih fourteen grams.
White Agaric, Spikenard, Ginger, Spanish Saferon, Treacle," Mustard Seed, Frankln- e even
cense, and Chian Turpentine, each ^^„ „
Camel's Hay, Costus Arabacus, Zeodary, Indian Leaf, Mace, French Lavender Long
Pepper, Seeds of Harwort, Juice of the Rape of Clstus, Strained Storax, Opponax
Stramed Galbanum, Balsam of Gilead, Oil of Nutmeg, Russian Castor, each eiaht "
Water Germunder, Balsam-Tree Fruit, Cubeb, White Pepper, Seeds of Carrot of
Crete, Foley Mont, Strained Bdellium, each.... gg^g^ «
Gentian Root, Celtic Hard, Leaves of Dittany of Crete, Red Rose, Seeds of Mace-'
donium Parsley, Sweet Fennel Seed, Seeds of Lesser Cardamom, Gum Arabic
Opium, of each „ „
Sweet Flag, Wild Valerian, Anise Seed, Sagapernum, each.... .........'.'."". t^ree "
Spigrul, St. John's Wort, Juice of Acacia, Catechu, Dried Bellies of Skunks, each '.'.'. 'two and one-half «
Clarified Honey. „.,» „
The roots, etc., to be finely powdered, and the whole mixed thoroughljt.
DEITGUE FEVEE. 84f>
twenty-four hours.' It is claimed that the tincture is retained by the stom-
ach when all other remedies are rejected. Prof. Maclean says that he has
seen the most hopeless cases — those manifesting a degree of severity which
seemed to preclude the jiossibility of recovery — commence to convalesce as
soon as the patient was brought under the influence of this remedy.'' No
special rules can be laid down in regard to the administration of stimulants
in pernicious fever ; the condition of the patient must be the guide.
They are only of service as means to aid in carrying a patient over a dan-
gerous period. Their continued use in large quantities is strongly objected
to by those who have had the most extensive experience in the management
of this fever. Do not wait for the action of a calomel purge. Do not resort
to any depleting measures. However mild the paroxysm, no time should be
lost ; bring the patient as rapidly as possible under the influence of quinine
and opium, or, if Warburg's tincture is used, administer it in full doses as
early as possible, and continue its administration until convalescence is
fully establishedo
DEJS^GUE FEVEE.
Dengue,^ hreah-hone, or dandy fever first appeared after the landing of a
cargo of slaves from Africa, hence its earliest name was African Fever. It
is neither an intermittent, a remittent, nor a pernicious fever. It is an
acute disease which appears as an epidemic in hot climates. It is charac-
terized by a febrile excitement remitting in its character, and is accom-
panied by more or less intense arthritic pains, attended by the develop-
ment of a papillary eruption resembling that of measles.
Morbid Anatomy. — The morbid anatomy of this variety of fever does not
differ essentially from that of the severer types of malarial fever, except that
a cutaneous eruption commences on the palms of the hands and extends
rapidly over the entire body. In most cases, arthritic changes of a rheu-
matic character are present ; usually the external lymphatic glands are
somewhat enlarged. This disease seems to be an exanthematous malarial
fever, with a rheumatic or neuralgic element.
Etiology. — Dengue or break-bone fever prevails epidemically in malarial
districts ; it may occur as a sporadic disease. Its infection has been carried
in clothing from one seaport to another.* Some claim that the disease de-
pends upon a specific contagion ; but its contagious character has not been
established. Its prevalence is not arrested by cold weather. The intensity
1 The tincture may be evaporated nearly to dryness, and put up in capsules containing from one to two
drams each.
2 Prof . Maclean's rules for its administration are as follows :—" One-half ounce (half of a bottle) is
given alone, without dilution, after the bowels have been evacuated by any convenient purgative, all fluids
being withheld ; in three hours the other half of the bottle is administered in the same way. Soon after-
ward, particularly in hot climates, profuse, but seldom exhausting, perspiration is produced ; this has a
strong aromatic odor, which I have often detected about the patient and his room on the following day.
With this there is a rapid decline of temperature, immediate abatement of frontal headache— in a word,
complete defervescence, and it seldom happens that a second bottle is required. If so, the dose may be
repeated as above. In very arlynamic cases, if the sweating threatens to prove exhausting, nourishment
in the shape of beef-tea, with the addition of Liebig's extract and some wine or brandy of good quality,
may be required."
3 El dengue means in Spanish, affectation, a dandified manner.
* Dengue seems to have a specific poison ; and the disease is in some degree infectious. Some regard it
as more highly contagious than even the exanthematous fevers.
54
850
ACUTE GE]!q"ERAL DISEASES.
of the malarial poison unquestionably lias some influence in increasing or
lessening the severity of this fever. In districts slightly malarial its type
is usually mild ; but in districts strongly malarial its type is severe. It at-
tacks all classes and all ages, rich and poor, black and white, the very
young and the very old. Occasionally it has occurred as the precursor of
yellow fever. In '1780 it was epidemic in Philadelphia. In 1827 a very
extended epidemic of this fever prevailed in the West Indies ; during the
prevalence of this epidemic, the specific poison of the disease was trans-
ported in clothing and merchandise to many neighboring seaports. In
our Southern States, in 1880, it prevailed as an epidemic. One attack
does not protect against a second.
Symptoms. — The period of incubation is estimated at from three to five
days. Its initiatory symptoms are sudden and well pronounced, and its de-
velopment is very rapid. In the majority of cases, the earliest symptoms
are headache, photophobia, great restlessness, chilliness alternating with
flashes of heat, and pain in the back, limbs and joints ; the small joints.
swell, and there is soreness and stiff-
ness of the muscles. The skin be-
comes hot and dry, and in some in-
stances the temperature reaches 107°
or 108° F. The pulse is rapid, rang-
ing from 120 to 140 beats per minute..
The face is flushed and the eyes red
and watery. Thomas says that in
children it often begins with a con-
vulsion.*
After the fever has continued about
twelve hours, the pains in the joints,
and back become intense, and shoot
down the sciatic nerve. Nausea^
vomiting, and pain in the epigastrium
are usually prominent symptoms.
Early in the fever the lymphatic
glands become involved ; the ingui-
nal are first affected, then those in
the axilla and neck ; they increase very rapidly in size, and become ex-
ceedingly tender. The testicles, or rather, the epididymes, enlarge, and
the swelling continues until the subsidence of the other symptoms. The
active febrile excitement continues from twelve hours to three or four days,
when it subsides, leaving the patient in an exceedingly feeble and prostrate
condition. Sometimes the fever abates suddenly, with critical symptoms,
as in relapsing fever, such as profuse sweats, diarrhoea, or epistaxis. Pro-
fuse diarrhoea may usher in the disease. The patient after being in a pas-
sive condition for two or three days, passes into the period of remission.
The pains now become less, the glandular swellings diminish, there is less
febrile excitement, but the fever does not entirely subside.
> Dengue. J. G. Thomas, M.D., Savannah, 1881.
Day: /.
2.
3.
4.
5.
6.
7. |;=
a OS
•SB
sa
„
_
1
■bJ
J)a^:
/0T
ws
/03''
/Oi
3.
i
I
9.
/O.
//
il
J2.
/3.
I
J4.
n
/s.
J6.
>'Aa.
&
Fig. 178.
Temperature Record in a mild case of Acute
Rheumatism.
Fig. 179.
Tsmperatnre Record from the eighth day in a
fatal case of Acute Rheumatism.
rises to 105° F., and 109° and 110° F. have been reached before death in
severe cases. There are distinctly marked exacerbations and remissions,
the minimum temperature being nocturnal. The pulse is full, bounding
and compressible, as a rule keeping pace with the temperature ; it often
reaches 120 per minute independent of the fever, seemingly on account of
the severe pain.
The joints attacked become red, swollen, and so tender that the weight of
the bed-clothes cannot be borne, nor can the patient bear the shaking of
the bed by the footsteps of attendants. Fluctuation can soon be made out
in those joints whose situation permits examination. Muscular cramps
usually accompany the joint symptoms. The face is flushed and the body
is bathed in a copious, sour smelling, and acid sweat, especially about the
affected joints. Sudamina are common. The saliva is said to become
acid, and inflammatory fluids poured out into serous cavities during rheu-
matic fever have been found distinctly acid in reaction. There is great
anxiety and restlessness, but the sufferer dares not move, so agonizing is
the pain in the joint.
The urinary secretion is diminished, its color being darker than normal.
On cooling it deposits a brick-dust sediment of urates. Its specific gravity
varies from 1.025 to 1.030. Urea and coloring matter are in excess, while
860 CHEONIC GENERAL DISEASES.
the chlorides are diminished. Sulphates and albumen are not infrequently
found. Uric acid is increased.' The tongue is covered with a thick
creamy fur. There is anorexia and great thirst, the bowels are usually
constipated and the fgeces are dry.
The large joints are usually involved first. The joint involvement is
remarkably symmetrical : thus one ankle joint swells, and as soon as this
subsides its fellow is immediately attacked, and the affection travels rapidly
from one joint to another in a symmetrical course. There is little oedema,
pitting or cuticular desquamation after the acute symptoms have subsided,
except in the very weak and feeble. As a rule, one joint remains swollen,
for three or four days, while others are being successively involved. By
the seventh or eighth day half a dozen articulations may be involved. The
hip-, finger- and toe-joints, the spinal articulations, and the symphysis
pubis are ral-ely involved. Not infrequently sudamina, herpes urticaria,
and miliaria accompany the articular symptoms.
There is usually little mental distui-bance ; but when the temperature
reaches 105° F. there is often great restlessness, insomnia, and a mild wan-
dering delirium. I regard this delirium (when not occurring in drunk-
ards) as indicative of extensive blood changes and a sign of great danger.
One of the characteristics of rheumatic fever is the intense auaemia devel-
oped in a few days after its onset, even when no antiphlogistic remedies
have been employed. Auscultation of the heart reveals ''blowing " hsemic
murmurs, even when no cardiac complications exist. The articular symp-
toms often subside suddenly, and cardiac or cerebral symptoms as suddenly
make their appearance. Cerebral symptoms are always attended by high
temperature. The cerebral and cardiac phenomena are not due to a metas-
tasis in the strict sense of the term, nor yet are they complications. There
is some bond of connection between these cerebral and heart lesions and
the joint affections, — the exact nature of the connection is not known. The
fibrous tissue of the heart is as liable to be involved as the joints ; and in
many young subjects the heart involvement precedes that of the joints.
Differential Diagnosis.— ^The connection between gout and rheumatism is
considered under the head of gout.
Pycemia may be mistaken for rheumatic fever ; but the recurring chills,
sickly, siveet breath, slow development, jaundiced skin, previous history,
and finally the presence of infarctions, multiple abscesses and thrombi are
sufficient to distinguish pygemia from rheumatic fever. Suppurative syno-
vitis may occur in pyaemia, but not in acute rheumatism.
JVow-rheumatic arthritis is to be distinguished by its persistence in one
joint, by the absence of the characteristic sweats, by the graver local and
more trivial constitutional symptoms, and by the absence of cardiac com-
plications.
Prognosis. — Apart from the complications, acute polyarticular rheumatism
is 7iot a fatal disease ; three per cent, is its average death rate. The disease
lasts from three to four days in one joint ; the whole duration of the fever
and attendant arthritis is from three weeks to thirty days. The rule is that
' Parkes and Garrod, respectively, found thirteen and eleven and one-half grains in a quart of urine.
ACUTE ARTICULAR RHEUMATISM. 8G1
no crippling of the joints follows the acute attack. If the course of the dis-
ease is prolonged, complications are usually present ; in many cases its course
is erratic in that just as convalescence is apparently established all the acute
symptoms reappear. It runs no cyclical course, — there is no definite limit
to its duration ; patients may recover in two or three days or a week, or it
may persist for a month or longer ; generally the milder the attack the
shorter its duration. I have seen six or seven weeks elapse before the joints
have returned to their normal state ; in such cases all the joints become
involved in succession and the articular phenomena are persistent. The
more robust the individual the sooner is convalescence established. Some-
times the fever subsides and the joint affections persist.
. The frequent occurrence of endo- and pericarditis leaves little doubt as to
their intimate connection with the rheumatism. The younger the subject
the more liable are the cardiac affections to occur. Statistics are most di-
verse on this point ; some say five, others seventy-five per cent, of all cases
of rheumatic fever are accompanied by cardiac inflammations. Endarteri-
tis, pleurisy, pneumonia, cerebral and spinal meningitis, laryngitis, bron-
chitis and peritonitis are its principal complications. A strange sequel of
rheumatic fever is chorea.
Another, graver, sequel is ulcerative endocarditis. Instead of comiDlete
recovery acute rheumatism may become subacute or chronic. Muscular
rheumatism frequently follows an attack of acute articular rheumatism.
The worst legacy acute rheumatism leaves is a crippled valvular apparatus
in the heart. ^
Treatment. — The hygienic surroundings of rheumatic patients should be
yery carefully attended to. The temperature of the apartment should range
from 68° to 70° F. ; all draughts should be avoided, and the patient should
be clothed in flannel and covered with flannel sheets. The diet should be
milk and seltzer- water. If this is not well borne, concentrated food, other
than animal, can be given. Animal food and alcoholic stimulants are con-
traindicated during the active period, of the disease. As soon as the fever
declines, nutritious and easily digested animal fOod may be freely given.
Only a few of the many external applications which have been made to
the affected joints will be referred to. Cold by the means of ice-bags to
the joints has been strongly recommended. Friction, with chloroform or
opium in glycerine combined with alkalies and the tincture of aconite is a
favorite plan with some. ''Hot-packs" by means of flannel compresses
wrung out in water as hot as the patient can bear, or bathing the joints in
warm laudanum and then covering them with oiled silk is always grateful
to the patient. Wunderlich and Niemeyer advocate, respectively, ethyl
chloride and ether to be rubbed over the affected joints. The " blister
plan," which consists in surrounding all the affected joints with fly blisters,
temporarily relieves the pain, but the rheumatic attack is not shortened,
nor do they afford any permanent benefit. My experience leads me to the
' Two casesof acute rheumatism wore recently (July 31st, ]882) reported by Mayer in "Henoch's Klinilc,"
where peculiar and piKnificunt complications were observed. The patients were children ; and both had
little. tnm/>rs develop about the joints (malleoli, elbo\v, etc.), that on section, after death, proved to be con-
nective-tissue neoplasms which had a tendency to necrobiosis or to osseous-like change.
862 CHRONIC GENERAL DISEASES.
opinion that if the affected joints are protected from changes of tempera-
ture by cotton batting and oiled silk, all is accomplished that can be by
local applications.
Internal Medication. — Innumerable remedies have been brought to the
notice of the profession as specifics in the treatment of rheumatism, yet it
is still the most unmanageable of all diseases. Garrod is of the opinion
that colored water is about as potent as anything. He claims that rheu-
matic fever is a " self-limiting disease," sometimes running a long, some-
times a short course. Bleeding, mercury, and antimony and mercury are
no longer employed. Some advocate the use of iodide of potassium ; some
colchicum, some veratria, some guaiacum, and some quinine. Garrod's
" quino-alkaline " plan, which combines quinine with the alkaline treat-
ment, is a favorite method with many. It is claimed that the so-called
alkaline treatment shortens its duration and diminishes the frequency of
cardiac complications. It consists in the administration of the soda salts
in from 3v to 3x daily until the urine becomes alkaline.
My experience inclines me to the opinion that while alkalies in the early
stages relieve the pain in the Joints, they do not shorten the duration of
acute rheumatism, and if long continued they do positive harm.' The
tincture of the chloride of iron, in one-half drachm doses, is especially ser-
viceable as soon as the temperature reaches 100° F. Within the past few
years salicin, salicylate of soda, and salicylic acid have been very exten-
sively employed. It is claimed that immediate relief follows the adminis-
tration of the salicylates — that the temperature falls, that the pain and
swelling of the joints subside, and that the duration of severe attacks has
been limited to thirty-six or forty-eight hours. But it causes great depres-
sion of the heart, increases the liability to cardiac complications, causes
irritability of the stomach, and places the patient in a weak and debilitated
state ; for the past year I have seldom employed it, for my experience
shosvs that while in some cases it may relieve the urgent symptoms of the
disease in two or three days, relapses are almost certain to follow, and the
duration of the disease is not shortened, and I have seen very serious toxic
effects follow its use. Benzoic acid and benzoate of soda are claimed by
some to act more efficiently than salicylic acid and to be less harmful. I
have not seen any good results follow their use.
My plan of treatment in a severe articular rheumatism, after regulating
the hygienic surroundings and the diet as already indicated, is to render
the urine neutral by the free administration of the carbonate of potash or
soda, and to administer regularly every six hours, sufficient morphia hypo-
dermically to relieve pain and to keep the patient comfortable. If this
plan is judiciously followed until the acute rheumatic symptoms subside,
and the patient then placed on iron and cod-liver oil, I am confident it
will recommend itself to every unprejudiced observer. The treatment of
the various complications is considered under their appropriate heads.
1 Gull, Sutton, and Lebert found marked diminution in the duration of rheumatism from steady
administration of lemon juice.
OHEOSriC ARTICULAR EHEUMATI8M. 863
SUB-ACUTE RHEUMATISM.
Sub-acute rheumatism is usually a sequela of acute, or occurs in one who
has at some time had an acute attack ; it is attended by slight if any fever ;
the pain in the joints is not severe, except on motion ; and the swelling and
redness are not excessive, and are limited to one or two joints, usually the
large ones. There is no tendency to disorganization or permanent crip-
pling of the affected joints ; and although it may last six or seven weeks,
or three or four months, the joints usually return to their normal condi-
tion. The blood changes are the same as in acute. The articular symjD-
toms are less metastatic than in acute ; angemia is always well-marked, and
cardiac complications are not infrequent.' The treatment is a milk diet,
iron and cod-liver oil, and a warm climate, and heat to the affected joints.
The so-called anti-stimulants have failed in my hands to relieve or cure.
CHRONIC ARTICULAR RHEUMATISM.
Chronic articular rheumatism usually involves only a few joints ; it oc-
curs most frequently in those who have had rheumatic fever in early life.
Although it may be of long duration it rarely induces extensive changes in
the joints.
Morbid Anatomy. — The parts affected are the iibrous tissue around the
joints, the fibrous envelopes of the nerves, the aponeurotic sheatlis of the
muscles, the fasciae, and the periosteum. The synovial membrane is thick-
ened, the fringe-like processes are hypertrophied and very vascular, and
the synovial fluid becomes turbid and cloudy. The ligaments are thick-
ened, the cartilages relaxed, shaggy, and sometimes in a state of fatty de-
generation. The more protracted the disease the greater the thickening of
the peri-articular structures, and the thicker and scantier will be the fluid
in the joint. The fibrous tissue developed about the joints causes more or
less stiffness and loss of motion, but not ankylosis.
Etiology. — It is a disease of adult and advanced life, occurring oftenest
in those whose hygienic surroundings are bad, and who are exposed to wet,
cold, or sudden changes of temperature. A residence in dark and damp
dwellings predisposes to it. Previous attacks of acute articular rheuma-
tism develop a tendency to chronic rheumatism. It is often hereditary, and
then there may be no appreciable exciting cause to its development. Both
sexes are equally liable.
Symptoms. — There is aching and constant pain in some one or more of
the larger joints, usually the knee or ankle, but sometimes those of the
upper extremities. The affected joints are tender and slightly swollen, and
their movements are constrained. No fever is present. The aching and
deep-seated pains are often worse at night. When it is the result of expos-
ure, heat will- give a grateful sense of relief ; when a rheumatic diathesis
exists, the heat' of the warm bed-clothes increases the pain, and relief is
I Barwell, who calls this disease " Sub-acute Eheumatic Synovitis," says it may lead to hydrops articuli.
—Diseases of the Joints, 1881, p. 138, et neq.
8b4 CHRONIC GENERAL DISEASES.
often obtained by exposure of the joint to dry cold. Old people with rheu-
matic Joints are great "weather prophets," often being able to foretell the
coming of a storm. After rest, motion gives great pain, but use renders
the joint temporarily more supple and less painful. The pains undergo
exacerbations and remissions, and the disease may continue for years with-
out causing much deformity or great crippling of the joints. The muscles
near the joint usually undergo more or less atrophy, and as a result the af-
fected joints appear larger than they really are.
Palpation may reveal fluctuation in the joint, and auscultation gives a
rough, grating crepitus during motion.
Differential Diagnosis. — Chronic articular rheumatism may be distin-
guished from arthritis deformans by the absence of deformity of the af-
fected joints, the history of previous acute rheumatic attacks, the large
joints being mainly involved, the partial or complete recovery during warm
weather, and its return on exposure to wet and cold ; arthritis deformans
is a steadily progressive disease, one joint after another being involved and
never recovered from.
Prognosis.— There is little chance of complete recovery after middle life ;
it is only possible in those cases treated at the onset under favorable
hygienic conditions. In long-standing cases, wasting of the muscles may
lead to great crippling of the joint. Muscular rheumatism is a frequent
accompaniment of articular. Chronic rheumatism never affects the dura-
tion of life, except as it may deprive the patient of exercise and sleep, and
thus interfere with nutrition.
Treatment. — This form of rheumatism is benefited mostly by local treat-
ment, such as blisters, iodine, belladonna, aconite, opium, and chloroform
liniments, veratrum ointment, etc., etc. Most rheumatic patients have
their favorite prescriptions for local use, which they claim afford them
almost instant relief. If there is but little pain in the joints, ammonia
and turpentine liniments are of service. Thick flannels should always be
worn about the joints. Some advocate, for both pain and stiffness, spong-
ing the joints with hot water. The Galvanic or Faradic current will tem-
porarily reduce the swelling and pain, and sometimes improves the mobility
of the joint. Local or general baths form an essential part in the treat-
ment of this form of rheumatism. Hot air, or vapor baths are not so
efficacious as hot water. Many of the hot saline springs for bathing have
acquired a great reputation in the treatment of this form of rheumatism,
cures being effected in cases that had resisted all other methods of treat-
ment.' Massage and rubbing are always beneficial ; and undoubtedly
much of the good that is claimed for certain liniments is due to the rub-
bing and manipulation of the joints during their application.
Internally, tonics should be employed, such as iron, quinine, strychnine,
etc. Cod-liver oil is the most useful of all internal remedies, and should
be administered continually. All the means for improving the general
health of the patient should be carefully considered, and if possible he
1 Those which I have found most efficacious in this country are the Hot Springs of Arkansas, the Vir-
ginia Hot Springs, and the Richfield Springs in New York State.
ARTHEITIS DEFORMANS. 865
should reside in a dry, warm climate. Colchicum, arsenic, iodide of po-
tassium, and guaiacum have gained reputation in its treatment, as have
also the turpentine and cajeput oils combined with sulphur ; but I have
been unable to find sufficient proofs of their beneficial effects to strongly
recommend their use. Recently, Rawson advises guarana, and Heller
liquor ammonii.*
The diet must be highly nutritious and absolutely non-stimulating ; I
am convinced that errors in diet and ''fits of indigestion" prolong, and
are powerful to develop this disease. Exercise is important, and if pos-
sible a sea voyage in a warm climate should be taken.
ARTHRITIS DEFORMAlSrS.
{Bheumatoid Arthritis.)
Arthritis deformans is a chronic inflammation of the synovial capsule,
the ligaments and tissues of the joint, unattended by suppuration and with
little fluid accumulation in the articular cavity.
Morbid Anatomy, — The synovial membrane and articular cartilages are
first involved. The fringes of the former are increased in number, and
are very vascular : they are called "the destructive vegetations" of the
synovial membrane. The central portion of the articular cartilages be-
comes roughened or villous, gets gradually worn down, and finally disap-
pears, and the bones thus laid bare undergo eburnation. The ivory-like
surfaces are striated, the strise running in the direction of the articular
movements.^ While the central portion of the cartilage is disappearing,
its margin forms nodular irregular outgrowths. The synovial fringes take
part in the hypertrophic processes, and form pyriform excrescences, which,
after a time, become converted into fibrous tissue. These outgrowths in
some cases blend with the osseous structure of the epiphysis, and in others
become detached and are free. Lateral expansion of the joint surfaces
with enlargement of the ends of the bones takes place and leads to de-
formity, dislocation, and immobility. All the joints may, in course, be
involved, especially those of the hands and feet. The thickened ligaments
sometimes undergo partial cartilaginous, osseous, or fatty degeneration.
The tendons are sometimes thinned and ossified. The fluid in the joint
cavity is thick, turbid and yellow, and alkaline in reaction. There are no
blood changes ; no urates are found in the joints. The adjacent muscles
undergo atrophy.
Etiology. — This disease is regarded by some as a peculiar form of chronic
rheumatism, while others regard it as an essentially different disease. It
may occur at any age ; but the tendency to it increases with advancing
years. Women are more liable to it than men. The smaller joints are
most often involved in women ; the larger in men. It is very rare in dry,
hot climates. Damp dwellings, poor food, and mental depression are
' Wien. Med. Presse, Dec, 1875.
* Charcot calls ebumatiou a " sclerosis of bone, accompanied by vascularization of the deep parts."
55
866
CHEONIC GENERAL DISEASES.
powerful predisposing causes. Thin people suffer oftener than the cor-
pulent. It is met with of tenest in the poorer classes. '
Symptoms. — The symptoms of arthritis deformans are all referable to
the changes which occur in the joints. It may come on insidiously, neu-
ralgic pains sometimes preceding stiffness and deformity. As the soft
parts atrophy, the joints stand out distorted and rigid from the flabby mus-
cular surroundings. There are usually severe inflammatory symptoms,
the joints are only slightly tender to pressure, but motion always gives
pain. Months and years may elapse before the articular changes are
completed ; but once started, they are progressive, until the joint is anky-
losed or deformed.^ The immobility of the joints depends upon the
osteophytes or fibro-cartilaginous transformation of the synovial mem-
brane or fibrous union of the surfaces of the bared bone.
In some cases the disease begins with all the signs of rheumatic fever,
with inflammatory symptoms of a mild
type. No cardiac signs are present,
and no excess of uric acid can be
found in the Uood. The acute symp-
toms gradually subside, leaving the
joint irreparably crippled. The small
joints are usually first involved. The
metacarpo-phalangeal articulations of
the index and middle fingers are
usually first attacked. In forty-five
cases, the smaller joints of the hands
and feet alone were involved in twenty-
five ; the great toe in four ; the hands
and feet with a large joint in seven ;
the large joint first, then the fingers in
nine. After a time large joints, the
temporo-maxillary articulation, or the
articular "processes of the vertebrae,
especially the cervical, become involved.
The hip, shoulder, elbow, knee, and
hands are its favorite sites. In many
joints abnormal mobility is developed,
i. e., the hip may slip up and down in
its socket. Subluxations are common,
in the fingers especially.
Early in the disease a friction crepi-
tus is heard as the articular surfaces
are rubbed upon each other, which becomes coarser as the disease ad-
vances. There are painful spasms of the muscles in the affected limb,
more marked at night and just before a storm. When the disease is local-
1 Charcot advocates a nervous origin, especially when it begins in the smaller joints. Barwell regards
it as due to colitis, originating in " some constitutional cachexia," which, in some of its tendencies, re-
eembles the rlieumatic diathesis.
^ Kemak believes that the painful swellings on either side of the Joint are " neurotic nodes,"
Fig. 180.
Deformity from Articular Rheumatism.
ARTHRITIS DEFORMAiTS. 8G7
ized in the hip joint, it has been called "morbus coxge senilis." In such
cases the limb is shortened and the patient limps. The greatest variety of
deformity takes place in the hands of those who have been long the sub-
jects of this disease. The constitutional disturbance is never commensur-
ate with the local signs. The skin becomes dry and harsh ; there is great
acidity of the stomach, cold extremities and a condition of extreme anse-
mia.*
Differential Diagnosis. — Arthritis deformans may be mistaken for chronic
articular rheumatism without deformity, and chronic gout.
Gout is hereditary, and occurs more in males. Arthritis deformans is
rarely hereditary, and occurs oftenest in females. Attacks of gout are
periodic, and the small joints are found involved. Arthritis is progressive,
and the large joints are generally first attacked. Kidney complications are
common in gout and rare in arthritis. Chalk-stones develop in the joints in
gout and are never present in arthritis. Uric acid is always in excess in
gout, and never in arthritis ; deformities and ankyloses are less marked and
extensive in gout than in arthritis.
Prognosis. — Arthritis deformans never destroys life, and is never recovered
from ; patients with this disease may attain very old age. The greater
the number of joints involved the more deplorable will become the condi-
tion of the patient. There is rarely complete ankylosis. When false joints
form there is a possibility that such patients may walk or move about with
comfort.'^
Treatment. — Treatment of this disease is very unsatisfactory ; for the
most part we must trust to local measures for relief, and to such constitu-
tional measures as shall improve the general health. Quinine, iron, cod-
liver oil, arsenic and strychnia are indicated. The diet should be nutri-
tious and easily digestible. Alcoholic stimulants, if they improve nutrition,
are of service. Change of climate and habits of life is often followed by
an arrest in its progress. Flannels should always be worn next the skin.
Mineral waters and warm salme baths, either artificial or natural, often
temporarily arrest its progress and relieve the pain in the joints. The
preparations of indi^ie and the acute rheumatism and gout remedies have
seemed to me to do more harm than good. Local frictions with iodine,
mercury, and iodoform sometimes relieve. If the pain is so severe as to pre-
vent sleep, it must be relieved by anodynes. Great care must be exercised
in their use that the patient does not become addicted to them. The con-
stant or Faradic current may be cautiously tried ; in many cases it is of
great benefit.' The parts should be moved as much as possible if the
joints are not painful. In the so-called acute attacks rest is necessary ;
and then leeches and blisters to the joints are indicated.
'The orly vrlnary change is diminution in the amount of phosphoric acid by nearly fifty per cent.—
{Drachnuinn.)
2 Charcot describes numerous cases complicated by asthma, megrim, cystitis, and such skin diseases as
eczema, Tiummnlar psoriasis, lichen, and arthritic prurigo ; but these complications are the result of the
long confinement and inability to excercise, rather than necessary sequelae.
* Bemak and AUhaua.
868 CHRONIC GENERAL DISEASES.
MTJSCULAE RHEUMATISM.
{Myalgia.)
Muscular rheumatism is a rheumatic affection of the voluntary muscles,
the fasciae, periosteum, and other fibrous structures, accompanied by pain
and tenderness, but by no other evidences of inflammation. It has been
named according to its seat, torticollis (wry-neck), cephalalgia, pleurodynia,
lumbago, etc., etc'
Morbid Anatomy. — The negative results of autopsies lead to the conclu-
sion that there are no constant anatomical lesions, except those due to
transient hypersemia, or to scanty serous exudations into the mugcles. In
a few cases there is evidence of inflammation of the fibrous sheath of the
muscles and of muscle-degeneration. Thickenings and adhesions of the
neurilemma of the nerves supplying muscles that have long been subject
to chronic rheumatism have been found.
Etiology. — Muscular rheumatism is not uncommon in the children of
the gouty or rheumatic. It is often intimately associated with articular
rheumatism, which sometimes precedes, sometimes follows it. Exposures
to cold and damp draughts are often the exciting causes of an attack, es-
pecially after the muscles have been over-fatigued. Sudden straining of
a muscle may induce it. It often seems to have a malarial origin. It may
come on suddenly in a rheumatic or gouty subject without any appreciable
exciting cause.
Symptoms. — An attack usually comes on suddenly with severe, deep-seated
pain in the group of muscles affected. The pain is of a stretching or tearing
character, increased by movement or pressure ; it is always more severe at
night, and remits or disappears during the day. It may be migrating or
remain fixed in certain muscles or fasciae. It is usually acute when the
muscle is in action, and dull when the parts are at rest. Certain positions
mitigate the pain. In many instances it will wholly disappear in a few mo-
ments, and the sufferer, who perhaps has been for hours enduring excrucia-
ting cramp-like pain, feels a sudden sense of relief. Such attacks are fol-
lowed by lassitude.
Lumbago, pleurodynia, and wry-nech are the most common forms.
Lumbago, or rheumatism of the muscles on either side of the lumbar
spine, usually is the result of straining the lumbar muscles, or sitting on
the damp ground, or is excited by a current of air across the back. The
patient is unable to bend backward or forward ; if the pain comes on while
he is in a sitting posture, he is compelled to walk with the body bent at
the hips. Lumbago comes on very suddenly, and the pains are more in-
tense than in any other form.
Intercostal rheumatism, ox pleurodynia, is attended by many of the symp-
toms of acute pleurisy. There is pain in the side, which is increased by
1 These different varieties are grouped by some in the list of the symptoms of chronic rheumatism;
others regard them as neuralgias.
MUSCULAE RHEUMATISM. 869
every respiratory movement ; the sufferer leans to the affected side. Cough-
ing, sneezing and defecation render the pain more intense.
In wry-nech the muscles on one side of the nape of the neck are involved.
The patient holds his head toward the muscles that are affected, so as to
relax them, and, in attempting to turn his liead, turns his whole body like
a pivot.
If the frontal, occipital, or temporal muscles are involved, it is termed
rheumatic cephalalgia.
If the abdominal muscles are involved, it is termed abdominal rheumO'
tism. In all cases there is ^am and rigidity of the muscles or groups of
muscles involved, accompanied by a fixed position. There is no fever or
constitutional symptoms.
Differential Diagnosis. — Lumbago may be mistaken for renal colic.
In renal colic there is no tenderness on either side of the lumbar spine,
which is always present in lumbago. The position of the patient is not
fixed as in lumbago. In renal colic the pain radiates along the ureter, to
the end of the penis, and is often accompanied by retraction of the testicle
on the .^^ected side. The urine is diminished during, and copious and
bloody after, the attack.
An examination per vaginam will decide between uterine disease and
lumbago.
Lumbago may be distinguished from disease of the spine by the fact that
in the latter affection pressure on the ends of the spines will produce pain,
while lateral pressure gives negative results ; in rheumatism of the muscles
the reverse is the case.
Pleurodynia may be mistaken for pleurisy and intercostal neuralgia.
Pleurisy is accompanied by fever, increased pulse-rate, cough and — on
physical examination — by physical signs of pleurisy. None of these condi-
tions are present in pleurodynia. In intercostal neuralgia there are three
(diagnostic) points of tenderness : at the exit of the nerve from the spine ;
at its termination near the sternum; and midway between these points, while
there is no tenderness over the muscles. In pleurodynia these points of
tenderness are absent, and the intercostal muscles are tender.
Abdominal rheumatism may be mistaken for peritonitis ; but in perito-
nitis there will be fever, increased pulse-rate, and well-marked constitu-
tional symptoms which are absent in abdominal rheumatism. In the lat-
ter, deep, firm pressure affords relief.
Trichinosis is accompanied by symptoms that resemble those of muscular
rheumatism ; but the history of the case, the oedema of the feet, and a
microscopical examination of a portion of the muscle, will decide the diag-
nosis.
Prognosis. — No danger attends this form of rheumatism. An acute at-
tack may last a few hours or days. If it become chronic, the muscular
pains may last for months. Wry-neck is the mildest and lumbago the se-
verest variety. One attack generally favors the occurrence of a second.
Treatment. — In the young, if there is an hereditary tendency to rheuma-
tism, cod-liver oil acts as a prophylactic. At the commencement of an at-
870 • CHEONIC GENERAL DISEASES.
tack a hot-air or Turkish bath will be of service. Guaiacum, sulphur and
arsenic are the favorite drugs in chronic cases. Quinine is almost a specific
in the malarial form. In vigorous persons subject to muscular rheumatism
the surface should be warmly covered with flannel, and the individual should
accustom himself to a morning rub-down with a dry, coarse towel after
a cold sponging. The bromides are useful in some cases.
In lumbago hot anodyne fomentations and anodyne liniments will often
give relief if vigorously applied. Hypodermics of morphia may be given
for temporary relief. These patients should remain quiet in the position
that gives them most relief.
In intercostal neuralgia, cupping, blisters, and hot poultices will often
relieve. But in severe cases hypodermics of morphia must be resorted
to.
In wry-neck, the cervical region should be swathed in warm flannel.
Gentle traction likewise aids in this. The constant and Faradic currents
may be passed alternately through the affected muscle. Showering with
water as hot as can be borne is very efficacious in some cases. Acupunc-
ture affords relief in many instances. Veratria and aconite are often used
in ointments. Manipulation by a skilled ''rubber" is one of the most
efficient means of local treatment. If angemia is present chalybeate waters
and tonics are indicated.
GOUT.
Gout is a constitutional disease of mal-nutritiou, characterized by an
excess of uric acid in the blood and the deposit of urates in the cartilages
and fibrous structures of Joints and throughout the bodv. The constitu-
tional condition is generally described as the "gouty diathesis,'- ^lith^mia •
and the term gout is applied only to the phenomena,, which may be either
acute or chronic, attendant upon the elimination of the urates and their
deposition in the joints. '
Morbid Anatomy.— The primary changes, so far as we are able to appre-
ciate them, are in the blood and consist in an excess of uric acid.' In just
what way the nutritive processes are at fault, and whether the urates found
in the blood are there as the result of an excess or a deficiency of activity,
are points as yet undetermined. In acute gout this excess occurs only just
previous to, and during the paroxysm, when the proportion of urates may
reach 1-20,000 or even 1-6,000, and the corpuscular elements are un-
changed, but in chronic gout it is permanent though in much smaller ra-
tio, and is accompanied by anaemia. Traces of oxalic acid are occasionally
found in the blood, and there is always decrease of alkalinity and increase
of the fibrin-factors.
Although the blood change is the essential one, the articular are the
more manifest and characteristic, and consist in the deposit of the urates in
» It has received the names of podagra, chiragra, gonagra and arthritis according as it affects the foot,
hand, knee, or several joints.
2 The precise combination in which uric acid occurs in the blood is undetermined. It is probably
*ither as the acid or neutral urate of soda.
GOUT.
871
the Joints with the attendant inflammatory and ulcerative processes. The
primary deposit occurs in the cartilage capsule and cells at the point of
least vitality and most remote from vascular supply, and gradually in sub-
sequent attacks invades the cartilage, periosteum, synovial fringes, and
fibrous tissues of and about the joint,
where it is found between the connec-
tive-tissue fibres. This deposit con-
sists principally of the urate of soda
in the form of minute needle-shaped
crystals, but to the unaided eye ap-
pears amorphous ; chloride of sodium,
urates of lime, magnesia or ammonia,
hippuric acid and phosphate or car-
bonate of lime are present in small
proportion. In the earlier stages the
articular surfaces are slightly granular
in appearance, with a thin amorphous
incrustation. But as the acute attacks
are repeated, or in the later stages of
chronic gout, the incrustation in-
creases, the surfaces are decidedly
roughened ; gradually erosions occur
from epithelial degeneration and attri-
tion, and all the adjacent structures
are infiltrated and covered with a thick
deposit of urates. The articular
changes may go on to entire destruc-
tion of the cartilages and articular surfaces, while the extra-articular de-
posits form large concretions or topM. These may induce ulcerative and
suppurative processes until they finally protrude through the skin, are dis-
charged from abscesses, or produce fibrous and osseous ankylosis. The
veins about the joint become dilated, varicosed, and filled with thrombi
which may at any time cause embolism. All these changes are gradual in
their development, but each attack of gout, even the first, leaves its per-
manent mark in the affected joint. Aside from the acute attack, inflam-
matory processes of a low grade are eventually engendered by the irritation
of the deposits, and molecular changes enter as an element in the destruc-
tive processes, or the inflammation may result in the production of ecchon-
drosis.
The small joints of the body are most frequently affected, and of these
the metatarso-phalangeal articulation of the great toe is so unquestionably
first as to render it the classical seat of acute gout. In order of frequency
after this are the joints of the fingers, knee, elbow, hip, and shoulder.
Other joints are but rarely affected. But all the cartilages and fibrous
tissues throughout the bodv as well as those of the joints may be the seat
of gouty manifestations. Tophi are frequently found in the cartilages of
tne ear, nose, or eyelids, and are then of the highest clinical significance.
Fig. 181.
Section of a Gouty Cartilage.
A. Articular smface.
B. Nominal Caitilage.
C Crystals of urate of soda in the stroma.
D. Dense deposit of urates, x 300.
873
CHROKIC GE]S"EEAL DISEASES.
They may be present also in the larynx, sclerotic, tendons of the hands,
and even on the spinal dura or outer coat of the arterial sheaths.
The most important visceral lesions are found in the kidney, and consist
in a similar deposit of urates and subsequent cirrhotic changes. The
primary deposits here are probably in the tubules and their epithelium,
and the interstitial deposits and fibrous changes are secondary. The
kidney presents a granular appearance,
and on section the fine strise of urates
may be seen throughout the tubular
structures. More abundant deposits
may aggregate in the pelvis as calculi
and incite pyelitis. The heart is event-
ually hypertrophied and may present
signs of fatty degeneration, while the
arteries present varying stages of athe-
roma from the primary fibroid changes
to distinct calcareous deposits. Fibroid
and cirrhotic changes also occur in the
liver and stomach, and finally uric acid
is present in both the normal and patho-
logical fluids found in the body.
Etiology. — The exact nature of those
changes which result in the gouty
diathesis is still undetermined, but cer-
tain etiological relations are quite clearly
established. Gout is pre-eminently a
disease of middle life, and although it can be developed in any constitution,
heredity can be traced in fully sixty per cent, of cases, and almost in-
variably so when it is present in children or early adult life.
Clinical experience proves that the direct exciting cause is the product
of the following factors in varying proportions. — First. An excess of nitro-
genized material in the system from over-eating and the use of alcohol.
Excess as applied to eating is a relative term, and in certain constitutions
an amount of food, which in others would be very moderate, may so exceed
the demands of the system as to be the cause of gout. Of alcoholic
beverages the sweet wines and malt liquors are considered more gouty than
spirits.
Second. Deficient or suddenly arrested oxidation. Lack of exercise and
its consequent abundant supply of oxygen are the most frequent causes
of such deficiency of oxidation, but it is also probable that the con-
stitutional and hereditary tendency exerts a powerful influence over the
assimilative function, and that impaired nervous energy may be the ulti-
mate cause of defective oxidation.
Third. Failure in the excretive power of the kidney. Such failure may
result either from deficiency of the eliminative power of the renal epithe-
lium or mechanically from obstruction of the tubules by deposits of urates,
and is the prime factor in producing the acute gouty attack. In a system
Fig. 182.
Vertical Section of a Malpighian Pyramid in
Gouty Nephritis.
Thestrice, consisting of urates, folloio the general
course of the tubules. Much of the deposit has
been ivashed out of the siJecimeii in hardening.
X 30.
GOUT. 873
already laden with urates, a few glasses of wine, a fit of dyspepsia, ex-
posure, severe mental effort, or a fit of anger may be sufficient to bring on
an attack of gout.
Symptoms. — Gout may be either acute or chronic, and appear as *' regu-
lar" in the joints, or as irregular, misplaced, retrocedent or anomalous
gout in the non-articular structures and the internal organs.
In most cases of acute gout premonitory symptoms precede the first
paroxsym ; there will be a history of occasional pains in one or both great toe-
joints, a feeling of malaise with sleeplessness, constipation, dyspepsia, and
perhaps pain in the side, a dry, hot skin, scaly eruptions and scanty urine.
Sometimes an attack is preceded by a peculiar sense of well-being, even ex-
citation ; at others by great anxiety, irritability, and depression of spirits.
Asthmatic symptoms often precede the outbreak of an attack. Usually
between midnight and four or five in the morning the individual wakes
with a burning, throbbing pain in the ball of the great toe, which the
slightest pressure greatly intensifies.
The affected joint becomes red, swollen, hot and shining ; the veins are
distended, and it resembles a joint about to suppurate. There is some fe-
brile movement which varies in intensity with the number of joints affected.
The temperature may in a severe attack reach 105° P. The pulse is full
and bounding but compressible. As the fever comes on the pain in the af-
fected joint is so great that the patient cannot move it; he becomes restless,
tossing for hours, until finally, in a profuse perspiration, he falls asleep. In
a few hours he awakes refreshed and comparatively free from pain ; but the
affected joint is swollen, tense, and vividly red. He continues comfortable
during the day,. but about the same hour the next night there is a recurrence
of the local pain and the fever, which is followed by another remission the
following morning.
These nocturnal exacerbations and morning remissions continue with
about the same severity for two or three days, then the maximum of pain
is reached. At the end of a week they have gradually subsided ; the af-
fected joint remains tender and swollen for a week or two longer. This
swelling is due to oedema, and pits on pressure, and as it disappears des-
quamation occurs. Following the attack, there is a feeling of well being
which has led to the popular belief that an attack of gout is beneficial.
There is usually marked digestive derangement during an attack, with
anorexia, a thickly furred tongue, and constipation. The urine is scanty,
high colored, and contains less uric acid than normal, dejiositing on cool-
ing a copious sediment. The bladder is irritable, and there is a scald-
ing sensation on urination. Intense cramps in the muscles adjacent to
the affected joint may occur. Occasionally during the first attack both
great toe joints are involved ; and instead of disappearing at the end of a
week, successive outbreaks occur in the other joints.
An individual may have only a single attack ; but usually a second su-
pervenes within a year. Gradually the attacks approach each other, and
are more prolonged though less severe, until a condition of chronic gout is
reached. In the second and third attacks the joint formerly involved, or
874
CHEONIC GENERAL DISEASES.
its fellow of the opposite side, presents the same phenomena as in the
primary attack.
Although all gout is strictly speaking chronic, by chronic gout is
understood those gouty manifestations which are developed as the parox-
ysms coalesce, and the patient is scarcely ever free from some gouty mani-
festation. Tophi form around the
affected parts, and the joints be-
come so distorted or crippled that
walking becomes difficult. Grad-
ually the health deteriorates, and
feebleness and a gouty cachexia be-
come marked and visceral derange-
ments become prominent. When
chronic gout follows acute, the ar-
ticular phenomena are always prom-
inent. But when, as not infre-
quently happens, gout is chronic
from the onset, tophi form early
without acute inflammatory symp-
toms, and the visceral affections are
prominent. In chronic gout the
urine is greater in amount, lighter
in color, of lower specific gravity,
and contains less uric acid than nor-
mal. In a few cases casts and al-
bumen make their appearance.
Misplaced gout — gout that has re-
troceded from a joint to an inter-
nal organ, also called visceral, masked, internal and metastatic gout —
may attack any organ and result in a long series of functional disturb-
ances.
The sequel* and complications of gout are numerous. Those referable
to the nervous system are vertigo, neuralgia, headache, stupor, convulsions,
delirium, apoplexy and lunacy. * Those referable to the vascular system are
arterial degeneration, angina pectoris, cardiac palpitation, and valvular dis-
ease. Those referable to the lungs are asthma, which alternates very
often with the articular phenomena of gout, and bronchitis, which some
regard as the commonest manifestation of gout, after arthritis. Eefer-
able to the digestive tract is a long list of gastro-intestinal catarrhs, cir-
rhoses of the liver, jaundice, and cirrhotic kidney.
Differential Diag^nosis. — Grout is generally easy of diagnosis. It may,
however, be mistaken for rheumatism.
Gout attacks the small and rheumatism the large joints. A rheumatic
attack is of longer duration than a gouty paroxysm, and has no perio-
dicity. In gout the fever is slight, 102° to 103° F., and is in inverse ratio
to the number and size of the joints involved ; in rheumatism there is usu-
i These are regarded by some observers as evidences of cerebral gout. — Garrod, Todd, Trousseau.
Fig. 183.
Deformity from Gout.
GOUT. 875
ally a higher range of temperature. Cutaneous affections are common m
gout and rare in rheumatism. The heart is frequently involved in acute
rheumatism, and rarely in gout. The gouty attack coming on at night m
the great toe joint is in marked contrast to the onset of rheumatic fever.
Acute articular rheumatism is a disease of early adult life, while gout is
rare before thirty-five. In gout there is a history of high living, or an
hereditary predisposition ; m rheumatism there will be a history of expos-
ure or exhaustion. In gout there is an excess of uric acid in the blood ;
this is never the case in rheumatism. When we are enabled by the mi-
croscope to see uric acid crystals derived from serum of a patient with an
arthritis, the diagnosis of gout is established. Tophi never form in rheu-
matism, but are always present late in gout.
The joint affection oi pyoemia may be mistaken for gout ; but the his-
tory, in connection with the constitutional signs of pyaemia, will remove all
doubt.
Prognosis. — Gout rarely kills, but complete recovery from it is also rare.
Death is generally the result of visceral complications or of the cachexia
induced by blood changes. The prognosis is less favorable in hereditary
gout, and in those who persist in high living and the use of alcoholic bev-
erages, and when the larger articulations are affected. The appearance of
albumen in the urine, and total absence of uric acid from the secretions
are grave symptoms. The prognosis is exceedingly unfavorable when there
is great crippling of the joints accompanied by an extensive cachectic con-
dition. Concerning the doctrine of antagonisms, it has been proved that
gout does not exclude cancerous or phthisical developments.
Treatment. — The treatment of gout will be considered under four heads :
(1) General hygiene ; (2) Dietetics ; (3) External, and (4) Internal treat-
ment.
I. Gouty subjects should take systematic exercise in the open air, espe-
cially horseback-riding. A country residence is to be preferred to the city ;
and a warm, dry climate at a moderately high elevation is preferable to a
severely cold one. They should always be clad warmly in flannel, and
should avoid sudden and violent physical exertion, severe mental strain, and
all unnecessary exposure to vicissitudes of temperature. They should retire
and rise early, sleeping in a large, well-ventilated apartment without drafts.
II. Dietetics. — Simple, nutritive food should be taken at stated intervals
and in small quantities. Starving will not cure gout. As vegetables may
be taken more freely than animal food, all pastry, eggs, tea and coffee,
and alcohol should be avoided, and great care should be taken not to over-
load the stomach. Game and highly seasoned food, cheese, dried meats,
tomatoes and strawberries are to be avoided. Vegetables that contain the
least starch, such as cabbage and the salads, are to be preferred. The prin-
cipal articles of diet should be beef, mutton, and chicken, bread, milk, and
fruits. Alkaline mineral waters, seltzer, vichy, lithia, etc., may be taken
with and after meals. When stimulants must be given on account of the
enfeebled digestion, light wines, whiskey or gin will be found least objec-
tionable.
876 CHEOKIC GENEEAL DISEASES.
III. External Treatment. — The affected limbs should be kept raised above
the leyel of the body during an acute attack, and wrapped in flannel or
cotton batting. Cold applications and leeches to the afliected joints do
harm. When the pain is intense opium may be applied to the joint, or
morphine may be injected near it. Tepid alkaline washes and horse-chest-
nut oil are strongly advocated by many/ Vapor and Turkish baths are
often of the greatest service and should be taken weekly during the inter-
vals between the paroxysms.
IV. Internal Treatment. — Colchicum and the alkalies are our chief
remedies during the paroxysm. For thirteen centuries colchicum has
been used in this disease ; it relieves the symptoms, but how we do not
know. Its efficacy has been attributed at various times to the elimination
of uric acid, its sedative action on the circulation, its purgative and nar-
cotic powers. My rule is to give one of the following pills' every three
hours until the specific purgative action of the colchicum is obtained ; or
five drops of the fluid acet. ext. of colchicum in alkaline water may be
given every two hours. The maximum dose of the latter should be given
at the end of the attack ; small doses only are admissible at the commence-
ment. When marked cerebral, circulatory, or gastro-enteric phenomena
occur, colchicum is to be discontinued. Carbonate of potash, Kochelle
salts, and the urate or citrate of lithia, are important adjuvants to the
colchicum treatment.' Chloral, opium, and hyoscyamus may be given dur-
ing the acute attack, to relieve the pain and restlessness of the patient.
Common ash leaves, cinchona and gentian, the sulphate of quinine, and
the iodide of potassium with tr. guaiac. ammo, have been extensively used
in the treatment of gout, not only during the paroxysm but during the
interval. The benefit derived by gouty patients at the different springs
which are so highly recommended seem to me to be due to the change of
air and scene and to the dietetic restrictions more than to the bathing. A
restricted diet, exercise in the open air, and a Turkish bath once or twice
a week have succeeded with me as well as a residence at some spring.
In chronic gout, tonics (iron, arsenic, etc.) are usually demanded. The
inhalation of oxygen has been advocated as a remedy for the impoverished
blood condition. Chemically active remedies — ammonia phosphate and
benzoic acid — have not proved as useful clinically as theoretically. It
should be remarked that the excessive use of mineral waters is contra-
indicated in those who are advanced in years, in individuals whose kid-
neys no longer have the power of elimination, and in those with whom
alkalies disagree on account of some peculiar idiosjTicrasy.
1 Charcot spenks highly of atropine and blisters as topical remedies.
3 ^ Pulv. ipecac gr. i.
Ext. colchi. acet gr. i.
H)'drarg. protochlor. (calomel) gr. i.
Ext, aloes fl gr. i.
Ext. nuc. vomic gr- H-
3 Strieker caused the tophi to disappear by giving 1% grains of lithia carbonate and S}^ grains of soda
bicarbonate in 16 ounces of carbonic acid water a day. — Virchow's Archiv., vol. xsxv.
DIABETES MELLITUS. 877
DIABETES MELLITUS.
The term diabetes mellitus is applied to a constitutional disorder arising
from malassimilation, in which the first appreciable change is the presence
of sugar in the blood. When the proportion of saccharine matter reaches
three parts in one thousand, it appears in the urine, producing the symp-
tom which has given the name to the disease.' It has at various times
been regarded as a disease of the kidney, alimentary canal, liver, and
nervous system, but its exact pathogeny has never been determined.
Physiological experiments and clinical facts, however, tend to show that
the abnormal condition may be the result of either of these pathological
processes or of their united action :
First. — Excessive activity in the glycogenic function of the liver or in
the primary assimilative processes may so overload the blood with sugar as
to cause it to appear in the urine. Whether this hyperactivity is the re-
sult of active hypergemia simply, or arises from disturbed nervous supply
is uncertain. The occasional appearance of diabetes following the use of
stimulants, and its very general occurrence as a result of irritation of the
vaso-motor areas in the floor of the fourth ventricle, would seem to indicate
that hypersemia, either from local or central irritation, is an important
factor, but what nervous influence is primarily at fault in producing this
mysteriously perverted functional activity is undetermined.
Second. — The secondary assimilation may fail to dispose of the sugar pro-
duced, and the kidneys are again called upon to eliminate it from the
blood. Until physiology can speak with more definiteness than to say that
sugar is disposed of in the system ''either by oxidation or, as seems more
probable, in other ways," ^ it is useless to speculate as to what organ or
functions are at fault in this form of diabetes.
Morbid Anatomy. — The only characteristic lesion is the presence of sugar
in the blood in varying proportions, up to nine or ten parts in a thousand,
and secondarily in all the organs, secretions and excretions. It is most
abundant in the urine. Glycogen, acetone and kreatin are generally pres-
ent in the organs and fluids, and the blood contains more fat than nor-
mally. The parenchymatous changes in the viscera are principally degen-
erative, the result of the blood change. The liver is usually hyper^mic,
with possibly some fatty degeneration. The lungs are nearly always tuber-
culous, with points of catarrhal pneumonia, or possibly of gangrene, at-
tended by pleurisy. The heart is soft and flabby, and, like the other mus-
cles, pale and dry. The spleen is hyper^emic, hypertrophied and firm.
Aside from hypersemia, the kidneys often present the usual changes of
chronic parenchymatous nephritis (large white kidney), possibly the result
of the excessive work thrown upon them. Softening, cirrhosis, and tumors
may be present in the brain, and when they involve the fourth ventricle
become of interest from an etiological standpoint. Emaciation becomes
' Synonyms : Glycosuria, Glucosuria, Mellituria, Glycohaemia.
2 Foster'8 Phys., 25 Am. Ed., 1881, p. 537.
878 CHRONIC GEISTERAL DISEASES.
marked early, and in protracted cases becomes extreme. The skin, which
is harsh and dry, is generally the seat of furuncles, carbuncles, bed-sores,
and gangrene.
Etiology. — Diabetes is a disease of early adult life, and is met with more
frequently in males than in females. In some cases it appears to be heredi-
tary. It is a well-established fact that mechanical irritation of a certain
area of the medulla, an area corresponding very closely with the vaso-motor
area in the fourth ventricle, invariably produces glycosuria, and clinical
facts prove with a great degree of certainty that diabetes is frequently the
result of lesions producing similar irritation. Such irritation may result
from general shock or concussion, cerebral hemorrhage, softening, cirrho-
sis, abscess or tumors, also from excessive mental labor, shock, grief, and,
possibly, from the excessive use of cerebral stimulants. Blows upon the
epigastrium are included in its list of causes. Pregnancy, impaired diges-
tion, and immoderate use of sugar, new wine, and alcohol have also been
named as causes.
Symptoms. — Although diabetes may be acute and result fatally within
two or three weeks from the time the increased flow of urine is first noticed,
it usually comes on insidiously. The patient notices that for some time he
has been passing more urine than usual, and has been unusually thirsty.
While his appetite has been good, and he has taken more food than he is
accustomed to, he is losing flesh and strength ; and there is an abnormal
dryness of the mouth, throat and skin, with intolerable itching, followed
by desquamation. His sleep is disturbed by a frequent desire to empty the
bladder.
As the disease advances he becomes listless and debilitated, and there is
decrease or abolition of sexual desire ; in women the menses are often sup-
pressed. The tongue is red or coated, and nearly always thicker than nor-
mal ; the gums are pale, retracted, and bleed easily, and the teeth become
carious. There are nausea, vomiting, and well-marked dyspeptic symp-
toms, with constipation, and most patients complain of a constant sink-
ing feeling at the epigastrium. In many instances the breath has a
heavy, sweet odor, and the taste is perverted. Attacks of profuse diarrhoea,
lasting for a day, occur in advanced cases, and may precede an unexpected
fatal issue. Headache, often amounting to intense hemicrania, is common.
There is derangement of the special senses, especially of sight (soft cataract
and amblyopia) ; dulness of mind, irritability and restlessness, melancholia
and hypochondria. The temperature, pulse-rate, and respirations are be-
low the normal.
In some cases the classical course of the disease will be varied from ; there
will be little thirst or loss of appetite and no emaciation; the patient may
even gain in flesh.* In diabetes from " over-production " the quantity of
urine passed is greater than in the other form, the skin affections are more
severe and frequent, the patient does not emaciate, but loss of sexual desire
1 Frank describes a " diabetes decipiens." in which the amount of urine passed is not above the normal,
while a large amount of sugar is present. Quincke relates some very interesting cases of diabetes where
delirium, stupor and coma have appeared before de&th.— Berlin. Klin. Woch. No. 1, 1880.
DIABETES MELLITUS. 879
comes earlier. In the variety clue to defective assimilation, the emaciation,
anaemia, loss of strength and flesh, and palpitation, vertigo, and dyspncea
are early and marked signs, while the nervous phenomena are not jiromi-
nent.
The Urine. — Very rarely the amount of urine passed is but little increased;
generally, however, it very rapidly rises to twenty, thirty, fifty or more pints
in twenty-four hours. The calls to urinate become very frequent both by
day and night, and the genitals are inflamed and excoriated. The urine is
acid, of a light straw color, with possibly a faint green tint, clear, without
sediment, and of a slightly aromatic odor and a sweet taste. The specific
gravity varies from 1.030 to 1.070 with an average of 1.040, and the propor-
tion of sugar from a trace to 5-0 to 100 or more parts in a thousand. In
rare cases, a low specific gravity of 1.008 or 1.010 is recorded, but a specific
gravity of 1.030, when the quantity of urine passed is normal or increased,
should always lead to an examination for sugar. Urea is always present in
increased amount, and uric and hippuric acid, kreatinin, sulphuric and
phosphoric acids, acetone, alcohol, and albumen are frequently found. In
certain cases where the patient continues to fail, although the quantity of
sugar lessens, inosite appears in the urine, and continues to increase as the
sugar lessens. It may amount to two or three hundred grains in twenty-
four hours.
In those cases where sugar and the starchy element of the food are the
sole sources of the diabetic sugar, diet may reduce the quantity and specific
gravity of the urine to the normal and remove all traces of sugar from the
urine and blood. In other and more advanced cases animal food is also
converted into sugar, and in such conditions dieting can only modify the
urinary symptoms. In a third class of cases the tissues of the body also
contribute to its formation, and the quantity of sugar eliminated is but little,
if at all, affected even by starvation.' Urea is excreted in abnormally large
quantities by diabetic patients ; some claim that there is increased decompo-
sition of albumen into urea and sugar. Albumen does not necessarily indi-
1 The following are the best tests to determine the presence of sugar in the urine : —
Trommer's Test. — To the suspected liquid add a few drops of a slightly alkaline solution of tartrate of
copper. Boil. Sugar precipitates copper as a yellowish red oxide.
Fe.hling's Test is founded on the fact that glucose has the property of precipitating the red cupreous
oxide from an alkaline solution of sulphate of copper.
Dissolve 36.64 grammes cupric sulphate in 200 c.c. distilled water. ; dissolve 80 grm. sodium hydrate
in 600 c. c. water, and add 173 grm. Rochelle salts. Mix the two solutions and add water to make one
litre. Keep in small, carefully sealed bottles. The copper in one c. c. is entirely precipitated by 5 milli-
grammes of grape sugar.
Pour 5 c. c. of the above test-solution into a test tube and heat to boiling ; add the suspected urine,
guttatim : If grape sugar is present the blue changes to green and the red oxide of copper is precipitated.
When the blue is discharged the copper is precipitated. — Draper.
Wnr)'en''s_ Test.— In a test tube containing three drams of urine add two drops of a solution of sul-
phate of copper and one-half as much liq. potass, as the amount of urine ; boil, and if the urine con-
tains unrjar.. the red sub-oxide of copper will be thrown down.
Maumsne's Test consisrs in heating saccharine urine in the presence of bichloride of tin, which
canaes it to throw down a black-brown "caramel " looking deposit.
yfoorf^n y'fcf/ consists in boiling liquor potassie with the suspected urine; if sugar is present a bistre
brown appears.
The Fenrtentatirm Test consists in putting German yeast in a test tube filled with the urine, and standing
It inverted, in a warm place : alcohol and carbonic acid ai-e formed and the bubbles of the latter, tested
With lime water, give evidence of its character. Non-saccharine urine does not ferment.
Tcn-uloi form during the fermentation as a scum, and, microscopically, are easily recognizable.
880 CHRONIC GENERAL DISEASES.
cate that there are grave kidney changes in diabetic subjects. The amount
of urine passed in twenty-four hours varies from fifty to one hundred pints.
The large amount of urine secreted distends the bladder ; and the large
amount passed, and its saccharinity, cause a constant itching, burning and
uneasy sensation at the prepuce, along the urethra, and at the neck of the
bladder ; in females, it may cause redness, irritation, excoriation, or an
eczematous condition of the vulva. Incontinence of urine is especially fre-
quent in diabetic children.
Differential Diagnosis.— Diabetes mellitus may be mistaken iov glycosuria,
for the atrophic form of Briglifs kidney, and for diabetes insipidus or
polyuria.
Diabetes occurs at all ages, and often from undiscoverable causes ; simple
glycosuria is very common in tJie aged, in the insane, in fits of ague,
after sudden excitement, blows on the head, the taking of chloral, etc. In
diabetes mellitus the amount of sugar seldom varies much from day to
day; while in non-diabetic glycosuria it varies greatly.' Polyuria, poly-
phagia, and polydipsia are marked symptoms in diabetic glycosuria. The
symptoms referable to the nervous system and skin are prominent in dia-
betes mellitus ; they are absent in simple glycosuria. Volumetric analysis
by Eehling's method is easy in diabetes mellitus ; while in simple gly-
cosuria it gives obscure results, owing to the presence of kreatinin.
Diabetes mellitus is at once distinguished from Briglifs disease or dia-
ietes insipidus by the presence of sugar in the urine, a condition which
does not occur in either of the other diseases.
Prognosis. — Although diabetes is a progressive disease, it has no regular
course, and the prognosis depends very largely upon the form which the
disease assumes. In that class of cases where diet reduces the amount of
sugar, or possibly at first removes it entirely from the urine, the fatal ter-
mination may be long delayed, but those cases which appear to depend
upon faulty assimilation are more rapidly fatal. Between these extremes
the disease may last from a few weeks to ten or twelve years. Pulmonary
tuberculosis (twenty-five to thirty per cent.) and uraemia (ten to twenty
per cent.) are the most frequent causes of death. Asthenic inflammation
with suppuration is frequent in all the tissues, and boils in successive crops,
and carbuncles, are frequent complications which influence the prognosis.
Pulmonary gangrene may occur with an odorless breath. Cataract, am-
blyopia, retinitis, and retinal hemorrhage are often present even in cases
not attended by albuminuria.
The prognosis is more unfavorable the younger the subject, the less
amenable to treatment the case proves to be, and the severer the gastro-
intestinal symptoms. It is always bad in those who emaciate rapidly.
Death may occur from marasmus, gangrene, dysentery, ansemia, or not
Infrequently in diabetic coma.
Treatment. — In spite of the fact that there are no " speciflcs " for dia-
betes, the greater number of cases can for a time be brought under control;
and to this end dieting is of first importance.
1 Gerin Rozes.
DIABETES MELLITUS. 881
All saccharine form of food, or any article that can be converted into
sugar, should be withheld. Hence, starchy foods, bread, arrow-root, tapi-
oca, sago— such vegetables as potatoes, parsnips, turnips, carrots, beans,
and peas are to be absolutely avoided or partaken of sparingly. Salads,
greens, acid fruits, all kinds of flesh and fowl, eggs, cheese and butter'
unsweetened tea and coffee can be taken. Alcohol in any form is harmful,
but should exhaustion demand stimulation a light sherry or claret may be
permitted.' Koumyss is sometimes given as a substitute for mild stimu-
lants. To allay the intense thirst acidulated drinks, cracked ice, or alka-
line waters may be used in as moderate quantities as possible ; while water
increases the amount of sugar passed, it is not certain that it increases the
amount formed, and the patient should use water in moderation rather
than attempt distressing self-denial. A meat diet is therefore to be en-
joined.
In the above bill of fare the patient will not find much that is unpleasant
or distasteful, except deprivation of bread. Gluten breads, bran cakes, and
biscuits and buns made from almond flour have been devised as substitutes
Some patients cannot eat bread thus made, and in such cases, if bread
must be taken, it should be well toasted. Moderate exercise must always
be advised, and the skin should be kept thoroughly active by means of
baths ; in the feeble, warm baths, and in the more robust, sea or cold baths.
But as pulmonary complications are so common, the body must always
be warmly clothed. The success of dietetic measures depends upon the
patients rigidly following them.
The drugs which exert a most beneficial influence are the extract of
opium, morphia, and codeia. They must be used sparingly, and usually
only when the meat diet is given up for a time. Small doses should alwaj^s
be administered at first. When arthritic muscular and neuralgic pains
are severe, narcotics are especially beneficial. Cures are reported by high
and trustworthy authorities from their use.
On theoretic grounds, lactic acid has been proposed as a substitute for
sugar. Ithas been given until arthritic (rheumatic) symptoms have appeared.^
Alkalies, bicarbonates, acetates, and citrates are highly recommended.
And since they are always most beneficial in the form of natural thermal
mineral waters at the springs, half their benefit may be ascribed to change
of air, mode of life, and the surroundings that attend a visit to watering
places. Carbolic acid and creosote have been used as antiseptics, and
salicylic acid has been proposed as an anti-fermentative ; sulphide of calcium
is of benefit where there is much suppuration {e. g., boils, carbuncles, etc.).
Ergot and jaborandi have apparently been beneficial in some cases ; the
constant galvanic current has been productive of good results. The
anaemia which attends it demands iron, cod-liver oil, strychnia, quinine
1 Donkin recommends the continuous administration of sl^immed milk, three or four quarts a day ;
whfin the patients are able to pursue this plan it is followed by pood results.
2 Two Neopolitan professors, Primavera and Caucani, claim that a meat diet with g ij-iv of lactic acid
and 1 88. of alcohol in 12 oz. of water at a meal, will furnish no materials for the formation of sugar,
yet will be a substitute for the saccharine and farinaceous elements of the food.
56
882 CHEOKIC GENERAL DISEASES.
and a change of air and scene. Surgical operations should on no account
be undertaken on diabetic patients.
DIABETES IlSrSIPIDUS.
Diabetes insipidus, or polyuria, is characterized by extreme thirst and
the secretion of a large quantity of colorless urine, of low specific gravity,
free from sugar and albumen. It is also called hyperuresis or polydipsia,
the latter term having reference solely to the intense thirst which attends
it.
Morbid Anatomy. — Polyuria has been produced both by mechanical and
pathological lesions of the brain just above the floor of the fourth ventricle.
Disease of the pineal gland, and cerebral disease extending into the medulla
have also been found associated with it.*
Etiology.— Diabetes insipidus may occur at any age and in either sex.
Some consider its immediate cause to be a dilatation of the capillary vessels
of the kidney, which has its origin in a disturbance of the sympathetic
ganglia. Blows on the head, injuries to the medulla or region of the fourth
ventricle, injuries to the spinal cord, violent emotions, have all apparently
caused its development. Drinking large quantities of ice-water when
overheated, and exposure to cold and wet are among its supposed causes.
Diabetes insipidus temporarily disappears during the course of acute febrile
disease.
Symptoms. — This affection may come on insidiously or suddenly. Its
chief symptom is the passage of a large quantity of limpid urine ; the quan-
tity varies from thirty to sixty pints j!?er diem. Its specific gravity ranges
from 1.003 to 1.008 ; it is remarkably clear, faintly acid, and of a greenish
opalescent hue. Urea, uric acid and kreatin are secreted in larger quanti-
ties than normal. It contains no sugar or other abnormal ingredients.
Intense thirst accompanies this increased flow of urine ; so great is it that
patients who have had all fluid withheld from them have drunk with avidity
their own urine. The quantity of urine equals the amount of fluid taken.
The skin becomes harsh and dry ; and the temperature becomes subnormal.
'The appetite, gastric and intestinal symptoms are all very variable. A
strong corroborative proof of its nervous origin is the occasional increased
salivation that is clearly due to nerve influence.^ The other symptoms
which attend this disease are variable. In some cases the patients are well
in all other respects : in others there is vomiting, rapid emaciation, and the
general signs of acute phthisis.
Differential Diagnosis. — A careful examination of the urine for one month
will distinguish this condition from all other diseased conditions which are
attended by the secretion of abnormally large quantities of urine.
Prognosis. — Recovery from diabetes insipidus is rare, although it may last
many years without any disturbance of the general health. Pleurisy and
acute rheumatism occurring during its course have been followed by com-
1 Dickenson found decjenerative changes in the solai- plexus. The blood is said to contain an abnormally
large amount of solid constituents.
^ See discussion of "submaxillary gland and chorda tympani nei've" in Foster's Physiology.
ANEMIA. 883
plete recovery.' In most instances death is caused by intercurrent dis-
ease.
Treatment. — When a cause can be reached, it should be removed. At all
times the body should be warmly clothed, and the skin kept active. The
food should be highly nutritious and easily digestible. Great attention must
be paid to the surroundings and general hygiene of the patient. Narcotics
have been advocated, but they are not so efficacious as in diabetes mellitus.^
Nitrate of potash, iron, alum, lime-water, tannic and gallic acid, creosote,
bromide of potassium, acetate of lead, jaboralidi and belladonna have all
been recommended, either for narcotic, astringent or vaso-motorial action ;
the chief idea in all being to constringe the renal capillaries. The constant
galvanic current passed between the loins and epigastrium is advocated, and
deserves more extensive trial. °
ANEMIA.
Simple anaemia is a condition in which the number of the red corpuscles
is markedly diminished ; when local it is called ischsemia. If the llood-
mass is diminished it is called oligcBmia. Spanc&mia and Jiydrcemia are
synonyms of ansemia.
Morbid Anatomy. — The density of the blood is diminished. There is
diminution in the number and size, and change in the form and color of the
red blood discs ; one hundred corpuscles may occupy no more space than is
normally taken by seventy-five, and the number may fall below one-half
the normal. Besides quantitative there are qualitative changes in the
blood ; the amount of haemoglobin in the red discs may be diminished
twenty-five per cent. When corpuscular abnormalities are due to imper-
fect development and formation, the condition is called ancematosis ; —
but when they have been perfect and have subsequently degenerated, the
name JicBmoplithisis is applied.
The heart in one who has died in a state of extreme anaemia is flabby
and pale ; the blood is of a lighter color than normal and more fluid ; if
coagula exist they are pale and crumbly. There may be a diminution
in the fibrinogen and fibrinoplastin. There is usually a small amount of
fluid in the serous cavities. Ecchymoses are common ; and minute hemor-
rhages may be found at various points.
Etiology. — Simple anaemia may be caused by anything that decreases the
number of red corpuscles or that interferes with their production.
Acute anaemia is the result of sudden and excessive loss of blood ; fe-
brile anaemia is acute.
Chronic anaemia may be the result of numerous small bleedings, or of
exhausting discharges other than blood, which attend many forms of
chronic diseases. It is a constant accompaniment of many forms of chronic
visceral diseases, of which Bright's disease is the best example. Chronic
blood poisons cause what is called toxic ansemia. Interference with nutri-
1 Dickenson and Dcsgranges.
* Rayer and Trousseau strongly advocate valerian ; and Sidney Ringer regards ergot and ergotin as effi-
cacious.
» Lay cock ; The London Lancet, vol. ii., No. 7, 1875.
884 CHROinc general diseases.
tion, from insufficient or improper quality of food, an ti -hygienic sur-
roundings, etc., are prolific causes of simple angemia. Women are more
liable to anaemia than men ; and the condition is much more frequent at
the two extremes of life, than during the period between twenty and sixty.
A tendency to an anaemic condition is not infrequently congenital. Struct-
ural changes in the cytogenic tissues, and disease of the lymphatics, induce
anaemia. Malignant growths and chronic tuberculosis are attended by con-
ditions of extreme anaemia.
Symptoms. — The symptoms of acute anasmia — such as results from pro-
fuse hemorrhages — are extreme pallor, pinched features, and cold sweats ; the
pulse is feeble, rapid, is quickly accelerated by slight mental excitement or
physical exertion ; a blowing cardiac murmur and even a '^ bruit de diable"
is present in severe cases. A condition of syncope is of frequent occur-
rence. Vomiting, delirium, tinnitus aurium, and other nervous phenomena
are common. The thirst is intense, and the urinary secretion is scanty.
In chronic ancemia there is a pale, waxy, or sallow hue of the skin, and
a pale, bloodless condition of the mucous surfaces. The skin becomes oede-
matous and the muscles flabby. The hands and feet are always cold. A
cachectic or marasmic condition is developed ; the skin becomes harsh, and
often desquamates in patches. As a result of long-continued anaemia a
hemorrhagic diathesis may be established. The urine is pale, contains
less urea and less pigment than normal. Dropsies are liable to occur when
anaemia has persisted for a long time. The temperature is frequently sub-
normal. Extreme exhaustion and muscular feebleness are among its ear-
liest and most prominent signs. Anaemic patients are irritable, excitable,
usually hyperaesthetic and suffer from neuralgias. Anaemic females com-
plain of a pain in the left side and a burning sensation on the top of the
head. They are often hysterical. Temporary aphasia may result from
anaemia. Anorexia and atonic dyspepsia result from deficiency either in
quantity or quality of the gastric juice. A morbid, craving appetite some-
times exists.
The constant and important signs of anaemia are haemic murmurs, which
may be cardiac, arterial, or venous. The cardiac murmurs are systolic
in rhythm, blowing or bellows-like in character, and have their point of
maximum intensity at the base of the heart. Arterial murmurs are heard
over the large arteries, and they may be accompanied by a thrill percepti-
ble in the radial vessels. Over the Jugulars, particularly the right, there
is heard a continuous venous hum. A deep inspiration intensifies, while
coughing diminishes the intensity of the venous hum. It is also dimin-
ished by the horizontal posture. It may sometimes be felt as a thrill on pal-
pation. The heart's impulse is always feeble ; the heart sounds are muf-
fled, and the radial pulse is compressible and small. Severe attacks of
cardiac palpitation are common.
Differential Diagnosis. — Acute ansemia from either internal or external
hemorrhage is not likely to be confounded with any other condition. The
diagnosis of chronic anaemia is readily made from the history and general
appearance of the patient, and by the presence of haemic anaemic murmurs.
CHLOROSIS. 885
Prognosis. — The prognosis in anaemia is determined by the conditions un-
der which it occurs. The earlier its cause is discovered, and the more readily
removed, the better the prognosis. Its duration varies from days to years ;
some individuals, especially women, are ana3mic during their entire lives.
When it is associated with, or dependent upou, organic disease, the prog-
nosis is unfavorable. Death, in acute, cases, results from annulling the
function of the medulla, or cardiac j^aralysis; in chronic cases, inanition and
exhaustion, or some complication, induce the fatal issue. Death may
occur in syncope, convulsions and coma.
Treatment. — The treatment of anaemia is always restorative, and must be
especially directed to improving the blood-making power. Acute anaemia,
the result of profuse hemorrhage from wounds, accidents, during labor,
etc., must be treated surgically rather than medicinally. The preventive
treatment of chronic anaemia when it depends upon exhausting discharges,
prolonged lactation, and anti-hygienic conditions, is the removal of its
causes. The diet should be most nutritious, embracing a large proportion
of nitrogenous elements. If the digestive organs are feeble, food must be
taken in small quantities and at short intervals. Alcohol is food to anaemic
patients. Burgundy, Madeira, and rich wines are to be preferred ; but in
anaemic females the malt liquors are often more beneficial. Daily exercise
in the open air and exposure to the direct rays of the sun are essential, and
should be taken regularly without producing excessive fatigue. The clothing
should be carefully regulated ; in winter warm flannels should always be
worn, and in the spring and fall great care should be exercised not to allow
the surface to become chilled.
Iron is the one drug that best combats anaemia. There are many prep-
arations,, but the chloride, Vallet's mass, Blaud's pills, and, in children,
reduced iron or the citrate are the forms that have given me the best re-
sults ; it should be given after meals. The combination of iron with quinia,
strychnia and phosphorus or arsenic is efficacious in many cases when iron
alone fails to improve. Emulsions of cod-liver oil are valuable adjuvants
when they can be borne by the stomach. It should not be given after it
produces headache or dyspeptic symptoms.' Eecently I have found malt
extracts combined with iron, pepsin and pancreatic preparations efficacious
when there is deficiency of stomach digestion. The operation for trans-
fusion of blood or milk in extensive anaemia has never proved successful in
my experience, although there is good authority for resorting to it. If the
bowels have a tendency to constipation, aloes should be given with vegetable
tonics. Travel and a change of climate, often act beneficially when all
other means have failed.
CHLOEOSIS.
Chlorosis is a special form of anaemia, which occurs almost exclusively in
young females about the age of puberty, without any assignable cause.
1 Goodhart, Fothergill, and others mniiitain that anasmia predisposes to cardiac dilatation, and hence
propose that digitalis should be combined with iron.
886 CHKONIC GENERAL DISEASES.
Morbid Anatomy. — The body is well nourished, the organs are abnormally
pale, the serous cavities contain fluid, and there is more or less oedema of
the lower extremities, the red blood corpuscles are diminished in number,
and the hsemoglobin is less in amount than normal. The amount of albu-
men in the blood-serum is often increased and the mass of the blood is
increased.
Virchow states that a constant and characteristic lesion of chlorosis is
imperfect development of the vascular system. The aorta and arteries are-
generally smaller in chlorosis than normal, and thin walled ; the aorta,
throughout its entire extent, may only reach the normal size of the caro-
tids. Fatty degeneration of the tunica intima is very common, and this:
coat may exhibit spots of superficial erosion. The intima exhibits fatty
change in little spots or streaks, not in large connected masses. The mid-
dle coat is seldom involved. The heart cavities are usually somewhat
dilated, and hypertrophy of their walls is not infrequent. Spots of extrava-
sation and ecchymoses may be found on the mucous surfaces and in the
serous cavities. The ovaries and uterus are usually abnormally small.
Etiology. — Chlorosis is regarded by some as a neurosis, the blood changes
being secondary to the neurosis. The unaltered state of the cytogenic or-
gans—spleen, lymph glands, and osseous marrow — shows that it is not,
strictly speaking, a disease of the hsematopoetic system. ' There is always
more or less anaemia, and there is nearly always some functional derange-
ment of the sexual organs. All of these causes, however, are not sufficient.
to account for its development in the majority of cases. In very many in-
stances its cause cannot be reached. It is met with most frequently in
young girls.^ There is a form called amenorrhoeal, and another menor-
rhagic chlorosis. Self-pollution is claimed as an exciting cause of chlorosis.
Symptoms. — With or without derangement of the menstrual function,
chlorosis comes on insidiously in precisely the same manner as simple
ansemia, with which, in its early stage it is so readily confounded. As it
develops, the mental condition changes, the individual becoming morose or
despondent. The countenance assumes a peculiar waxy, yellow, or yellow-
green pallor. The face is puffy, the eyes are surrounded by deep, blackish
circles, the sclerotic is pearly, and the mucous membranes are pale al-
most to the verge of bloodlessness. The puffy look of the face is soon
shared by the rest of the body ; but it is not oedematous. ^ Sometimes the
cheek will retain a slight degree of color ; and on excitement, mental or
physical, the face is suffused.
In some cases the onset is sudden, and the above-named signs appear soon,
after some menstrual derangement. In all cases lassitude, muscular weak-
ness, dyspnoea, and fits of cardiac palpitation are common. Muscular pains
follow violent physical exercise. The appetite is capricious ; the patient
1 Virchow regards the predisposition to it as dependent upon congenital abnormalities of the heart or
aorta. Immermann regards chlorosis as due (in part) to functional derangement of the cytogenic organs.
2 Niemeyer says that " obstinate chlorosis attacks all youns girls, without exception, in whom the-
menses have appeared in the twelfth or thirteenth year, and before the development of the breast and.
pubes."
' Immermann states that a tendency to obesity exists in chlorosis.
CHLOROSIS. 887
will crave the most indigestible substances, and will eat with avidity chalk,
slate pencils, ashes, dirt, or strongly acid and spiced food. Sometimes
there is anorexia, sometimes Miliinia. Cardialgia is a common symptom ;
it is accompanied by a sense of weight over the stomach and by belching
large quantities of inodorous gas. It is to be remembered that gastric ulcer
is frequently met with in chlorotic females. Chlorotic girls are usually
melancholy, abstracted and irritable. In some cases they have attacks
of nervousness, so that the term chlorotic hysteria is used to denote a
hysteroid attack in young females. The sexual desires are diminished
rather than increased. The rapid breathing, dyspnoea, and palpitation are
undoubtedly in most cases purely nervous. Dyspnoea is often a very promi-
nent symptom and is accompanied by a short, dry cough ; the respiratory
murmur is feeble, and a full inspiration causes a fit of coughing, which
may lead to the suspicion of phthisis. There is rarely fever ; when fever
occurs there is something more than chlorosis. Often late in the disease,
oedema of the feet and ankles occurs.
The urine is pale and watery. The specific gravity is below normal. Urea
and coloring matter are deficient in quantity. Leucorrhoea, and amenor-
rhoea or menorrhagia are common attendants of chlorosis. The heart is
feeble and excitable. A systolic haemic murmur is present which is heard
in the carotids as in anaemia, but the venous hum in the neck, though not
infrequent, is still not so common as in angemia.
DiflFerential Diagnosis. — Chlorosis may be mistaken for progressive perni-
cious ancemia, for simple aiicemia, Brighfs and cardiac disease.
In ancemia emaciation is marked ; in chlorosis there is no loss of flesh.
The peculiar greenish color and the mental state are important points in its
differental diagnosis. The age, sex, and presence of uterine complications
are all important in distinguishing chlorosis from ansemia.
An examination of the urine in the one case and a physical exploration
of the chest in the other, will soon decide as to the existence of kidney or
cardiac disease.
Prognosis. — The course of chlorosis is influenced by the hygienic and social
surroundings of the patient, and by the treatment employed. It is not a
self-limiting disease, and shows no tendency to spontaneous cure. Its dura-
tion is very uncertain. As a rule the prognosis is unfavorable, on account
of the liability to serious complications, as phthisis, valvular endocarditis,
ulcer of the stomach and thrombotic formations. Eheumatism, septicaemia,
typhoid fever, and pneumonia are nearly always of a malignant type and
fatal in one who is chlorotic. Hysteria, chorea, paralysis, and epilepsy
sometimes complicate, and sometimes are sequelae of chlorosis.' It is to be
remembered, in giving a prognosis, that relapses are common after intervals
of seeming health.
Treatment. — When a cause can be reached, such as self-abuse, masturba-
tion, or disease of the functions of the uterus or its appendages, the removal
of such cause will be the first step in the treatment. Chlorotic patients
should have an out-of-door life with cheerful companions and surroundings ;
1 Friedreicli and others state that BasedotJo's Disease is unmistakably connected with chlorosis
888 CHRONIC GE]srEEAL DISEASES.
they should eat regularly of a diet of which meat and vegetables form the
chief part. Late hours and bad air and gaslight should not be allowed.
Mental is as important as physical hygiene. The patient should not be idle;
something pleasant must always occupy the mind. I have found that iron
does not act as well here as in ansemia ; indeed, in many instances it is not
well borne.' When there is a tendency to fulness about the head it does
harm ; some authorities state that only small quanities of iron are absorbed
by this class of patients, others say that large doses are of much more service
than small.
Arsenic I regard as the most valuable medicinal agent, either alone or
combined with iron. Constipation is to be overcome by the careful but
persistent use of small doses of aloes and nux vomica. Quinine, calumba
and quassia may be given alone, or in combination with ferric preparations.
Zinc and the mineral acids will often prove valuable adjuvants to the
iron plan of treatment. In cases of long standing the rest treatment com-
bined with massage are followed by good results when all other means
have failed.
PEOGEESSIVE PERNICIOUS ANEMIA,
This form of anaemia has received many names ;° but progressive perni-
cious anaemia is the term now most generally accepted.^ It may be de-
fined as that form of anaemia which occurs without discoverable cause, re-
sists all treatment, and steadily progresses, with greater or less rapidity, to
a fatal termination. The degree of oligocythaemia is greater than in
simple anaemia.
Morbid Anatomy. — The Hood is scanty and pale with a specific gravity in
some cases as low as L030, and shows but slight tendency to coagulate.
The number of red corpuscles is greatly diminished and their size and out-
line are altered. There is no increase in the white corpuscles, but they
seem to be in excess, solely from the great loss in the red. It is stated
that the amount of haemoglobin in each red disc is diminished ; and that
the white globules contain traces of it. Myelogenic pseudo-leukaemia was
the name proposed by those who found that in this disease the adult mar-
row became fcetal, red and adenoid." But the change in the medullary
structure of the bones is a secondary, not a primary change. Large nucle-
ated embryonic corpuscles, lymphoma, and multiple sarcomatous growths
have been found in the marrow.^ Secondary to the anaemia the heart un-
dergoes circumscribed or diffuse fatty degeneration. When this is partial
the papillary muscles and inner part of the heart seem to suffer most. In
' Immermann and Niemeyer both regard all else as subservient to iron. The former says a couple of
boxes of iron pills do more good than anything else. They both regard iron as of more benefit than in
any other (allied) malady.
^ Addison called it idiopathic ansemia ; Lebert, essential anaemia and puei^eral chlorosis ; and Ponflck
the ancemia of fatty heart. Ansmatosis and pseudo-leucocythemia, have also been proposed for it.
3 Andral, Wilks and Wagner describe it under other names.
* Cohnheim, Gardner, Litten, Fede, Pepper and Eichhorst all found the bone-changes prominent in
this disease ; and the last named found microaytes in the marrow.
» See a case described clinically by Ehrlich, and pathologically by Growitz, in Charite-Annalen, 1880.
Berlin.
PROGRESSIVE PERNICIOUS AN^IIMIA. 889
many cases there is more or less dilatation, but no change occurs in the
valvular apparatus. The inner coat of the larger arteries and certain
capillary tracts also exhibits fatty degeneration.
The liver, spleen, kidney and stomach are ansemic, — even bloodless in
severe cases — and their epithelial elements present similar fatty changes.
In the kidney multiple sarcomatous formations have been found.' The
liver and spleen may be enlarged ; although some observers maintain that
anemia attended by splenic enlargement, disease or swelling of the lym-
phatics, or any change in the medulla of the bones is to he excluded from
the class called progressive pernicious ancemia. The body is commonly
covered with small — rarely large — spots of ecchymosis, and internal hem~
orrhages are not uncommon.
Retinal Jiemorrliage, demonstrable during life, is so common as to have
been regarded as affording almost positive proof of its existence. These
hemorrhages are due to fatty degeneration of capillary aneurisms. The
serous sacs of the body contain more or less blood-stained fluid, and may
also exhibit ecchymotic spots. There is not much emaciation, though the
skin, membranes, and internal viscera are much paler than in simple anae-
mia ; and rigor mortis is late and slight.^
Etiology. — The essential nature of progressive pernicious anaemia is un-
known. It has been suggested that at times an endemic and specific cause
may be at work, since the disease has been found to occur with compara-
tive frequency in certain localities.^ "Women suffer more than men, and
are liable to it especially during pregnancy.^ The period between twenty
and forty is the age when most cases occur ; the disease being rarely seen
in early youth or extreme age. When no cause can be found for extreme
anaemia, and when no treatment retards its progress, the case is probably one
of progressive pernicio us ancem ia.
Symptoms. — It comes on insidiously. Whether the patient has been ill
or in perfect health, the course is the same, and it begins with a sense of
languor, which increases from day to day. The skin and mucous membranes
become very pale and assume a dusky yellow color quite distinct from the
green of chlorosis. The muscles are soft and relaxed, and muscular weakness
may be so extreme as to force the patient to take to his bed ; and yet there is
often little or no emaciation. Cardiac palpitation, dyspncea, and attacks
of syncope are the results of the oligocythemia and attendant exhaustion.
More or less cedema and puffiness appear about the legs and ankles, as-
sociated with hemorrhages from the nose, gums, bronchi, and female gen-
itals. At the same time the body exhibits ecchymotic and petechial spots
and vibices, due to subcutaneous or external hemorrhage/ Ketinal apo-
plexy is not uncommon, and an ophthalmoscopic examination should never
> Quincke found an abnormal quantity of iron in the liver, and regarded that as a proof of great destruc-
tion of red discs.
* Brigidi found that the coeliac ganglia showed fatty and pigmentary degeneration of the nerve cells.
Le Sperimentale. May, 1878.
' Cf. Biermer In the Zuch Canton,
* Gusserow proposes the name " extreme anaemia of pregnant women." Lebert also calls it " puer-
peral chlorosifi."
* Immermann says the bleedings are due to the intense oligocythfemia.
890 CHRONIC GEISTEEAL DISEASES.
be omitted in any suspected case. Persistent diarrhoea is often present quite
early, and the urine is darker than normal.
There are early signs of atonic dyspepsia ; and anorexia, nausea, and
vomiting evidence the great irritability of the gastro- intestinal tract. To-
ward the end there are periods of pyrexia during which the temperature
is remittent and may reach 104° F. The rise in temperature is attended
by other febrile phenomena, such as thirst, furred tongue, etc., etc. Still
later there is a time of absolute apyrexia, and toward the very last moments
of life the temperature runs far below normal. Cardiac, venous, and arterial
murmurs are present and are far more intense than in simple anaemia. The
cardiac systolic murmur is associated with the fremissement cataire. The
heart is always feeble, and in severe cases intermittent ; sometimes it is-
slightly dilated from fatty degeneration.
Differential Diagnosis. — Progressive pernicious anaemia may be mistaken
for simple ancemia, leucocytlicBmia, pseudo-leukcemia, and chlorosis.
Ordinary ancemia presents a discoverable cause, is attended by marked
emaciation, has no febrile symptoms and no evidence of retinal hemorrhages
or purpuric spots. In progressive pernicious anasmia the case is Just the
reverse. Finally, simple anaemia is amenable to treatment, while pernicious-
anaemia is not.
In leucocythcemia the spleen and lymphatics are enlarged, often enor-
mously ; and the bones, especially the sternum, may be tender and some-
what swollen, and the blood will contain an actual as well as relative — 1-20
excess of white globules. None of these conditions are present m progres-
sive pernicious anaemia.
In pseudo-leukcemia the spleen and lymphatics undergo the same en-
largements as in leucocythaemia, but there are no blood lesions, while in
pernicious anaemia there is no enlargement of lymph-structures, and the
diminution of red discs is greater than in a.ny other disease.
Chlorosis is a disease of young females ; it is uncommon except at the
time of puberty. Pernicious anaemia is common among women in the pu-
erperal state, and occurs between twenty-five and forty as a rule. Chlorosis
is unattended by dropsy, while dropsical symptoms are common in perni-
cious anaemia. Hemorrhages, spots of extravasation, and febrile phenomena
form no part of the natural history of chlorosis ; while they are constant
symptoms in pernicious anaemia. Chlorosis is curable and does not pro-
gress beyond a certain point ; pernicious anaemia is incurable and progres-
sive. In chlorosis the face has a yellow-green hue ; in progressive pernicious
anaemia it is of a dusky yellow.
Prognosis. — Death occurs in 90 per cent, of all cases. Of course those
who make death a necessary factor in their acceptation of the definition,
justly hold that it is a fatal malady. The duration varies from six weeks
to six months. Whether it may supervene on a benign ansemia or a chloro-
sis is uncertain. In very rapid cases hemorrhage and diarrhcea will be ex-
cessive. Death may occur from inanition, exhausting hemorrhages or apo-
P^exy.'
1 Bramwell states that the end is often ushered in by diarrhoea, coma, or dehriuin.
LEUCOCYTH^MIA.
891
Treatment. — The treatment is purely symptomatic and supporting. Iron,
quinine, strychnia and arsenic, in combination with a highly nutritious,
mostly fluid diet, will be found the most available moans in such a line of
treatment. Change of air and, when the strength allows, sea-bathing are
highly recommended. Transfusion of blood has been tried, and has failed. '
One case was reported as cured by transfusion of two ounces of human
blood by the Dieulafoy aspirator.^ Though the outlook is discouraging
from the onset, yet vigorous supporting treatment should be the rule from
first to last.
LEUCOCYTHJEMIA.
Leucocythsemia is an abnormal blood condition marked by increase in
the number of the colorless corpuscles, and associated with new formation
of cytogenic tissue in different parts of the body.' It may assume either a
splenic or lymphatic form, associated, in some cases, with a myelogenous
leukgemia, in which' the medulla of the bones is involved. When two of
the adenoid structures are simultaneously involved, it is spoken of as
medullo-splenic or lymphatico-splenic leucocythsemia.
A temporary increase in the colorless corpuscles (leucocytosis) is not in-
frequent during and immediately after full digestion, in pregnancy and
fevers. It is not leucocythsemia.
Morbid Anatomy. — The blood in leucocythgemia is pale, its specific
gravity is diminished, and it does not readily coagulate, although the
amount of fibrin is said to be
increased. These changes are
due to a very marked increase
in the number of white corpus-
cles, which sometimes equal the
red. In splenic leukaemia the
white discs are larger and more
granular than normal ; while in
the lymphatic form they are
smaller. In some instances cor-
puscles containing several nuclei
preponderate ; in others the
white discs are found with only
one nucleus. Fat is sometimes
found in the white discs. The
red blood globules are dimin-
ished in number, and they lose
their normal outline. When
leuksemic blood is defibrinated
the corpuscles sink and form two
distinct layers — an upper wliite layer, and a subjacent red.
Fig. 184.
Blood from a case of Leucocythsemia.
A. A. White Blood Corpuscles.
B, B. Red Blood Corpuscles, x 300.
Some state
' Dr. Weldon states that he has cured four cases by the intra-venous injection of milk.
* Dr. Cary, in the Buf. Med. and Surf/. .lour., Jan., 1881.
3 Prof. J. Hughes Bennett, in 184.5, described this condition as suppuration of the blood. Virchow, the
eame year, called it Icukcerrda. Six years later, Prof. Bennett used the name leucocythsemia.
892
CHROKIC GENERAL DISEASES.
that the reaction of leuksemic blood is acid, others that it is alkaline.
Elongated, octahedral, colorless crystals of albuminoid material are often
found in the blood ; chemical analyses have resulted in the discovery of
multifarious ingredients, as lactic, uric, formic, acetic, and glycerin-phos-
phoric acids, leucin, tyrosin, etc., etc., some of which are present (nor-
mally) in the spleen.' It is, however, only when the blood persistently
shows a proportion of white to red of one to twenty that leukaemia can be
diagnosticated.
The spleen usually uniformly enlarges in all cases, and it may reach
Fig. 185.
Section of a Leucocythsemic Spleen.
A, A. Fibrous trabeculce of the vascular sim/ses—f>Hg/My thickened.
B, B. Dilated venous sinuses cotitaining hjmphoid. cells C, C. swolkn and proliferating
D, D, and large multinucleated cells E, E.
endotMM ceUs
eighteen pounds in weight. It is usually fii-mer than normal ; never
softer. On its cut surface the trabeculae stand out as whitish striae, and the
Malpighian bodies as whitish dots. These last are lymphadenomata of the
Malpighian bodies, which resemble hypertrophies, the tumors having an
encephaloid look, and yielding a cancer-like juice.^ The organ is some-
times " mottled " with infarctions, the vessels being plugged by white
blood-cells. In these cheese-like islands the vessels are changed into
granulo-fatty tracts. Large multinuclear cells and many lymphoid ele-
ments are found in the venous sinuses. The capsule is somewhat thicker
than normal, and inflammatory adhesions may bind it to surrounding
parts. In the hilus of the organ lymphomata the size of an egg are
sometimes found.
Virchow thus sums up the splenic changes : "Hyperplasia of this lym-
^ Physiology, M.. Foster. " Metabolic Phenomena," etc.
* Cornil and Ranvier saj' that the diagnosis of lymphadenomata (which may affect other glands than
the splenic Malpighian bodies) is to be made from cancer, by the fact that the capillaries in leukcemia are
full of white discs which carmine stains.
LEUCOCTTH^MIA. 893
phatic organ induces chemical and morphological changes in the blood."
In the lymphatic variety the splenic enlargement is slight, and the princi-
pal change is hyperplasia of the lymphatics. The inguinal, axillary, and
cervical glands are enlarged and soft, and present a red, pulpy appearance.
The meshes of their connective-tissae are crowded with lymphoid elements.
In myelogenic leukmmia the marrow in the long bones and the spongy
tissue of the sternum, ribs, and vertebra is changed to a creamy-white
]niruloid mass. lu some cases this hyperplasia produces, or is attended by,
a red, fleshy appearance, like foetal marrow. The larger vessels in these cases
have their walls infiltrated with lymph-cells, and the small vessels that re-
main in the changed marrow are chiefly filled with red cells.'
Between the liver cells are found circumscribed or diffused patches of
white blood cells that have escaped from the overfull capillaries — this is
called " apoplexy of the white blood corpuscles " — and in connection with
connective-tissue hyperplasia form the whitish masses found in the organ.
The liver is enlarged from hypersemia and from inter-lobular and inter-
cellular infiltration.
In the kidneys the infiltration of lymphoid elements appears in lines
parallel to the tubules. Here also lymphadenomata start from the con-
nective-tissue. Similar new growths are common in the stomach and
intestines, often measuring from 1 to 1^ inches in diameter, and present-
ing many of the characteristics of cancer.
The lungs, brain, skin, testicle, and retina are sometimes the seat of the
leuksemic developments. The heart may suffer fatty degeneration, and
there may be effusions into the pericardium. Indeed, effusions are fre-
quent in all the serous cavities. Cerebral embolism occurs in about five
per cent, of all cases. Hemorrhage from mucous surfaces or into serous
sacs is a very common pathological accompaniment of leucocythfemia.
Etiology. — Leucocythgemia occurs at all ages and conditions, but it is
most frequent in early adult life. It is twice as frequent in men as in
■women. In women there is a notable connection between the generative
functions and leucocythaemia. Cold, wet, and all anti-hygienic conditions
predispose to it. When the Peyerian patches are lymphadenoraatous, it is
possible that previous intestinal catarrh was the etiological factor. In the
majority of instances the etiology cannot be determined.
Symptoms. — The early symptoms of leucocythaemia are almost identical
with those of simple anmmia, accompanied by swelling of the abdomen with
a sense of fulness in the left hypochondrium and wandering pains in the
splenic region. The splenic enlargement may or may not be attended by
fever.
In the lymphatic variety, enlargement of the glands in the groin, neck,
and axillary regions may be the first symptoms which will attract atten-
tion, and may exist for months before the blood changes can be detected.
In the myelogenic variety, the bones, especially the ribs and sternum, be-
1 Neuman regards the myelogenous chnnges as primary, and states that hyperplasia of the man-ow
canses immature corpuscles to enter the blood. TJeber Myelogene Leukcemie, Berlin, Klin. Woch., 1878,
(6-10).
894 CHRONIC GEiq-ERAL DISEASES.
come tender upon pressure, and as the disease advances the patient becomes
pale and assumes a waxy appearance. There will be more or less pyrexia
with evening exacerbations, the fever being usually in proportion to the
rapidity of the leuksemic development. The pulse is accelerated, feeble,
and marked by a peculiar throb. The appetite is capricious, and the tongue
and pharynx may be the seat of ulcerations. Early in the disease the
bowels are constipated ; but its late stages are attended by exhausting
diarrhoea. Dyspnoea, arising from the blood condition and from the
splenic enlargement, is associated with a chronic bronchitis. As a result
of the blood changes, a hemorrhagic tendency is developed, which may
cause hemorrhages from any mucous surface, or apoplexy. Eetinal hem-
orrhages and whitish patches due to apoplexy of the white blood corpuscles
can be detected by the ophthalmoscope. Ecchymotic spots often appear
over the body, and the fatal termination is hastened by this hemorrhagic
tendency.
If a hemorrhagic diathesis is not developed the disease runs a tedious
course. In such cases the enlargement of the spleen and lymphatics is very
great and leads to symptoms of pressure. General anarsarca is of frequent
occurrence toward the end of the disease, and under these circumstances the
dyspnoea becomes extreme. The urinary symptoms are not important,
though the abnormal constituents present the greatest variety. The
amount passed diminishes with the progress of the disease.' As leuksemic
patients emaciate the dyspnoea increases, and the fever, which was at first
intermittent, becomes continuous. If no complication occur death results
from exhaustion, preceded by delirium, stupor, and coma.
Differential Diagnosis. — Leucocythaemia may be mistaken for progressive
pernicious anmmia, for chlorosis, and in its early stages for infiammatory
and cancerous enlargements, and for pseudo-leukaemia, or Hodghin's
disease.
In all cases the difEerential diagnosis rests upon the result of a micro-
scopic examination of the blood. When the ratio between the white and
red globules reaches one to twenty the case must be regarded as one of
leucocythsemia.
Prognosis.— No case of recovery from leucocythaemia has yet been re-
corded. It varies, however, in its duration. If it comes on abruptly with
active symptoms it may prove fatal in three or four months ; but when in-
sidious in its approach three or four years may elapse before the fatal
result is reached. The average duration of the cases under my observa-
tion has been about fourteen months. Sometimes the disease does not
progress steadily, but advances by stages, progressing rapidly for a few
months, and then remaining stationary for as long a period.
The more rapidly the patient emaciates, the more frequent and profuse
the hemorrhages, and the higher the temperature, the more unfavorable the
prognosis. Dropsy is always an unfavorable symptom. The most frequent
complications are effusions into the serous cavities and hypostasis in the
' A number of cases are recorded where priapism, venereal excess, and seminal emissions have marked
the onset and course of the disease, but the value of such symptoms is yet to be determined.
hodgkin's disease. 895
lungs. Pneumonia, pleurisy, and intestinal catarrh stand next ; then follow
a long list of visceral diseases which appear as coincidences, rather than
complications. Death may occur from profuse hemorrhage, from cerebral
apoplexy, from pulmonary and serous inflammation, or from exhaustion.
Treatment. — None of the many measures proposed and tried have as yet
produced a cure or proved successful in arresting its progress. Quinine in
large doses is, however, advocated by all ; it is tonic, and also has a direct
influence upon the spleen. Arsenic and iron should also be steadily given,
either alone or in combination with quinine. Faradization of the spleen,
extirpation of the spleen and transfusion of blood have been tried, the
latter witJi, the two former without, success. Mtric and nitro-muriatic
acid, internally and in the form of baths (locally) are recommended.
Iodine preparations do not seem to have any efficacy, and the water-cure
plan has been abandoned. The malady is delayed hj cheerful surround-
ings and simple and nutritious diet. Ood-liver oil and phosphorus are
valuable adjuvants to the dietetic plan. But the chief indications for
treatment are found in the accidental complications.
(Pseudo-Leukcemia.)
Pseudo-leukaemia is a disease resembling leucocythaemia in all its ana-
tomical characteristics except the 'blood changes. It consists in enlarge-
ment of the lymphatic structures and development of lymphotnata ; it so
invaribly terminates fatally that the term malignant lymphoma has been
suggested for it. '
Morbid Anatomy. — Histologically the lesions of this disease in no wise
differ from lymphomata. They are divided into hard and soft tumors.
The soft lymphomata are of encephaloid consistency. Their color is a
reddish gray, studded with spots of extravasation. The glands undergo
simple hy23erplasia, and as they enlarge become confluent, forming a
large, soft, fluctuating, lobulated tumor. The capsule is in some cases
attacked ("periadenitis"), and then the process is not confined to the
lymphatics, but extends to, and infiltrates the adjoining tissues. The fluid
expressed from a cut surface resembles cancer- juice. Hard tumors have
a fibrous feel, and on section exhibit a shining, waxy appearance. The
capsule and medullary structure are indistinguishable and no fluid can be
expressed. Many regard the extensive hyperjolasia of the soft as the
initial stage of the hard ; while others consider the greater proportion of
cellular elements as the cause of the difference. These tumors are rarely
larger than a hen's egg. Unlike scrofulous glandular enlargement they
undergo no caseation, suppuration, or retrogressive changes.
As a sequela of this disease the number of red globules in the blood is
diminished. The disease first attacks one group of lymphatics and later
1 Hodgkin, whose name the disease bears, was the first to describe these peculiar Ij'niphatic changes
0832). Trousseau called it " Adene." Anaemia lymphatica, Lymph o-sarcoma, Progressive glandular
hypertrophy, and Lymphadenosis are terms also applied to it.
896 CHRONIC GENERAL DISEASES.
invades those of the whole body. The glands at the angle of the jaw, in
the axilla and groin are usually first affected.
The spleen is enlarged, but rarely to such a degree as in leucocythaemia.
On section, it is seen studded with grayish nodules, the Malpighian bodies
having undergone hyperplasia. The lymphatic enlargements may be fol-
lowed by similar developments in the liver, kidney, stomach, lungs, ovaries,
testicles, brain, retina, muscles, subcutaneous tissue, and in the serous
membranes. These are called metastatic or secondary deposits ; and de-
velop especially in and along vascular walls.
Etiology. — Lympho-sarcomata were formerly thought to be carcinoma-
tous or a malignant form of tuberculosis. There is no connection between
pseudo-leuksemia and scrofulosis, or between it and syphilitic affections of
the lymphatics. The disease has been found in men oftener than in women ;
but no etiological relations have been established.
Symptoms. — When pseudo-leukaBmia runs its regular course, and begins
by swelling of the glands in the neck, armpit, or groin, it can be recognized
without difficulty, and the time of its commencement can be fixed with
considerable certainty. But when the enlargement commences in the ton-
sils, the retroperitoneal, mediastinal, or other deep-seated and impalpable
glands, its diagnosis is difficult. In all forms, however, emaciation and
anaemia are marked and progressive. In the majority of cases the spleen
will be more or less enlarged ; and d\iH pains, with a sense oi fulness and
distention, will be felt in the left hypochondrium. Attacks of cardiac pal-
pitation are common. The pulse is small and rapid. In the majority of
cases there is a steady pyrexia (100° to 101" F.) towards the end, attended
by slight evening exacerbations. With the increasing anaemia there will
be dropsy, and when the disease is well advanced the muscular weakness is
marked. When nausea, vomiting, and diarrhoea are prominent symptoms,
lymphadenomata of the stomach or intestines may be suspected. When
dyspnoea, cough, impeded venous return, and all the signs of a bronchitis
exist, the bronchial or mediastinal glands are probably so enlarged as to
diminish the calibre of the bronchial tubes or venous trunks near them.
The symptoms of laryngeal paralysis may be induced by a lymphadenoma
pressing upon the recurrent laryngeal. Pressure on sensory nerves will
cause more or \e&& pain in the regions supplied.
The impoverished blood condition is evinced by hemorrhages from the
various mucous surfaces and by the appearance of petechise over the sur-
face of the body ; or in children by the occurrence of convulsions or coma.
Jaundice has occurred in a few cases from pressure on the common bile-
duct. A large inguinal tumor may exert such pressure on the femoral vein
as to cause oedema of the legs.'
LifFerential Diagnosis. — Pseudo-leukaemia may be confounded with leuco-
cytJicsmia ; the points of differential diagnosis have been considered in leu-
cocythsemia. It is to be remembered that pseudo-leuksemia has all the
symptoms of leucocythaemia except blood changes mentioned ; and in
1 A rare case is reported where a lymphadenoma about the Eustachian tube caused deafness. Another
is mentioned where paraplegia resulted from tumors pressing on the cord.
Addison's disease. 897
ctridition the cervical, axillary and inguinal glands are early and notably
enlarged.
Prognosis. — No case of recovery is reported where the diagnosis has been
cprtain. One year is its average duration ; two months and three years are
it^ extremes. As in leukaemia, so in pseudo-leukaemia the course may be
rapid and attended by pyrexia and well marked constitutional symptoms ;
or it may be slow and essentially chronic. Pseudo-leukaemia is frequently
complicated by pleurisy, pneumonia, so-called diphtheritic sore throat, ne-
phritis, lardaceous degeneration of the lymphatic glands, and pulmonary
tuberculosis. Death may occur from asthenia, exhaustion, anaemia, or from,
complications.
Treatment. — The general treatment of this disease has been mainly surgi-
cal, the theory being that if the glands are excised the disease will be
checked. It is true that the removal of the enlarged glands relieves the
pressure symptoms, which are often exceedingly painful, but it is of no
permanent service. Electrolysis, galvano-puncture, the injection of caus-
tics, iodine, arsenic, and phenic acid have been tried without avail. If
excision is practised, it should be when there is little or no anaemia and no
fever. All forms of topical remedies have been tried, but to no purpose.
Internally, arsenic seems to have some controlling effect. ' Iron and cod-
liver oil should be given in all cases, and sea-bathing sometimes arrests for
a time the progress of the disease.
ADDISOlSr's DISEASE.
Addison's disease, or melasma suprarenalis, is a cachexia accompanied
or caused by degenerative changes in the suprarenal capsules, that re-
semble tubercular infiltration. Many believe that any of the three condi-
tions, viz. : tuberculosis, chronic interstitial inflammation, or fibro-caseous
metamorphosis, or the three combined, may be present in this disease. But
its real pathogenesis is still in obscurity, for the reason that the physiology
of the suprarenal capsules is still unsettled. Histologically Miese capsules
closely resemble a lymphatic structure.^
Morbid Anatomy. — In the early stages of this disease the capsules are
enlarged. In the centre of the medullary portion of the glands are found
small, gray, tubercle-like granules. As the development of these masses
progresses towards the cortex, those at the centre become fused and suffer
caseous metamorphosis. This change may be so uniform that the ivliole
capsule becomes a uniform caseous mass. At other times the process, be-
ginning in several foci at the same time, causes the gland to assume a more
or less lobulated appearance. The line of demarcation between the corti-
cal and medullary portions of the gland is lost, and either the whole cut
section may be of a yellow color, or yellow masses may be entwined by gray
tuberculoid fibrous tissue. The gray or yellow color predominates, ac-
1 Warfynge reports improvement in four cases from its use. — London Medical Becord, March 15, 1881.
2 Kollikcr describes the renal capsules as both vascular glands and as appendages to the nervous
system. Brown-Sequard's jihysiological experiments accord with tliese views of Kolliker.
57
898 CHEOKIC GEN'ERAL DISEASES.
cording as the condition has existed for a sliort or a long time. As the proc-
ess extends to the cortex the centre begins to soften. In some cases- the
gland is a shell of hard, cheesy material, with diffluent creamy contents.
Instead of this liquefaction it is not uncommon to find the centre of the
capsule in a state of calcification. In either case no sign of normal gland
structure remains.' In the stage where gray matter predominates the
capsules are enlarged ; where yellow material is in excess, especially if as-
sociated with chalky, degenerative changes, the gland is hard and indurated.
In some cases the suprarenal glands may become a mass of cicatricial
tissue, the central portion of which is in a state of caseous degeneration.
The capsules are usually bound to all the surrounding organs or parts by
^rm connective-tissue.
The sTcin is discolored. In the lower layers of the rete MalpigMi there
are granules of pigment matter which vary in color from a very light to a
dark brown. The coloration is deepest in those parts in which the pigment
is normally most abundant. In some instances granular pigment is found
in the papillae and in the cuticular connective-tissue cells. It may be dis-
tributed along the line of the nerves and blood-vessels.
The spleen may be enlarged and softened. The adjacent mesenteric and
retroperitoneal glands are often tuberculous or in a state of cheesy meta-
morphosis. Peyer's patches and the solitary glands of the intestine are
enlarged, and the testicles and the prostate are in some cases tuberculous.
The same changes occur in the liver as in the spleen. Scattered tubercu-
lous nodules are often found in the brain and apices of the lungs. The
heart may undergo fatty change and the kidneys are occasionally the seat
of parenchymatous degeneration. Connective-tissue hyperplasia is marked
about the nerve-sheaths in the sympathetic nerves near the capsules. There
is hypersemia of the nerve trunks and ganglia of the large adjoining plex-
uses." The blood is ansemic, fibrin is diminished, the red discs are altered
in size and form, and do not run together in rouleaux as normal discs do.
The white blood globules are increased.
Etiology. — There is an undoubted connection between tuberculosis and
morbus Addisonii. In over 80 per cent, of reported cases, tuberculosis ex-
isted in the capsules or in other organs.' The latest and by far the most
reasonable theory is that the highly nervous capsule contains gland-cells
which have a close connection with the vascular and liaBmatopoetic system.*
Buhl thinks that not only is it a blood disease, but that it is infectious.
It has been regarded as analogous to leukaemia and pernicious anaemia.
1 G. Merkel states that there is cell proliferation attended by the formation of a delicate reticulated
structure containing many furiform lymphoid and giant cells. In opposition to most anthorities, Cornil
and Ranvier affirm that the process ./??•«< invades the cortex, and the medullary portion suffers secondarily.
Upon microscopical examination the yellow and gray matter present the same pathological aspects as
tubercle.
2 Cornil and Ranvier say that "the lesions of the nerve centres of the suprarenal capsules and of the
great sympathetic in part account for the phenomenon of pigmentation."
3 Letnlle points to its association with tnberctilous disease of the spinal column. Wilks and Moson
found pulmonary tuberculosis in 80 per cent, of their cases. Riesel claims that there is a paralytic state of
the vaso-motor fibres of the sympathetic, and as a consequence the blood is imperfectly and unequally dis-
tributed. La France Medicale, No. 40, 1880. Also see Ziir Pathologic des morbus Addisonii. Deut. Arch,
fur Klin. Med. 18^0, Be. 7.
4 Henle and Von Brunn.
Addison's disease. 899
It attacks males oftener than females, and is essentially a disease of adult
life. It has been found associated with cancer, apoplexy, fatty and waxy
degeneration of the suprarenal capsules, and in some cases the suprarenal
capsules have been found perfectly normal.
Symptoms. — This disease may come on so insidiously that the patient
will be unable to determine the date of its commencement. A feeling of
extreme languor is its most constant symptom. Its progress may be unin-
terrupted, either slow or rapid ; or it may progress by stages ; in the lat-
ter case there will be periods when the disease remains stationary for
months. The countenance becomes pale, the muscles flabby, the pulse fee-
ble ; there is extreme muscular weakness, asthenia, indigestion, anorexia,
dyspnoea, and fits of palpitation. Melancholia is not uncommon ; the pa-
tient is not easily aroused from a drowsy, dreamy languor into which lie
habitually falls. Dizziness and long fits of syncoj^e are not infrequent.
Gastric irritability, nausea, and vomiting are common. There is a sense
of distention over the epigastrium, acid eructations, and fits of cardialgia.
The tongue remains normal in appearance throughout. Sometimes there
is obstinate diarrhoea.' In most cases there is intense pain in the joints,
and along the spine and sacrum. As the disease advances the heart action
becomes more and more feeble, the pulse more rapid and weak, and arte-
rial anaemic murmurs are heard.
Meanwhile the skin changes its appearance. At first its hue is like
that of melansemia, then it is distinctly icteroid, then it j)resents the
color of a mulatto ; finally, it becomes a lustreless bronze. Not only
the whole cutaneous surface, but the mucous membranes of the lips,
tongue, gums and mouth are strongly pigmented. The parts most exposed
change in color first, then the parts subjected to pressure and the flexures of
the joints. Superficial cicatrices are strongly pigmented, while deep ones
remain unaltered. The roots of the nails and the sclerotic remain un-
changed, and the soles of the feet and palms of the hands are not discolored
until late, and then not markedly. As these patients approach death,
sight and memory fail, convulsions and choreic symptoms and delirium are
followed by comatose jieriods. But even when they reach a state of com-
plete asthenia there is but slight emaciation ; the body often presents the
appearance of obesity.
The temperature is slightly sub-normal throughout its course. The
urine is normal in amount; uric acid, coloring matter, and indican are
in excess, and urea is decreased.
DifFerential Diagnosis. — It may be mistaken for ptyriasis nigra, but
the itching of the surface and the desquamation of the cuticle in the latter
disease readily distinguish it from Addison's disease. Anaemic jaundice,
and the discoloration of the skin from nitrate of silver or from exposure to
the sun will readily be distinguished from the bronzed skin.
Prognosis. — It is an incurable disease, and no case of recovery has been re-
ported. Its duration varies from sixteen to eighteen months to four or five
' In 1871 Prof. Flint stated that degenerative changes in the gastric and intestinal tubules were prob-
ably the cause of the intense ansemia. N. T, Med. Journal, March, 1871.
900 CHRONIC GENERAL DISEASES.
years. Death may occur from asthenia, diarrhoea, convulsions or coma,
or from complications.
Treatment.— All remedial measures have thus far proved unavailing.'
Faradization and galvanism of the sympathetic have been proposed. Qui-
nine combined with iron, and iodide of potassium have been strongly rec-
ommended. In all cases perfect rest, quiet and good hygienic surround-
ings are important. It must be remembered that sudden and unexpected
death at any period of the disease may occur when treatment is apparently
arresting its progress. I have never obtained any positive beneficial results
from any plan of treatment.
AMMOlSTiBMIA.
Ammonaemia is a condition in which an excess of carbonate of ammonia
is found in the blood, the result of the decomposition of urine retained in
the urinary tract.
Morbid Anatomy. — The intestines are the seat of chronic catarrh and
contain a greenish yellow alkaline fluid. Sometimes- ulcers are found in
the intestines similar to dysenteric ulcers. When ammongemia occurs with
anmmia, it is possible for the urea excreted by the intestines to change into
carbonate of ammonia.^ K ferment has been obtained from cystitic urine
that is said to be capable of changing urea into carbonate of ammonia.'
Etiology. — The one essential condition necessary for the development of
ammonaemia is the retention of urine in the body sufficiently long for the
urea to undergo decomposition. The conditions under which it most fre-
quently occurs are, stricture of the urethra, enlargement of the jDrostate
gland, atony and paralysis of the bladder, pyelitis, pyonephrosis, hydro-
nephrosis, sacculated kidney and chronic cystitis.
Symptoms. — There are, clinically, two forms of ammonsemia ; in one the
conditions which give rise to it come on suddenly ; in the other the causa-
tive condition comes on slowly but continuously.
In the first, or, as it is called, acute ammoncBmia, there are nausea and
vomiting, intermittent and irregular chills, acceleration of the pulse, and
rapid rise of temperature. Diarrhoea and vomiting, if excessive, lead to
exhaustion and a typhoid condition. The complexion assumes a dingy
bronzed hue ; there is great muscular weakness with a tendency to
lethargy. (Edema of the face and ankles is of very rare occurrence. De-
lirium may occur. The tongue is dry, brown and shining — the beefy
tongue — and the mucous membranes that are exposed to the air, that of
the throat especially, are remarkably dry. The breath and the perspira-
tion are ammoniacal.
Chronic ammonaemia which accompanies atony and paralysis of the blad-
1 Greenhow asserts that glycerine 3 ij. combined with spts. chlorof onn. et tr. ferri chloridi, aa tii,xv.,
is highly advantageous.
sRosenstein denies any connection between ammonsemia and carbonate of ammonia ; but the weight of
opinion is in favor of it. Rosenstein, " xieber Ammon(Bmia, " Deutsche Zeitschrift f. pr. Med. No.
20: 1874.
3 Pasteur only succeeded in finding a ferment when bacteria were present ; but those who follow PaS'
teur's teachings claim that a specific ferment is the cause of amraonasmia.
AMMON^MIA. 901
der and enlargement of the prostate gland, comes on very insidiously. The
complexion becomes sallow, then of a dingy brown hue. There is pro-
gressive emaciation and restlessness, headache and insomnia. Irregular
chills occur at infrequent intervals ; the temperature is constantly above
normal, and the pulse is accelerated. Vomiting is persistent. The
mucous membranes assume a dry, glazed, shining apj^earance ; the skin be-
comes dry and harsh ; the breath and persjiiration are distinctly ammo-
niacal. JBut it should be remembered that the amount of perspiration in
ammongemia is probably less than in any other disease. When the disease
is far advanced convulsions may occur. At this time the complexion may
become quite dark, and emaciation is marked. Diarrhoea alternates with
constipation.
As a cachexia develops, insomnia and restlessness give place to som-
nolence, delirium, lethargy, stupor, or coma, and the patient passes into a
typlioid state. Old men with enlarged prostates pass into a condition of
stupor ; and then low muttering delirium, rapid, feeble, and irregular
pulse and subsultus tendinum terminate in a fatal coma.
The urinary symptoms are important. The urine is ammoniacal and
strongly alkaline when passed. It often contains pus, and there is a deposit
of amorphous phosphate of lime with crystals of ammonio-magnesian phos-
phate. The odor is offensive and pungent.
Differential Diagnosis. — Ammonsemia may be- mistaken iov typlioid fever,
sub-acute gastritis, pycemia, or septicmmia. In gastritis the urinary symp-
toms are negative, while in ammonasmia they are diagnostic. Nausea and
vomiting are persistent in ammonaemia, and intermittent in gastritis. Ca-
theterization, or a rectal examination, will rarely fail to discover some
organic genito-urinary obstructive cause for urinary retention; while a
physical exploration in gastritis gives negative results.
In pycBinia there will be an initiatory chill, profuse, exhausting, and re-
curring siveats, a high temperature (103° to 104° F.), a sweet, sickly odor
to the breath, and the evidence of thrombi, infarctions, and multiple ab-
scesses in some central organ or organs. All these symptoms are absent in
ammongemia ; and the ammoniacal breath and urine, and i\\e parched, diy
skin are in direct contrast to the symptoms of pysemia.
In septicmmia the temperature is very high— 105° to 107° F. Besides
there is no ammoniacal odor to the breath or urine; the skin is not dry,
and genito-urinary obstructive conditions will not be found. The history
of the case will also greatly aid in making a diagnosis.
Prognosis. — The prognosis in ammonaemia is determined to a great extent
by the condition which causes it ; when it is possible to remove the cause
the prognosis is good, but when the cause cannot be removed the prognosis
is very bad. In all cases there is slow but progressive impairment of the
general health. Aged patients rapidly become exhausted, and sink into a
typhoid state if the causative condition cannot be speedily removed.
Treatment. — The most important thing to be accomplished in the treat-
ment of this condition is the removal of its cause. And, since atony of
the bladder and enlarged prostate are its most common causes, the first
902 CHROI«riC GE^^TERAL DISEASES.
step is to empty and wash out the bladder. Very often when the patient
seems to be sinking into a typhoid state, when there has been nothing
to direct attention to the bladder, on the introduction of a catheter a large
quantity of stinking urine will be evacuated ; and after having thoroughly
washed out the bladder, rapid improvement takes place, and the gastric
symptoms subside. The diet should always be supporting and stimulating.
If tepid water is used to wash out the bladder, carbolic acid, bicarbonate
of soda, borax, or glycerine may be added ; and the washing should be
continued till the withdrawn fluid is perfectly clear and free from odor.
Iron and vegetable tonics are indicated.
HEMOPHILIA.
The hemorrhagic diathesis is an hereditary disease marked by a tendency
to immoderate bleedings — spontaneous or traumatic — and to obstinate
swelling of the Joints.
Morbid Anatomy. — No changes in the blood or vessels have been found
in the few post-mortems that have been made. The swellings of the joints
are probably due to blood extravasations within the articulation.
Etiology. — Its most marked cause is hereditary predisposition. It attacks
men far oftener than women.' The tendency descends to sons through
the mother, who herself may give no evidence of the disease. Fathers do
not transmit the tendency to their sons. Pregnancy is said to be a devel-
oping cause. There is often nothing to indicate the existence of this dia-
thesis prior to the occurrence of the hemorrhage. Whether the hcemophilia
of the new-born is a distinct disease is an unsettled question. Their blood
has been found to contain fungoid organisms which afford an apparent
explanation of the hemorrhages. The hemorrhagic diathesis has been re-
garded as allied to scrofula, chlorosis, gout, and similar dyscrasise, and
again as a pronounced manifestation of a rheumatic diathesis, as both these
conditions occur under the same influences. One of the most recent theories
is that it is dependent on deficient capillary innervation with resulting
dilatation. This neurotic theory is favored by the frequency of nervous
disorders in bleeders and the fact that neurotic remedies exert the greatest
control over it.^ In its transmission from parent to offspring it often skips
one generation.
Symptoms. — The symptoms appear as a rule during the first or second
year of life. There is nothing about the appearance that indicates the ex-
istence of any diathesis. The disease remains latent until a cut, a fall
on the nose, or the pulling of a tooth starts a hemorrhage, which at times
is uncontrollable. The blood will ooze for days, and death from acute
anaemia may result. Usually the bleeding slowly ceases and after a long
time the patient recovers. The bleedings may come on spontaneously.
Then there may be prodromata : signs of plethora, of cerebral congestion.
' Legg (in QuaMs Dictionary, p. 569) gives the proportion as high as 11 to 1.
* Mosler states that over fifty per cent, of his cases of leiilifemia were complicated by it, and in one
hundred and fifty cases collected by Gowers, eighty were bleeders.
SCURVY. 903
stupor, cardiac palpitation, and painful swellings of the joints. In child-
hood bleeding from the nose is the commonest form of hemorrhage. The
joints affected are the larger ; the knee is most frequently attacked.
In bleeders a slight bruise will be followed by extensive blood extrava-
sations into the connective-tissue. Hemorrhages may take place into the
stomach, intestines, lungs, bronchi, kidney and brain. Extensive blood
tumors may form in any part of the body.
DiiFerential Diagnosis. — There is no condition which is liable to be mis-
taken for haemophilia, if the history of the patient is accurately taken.
Prognosis. — Complete recovery is rare, but life may be prolonged by ju-
dicious management ; an example of which can be cited in the case of
Prince Leopold, who was thirty-two when he died of haemophilia.
Treatment. — For tlie traumatic forms styptics and mechanical surgical
measures should be promptly made use of. When hemorrhage arises spon-
taneously little can be done. The diet of bleeders should consist largely
of animal food. Chalybeate tonics should be constantly administered, and
the patient should lead a quiet life in a warm climate. Niemeyer rec-
ommends cathartic doses of Glauber's salts and ergot. Harkin, of Bel-
fast, recommends the chlorate of potash, — one ounce of the saturated
solution three times a day — combined with the muriated tincture of iron,
and claims to have had excellent results. He states that this plan will
eradicate the constitutional tendency.
SCTJEVT.
Scurvy or scorbutus is a chronic blood disease, which may be regarded
as a peculiar form of anaemia arising from deficiency of vegetable diet.
Until recently it prevailed very extensively in armies and among crews of
sailing vessels. Improved means for the preservation of supplies have ren-
dered it of much less frequent occurrence, and greatly mitigated its severity
even during long campaigns, and at the present time it is seen but infre-
quently among sailors.
Morbid Anatomy. — The red blood corpuscles are diminished and the al-
bumen and fibrin-factors are increased, although the albumen does not
coagulate readily, and there is a peculiar viscidity to the blood. There
is said to be a deficiency of potash salts.' The capillaries have been found
choked with red corpuscles and their endothelial cells altered. Some de-
scribe the blood as thicker, others as thinner than normal — at one time
lighter, at another darker. Ecchymoses are very characteristic of scurvy,
and occur in and beneath the skin, in the muscles, between the periosteum
and the bone, and within the joints. In these situations they may be very
extensive. They are also found on all the mucous and serous membranes
and may partially fill the pleura or pericardium. °
The heart, kidney, and liver often undergo fatty or parenchymatous de-
' Cornil and Ranvier.
^Dr. Ralfe regards diRproportion bptween the various acids and bases of the blood as the cause of the
disorganization of the blood corpuscles and subsequent mucous ecchymoses.
904 CHKOKIC GENERAL DISEASES.
generation. The spleen is enlarged, softened, and exceedingly friable.
Ulcers occasionally form on tlie mucous surface of the large intestine, re-
sembling those of dysentery. The changes in the gums are even more
characteristic lesions. In nearly all cases they become soft, spongy, and
•oedematous, and ulcerated masses overhang the teeth and bleed upon the
slightest provocation.
The bodies of those who have died of scurvy are emaciated, the skin is
ashen gray, and there is more or less oedema, especially of the lower ex-
tremities.
Etiology. — Deprivation of fresh vegetable food for a long time will very
surely induce scurvy, independent of climate, latitude, race, or sex. ' It is
rarely met with from any other cause, although an unvaried diet of poor
quality may induce it. Sudden atmospheric changes, mental disturbance,
severe and prolonged physical labor with insufficient food, and bad hygi-
enic surroundings may predispose to scurvy, but seldom develop it so long
as fresh vegetables in moderate amounts are eaten.
The theory that scurvy is due to a specific infection, while improbable,
cannot absolutely be rejected.^
Symptoms. — The earliest noticeable changes are in the skin of the face
and eyelids, which changes color and appears bruised and swollen. The
pulse is soft and the temperature lower than normal. The patient rapidly
becomes less and less capable of mental or physical labor, the face grows pale
and bloated, there is great despondency and a sense of weight in the lower
limbs. The skin is dry, rough, and of a muddy pallor ; later it becomes
sallow and leaden. The conjunctivae are pearly white, the tongue is clean
and pale, the teeth loosen and are surrounded by bright red ulcerated or
fungous-looking gums that present a purple line where they join the teeth,
and contrast strongly with the pale or livid lips. The breath is exceed-
ingly offensive, frequently from necrosis of the jaws. The eyes are sunken
and surrounded by a dark blue circle.
Ecchymoses and petechial spots cover the body and extend over a large
surface on the slightest blow or injury. Severe darting pains which simulate
rheumatism are felt in the limbs, about the calf of the leg and the popliteal
space. The legs may become fixed, owing to the hardness of the muscles
of the calf and thigh. Node-like swellings occur over the tibia from sub-
periosteal ecchymoses. The pulse is slow except upon excitement, when
palpitation and dyspnoea are also marked. Slight exertion may occasion
syncope in those in whom the disease is advanced. Ansemic murmurs are
heard upon" auscultation. The bowels are constipated, unless there be scor-
butic dysentery. The urine is high colored, sometimes albuminous, and
there is a diminution in its normal ingredients except potash salts and
phosphoric acid. The chlorides are abundant. Insomnia and disordered
vision are common.
Differential Diagnosis. — The history of a case and a close inspection of
1 In the Crimean war more died from scurvj^ than from any other cause. It was the cause of death in a
large proportion of those who died during the potato famine in Ireland.
* Fabre regards scorbutus as a miasmatic afEection which especially affects the nervous system.
PURPURA. 905
tlie gums will enable one to clistingoiisli scurvy from mercurial poisoning.
Scurvy is distinguished from purp^ira by the sjiongy gums, painful
swellings, and more j^rofuse though less numerous hemorrhages. Purpura
frequently occurs in those whose health has not been impaired by faulty
nutrition ; scurvy very rarely Purpura is not affected by lime juice or
change in diet, while either will at once produce marked improvement in
scurvy. Purpura occurs in isolated cases ; the vital powers are not as de-
pressed as in scurvy, and muscular swellings are aljsent.
Prognosis. — Scurvy is not a fatal disease ; appropriate treatment in un-
complicated cases always effects a cure. It may be complicated by dysen-
tery, syphilis, the various forms of malaria, typhus, typhoid, and chronic
alcoholismus. The former diseases assume a scorbutic character. Death
may occur from complications, exhaustion, general dropsy, hemorrhage,
diarrhcea, dysentery, pleurisy, pericarditis, or pulmonary oedema. It is
said that meningeal hemorrhage is sometimes a cause of death. Hemera-
loj^ia often occurs as a sequela.
Treatment. — In long voyages or campaigns lemon or lime juice or cit-
ric acid should be taken daily when fresh or preserved vegetables cannot
be obtained. By their use in the English navy scurvy has been diminished
nearly ninety per cent. One who is seriously ill of scurvy should be kept
in bed, and the diet at once be made to consist largely of fresh yegetables
and acid fruits with fresh meats in such proportion as the patient can
easily masticate and digest. Mustard, radishes, cabbage, and water-cresses
are anti-scorbutics. Three or four ounces of lime or lemon juice, largely
diluted with cold water, should be taken daily. If stimulants are required
malt liquors are to be preferred. A wash of chlorate of potash will afford
relief to the oral symptoms, and potash may be given internally ; quinine,
iron and strychnia act both as tonics and appetizers.
PTJEPUEA.
Purpura is a general disease, characterized by sanguineous effusions into
the upper layers of the cutis and beneath the epidermis.^
Morbid Anatomy. — Either from changes in the walls of the vessels or in
the blood itself (excess of salts, or water, etc.), or quite probably from both
combined, extravasations occur into the connective-tissue spaces of the
rete mucosum and papillary laj^er of the cutis or in the spaces between the
ducts and hair follicles. The serum is soon absorbed and the more solid
elements may gradually undergo complete absorption or result in perma-
nent pigmentation of the parts. Similar lesions are found in the mucous
membranes, attended by hemorrhage from the free surfaces. Such hemor-
rhages are more common in the nares and along the alimentary canal.
Serous membranes are less frequently affected, but extravasations have been
found in the pleural, pericardial and peritoneal cavities and in the meshes
of the pia mater.
1 It may be simple, rJievmatic, hemorrhagic or symptomatic. Purpura hemorrhagica is also called
" Morbus MaciUoi'M WerlhoJU."
906 CHEONIC GENEEAL DISEASES.
Earely are the muscles, periosteum, bones, conjunctiva, and retina the
seat of extensive blood effusions.
Etiology. — Age appears to have no bearing upon the development of pur-
pura, but it is found more frequently in women than in men. It appears
in some cases without any discoverable cause in the healthy and robust ;
sometimes its causes seem almost identical with those of scurvy. Rheu-
matic purpura may complicate acute polyarticular rheumatism or occur
in those of a rheumatic diathesis. Purpuric spots are not infrequent with
valvular disease of the heart, Bright's disease, phthisis, cirrhosis of the
liver, and various forms of malarial fever.
Its occurrence with leucocythsemia is interesting on account of Pen-
zoldt's discovery of the peculiar form of the blood discs in Werlhof's dis-
ease/ Purpuric spots have followed large doses of chloral and iodide of
potash. Distinct exciting causes, if such exist, are obscure ; fright, severe
coughing fits, and epileptic attacks are said to have induced it. There is
no doubt but that the enfeebled condition of the vessels often depends
upon a state of general debility either hereditary or acquired.
Embolism and thrombosis have been suggested as causes, while disor-
dered vaso-motor innervation, which might possibly account for its occur-
rence after exhausting diseases, has also been considered the primary
lesion."
Symptoms. — In many ^ases for days or weeks before the eruption occurs
there will be a general feeling of malaise accompanied by digestive derange-
ment. In all varieties of purpura the eruption has the same general char-
acters. The spots appear upon the extremities and trunk as a rule, but in
severe cases the}^ cover the head and face as well. They vary in color from
a bright red to a livid or purple ; they are round or irregular with serrated
edges, and vary in size from a pin's head to a large pea, or a spot may
measure an inch or more in circumference. They do not disappear upon
pressure. The smaller extravasations are spoken of as petechise, and the
larger as fecchymoses, and when they occur in lines or stripes they are
called vibices.
If the hemorrhage is so extensive or of such a form as to cause the spots
to be elevated above the level of the skin the disease receives the name pur-
pura papulosa, or lichen lividus when they are conical and located around
a hair follicle. The elevated wheal-like nodules are designated as purpura
urticans, and if they form bullae containing serum and blood the name
purpura bullosa is given.
While the primary spots are undergoing absorption, as indicated by the
gradual change of color from the dark blue through the green to yellow,
another livid red crop is appearing. In ordinary cases a crop lasts from a
week to ten days. Desquamation never follows, and once formed a spot
does not increase in size, except by fresh hemorrhage in its vicinity.
Sometimes there are no constitutional symptoms whatever in jsMrjowrfl!
simplex; but vci purpura r7ie?i7wa^/ca slight fever and rheumatic pains in
1 Blufbefvnd bei derWeiihofschen Krankheit, 1878, Erlanger.
2 Cavalie reports a case associated with organic disease of the brain.
MTXOEDEMA. 907
the knees and ankles are accompanied by red and swollen joints, gastric
and intestinal disturbances, colicky pains, etc., in addition to the usual
eruption. In purpura hemorrhagica, preceding and accompanying the
eruption, there is great constitutional disturbance ; the spots are large and
numerous, and invade the whole body ; there are free hemorrhages from
all the mucous tracts and from the lungs. So extensive may these hemor-
rhages be that acute ansemia is rapidly followed by typhoid symptoms and
death. The amount of hemorrhage does not depend upon the extent of
the eruption. Cerebral symptoms may occur from ventricular or menin-
geal hemorrhage.
When purpuric spots accompany the exanthems and contagious fevers the
usual symptoms of those diseases and the eruption are purely symjotomatic
of the extensive degenerative changes engendered by the primary infec-
tion.
Differential Diagnosis. — The points of diagnosis between purpura and
scurvy have already been given. The fact that there is no itching, no
desquamation, no suppuration or discharge, and no change in purpuric
spots upon pressure suffices to distinguish them from the eruption of any
form of sTcin disease.
Prognosis. — In uncomplicated purpura the prognosis is good ; but when
venous thrombosis, scurvy, diarrhuea, or an incurable organic disease exists,
life is endangered by the liability to hemorrhage from mucous surfaces, and
the occurrence of extravasations into the serous cavities or brain. Anaemia
and dropsy are often causes of death.
Treatment. — At one time the treatment consisted in administering quinine
and sulphuric acid. At the present day rest, a highly nutritious concen-
trated diet, and moderate stimulation with a nutritive wine are the princi-
pal measures employed. Tinctnra ferri perchloridi, — 15 to 20 minims
three times a day, — is very efficacious, and should be given in connection
with some one of the mineral acids, preferably sulphuric. Ergot, turpen-
tine, gallic acid, and other haemostatics are all highly recommended when
the hemorrhages become dangerous. When hemorrhage from the lungs
occurs, the treatment is the same as in other forms of bronchial hemorrhage.
Eecently, small doses of mercury have been given, and apparently effected
a cure. Shand has obtained excellent results from Faradization {Lond.
Lancet, July 9, 1879).
MYXCEDEMA.
Myxoederaa is a name given by Prof. Ord to a progressive disease where
the tissues of the body are invaded by a Jelly-like, mucus-yielding dropsy.
Morbid Anatomy. — All over the body the connective-tissue is found ab-
normally abundant, the fibrillar element being especially increased and un-
usually well defined. In Prof. Ord's cases the corpuscular elements were
enlarged and multiplied, and the interstitial element greatly augmented.
The skin in myxoedema yields many hundred times as much mucin as nor-
mal or ordinarily dropsical skin. Besides the overgrowth of connective-
tissue, it seems to have undergone a retrograde degeneration. In the skin
908 CHEONIC GENEEAL DISEASES.
the mucous infiltration causes swelling, translucency and defective secre-
tion. The connective-tissue stroma of the mucous membranes, of the outer
coat of the arteries, the glands, muscles, and the central nervous ganglia
is similarly infiltrated and degenerated.
Prof. Ord states that the structure of the thyroid glands maybe entirely
destroyed by the material ; and he thinks its inroads on the Malpighian
bodies and tub ales of the kidney cause the albuminuria which occurs late
in the disease. Dr. Mahomed, on the other hand, argues strongly in favor
of the identity of myxoedema and Bright's disease. Eecently it has been
almost conclusively proven that the central nervous system is affected, and
in two cases marked bulbar paralysis has been found.
Etiology. — Myxoedema, in the few cases first described, only occurred in
adult females, and of these more married than single women were affected.
Eecently, however. Dr. Andrew Clark states that in his experience males
suffer oftener than females, in the proportion of seven to three. The
number of recorded cases is, however, too small to admit of positive
statements. '
Symptoms. — The face is swollen as in real dropsy ; but the skin has a
waxy anaemic look, and the oedema involves not only the dependent por-
tions, but every feature of the face. Both lips are equally enlarged ; the
nose is thickened, and the rounded cheeks have a pinkish hue, contrasting
peculiarly with the rest of the waxy white skin. There is no pitting on
pressure ; on the contrary, the skin is rather elastic. The shape and form of
the hands is lost.^ The dry, rough, translucent skin seldom or never per-
spires. The thyroid body disappears or diminishes, while there is elastic
tumefaction of the skin in the lower triangle of the neck above the clavicle.
The expression of the face is stolid and sad ; the speech is monotonous,
slow, and leathery ; the limbs move slowly and lazily ; a fixed attitude
cannot be maintained, and consequently the patient is apt to suddenly fall.
The intellect becomes dull, sensation is slow but finally sure, and the mus-
cles are so relaxed at rest that a long contraction occurs before a proper
equilibrium can be maintained ; hence a quiver often runs through the
body as one foot is raised from the ground and the body is balanced on
the other. The muscles of the neck are so lax that the head droops on
the chest. Sometimes the patella is fractured by the forward bending of
the body. There is no real loss of muscular power, no wasting, and no loss
of sensation.
Thoughts and expressions are tardy and deliberate, but correct. The
bodily temperature ranges between 98" and 94° F. These patients are
constantly chilly. Late in the disease patients grow morose and irritable,
and are subject to delusions, hallucinations, loss of memory, and finally
complete mental failure.
Differential Diagnosis. — There is no disease with which myxoedema can
be confounded when the mucoid oedema is well marked.
^ In the sixteen cases on which Ord based his descriptions, pregnancy ia one or two cases preceded the
myxoedema.
= Sir William Gull calls them spade like.
SCROFULA. 909
Prognosis. — This is always unfavorable ; its duration varies from six to
eight years. Death may occur from coma, uraemia, or inanition.
Treatment. — Besides warm clothing, tonics, and good food little can be
done. Prof. Ord found that ten to sixty minims of the fluid extract of
jaborandi, administered four times a day, was followed by marked relief.
He says the signs of myxoedema almost entirely disajopeared under this
treatment. JSTitro-glycerine benefited one case. Vapor baths are advo-
cated. Dr. Andrew Clark says that baths, assiduous friction, a careful
diet, and arsenic and iron as tonics, may sometimes cure the disease.
SCROFULA.
Scrofula is a term applied to many different physical conditions de-
pending upon a diathesis which is regarded as identical with the tuber-
culous.
Morbid Anatomy. — The characteristic lesions of scrofula are to be found
in the lymphatic glands, although the skin, mucous membranes, bones,
joints, and organs of special sense may be involved.' Inflammation ante-
dates the scrofulous change, and whether occurring in the glands, skin,
mucous membrane, subcutaneous connective-tissue, bones, joints, kidney
or testicle, the inflammatory product is the same. When fresh it is rich
in cells, consisting of a dim, glistening protoplasm with a large single or
double nucleus. The exudation is either nodular or diffused. It may
undergo resolution, suppuration or organization ; all taking place slowly
and imperfectly, on account of poor vascularity. Anemic necrosis some-
times occurs in the glands.
On the skin the lesions appear as eruptions. Impetigo of the eyelashes
and external otitis are common strumous diseases. In one who has this
diathesis any skin disease takes on a scrofulous character. Scrofulous in-
flammation of mucous membranes is marked by a thick, sticky exudation,
with a tendency to form scabs. The bones most frequently involved are
those of the ankle, lower part of the femur, the vertebrge, and rarely the
fingers and toes. The scrofulous development may assume the form of
synovitis, osteitis, periosteitis, or general arthritis.
Etiology. — The scrofulous diathesis is very largely an inherited condition
whose exact nature is unknown, and whose etiology is perhaps equally ob-
scure. It usually has been considered a functional disturbance of impaired
vitality, but some recent' observations afford ground for the suspicion that
it may possibly possess an anatomical basis.
The children of intemperate, phthisical, syphilitic, very old or very
young parents develop early all the characteristic features of the scrofulous
diathesis. It is also very apt to appear in the children of parents closely
1 Virchow taught that the primitive strumous lesion is a simple h}'perplasia of the gland tissue, but
Schiippel has proven ihaX. a scrofulous gland is a tubercvlous gland. Tubercles stud the glands, which
soon become enlarged and soft. When cut they eii her resemble a normal gland or contain a white, soft
cheesy mass mixed with thick pus. Abscess or ulceration may ensue and leave an unsightly scar. Simple
chriinic hypertrophy results in tlie formation of knotty groups of glands. Of all the tissues the lymphatic
is the most embryonic, the most plastic or potential.
910 CHRONIC GENERAL DISEASES.
related by blood. Heredity is by no means always present, however, for a
marked scrofulous diathesis is acquired in early infancy by healthy children
from improper food, over-crowding, and anti-hygienic surroundings.
Lack of fresh air, exercise, and sunlight exerts an equally powerful influ-
ence in reducing the vitality and the reactive power of the system under
irritation.' Scrofula and the tuberculous diathesis, if not identical, are so
closely related as to be interchangeable.'
Symptoms. — Scrofula presents no lesions that may not occur in other dis-
eases, and the scrofulous inflammation has no characteristics, beyond a
tendency to extreme clironicity and to undergo caseous changes. It is
principally a disease of childhood ; rarely, however, appearing before the
second year.
Children with a scrofulous habit are markedly different in appearance
from their healthier mates. Most of them have a transparent, white skin,
with delicate blue veins ; large, lustrous eyes ; bright red lips, and alto-
gether look more like wax figures than healthy children. They are apt to
show abnormal mental development, with an irritable nervous system. On
the other hand, they may have a large head with coarse features, a thick
skin, which has a flabby, spongy feel, an enlarged abdomen and cervical
glands. About the upper lip and the nose there is frequently ah over-
production of fat.^ In their development no two cases present the same
characteristics. Chronic inflammations of the skin, especially about the
face and scalp and at the junction of skin and mucous membranes, are
frequent, either alone or associated with persistent chronic catarrh of the
adjacent mucous surface. Coryza, conjunctivitis, ulceration of the cornea,
and otorrhoea often follow an eczema of the face and neck or alternate with
it. Laryngitis and bronchitis are obstinately persistent, and may extend to
the alveoli and eventuate in phthisis. Pyelitis, cystitis, and vaginal or
vulvar catarrh are rarer indications of the depraved condition.
The articular manifestations may appear as a simple synovitis or tumor
albiis, or some slight injury may be the starting-point of caries and ne-
crosis, with suppuration, burrowing of pus, and complete destruction of the
joint.
Glandular enlargements so invariably develop sooner or later in scrofulous
patients as to be accepted as the most characteristic lesion. This enlarge-
ment, which is non-inflammatory and due to cellular hyperplasia, is very
gradual, and forms a smooth, firm tumor, which, with similar adjacent
glands, may unite in an irregular, shapeless mass. Occasionally these
hypertrophied glands subside, but more frequently they finally excite in-
flammation with suppuration or caseous changes.
The disease progresses slowly with periods of apparent well-being, bub
toward puberty pulmonary disease is apt to be established ; or, if there has
been much suppuration, waxy degeneration may occur in the viscera or in-
1 BuW favors a specific virus theory, but the parasitic origin rests on no certain anatomical facts.
2 Birch-Hirschf eld found tubercles in nine out of ten lymphatic glands removed from the necks of
scrofulous patients.
s Canstatt calls this latter the torpid, and the former the erethitic form of scrofulosis.
RICEETS. 911
testinal tract. Such a condition will not long continue without the devel-
o^ament of extreme ansemia and a characteristic cachexia.
DifiFerential Diagnosis. — Scrofulous developments per se can hardly be
mistaken for any other disease, and a question of diagnosis can only arise
as to the nature of chronic degenerative changes other than glandular.
Such a diagnosis can be made from the obstinacy of the disease and coinci-
dent evidence of the j)eculiar diathesis.
Prognosis. — The prognosis is good when the patient is seen early, and
means exist for a change of diet and surroundings. Scrofulous children
may die from tuberculous intestinal disease, acute hydrocephalus, or croup.
Treatment. — The prophylactic treatment embraces a consideration of all
the laws of health. Until unhealthy, old and closely related individuals
cease to marry, until children receive the proper amount and kind of food
for the first two or three years of life, scrofula will exist.
The diet of scrofulous children should be the same as that advised in the
treatment of chronic phthisis {q. v.). Cod-liver oil will be the chief agent
for arresting its progress and development, and should be given daily dur-
ing the greater portion of infantile and adult life. Iodine is no longer re-
garded as a specific. Chloride of calcium and the sulphites have been recent-
ly highly recommended. Sea or brine baths or even ordinary cold water
baths are frequently of the greatest benefit. The treatment of the skin, joint,
and eye complications, and the question of extirpation of scrofulous glands,
belong to the domain of surgery.
EICKETS.
Eickets or rachitis is a disease of general malnutrition with characteristic
lesions in the osseous structures.
Morbid Anatomy. — Deficient ossification is the essential pathological
change ; bones already ossified are softened, and ossification in parts still
cartilaginous is prevented or delayed. G-rowth of the bone is retarded or
advances in an irregular manner, and while the medullary cavity increases
the osseous shell becomes deficient, owing to proliferation of unossified
matter at its circumference. There is an undue development of the car-
tilaginous epiphyses and fibrous periosteum,' causing the clumsy appearance
of rachitic bones. The flat bones are greatly thickened at their circumfer-
ence, from proliferation of the periosteum, but thinned at their centres, — a
condition called craniotabes: — this is especially marked in the occipital and
other cranial bones. In the lower jaw the anterior wall of the alveolus is
sometimes perforated by the milk teeth.
The liver, kidneys, sjDleen and lymphatic glands are often enlarged from
irregular hyperplasia of their fibroid and epithelial elements, conjoined
with a deficiency in earthy salts. The brain enlarges from increase in its
neuroglia. The muscles are small, pale, flabby, and soft, and their striae are
1 Virc'now thii« describes the changes in the diaphyses: — (1) Increasing density of perioste'il prolifera-
tion and progressive rarefaction of tlie substance in the areolje and cancellated tissue. (2) Deficient os-
eification of the cancellated tissue and continuance of the deep layers of compact exterior substance. (3)
Partial formation of cartilage in tlie areolae.
912 CHKOKIC GENERAL DISEASES.
very indistinct. The ligaments are also wasted. The fontanelles close
very late in rachitic children, and, on this account, chronic hydrocephalus
maybe suspected.
Etiology. — Our knowledge of the primary blood changes which result in
deficient ossification is largely theoretical. It has been supposed to be :
(1) the presence of lactic acid holding the salts in sojution ; (2) deficiency
of lime salts ; (3) an inflammation of the epiphyseal cartilages and perios-
teum ;' (4) some irritant in the blood.^ Clinically, rickets is caused by
anti-hygienic surroundings. Poor or deficient food and foul air are the
most potent factors. Acute disease and troublesome dentition predispose
to it. It is more apt to occur in children of rachitic, syphilitic, or phthisi-
cal parents.
The disease usually develops during the first year of life, and is rare be-
fore the seventh month or after the seventh year of life.' Foetal and con-
genital forms occur, and in many cases no cause can be ascertained.
Symptoms. — Usually gastro-intestinal disturbances are the earlier symp-
toms of rickets. There may be vomiting, and the motions are frequent,
pasty and offensive. The child, when awake, is listless and drowsy, and
when asleep is restless and sweats profusely, mainly about the head and
upper parts of the body, regardless of the temperature of the room. He
dislikes to be disturbed and frets when any one approaches his cot. There
is an intolerance of the bedclothes, which the child is constantly throw-
ing off.
The final distinct evidence of the osteal changes is the enlargement
of the lower extremity of the radius and tibia and of the corresponding
portion of the ulna and fibula. The softened bones yield readily to
pressure, and if the child is allowed to stand or walk, the legs become bent
and twisted, and the gait unsteady and swaying. The limbs may remain
perfectly straight, though stunted, thin and flabby, when the disease oc-
curs very early in life. The head is large and elongated antero-posteri-
orly, the fontanelles are wide and the sutures thick. The forehead is very
prominent, while the face is small and wizened, with the skin wrinkled as
in old age. The lower Jaw is shortened, so that the upper teeth overlap
the lower. The teeth appear late, the incisors may not appear until the
end of the first year, and dentition proceeds very irregularly. The spine
is curved, and distortions of the ribs induce an unsymmetrical or oblique
thorax.
Eachitic children are usually pigeon-breasted, and there is often marked
deformity of the pelvis. The joints are large, loose, and lax. The child is
short for his age, and the limbs are short in proportion to the trunk
and head. The abdomen is prominent, and the liver and spleen will
usually be enlarged ; sometimes their enlargement gives the first indication
of rachitis. The large cranium, thin face, and distorted limbs cause a
rachitic child to present the appearance of a monstrous deformity, when
intellectually it is bright and mature beyond its years. Eachitic children are
' Niemeyer. 2 Wagner.
5 Rehn states that lie never saw it develop after the third yewc.— Centralb.f. Kindr/i., 1877 to '78.
ALCOHOLISM. 913
anaemic and very sensitire to changes of temperature.' The nervous sys-
tem is very im j)ressionable, and general convulsions or spasms of the larynx
are frequent. All rickety children do not emaciate, and some only suffer
pain when they attempt an exertion.
Persons who were rachitic in infancy not infrequently become very
strong as they reach adult life. They remain of short stature and the
deformities persist. In foetal rickets the body is large and plump, the ab-
domen protrudes, all the abdominal organs being large, the skin is thick,
and the extremities are short and thick. In these cases the chicken-
breast is not present. *
Differential Diagnosis. — The nocturnal sweats about the head, the osseous
changes, the enlargement of the spleen and liver, the weakness of the legs,
the rims around the cranial bones, the large, lax joints, and the gastro-
intestinal disturbances form a train of symptoms that prevent rickets
from being confounded with any other disease.
Prognosis. — As a rule, when the cause is removed the disease will dis-
appear. The greater the thoracic deformity and the longer the disease has
existed the worse the outlook. Bronchitis, pneumonia, enteritis, laryn-
gismus stridulus, convulsions, difficult dentition, diarrhoea and chronic
hydrocephalus are not infrequent complications. Death may occur from
the wasting and anaemia, from the complications, or from asphyxia due to
thoracic deformity.
Treatment. — Cleanliness, fresh air, and nutritious food suitable to the
age of the patients are of the utmost importance. Children kept too long
at the breast often become rickety ; they should be weaned at once and have
liquor calcis saccharatus added to their food. Cod-liver oil should be taken
as early and in as large doses as the child can digest. Scraped raw beef^.
with a small amount of wine, often produces marked improvement. The
intestinal derangements are best corrected by castor oil or rhubarb and
soda. In older children quinine, iron, and lime preparations may be ad-
ministered.' The hydrate of chloral is to be used for any nervous derange-
ments. Eickety children should not sleep on feather beds or high pillows,
and must not be allowed to run about or exert pressure on any part thai;
may become deformed. Orthopaedic measures are treated of in works on
Surgery.
ALCOHOLISM.
Alcoholismus may be acute or chronic. Acute alcoholismus often mani-
fests itself as delirium tremens.
Morbid Anatomy. —In acute alcoholismus the mucous membrane of the
stomach and duodenum is intensely injected. Patches of aphthae are found
upon it, and the mucous surface of the stomach is covered with ropy mucus
slightly tinged with blood. The gastric juice is altered in quantity and
quality. The brain, lungs and kidneys are the seat of active hyperaemia,
1 Barthez regardw a blowing sound audible over the cranial sutures, as diagnostic of the affection.
" Recently the phonphates have been more recommended than cod-liver oil. The fluorides and arsenic
are esteemed highly by German phytsicians.
58
914 CHEOKIC GENEUAL DISEASES.
and the pericardium and .pleura are often filled "with bloody serum. In
chronit alcoholismus there is chronic gastritis, congestion or cirrhosis of
the liver, emphysema and bronchitis, fatty degeneration and dilatation of
the heart, atheroma of the vessels, and Bright's disease of the kidneys.
Chronic meningitis and pachymeningitis are common. In long-standing
cases cerebral softening occurs, and in such the viscera are fatty and the
subcutaneous tissue and omentum are loaded with fat if the subjects are
beer or wine drinkers ; those who drink s|)irits are emaciated and grow pre-
maturely old, on account of the increase in connective-tissue. Frequently
the abnormal accumulation of fat in the abdomen is in striking contrast
with tlie thin, wasted limbs.
The blood m chronic alcoholismus contains more fat than normal ; one
of the first effects of alcohol is a true chfimical combination with nerve-
tissue, and as the ingestion of spirits is constant, the nerves progressively
atrophy and harden. This is hastened by general interference with nutri-
tion from poor blood. The face of the confirmed toper shows turgid and
varicose veins, — especially about the nose, which becomes clubbed, — in-
jected conjunctivge, and pimples of acne rosacea. Puffiness under the
eyes indicates the changes taking place in the kidneys.
Etiology. — Even more deleterious than alcohol itself are the adulterations
of fusel oil, wormwood, and cocculus indicus. Delirium tremens comes on
after a prolonged debauch in an old drinker, or when one unaccustomed to
alcohol takes a comparatively large quantity of raw spirits. After ex-
posure to cold, prolonged abstinence from food, or some exhausting dis-
ease, a small amount of alcohol may induce acute alcoholismus. Chronic
alcoholismus is often met with in families where epilepsy, hysteria, in-
sanity, and allied disorders show themselves. In such cases a peculiar
constitutional condition which renders abstinence from alcohol especially
difficult, is undoubtedly present.
Symptoms. — In acute alcoholism, after a period of exhilaration and semi-
delirium, acute coma is very apt to supervene ; in this condition the breath-
ing is stertorous, the face is pale, and the pupils as a rule are dilated.
The skin is cold and clammy, and the temperature below normal. The
urine may be albuminous, and always contains more or less alcohol. Some-
times control over the sphincters is lost. In rare cases delirium tremens
occurs after the first debauch.
In chronic alcolioUsmus there is muscular tremor and pyrosis, or vomit-
ing on waking, with entire loss of appetite, the sleep is disturbed, and there
is headache and vertigo ; the will-power and memory are progressively
weakened until entirely lost, the gait becomes ataxic, the face is flabby and
the eyes watery. The breath and sweat have a peculiar, offensive odor,
the generative functions are enfeebled, muscular ti'emors become constant,
and the patient is in a continued state of dread or anxiety.
Delirium tremens occurs most frequently in old topers after a severe
drinking bout : — there is complete anorexia, marked tremor, especially of
the tongue, insomnia, or sleep disturbed by bad dreams, disorders of vision
and hearing, a soft, weak pulse, cold extremities, and extreme mental de-
ALCOHOLISM. 915
jection. In a day or two a wild delirium comes on characterized by the
most terrible hallucinations, snakes and all forms of repulsive reptiles
bemg seen and causing the most intense horror and abject fear. The
patient talks incoherently and incessantly, moves constantly and quickly,
has a wild or vacant expression of the eye, and all the muscles are mean-
while in a continual tremor. The pupils are contracted, the pulse is rapid,
feeble, and dicrotic. Insomnia is continuous. After a day or two, coma-
vigil and all the typhoid symptoms appear as the precursor of death, or a
sound sleep ends the delirium and establishes convalescence.
Acute alcoholic mania, acute melancholia, or chronic dementia with sui-
cidal tendencies, are common exhibitions in chronic, but rare in acute
alcoholismus. ^
Differential Diagnosis. — The coma of alcoholism may be confounded with
urmmic coma, which has already been considered. Its diagnosis from apo-
plectic coma will be considered under apoplexy.
It can only be distinguished from opium poisoning by an examination
of the contents of the stomach, and by an examination of the uriue.
The delirium of acute diseases will not be confounded with delirium tre-
mens if the history of the case and the j)atient's temiaerature be taken.
Meningitis is distinguished from alcoholismus by the firm, hard pulse,
the pyrexia, the projectile vomit, the retracted abdomen, the j)hotophobia
(absent in alcoholismus) and the agonizing headache.
Chronic alcoholic tremor has been confounded with shaTcing palsy (q. v.),
with locomotor ataxy, and softening of the brain ; their differential diag-
nosis will be considered in connection with the history of these diseases.
Prognosis. — The prognosis is good if the patient is manageable. Death
may occur in acute alcoholic coma, and from acute lobar pneumonia which
so often complicates it. A patient in delirium tremens may suddenly j)ass
into a comatose state, which will soon be followed by death. The degenera-
tive changes which take place in the vessels and viscera in chronic alcohol-
ism predispose to a long list of diseases and tend to shorten life. Insanity,
impotence, epilepsy, melancholia, and organic brain diseases are its fre-
quent seqaelge.
Treatment. — In acute mania, delirium, etc., w^ash out the stomach and
give a simple saline purge. Cold affusions and galvanism with energetic
friction are beneficial. In delirium tremens nothing but milk must be
given in the way of food. Bromide of potash, hydrate of chloral, oj^ium,
and hyoscyamus are all favorite drugs for inducing sleep. Tartar emetic
sometimes acts in this way.^ Inhalation of chloroform should be practiced
with great care. Sometimes stimulants are necessary if the vitaj powers
are much depressed. In chronic alcoholismus bromide of potash, or better,
hydrate of chloral, is to be employed for the insomnia. For the craving
for alcohol, opium is sometimes given, but is apt often to engender a still
worse habit. A variety in the diet, pleasant surroundings, and strong
will-power are about the sole means of combating this condition.
1 Oinomania is a condition where at long intervals an individual has paroxysms of alcoholic excess, be-
tween which he neither touches nor craves alcohol. This form is truly a disease.
a Jones, of England, advocates digitalis.
916
CHRONIC GENERAL DISEASES.
TRICHIlSrOSIS.
Trichinosis is a parasitic disease, classed by some among the acute in-
fections diseases.
Morbid Anatomy. — Trichina spiralis, in the form of a minute worm, meas-
uring about one thirty-fifth of an inch in length, enters the human system
through the intestinal tract after the ingestion of trichinous flesh. The
muscle larvse mature two days after, and in six days the embryos are born.
In about fourteen days the migrating progeny reach the muscles. Some
believe that the blood-vessels are the channels of their conveyance. The
most prevalent idea, however, is that they pass through the intestinal walls
and peritoneal cavity and then enter the muscular system. Once in the
IMW
Fig. 186.
Encapsulated Trichinte in voluntary muscle.
X 300.
Fig. 187.
Trichinte with calcareous deposits and de-
generation of the capsules, x 300.
muscles, ovoid protective capsules are thrown around the entozoa, each of
which is curled up spirally like a hair spring. The muscular fibrillse sub-
sequently break down into a granular debris, interstitial connective-tissue
forms in abundance, and in the neighborhood the muscles have an inflamed,
gray-red appearance.
The voluntary muscles are those usually invaded. The ends of the
muscle^where it becomes tendinous — exhibit the greatest number. The
diaphragm, lumbar, intercostal, cervical, and laryngeal muscles, and those
of the eye are the favorite sites. As a rule, the farther from the trunk the
fewer the trichinae. At times the heart has been infested with them. The
number of the trichinae in the muscles is greater the longer the disease has
lasted.* Later the capsules become dense, fibrous, cheesy, and even chalky.
I Oohnheim states that the muscles have no ather changes exceut those met with in acute infectious
diseases.
TEICHINOSIS.
917
At the autopsy of one who has died of trichinosis during the first week,
only the signs of more or less intense intestinal catarrh are found ; after
the fourth or fifth week, distinct signs of interstitial and parenchymatous
inflammation of the muscles are found as fine gra3''ish-red striae. Intestinal
catarrh, enlarged mesenteric glands, peritonitis, venous thrombosis, and
hypostatic congestion of the lungs are also quite frequently found. En-
cysted trichinae retain their vitality for a number of years.
Etiology. — Trichinosis in the human being results almost exclusively
from eating trichinous pork. The raw flesh is most dangerous ; the more
underdone the pork the greater the danger. Pork cooked in any way that
does not kill the trichinae is dangerous. Sausages, ill-smoked ham, or
quickly-broiled ham, or any form of pork that has not been subjected to a
moist heat of ] 70°, is liable to induce it. Salting meat does not necessarily
destroy the trichinae. Each trichina may give birth to a thousand young ;
about one-half a pound of pork containing trichinae could rapidly produce
thirty millions of trichinse. *
Symptoms. — The symptoms of trichinosis are first gastro-intestinal and
then muscular ; associated with these there is more or less fever. After a
varying time following ingestion of trichinous meat, nausea, vomiting,
vertigo, anorexia, a feeling of malaise, and a slight febrile movement
occur. There is almost always diarrhoea, the passages being first brownish,
then yellow ; after a short time there are wandering pains in the limbs,
which become stiff and painful to the
iouch, and the muscles are swollen
And. rigid. In from four to ten days
cedema of the eyelids, perhaps of the
entire face, occurs. The temperature
ranges from 101° to 106° F., the
pulse from 110 to 120 ; there is photo-
phobia, and movements of the limbs
or of the eyes are accompanied by ex-
cruciating pain. The pain in the
limbs becomes so great that the patient
cannot sleep. (Edema of the lower
extremities is common ; and there
may be general anasarca. Copious
perspiration with sudamina charac-
terize the fever of trichinosis. The
diarrhoea becomes exhaustive, the
limbs are paralyzed and the patient
lies in a state of utter helplessness.
Abdominal pains are sometimes
present and the muscles of the ex-
tremities may become strongly flexed. Deafness and aphonia occur when
trichinosis of the stapedius muscle or of the muscles of phonation respect-
Bay
S.2.
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Fig. 188.
Temperature Record in the fourth week of a case
of Trichinosis. Death on the 29th day.
» Trichinae have been found in rats, mice, dogs, cats, badgers, etc., and swine get them by eating Van
excrements of them; auiuiulB or the dead animals themselves, rats and mice especially.
918 CHROIS"IC GENERAL DISEASES.
ively takes place. ^ When recovery is to occur the symptoms all gradually
abate. This occurs in from four to five weeks after the first evidence of
its commencement. When death occurs it is usually during the fourth
week, and it may or may not be preceded by delirium.
Differential Diagnois. — Trichinosis may be confounded with typhoid
fever, myalgia, Asiatic cholera and inflammation of the muscles. The
points of diagnosis between trichinosis and typhoid fever have already been
considered.
From myalgia, or inflammation of muscles, trichinosis is distinguished by
the abdominal pains, the diarrhoea, febrile movement, and the history of
the case.
Cholera is distinguished from it by the sub-normal temperature, absence
of sudamina and copious perspiration, and by the presence of the charac-
teristic rice-water discharges. It is said that the nematoid can be found
in the faeces. In all cases a diagnosis can be reached by excising a piece of
the deltoid muscle and examining it microscopically.
Prognosis. — There are no reliable statistics by which its rate of mortality
can be determined. It may be complicated by hydrothorax, pneumonia,
bronchitis, haemoptysis, gastritis, enteritis, peritonitis and anasarca.
Treatment. — Preventive treatment consists in eating no pork that has not
been so prepared as to kill any trichinae that might exist. The first indi-
cation for treatment is to support the patient by a nutritious diet and mod-
erate stimulus. We know of no means of destroying the trichinae after
they have once entered the muscles. Very early in the disease a prompt
emetic or a brisk purge may remove the trichinae from the intestinal tract.
Calomel, jalap, scammony and colocynth are efficient for such purpose.
To allay the fever and overcome the subsequent anaemia quinine and iron
are of service. The treatment is mainly symptomatic.
SYPHILIS.
Syphilis is a specific infectious disease produced only by inoculation. It
presents a characteristic acute, initial lesion, and multiform chronic mani-
festations, which follow a uniform order of development, and are of two
distinct forms, called secondary and tertiary lesions.
Morbid Anatomy. — The pathological changes in the primary and second-
ary stages are essentially inflammatory. About the point of inoculation
there is hyperaemia and cell infiltration, followed by necrosis or ulceration,
and resulting at first in a papule, and later in a simple excoriation or a
shallow, indolent ulcer, with characteristic induration and a dirty-gray base,
which eventually leaves a discolored, retracted cicatrix. This ulcer is the
typical Hunterian chancre. For its many deviations due to adventitious
circumstances reference must be made to surgical works. In connection
with the inflammatory changes of the secondary stage there is proliferation
1 Cohnhelm states that the position of one suffering from trichinosis is that in which the various
groups of muscles are least extended.
SYPHILIS. 919
of connective-tissue with new formations which soon subside or merge with
the tissue in which thej occur, producing ostoses, or in vascular organs in-
duration and atrophy. In the tertiary stage the process assumes the form
of specific neoplastic formations termed gummata, which may be circum-
scribed and isolated, but more frequently are infiltrated through the af-
fected tissue. They may appear as firm, gray, opaque nodules, or as soft,
translucent masses. They consist histologically of a cell-growth, resembling
granulation tissue, and, unlike the earlier manifestations, show little tend-
ency to resolve, but evince a marked tendency to undergo caseous and
calcareous changes and to produce necrotic processes in the infiltrated tis-
sue.
In the skin, mucous membranes, and smaller cartilages and bones, this
degenerative process results in fatty degeneration, ulceration, and slough-
ing, and may result in widespread destruction of tissue. In the deeper
organs it produces more or less circumscribed tumors, composed of ca-
seous matter, granular detritus, calcareous deposits and fibroid indura-
tion. The distinction between secondary and tertiary lesions is often more
distinct clinically than pathologically. The glandular changes which
appear soon after the initial lesion are permanent, and are due to cellular
infiltration and hyperplasia, but are not usually attended by suppura-
tion.
Etiology. — There is no doubt as to the specific nature of syphilitic poison,
or its transmission solely by inoculation, which may be mediate, immediate,
or through the processes of conception. The poison is most frequently
communicated during sexual intercourse, but inoculation may occur from
deposition of the poison upon any abrasion of the surface or upon delicate
membranes, as those covering the sexual organs, without any solution of
continuity. Thus infection may take place in kissing, or from the use of
pipes, drinking vessels, etc., upon which the poison has been deposited.
Nursing children may infect, or receive the poison from their nurse.
Physicians not infrequently receive it accidentally upon the fingers, or are
the agents in its transmission by vaccination.
Even more unfortunate are the victims of syphilitic parents. The poi-
son in the mother invariably manifests itself in the child, and when in the
father, infects the offspring and, secondarily, the mother through the foetal
circulation. The syphilitic poison is most virulent in the primary sores and
glandular affections, but is present in the blood in decreasing quantity
through both the secondary and tertiary stages. Late in the disease it is
found only in the discharges from those organs which are involved in the
specific processes. One inoculation of syphilitic poison, with rare excep-
tions, confers protection from all subsequent poisoning.
Symptoms. — Primary. The period of incubation is variable, but is sel-
dom less than ten days and averages about twenty-five. The first change
is the appearance of a dark-red papule, which slowly enlarges, becomes in-
durated early, is not painful, and may even escape notice. Although it
may run its full course without becoming moist, generally the apex be-
comes eroded, leaving a moist surface, or undergoes ulceration. The true
920 CHEOXIC GENERAL DISEASES.
chancre does not secrete j)us unless it becomes inflamed, but remains a sim-
ple excoriation, either moist or scabbed, through its entire course. The in-
duration may be thin and superficial, may simply underlie the excoriation,
or may spread extensively into adjacent parts. In the course of six or eight
weeks the sore begins to heal, the induration subsides, and finally there is
no trace left, or if ulceration has been present, there remains a white or
slightly pigmented cicatrix. Soon after the appearance of the primary
sore, the nearest lymphatic glands indurate and enlarge but rarely suppu-
rate. Nor do they resolve with the healing of the chancre, but remain en-
larged for months and years, and are eventually joined by other glands
throughout the body.
Secondary syphilis includes the earlier and generally lighter affections of
the skin and mucous membranes, with some of the affections of the organs
and nerves. The most prominent are those of the skin which usher in the
eruptive stage of syphilis. They appear from six weeks to three months
after inoculation, and in nearly one-half the cases before the initial lesion
has healed. This stage is often attended, at its invasion, by some slight
fever and constitutional disturbance, marked by weakness, emaciation, and
wandering pains in the limbs and joints. The cutaneous syphilides assume
nearly all the types of skin diseases, and present in this multiplicity of
form a distinctive characteristic. The earlier eruptions are generally the
simpler forms of erythema, and papules, and are diffused over the surface
quite uniformly. Later, there appear vesicles, pustules, tubercles, and
scaly eruptions which are more apt to be gathered in groups. Not infre-
quently several or all the forms may be present. In all syphilides there
is a general roundness of form, an absence of pain and itching, and a pe-
culiar livid coppery color which gradually changes in cicatrices to a glis-
tening white.
Secondary syphilis most frequently affects the mucous membranes of the
fauces and pharynx. In connection with the earlier symptoms there may
be only a diffuse hypergemia and a redness with or without ulceration ; but
with the later secondary and earlier tertiary, there is a peculiar dusky red
appearance, the result of chronic congestion, and more or less thickening
and induration about ulcers and mucous patches. This condition seldom
causes any pain or discomfort, and the ulcers may disappear spontaneously.
Mucous patches appear most abundantly about mucous orifices, as the
mouth and anus, but may appear on the skin. They are round or
oval, slightly elevated spots of varying size, with a moist excoriated sur-
face, which does not ulcerate unless irritated. They appear with the
earliest eruption and continue with decreasing frequency into the tertiary
stage.
The secondary affections of the eye assume the form of iritis with ex-
tensive exudation, and retinitis, which, appearing with but little pain or
photophobia, is attended by extravasations and partial or complete abolition
of function. In connection with the general tegumentary inflammation
the hair-bulbs are involved, and the hair becomes thin or is lost en-
tirely.
SYPHILIS. 921
Tertiary. — Secondary symptoms usually pass away after a few months
and the patient may never suffer further, or, more frequently, he enjoys a
period of apparent health of from two months to two years, in some cases
extended to twenty or more years. In other instances there is no break, but
the secondary lesions merge into those of the tertiary stage. The special
characteristics of tertiary lesions, as already stated, are the formation of new
tissue — gummata — and the tendency to cause degenerative and necrotic
changes. Fibroid < change and induration are less frequent results. They
involve deeper parts, and are not symmetrical, but are persistent and re-
current. Tertiary syphilis is rarely attended by any fever, and even a ca-
chexia is wanting in most cases. When present this cachexia is indicated
by anaemia, with possibly some anasarca and general depression, both physi-
cal and mental. The skiu is dry, harsh, and dirty looking, the face thin,
the eye dull, and the general appearance that of decay. In the skin,
gummy tubercles, which may be single or in groups, result in ecthyma,
rupia, and extensive ulcers, which leave characteristic cicatrices. Sub-
cutaneous gummata may soften, break through the skin, and form deep
ragged cavities which heal slowly. Similar processes occur in mucous
membranes, more particularly of the mouth, pharynx and nose, and may
destroy the tonsils, fauces, and soft palate, or entirely clear out the nasal
cavities. The resulting cicatrices produce permanent stricture of the fauces
or oesophagus, and other deformities.
Syphilis of the viscera is most frequent in the liver, where it appears as
gummata or general fibroid induration. All the organs are liable to sim-
ilar deposits, as the heart and arteries, lungs — syphilitic j)n€umonia — and
bronchial tubes, or any abdominal organ. In the bones, caries and necro-
sis are often chronic states, and diffuse or circumscribed periostitis with
the formation of painful, tender nodes is very characteristic. These
nodes do not often suppurate, but are quite permanent. Of even greater
importance are the lesions of the nerves. The cranial bones and cerebral
membranes are the seat of nodes and gummy tumors which cause convul-
sions or paralysis and disturbances of function, as epilejisy and insanity,
by direct pressure or through inflammatory processes. In the brain sub-
stance inflammatory softening and induration are the most frequent changes.
In the eye the cornea, iris, and retina are more frequently affected, and
the changes differ in degree rather than in form, from those found in the
secondary stage.
Inherited Syphilis. — Syphilis may be inherited from either the father
or the mother. If from the father, the mother will not escape infection
during pregnancy unless he is in the tertiary stage. Syphilitic mothers
usually abort two or three times, then produce a weak, unhealthy child
that dies within a few days. Finally, an apparently healthy child is born.
It does not develop properly, however, looks old and withered, and in a
few months secondary eruptions make their appearance with excoriations,
mucous patches and ulcers about the mouth, nose, anus and genitals. At
the same time it develops the characteristic snuffles. The nose discharges
an irritating secretion at first, producing excoriations on the lips. Becom-
922 CHRONIC GENERAL DISEASES.
ing closed it fills with mucus and pus which produce ulceration and ne-
crosis. Tertiary symptoms appear early, and gummy tumors and fibroid
indurations may occur in the yiscera in connection with the secondary erup-
tions. Such children have a very characteristic appearance ; they are thin
and poorly nourished, the skin is pale, coarse and wrinkled, the forehead
and cheek prominent, the eyes and nose sunken, and the teeth present the
peculiar pegged appearance. Interstitial keratitis causes defective sight
and photophobia, and the child, with some deafness, a coarse, harsh voice,
wrinkled brows and apathetic look, presents a pitiable sight.
Differential Diagnosis. — For the diagnosis of the primary lesions reference
should be made to surgical works. As the diagnosis of secondary and ter-
tiary lesions depends so largely upon their location, they are considered in
connection with the diseases of the various organs. In inherited syphilis
the coryza and snuffles, the cracks, excoriations and fissures about mucous
orifices, with mucous patches, are the early characteristics. Later there are
the scars on the face and in the throat, the sunken nose, and peculiar teeth.
In many cases, however, the differentiation can be made only by the results
of treatment.
Prognosis. — As a rule the prognosis is favorable before destruction of tis-
sue has begun, and even afterward the necrotic process may be arrested.
It varies greatly, however, with the nature of the lesions and their situation.
In confirmed drunkards, and when the disease assumes a rapid or malignant
form, the prognosis is grave. In inherited syphilis the prognosis varies
with the date of the appearance of symptoms. If the eruption is present at
birth or occurs early the child seldom lives. The longer the disease remains
latent, the more favorable the prognosis.
Treatment. — The treatment of syphilis is primarily specific, and confined
to the use of two drugs, — mercury and iodine. Secondarily it is hygienic
and tonic, a relation which for a time is reversed in some cases. Specific
treatment is often unavailing when used alone, but becomes brilliantly suc-
cessful when assisted by fresh air, good food, exercise and rest, with oil,
iron, quinine and other tonics.
As a rule mercurials are more efficacious in the earlier, and iodine in
the later manifestations. Mercury should be given as soon as a diag-
nosis of chancre is established, but were better omitted until the appear-
ance of secondary symptoms than used on an uncertain diagnosis. When
treatment is begun thus early, it should be continued for at least a year,
and followed by one or two years of a mixed treatment of mercury and
iodine.
When treatment is begun late in the course of the disease either iodides
alone or a mixed treatment will most speedily remove the lesion, after
Avhich the patient should continue treatment for a year or more. Gener-
ally it is well to continue a mild mercurial course for at least six months
after all lesions have disappeared. The present tendency is toward a more
extended use of mercury in the later stages of the disease. The methods
of administering mercury are too numerous to be described in detail : the
more common, aside from tliat by the stomach, are, hypodermically, by
SYPHILIS. 923
fumigation, baths and inunction ; the latter being the most desirable for
children with inherited syphilis. Iodine may be used in its combinations
with potash, soda, ammonia, mercury, iron, etc. The doses of both
mercury and iodine must be determined by trial for each case. With
mercury they should fall short of salivation, but with iodine should
increase to the limit of the patient's endurance, or until the lesions yield to
treatment.
SJi^CTION Vl.
DISEASES OP THE NERVOUS SYSTEM. '
{Including Diseases of the Brain, Spinal Cord, and Functional Weriaous Diseases.)
GEl^EEAL SYMPTOMATOLOGY.
The symptomatology of nervous diseases presents many peculiarities which
render their diagnosis especially difficult. Nearly every pathological con-
dition may be the result of so many different lesions that at best it is
indicative of the seat and extent of the lesion only, and not of its nature,
and often only determines the division of the nervous system which is
affected. Symptoms are, therefore, entirely negative when taken singly,
and find their significance only in the order and manner of their develop-
ment, or in their combinations with others equally valueless per se. All
symptoms of nervous disease appear as (1) impairment or abolition, (2) ex-
altation, and (3) perversion of function, and may manifest themselves
through the motor, sensory, co-ordinating, or psychical systems by symptoms
which will vary with the location, nature, and extent of the lesion. I shall
first consider some of the more important symptoms in their general rela-
tions to nerve lesions.
Motor Paralysis. — Loss of motor power, or voluntary nervous control
of muscular movements, may exist in all degrees, from the slightest weak-
ening or delaying of the nervous impulse to absolute abolition of the im-
pulse or its complete arrest in transit to the muscles. The lighter and
intermediate grades are termed paresis, while paralysis is applied to ex-
tensive or entire loss of motor power. The nature and extent of the
paralysis is evidenced in the muscles, so that the muscular condition be-
comes a matter of primary importance.
(a) Reflex Action. — In many instances, and more especially in spinal
paralysis from circumscribed lesions, the muscular force, as indicated by
reflex movements, is not diminished. Under suitable irritation the ap-
parently powerless muscles execute violent movements and become power-
fully contracted. These reflex movements are not always limited to the
irritated limb, but may appear in other paralyzed muscles. For diagnostic
purposes, then, reflex action indicates unimpaired nervous connection be-
tween the paralyzed muscles and the spinal centres, and can never be
present when the paralysis is due to a disseminated destructive lesion of
the nuclei of origin of the affected nerves, but is generally most distinct
in disease interrupting the transmission of voluntary motor impulses. A
very common and patent form of reflex action is known as tendon reflex.
GENERAL SYMPTOMATOLOGY. 925
If in health the tendon of any muscle be struck a sharp, quick blow, there
will immediately follow distinct contraction of its attached muscles, most
marked, of course, in the larger muscles, as those attached to the patella
or tendo Achillis. Abolition or exaggeration of tendon reflex is an im-
portant point in diagnosis. Either may be associated with decrease or
increase of reflex action from irritation of the skin. A third form of re-
flex action is called ankle clonus. This consists in a clonic tremor of the
muscles, particularly of the leg, occurring whenever the muscle is stretched
by flexion of the foot, aud continues during flexion. In severe cases it
may be excited by putting the toe to the floor, and then often involves the
entire limb. Abolition of reflex action maybe due to degenerative changes,
either in the nerve trunk or spinal centre, but exaggeration is generally the
result of central irritative lesions.
(b) Electrical Irritability. — Electrical contractility of paralyzed muscles
may remain normal, be increased, or impaired. When muscles atrophy
from disease, or are the seat of degenerative changes, Faradic contractility
is proportionately decreased. As dependent upon nerve changes it is not
only generally retained in both cerebral and spinal paralysis due to inter-
ruption of nerve-currents, but is frequently, and especially in thie latter
form, increased. When disease involves central nuclei or nerve-trunks,
Faradic contractility is often rapidly and extensively lost. Such muscles
may still react, however, t0 the slowly interrupted galvanic current, even
after they fail entirely to respond to the Faradic. Indeed, galvanic con-
tractility may increase as Faradic decreases, and eventually become more
marked than in healthy muscles.
(c) Muscular Nutrition. — Muscular nutrition and tonicity generally keep
pace with contractility ; and the muscles remain firm and are but slightly
reduced in bulk, or they may become small and flabby, or in some cases
contracted and rigid. The former condition prevails when disease lies
above the origin of the implicated nerve, but sudden onset of the disease
or implication of nuclei or nerve trunks results in flaccid and wasting
muscles. Rigidity and contraction follow irritative lesions or complica-
tions and also occur in paralysis of long standing, in which case they
are mostly due to secondary descending degeneration of the cord.
General Paralysis. — Lesions resulting in general paralysis of necessity
involve such important parts as to be followed in most cases by immediate
death. General paresis occurs in connection with insanity from diffuse
disease of the cerebral cortex. It implicates all the voluntary muscles, not
excepting those of deglutition and phonation, but is slight in degree, sel-
dom extending beyond weakness and sluggishness of movement.
Bulbar paralysis is perhaps the nearest approach to general paralysis.
Disease of the pons or medulla generally results in bilateral paralysis, and
is the cause of the mixed and crossed paralyses occasionally met with, as
paralysis of both arms, both legs, or one side of the face and the oppo-
site side of the body. Motions of the eye, phonation, deglutition and res-
piration are especially liable to be interfered with, and death is seldom
long delayed.
Cerebral Causes.
926 DISEASES OF THE ]S"ERVOUS SYSTEM.
Hemiplegia is a motor paralysis limited to a lateral half of the body.
It is generally the result of a lesion above the medulla, and most fre-
quently of the corpus striatum, but may result from injury to a cerebral
hemisphere or crus. It occurs on the side opposite to the disease or in-
jury. Its most frequent cause is undoubtedly apoplexy, but it may be
due to other cerebral injuries or disease, and not infrequently is functional.
The causes of hemiplegia may be classified as follows :
' Compression from bone, blood, pus, or inflamma-
tory exudations.
Tumors, especially carcinoma, sarcoma, gummata.
Partial ansemia from thrombosis, embolism, soft-
ening, aneurism, apoplexy.
Encephalitis, — abscess.
Atrophy and sclerosis.
^ . 1 p j As above, or any disease affecting a lateral half of
■^ ( the cord.
-p, , . , p j Hysteria, chorea, epilepsy, diphtheria, malaria,
( poisons, etc.
Although the paralysis is of central origin, the muscles are seldom af-
fected uniformly, and ,it has been noted that those which suffer least are
such as act in conjunction with their counterparts on the non-paralyzed
side. The muscles of the arm and leg are chiefly affected, while those ol
the trunk and neck often escape entirely, so that the body and head remain
erect and firm. The paralysis is generally descending in its onset, and as-
cending in its recovery, the leg being last involved and the first to regain
its power. Occasionally, however, the leg escapes entirely, or it may suffer
a more complete paralysis than the arm. Of the cranial nerves the third,
fourth and sixth seldom suffer unless the lesion is in the crus, when the
third will probably be involved. The fifth, also, as a rule, suffers but
little, but may be paralyzed in either or both roots, a condition indicated
by anaesthesia of the face and cornea and paralysis of the muscles of mas-
tication on the affected side. The facial, on the other hand, seldom
escapes entirely in lesions at the base. The face becomes blank and mo-
tionless, the mouth is drawn toward the healthy side, and the j)aralyzed
cheek puffs on expiration. The muscles of the tongue may escape or suf-
fer with the others, and the tongue will then be protruded with the tip
pointed toward the affected side. When hemiplegia is uncomplicated its
diagnosis is evident, but if associated with coma it may not be readily ap-
preciated. The paralyzed limbs, however, will be more flaccid, and when
raised and released will drop more heavily and limply than on the unaf-
fected side. If the face is implicated the peculiar expression and retrac-
tion of one angle of the mouth will be readily appreciated. In the differ-
ential diagnosis of the causes of hemiplegia the location, nature, and ex-
tent of the paralysis will be of value, but the most important points will
be found in the history of the case, the manner of invasion, and the pe-
culiar combination of other symptoms.
GENERAL SYMPTOMATOLOGY. 937
Paraplegia. — Bilateral paralysis, of whatever, extent is termed paraple-
gia, and when of organic origin aif ects only those parts of the body supplied
by nerves leaving the spinal cord at or below the seat of the lesion. Or-
ganic paraplegia, therefore, is commonly of spinal origin, and in extent
varies with the seat of the lesion.' If this is located in the dorsal region
the lower extremities alone are affected ; the paralysis becomes more exten-
sive the higher in the cord it has its seat ; when it has its seat in the cervical
region the entire body, including the diaphragm, may be paralyzed. In all
forms, however, the sphincters are liable to be involved. Generally if the
disease is high up there will be spasm and retention ; if low down, paral-
ysis and incontinence. Paralysis may be of all grades and varieties, ac-
cording as more or less of the thickness of the cord is involved. There
may be simply slight paresis, decided paralysis with sensation unimpaired,
or complete paralysis of both motion and sensation. Disease of the cord
has a special tendency to be unsymmetrical, and confined to particular
tracts. As a result the effects are very varied. When the changes are
confined to a lateral half, motor paralysis affects the parts below on that
side, but owing to the immediate decussation of sensory fibres on entering
the cord, and their consequent implication with motor fibres of the other
side, anaesthesia is found on the opposite side of the body below the lesion,
with possibly a distinct line of anaesthesia marking the upper boundary
of motor paralysis. The limitation of spinal lesions to distinct tracts has
given rise to such characteristic combinations of symptoms as to lead to
their being considered as special diseases.^
Aside from the foregoing forms of paralysis for the most part due to in-
terruption of the connection between nerve-nuclei or trunks and the higher
centres, paralysis may result from direct injury to, or destruction of, these
nuclei or trunks. In such cases the paralysis is confined to the distribu-
tion of the affected nerves, is generally more complete and permanent than
in other forms, and is attended by rapid loss of Faradic irritability with
wasting of the muscular tissue.
Spasms, Convulsions. — In determining the seat and nature of the disease
causing spasms the same anatomical facts are to be considered as in the
diagnosis of paralysis. It is probable that irritative lesions of the same
centres as are affected in paralysis result in motor disturbances ; hence con-
vulsions of a lateral half of the body may be ascribed to irritation of the
opposite cerebral hemisphere, corpus striatum or crus. In a similar man-
ner spasms confined to the lower portion of the body and bilateral are to
be considered of spinal origin, while general convulsions may be the result
of general cerebral disturbance or of a general affection of the cerebro-spinal
> Etiology :
Brain \ Small clot in the pons.
r Compression of a lateral half of the cord from bone as In fracture, caries, dislocation,
Spinal -j spinal bifida, from blood (traumatic), pus, exudations, tumors, all diseases of the cord,
1 shock and concussion.
Functional -{ Hysteria, catalepsy, rlieumatism, syphilis, poisons.
Reflex -j Diseases of geniro-urinary organs, diseases of intestines.
' See locomotor ataxia, profjresdve muscular atrophy, etc.
9']Q DISEASES OF THE NERVOUS SYSTEM.
system. Basing the diagnosis upon our knowledge of the motor areas of the
cerebral cortex, it is possible in many cases to locate the lesion quite exactly
by careful consideration of the location and extent of the convulsive move-
ments. Spasms are even more varied in their distribution than paralysis,
affecting single muscles, muscular groups, a single limb, half the body or
all the muscles, not excepting those of respiration and deglutition, and
they vary in degree from light fibrillary twitching to such violent cramps
as to rupture muscles or to fracture bones. When the contractions are
persistent they are termed tonic, but when rapidly alternating with relaxa-
tion are called clonic. Convulsions appear as symptomatic of both organic
and functional disease. Tremulousness of the muscles often accompanies
paresis, and paralysis is frequently followed by tonic contractions. Fibril-
lary twitchings are common in debilitated conditions, in general paresis,
the typhoid state, paralysis agitans, etc. ; while the severe forms are illus-
trated in inflammatory conditions of the brain and cord, epilepsy, tetanus,
strychnia poisoning, hydrophobia, etc.
Seiisory Paralysis, Anmstliesia. — Anaesthesia, like motor paralysis, may
be located in any part of the body, may be of all degrees, and may be super-
ficial or extend to deep parts. When slight it is only a sense of numbness
which gives the impression of some soft substance covering and protecting
the parts, and is generally attended by formication or burning prickly pains.
In complete anaesthesia the patient is unconscious of the severest injury,
and bed-sores may denude the bones without his being aware of their ex-
istence. In some cases sensations of heat and cold are still appreciated,
while all other sensibility is lost. Among perverted sensations may be
placed those conditions in which sensation is delayed, and the patient ap-
preciates the impression only after the lapse of some seconds, or is unable
to determine its nature. In many cases he suffers severe neuralgic pain in
the anaesthetic parts, due to the central nervous irritation. Anaesthesia
may be general with general paresis in insanity, but rarely so in other con-
ditions. It more commonly appears as hemi-aneesthesia, from causes sim-
ilar to those of hemiplegia, but is less frequent than the latter. It most
frequently depends upon lesion of the external capsule or fibres of commu-
nication between the optic thalamus and hemisphere, and frequently impli-
cates some Qf the nerves of special sense. Lesions of the tegmentum of the
crus also result in opposite hemi-ansesthesia. Spinal anesthesia is also far
less frequent than paraplegia, but when present is almost always associated
with it. The condition of reflex action will indicate somewhat its nature.
When paraplegia and anaesthesia are the result of destruction of nerve nu-
clei in the cord, or of injury to the nerve-trunks supplying the paralyzed
part, reflex activity will be abolished. When, however, the paraplegia is of
parts below a spinal lesion, reflex action is normal or often increased. As
noted before, a lesion of a lateral half of the cord may give a joaraplegia
compounded of motor paralysis on the side of the lesion and sensory ])aral-
ysis on the opposite side.
Hyperesthesia. — Hyperaesthesia, either general, partial, or .of the nerves ■
of special sense, is of common occurrence in nervous disease, since it may be
GEKERAL SYMPTOMATOLOGY. 929
the result of the most trivial disturbances. It is present in the congestive
or early stages of inflammatory conditions of the brain and cord, and in
functional disturbances. It is often a symptom in the earlier stages of fe-
brile diseases and in inflammation of the skin*. When normal sensation
becomes painful, it is termed dysaesthesia, and appears as gastralgia, enteral-
gia, or, in the nerves of special sense, as sparks and flashes of light or even
the appearance of distinct forms of men and animals, ringing or violent ex-
plosive sounds, and, in some cases, continuous conversation, or as disturb-
ances of taste and smell.
Disorders of co-ordination are of rare occurrence except in connection
with sclerosis of the posterior columns of the cord. Disease of the cerebel-
lum is indicated by lack of co-ordination, a staggering gait, or entire ina-
bility to maintain the erect position.
Mental Disturbances. — All forms of cerebral disease are attended by
more or less perversion of the mental powers, but such symptoms are sug-
gestive only of the general nature of the cerebral changes, and but remotely
of the character of the lesion. Hypersemia and inflammatory conditions
generally produce at first exaltation of mental processes which may vary
from simple excitement to the wildest delirium. On the other hand, any
lesion which causes sudden shock to nerve centres or interferes with nutri-
tion, either by simple pressure or through destruction of the cerebral tissue,
is generally indicated by depression or abolition of mental power. Patients
evince the most varied forms of mental disturbance, and at different times
suffer in their emotions, intelligence, or will. They may be happy,
hilarious, angry, or sober, melancholy, sullen and distressed. In intel-
ligence they may appear brilliant, vivacious, and the exaltation may extend
to delusions and hallucinations, or they may lose all reasoning power and
memory and become idiotic. Delirium of meningeal origin is generally
active or even maniacal, but becomes low and muttering, as in the typhoid
state, when the lesions implicate the cerebral ganglia and result in general
nervous depression. Like all other symptoms of similar origin it com-
monly ends in coma, with abolition of sense, sensation and voluntary
motion. Although coma is the usual termination of cerebral disease, it is
dependent upon many other and diverse causes, and often demands a dif-
ferential diagnosis as to its origin.'
Trophic Clianges. — Many forms of nervous disease are attended by peculiar
and rapid trophic changes throughout the body. They appear in the skin,
muscles, joints, bones, and viscera. The more common are bed-sores and
inflammations of the urinary tract. It may suffice to say generally that
trophic changes are associated only with inflammatory or irritative lesions,
which implicate the nerve trunks or their nuclei of origin in the case of
motor nerves, but in the case of sensory nerves may be located in the gray
matter of the posterior portion of the cord. Injury of motor nerves gener-
1 Etiology of coma :
Cranial i Hypersemia, Anemia, OSdema, Compression, Tumors, Thrombosis, Embolism, Apoplexy,
/ Abscess, Softenings, Shock, and Concussion.
Extra-cratial J Epilepsy, Ursemia, Ammonaemia, Cholremia, Poisons of drugs, Narcotics and Ansesthet-
( ics, Antispasmodics, Alcohol, Poisons of fevers. Malaria. Hysteria, etc.
930 DISEASES OE THE NERVOUS SYSTEM.
ally results in muscular or arthritic changes, while cutaneous changes are
dependent upon lesions affecting sensory nerves.
DISEASES OF THE
BRAIN
will be considered under the following heads
: —
I. Cerebral Hypercemia — active or V.
passive. VI.
II. Cerebral Ancemia. VII.
III. lieningiti^. VIII.
IV. Cerebral Thrombosis and Em- IX.
holism. X.
Cerebral Softening.
Cerebral Apoplexy.
Abscess of the Brain.
Cerebral Tumors.
Sclerosis of the Brain.
Hypertrophy of the Brain.
CEEEBEAL HYPEREMIA.
{Congestion of the Brain).
Cerebral hyperaemia is an increase in the quantity of the blood within the
capillaries of the brain. It may be active or passive. In active hyperge-
mia there is increased current, and the blood is arterial, while in passive
hypergemia the current is retarded, and there is an excess of venous blood.
Morbid Anatomy. — In passive hyperaemia, the veins and sinuses are en-
gorged with blood, and, when long continued, the dura mater appears
distended, and sometimes the cerebral convolutions are flattened, with a de-
cided pinkish color in the gray substance. On microscopical examination,
the perivascular lymph spaces are seen greatly diminished, or possibly ob-
literated. In the former case, large pigment granules are scattered outside
the vessels along their line.
On section, the white substance is seen dotted with numerous blood
points, and the cortex is grayish red. At the lower portions of the cere-
bellum there are dark red patches. In active hypermmia the small arteries
5,re enlarged, and the capillaries of the meninges are distended. This may
be accompanied or followed by oedema of the pia mater and distention of
the ventricular cavities.^ The condition of the membrane is no guide,
•either to the existence or degree of hypergemia, and transitory active or pas-
sive hyperaemia often leaves no trace discoverable at the autopsy.^
Etiology. — Active hyperasmia may be due to increase in the blood press-
ure, from excessive action of the heart, from contraction of the surface
capillaries during a chill, from prolonged mental labor, intense emotion,
digestive disturbances, acute blood poisoning, increased atmospheric press-
ure, and gravitation from a prolonged recumbent posture. Local arterial
anaemia in other parts of the body, such as arises from sudden cold to the
surface, intense muscular exertion, and pressure of tumors or dropsical
fluids on the main branches of the aorta, may also induce active hypergemia.^
1 Ecker states that the capillaries and small vessels are sometimes double their normal calibre. Niemeyer
and Nothnagel state that atrophj' of the brain may result from chronic passive hyperemia.
2 Many pathologists, while admitting the possibility of partial congestion, ascribe to post-mortem
changes what others denominate local congestion.
' Watson states that men have been arrested as drunk on cold nights, when they were only suffering
from active cerebral hyperaemia.
CEREBKAL HYPEREMIA. 931
Paralysis of the vaso-motor nerves of unknown origin, or severe nervous
shock, and poisons, alcohol and certain drugs, especially nitrite of amyl,
will give rise to active cerebral hyperemia. It occurs more frequently m
hot climates than in cold, and is said to follow breathing exceedingly rar-
efied air. Insolation is probably more than intense active hyperaemia. '
Passive cerebral hyperemia, when general, is the result of obstructed
venous circulation, itself the result of pressure upon the jugular or vena
cava descendens. Prolonged fits of coughing, playing on wind instruments,
and prolonged straining at stool may induce it. Any cardiac valvular le-
sion that obstructs the blood in the pulmonary vessels, or any disease of the
lungs which offers obstruction to the onward current, will lead to passive
hyperaemia of the brain. Tricuspid regurgitation stands iDre-eminent among
these causes. Partial or complete stenosis of the larynx will induce it, as
in croup and oedema glottidis. Thrombi in the cerebral sinuses may induce
passive hyperaemia; and it sometimes occurs from feebleness of the incoming
arterial flow.
Symptoms. — The symptoms of cerebral hyperaemia may be grouped in two
classes : — those of excitement and those of depression. In all cases these
symptoms are increased by a recumbent posture, by a forced inspiration and
by stimulants. The symptoms of excitement are a diffuse pain and throb-
bing in the head, accompanied by dizziness, vertigo, flashes of light, ringing
in the ears, restlessness, insomnia, and perhaps delirium and convulsions.
Photophobia is present ; and there may be nausea and vomiting. Sleep is
usually broken and disturbed from the onset. The gait is unsteady, the mind
confused, and sometimes the speech embarrassed. In active hyperaemia the
pulse is accelerated, full, bounding, and hard, and the carotids and tempo-
rals pulsate forcibly. An ophthalmoscojsic examination reveals injection of
the retinal vessels, and the conjunctivae are often suffused. In most cases
there are both motor and sensory disturbances. As a rule, the mental state
in active hyperemia is one of exaltation. These patients are irritable,
peevish and highly excitable. They are apt to talk a great deal. When
coma occurs, the hyperaemia is described as apoplectic ; when convulsions or
spasms are present, it is called epileptic ; and when there is delirium we
have the maniacal form. The latter is mania epliemera or impulsive insan-
ity."^ Paralytic symptoms are rare in active hyperaemia.
The symptoms of depression are dull headache, vertigo, ringing in the
ears, with confusion of mind and dulness passing into somnolence, stupor,
or complete coma. Illusions and hallucinations are uncommon/ Con-
vulsions may occur in children. When due to passive hyperaemia, as is not
uncommon, there is a cyanotic hue to the face and neck, the jugulars and
venous system are over-distended, and the arterial system is scantily filled.
The pulse varies with the etiological (cardiac) lesion. In old people, after
' See the inleresting experiments of S. Mayer and Pribram (Sitz. der Wien. Akad., 1873), in which elec-
trical or mechanical irritation of the walls of the stomach produced a reflex increase of the vascular press-
ure and considoruble diminution in the frequency of the pulse.
2 Trousseau and Nothnagol both claim that the epileptic and apoplectiform varieties are either true epi-
lepsy or are due to actual cerebral hemorrhage.
s Griesinger describes a peculiar /ear of places that seizes patients when in the midst of a crowd or
while in a certain place or street.
933 DISEASES OF THE NERVOUS SYSTEM.
depression of spirits, or a long period of taciturnity, there follows wander-
ing delirium, usually nocturnal, talkativeness, and a state often bordering
on hysteria. The mind becomes more and more inactive, and sensation as
well as motion is diminished. This condition is followed by coma, with
stertorous breathing and relaxation of the sphincters. This coma, which
is frequently interrupted by local or general convulsions, generally ends in
death.
Differential Diagnosis. — Cerebral hyperaemia may be mistaken for apo-
plexy, embolism, urcemia, acute alcoholismus, ejjilepsy, and cerebral an-
CBmia.
In cerebral hemorrhage the onset is more sudden ; the coma is more com-
plete and prolonged, and following the attack there is always hemiplegia.
In cerebral embolism the onset is sudden ; the face is pale, the head cool,
the respirations and pulse-rate are rapid and irregular, there is usually evi-
dence of cardiac valvular disease, aphasia follows the attack, and the symp-
toms are more permanent than in acute hyperasmia.
In urcemia the coma is deeper and generally preceded by convulsions.
There is oedema of the eyelids or of the lower extremities, and the, urine
will be found to contain albumen and casts.
In epilepsy there is usually an aura, and the patient falls as if from a
blow, uttering the epileptic cry. In the fit, which is of short duration, the
convulsions are first tonic and then clonic, and there is a bloody froth about
the mouth.
The diagnosis between stomachic and cerebral vertigo will be found under
Diseases of the Stomach.
It is often impossible to distinguish between acute meningitis and cere-
bral hypersemia in children, except from the results of treatment, until .the
disease is well advanced.
In cerebral hypersemia the headache is generally diffused and the pupils
are contracted, while in cerebral ancemia the headache is vertical and the
pupils are dilated. In hypersemia there are loss of memory and hallucina-
tions, in anaemia we have simply incapacity for mental work. In anaemia
the respirations are hurried, the pulse is quick, feeble, and irritable, there
are murmurs at the base of the heart and in the vessels of the neck, and
the face is pale and cold.
Prognosis. — The prognosis depends upon the cause ; as a rule, therefore,
passive is less favorable than active hypersemia. The maniacal or apo-
plectiform variety is the most, the convulsive the least, dangerous. The
outlook for recovery is best in those whose habits are good, who can ex-
ercise mental control and avoid excitement, and in those between twenty-
five and fifty. In youth and old age the prognosis is more unfavorable on
account of the condition of the cerebral vessels. Accompanying cardiac
and pulmonary disease, passive hypersemia is a symptom of secondary im-
portance.
Treatment. — During an attack of cerebral hyperaemia from whatever
cause, the patient must be kept absolutely quiet in bed with the head
raised, and the diet should be the simplest and most easily digested, and
CEREBRAL ANEMIA. 933
taken in small quantities at short intervals. In active hyperremia cold
to the head and heat to the feet, with the administration of a brisk purge,
are to be the first measures. The bromide of potassium is beneficial in
most cases. In severe active hypereemia blood-letting is permissible in the
form of leeches to the temples or nose. The constant current maybe used
to stimulate the sympathetic nerve, and thus contract the cerebral blood-
vessels. Some advise zinc in combination with bromide of potassium.
Ergot and antimony have been used with some success in active hyperfemia.
In passive hypersemia stimulants may be given with bromide of potash
or soda. Digitalis is usually indicated. Sulphuric ether, inhaled or given
internally, often produces good results. In coma due to jjassive cerebral
hypersemia, all remedies will prove ineffectual, except quinine, which
should be given in small doses at short intervals. When cessation of the
menses or of an old hemorrhoidal flux is followed by cerebral congestion,
leeches to the anus, sitz-baths, emmenagogues, etc., should be given in
connection with the other remedies. A change of residence with rest
from mental work is often of great benefit.
CEEEBEAL ANEMIA.
Cerebral anaemia is a condition in which there is a deficiency in the
quantity or quality of the blood in the capillaries of the brain.
Morbid Anatomy. — The principal change in cerebral anaemia is pallor of
the brain, which may be partial or general, accompanied by serous effusions
into the meshes of the pia mater. The ventricles are often distended with
fluid and the veins and sinuses are engorged.' In some cases hypersemia of
the meninges coexists with cerebral ansemia. Partial cerebral anaemia is not
often demonstrable. It exists about neoplasia and adventitious jDroducts ;
and may be the result of local pressure, or partial occlusion of an artery.
Etiology. — It may be due to general systemic anaemia from excessive
hemorrhages, or to sudden pulmonary hepatization and congestion in
other organs. Exhausting discharges, prolonged lactation, etc., induce
it. Spurious hydrocephalus following infantile diarrhoea is a condition of
cerebral anaemia. It may result from defective blood nutrition, as in
chlorosis, or cardiac weakness, mitral or aortic valvular disease, or cardiac
insufficiency occurring in acute febrile diseases. Fatty heart is even more
potent than valvular lesions in producing it. Any mechanical interference
with the supply of blood to the head, as pressure on, or ligation of, the
carotids, may induce cerebral anaemia. The arteries that form the circle
of Willis are, in twenty per cent, of cases, so distributed that only im-
perfect communication exists between their two lateral halves. Mental
influences through vaso-motor spasm may produce it ; thus fright, joy, or
anger will, in many, produce syncope dr.e to cerebral anaemia.
Cerebral anaemia sometimes follows the application of strong electrical
currents to the spinal region and irritation of the peripheral nerves. It is
claimed that zinc oxide, the bromides, tobacco, calomel, and tartar emetic,
' Golgi claims that there is enlargement of the perivascular lymph-spaces.
934 DISEASES OF THE NERVOUS SYSTEM.
if long continued, will cause cerebral anaemia. Partial cerebral anaemia is
always due to local obstructions, which may result from narrowing of the
vessels from disease of their walls, from spasm of their muscular coats,
from embolism or thrombosis, and from pressure of tumors, blood, bone
or inflammatory products.
Symptoms. — The symptoms of cerebral anaemia may appear suddenly or
slowly. In the former case they are the ordinary phenomena of a fainting
fit ; the individual becomes dizzy, nauseated, and the sight is obscured ;
there is ringing in the ears, the pupils dilate, the gait is unsteady, cold
perspiration covers the surface, the pulse becomes feeble, rapid, and thready,
and the respirations hurried ; and the patient may fall to the ground with
slight spasmodic twitchings. Such a condition is common from reflex
causes. If due to extensive hemorrhage the loss of sight in those that re-
cover may be permanent.
When cerebral angemia comes on slowly it is attended by headache,
drowsiness, vertigo, muscse volitantes, tinnitus aurium, sometimes attacks of
total blindness, inability to perform work, insomnia, extreme sensitiveness
to light and noise, and at times delirium and hallucinations. Notwith-
standing the maniacal character of the delirium, melancholia is often its
predominant feature. Though usually of brief duration, it may end in per-
manent insanity. In most cases the pupils are sluggish and dilated, the
retina is anaemic, and the headache is confined to a small circumscribed
spot. The recumbent posture induces insomnia, and the erect position
often causes a sense of general muscular weakness and faintness. The face
is pale and cold. In the cerebral anaemia of children — spurious hydro-
cephalus — restlessness, jactitation, grinding of the teeth, and muscular
twitchings are followed by symptoms of collapse and coma.
Diiferential Diagnosis. — The points of differential diagnosis may be found
under the heads of Tubercular Meningitis and Cerebral Hyperaemia.
Prognosis. — The prognosis in cerebral anaemia will be determined in most
cases by its causes. Where acute anaemia results from hemorrhage, death
may result, although the hemorrhage has been arrested. The prognosis is
more favorable when there is no organic disease of the heart or vessels. The
more speedily the cause can be removed the better the prognosis. In the
so-called spurious hydrocephalus the prognosis is favorable, if met by
prompt and suitable treatment.
Treatment. — In acute anaemia with syncope the head must be lowered at
once and the patient may even be inverted, cold water may be dashed over
the face, the vapor of ammonia inhaled, and bandages applied from the
feet upwards. As soon as consciousness is regained, champagne, ether,
ammonia, coffee, or other cardiac stimulants maybe administered. If these
measures fail transfusion should be resorted to. Alcohol is to be given
very cautiously in cerebral anaemia ; and exercise of either brain or body
must be carefully undertaken. Bromides are never to be given.^ For
chronic anaemia the treatment can only be determined by causal indica-
tions.
1 Nothnagel advises small doses of morphine for the excitement that precedes anaemic delirimn.
MENIlfGITIS. — ACUTE MEKIKGITIS. 935
MENINGITIS.
The membranes covering the brain are the pia and dura mater ; the pia
mater is a delicate and exceedingly vascular membrane which is intimately
adherent to the brain, sending jDrolongations into the sulci and fissures ;
its connective-tissue is very extensive. The external layer of the pia mater
is the structure formerly called the arachnoid. The meshes of the pia
mater-were formerly denominated the subarachnoid space.' The dura mater
acts as the periosteum of the cranial bones ; it is firm, not very vascular,
and encloses venous sinuses between its folds. Its inner surface is covered
with a layer of endothelial cells.
Inflammation may have its seat in the dura mater, the pia mater, or both
may be involved. Inflammation of the pia mater is usually called menin-
gitis. The term pachymeningitis is applied to inflammation of the dura
mater.
When inflammation of the pia mater is attended by rapid changes in the
membrane and by the eJSusion of sero-fibrin and pus, with varying quanti-
ties of red blood globules, it is called acute meningitis.
So-called sub-acute meningitis is a mild tyj)e of acute, in which extensive
serous effusions are the chief, and at times almost the sole, event, although
small quantities of lymph, white and red blood cells, and fibrin are usually
present.
Inflammation of the pia mater, when chronic, results in thickening,
opacity, and adhesions. It might be called interstitial meningitis, while
the acute and sub-acute belong to the class of exudative inflammations.
The dura mater has an external and an internal layer, the external is in-
timately connected with the inner surface of the calvarium. Inflammation
of this layer is c,sWe(i pachymeningitis externa, and is marked by thickening,
opacity and localized adhesions of the dura with the skull.
Pachymeningitis interna is an inflammation of the inner surface of the
dura mater, and may be acute or chronic ; it is usually localized. Chronic
pachymeningitis interna often results in the formation of flat, oval, lami-
nated sacs containing blood which lie between the dura and pia mater,
and is called hcematoma of the dura.
ACUTE MENINGITIS.
Acute meningitis is also callerl simple meningitis of the convexity (from
its usual site), cerebral fever, and arachnitis. When the unqualified word
meningitis is used, acute, non-sjoecific inflammation of the j)ia mater is
understood.
Morbid Anatomy. — The inflammatory process may be established in any
portion of the pia mater ; but it usually involves the hemispheres. Only
in rare cases is it confined to the base of the brain. There is always more
or less thickening and redness of the membrane, and it loses its glistening
1 Ilandb. d. Hist.— Strieker.
936
DISEASES OP THE NEEVOUS SYSTEM.
appearance. Around the vessels where the connective- tissue is most abun-
dant, there is first a slight serous effusion, which is quickly followed by
cellular infiltration. An opaque zone of exudation surrounds the vessels.
In mild cases the exudation is limited to the perivascular lymph spaces.
Fig. 189.
Acntc Meningitis.
Portion of the under surface of the Brain, including the middle lobe of the Cerebrum and the
Cerebelluni.
TTie opaque exudation is seen upon the cerebral meninges completely covering the pons and surrounding the
medulla. The basilar artery is dimly seen through the exudation.
The character of the exudation varies ; it may be serous or sero-purulent,
and occupy the deeper meshes of the pia mater, or a thick puro-fibrinous
exudation may cover the convexity of the brain as a firm membrane or a
creamy diffluent mass.' This layer of fibro-pus or false membrane is
thickest and most abundant in the fissure of Sylvius and the sulci and
along the vessels, which are visible as red, inosculating lines in a yellow-
green or distinctly green mass. On raising this layer the brain beneath is
found studded with minute hemorrhages from the ruptured vessels con-
necting the pia and gray substance. The wJiite substance may also show,
on section, numerous puncta vasculosa. The convolutions are flattened,
the sulci deepened, and the ventricular cavities will contain very little, if
any, fluid.^ "When the cerebellar pia mater is involved, as in young subjects,^
the roots of the cranial nerves about the medulla are sheathed in the exuda-
tion, and there is inflammatory infiltration of the neighboring plexuses.
Etiology.— Meningitis of the convexity is most frequent in early adult
life and in young children. It is more common in males than in females.
Acute alcoholismus and prolonged and intense mental anxiety and grief are
among its predisposing causes. Injuries of the cranial bones, as fractures,
severe blows, or punctured wounds are the most frequent exciting causes.
1 Klob is of the opinion that the pus is furnished in great measure from the arachnoidean epithelia.
2 Huguenin states that in meningitis of unknown origin the pia mater is often so adherent that it tears
Bway portions of the brain substance when it is removed.
' Beduar.
ACUTE MElsriNGITTS.
937
Disease of the cranial bones and suppurative inflammation of the middle
ear may induce meningitis, and inflammation of the dura mater is often
complicated by simple meningitis. Diabetes and irritation caused by cere-
bral tumors, or supj)uration in the eyeball, and large carbuncles about the
cranium have caused it.
Meningitis occurs as a complication in certain diseases — as measles, small-
pox, scarlet fever, ulcerative endocarditis, Bright's disease, acute croupous
pneumonia, typhus, typhoid fever, diphtheria, pyaemia and rheumatism.
Acute alcoholism is said to induce meningitis in children.' Long-continued
exposure to intense heat of the sun under conditions favorable to the de-
velopment of miasmatic contagious diseases may result in meningitis.
Finally, meningitis is sometimes idiopathic.
Symptoms. — The symptoms of meningitis may be divided into the tbree
stages of headache, delirium, and coma. Premonitory symptoms, such as
general malaise, wandering pains in the head and limbs, irritability, in-
somnia and a sense of imjoending trouble, are all indefinite "ijrodromata."
It may be ushered in by a distinct chill or by repeated rigors.
Usually the first prominent symptom is intense and persistent headache,
localized in the frontal, temporal, or occipital region, which increases in
severity from hour to hour. In severe cases the headache is diffuse, al-
though it may extend obliquely across the head, or shoot from temple to
temple. Accompanjnng the headache
there is vertigo, intense photophobia,
loud ringings in the ears, nausea, and
projectile vomiiing. There is cuta-
neous hyperaesthesia, and convulsive
movements of certain groups of mus-
cles. The upper and lower extremi-
ties, and the posterior cervical mus-
cles suffer most. The face is rarely
flushed, but has a pale, anxious ex-
pression. The conjunctiva are in-
jected, and the pupils are contracted
and respond slowly to light. The
degree of contraction of the pupil varies
considerably in different patients dur-
ing the twenty-four hours. It may
only be contracted on the same side
as the meningeal inflammation.
Aphasia has been noticed as occurring
in a few cases ; loss of co-ordinating
power is a marked symptom, so that
the individual has an unsteady, tot-
tering gait. The temperature, which rises rapidly, reaches 102° or 103° F.,
rarely higher ; it may have a morning remission and evening exacerbation.
" Ramskill states that in some inscances when impetigo and eczemn about the face and head suddenly
disappear, the symptoms of acute meningitis of the convexity are developed.
J)ai/: 1.
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Fi(i. 190.
Temperature Record in a case of Acute
Meningitis.
938 DISEASES OF THE NEEVOUS SYSTEM.
In those cases which are rapidly fatal there is continuous high tempera-
ture. The pulse is firm, hard, wiry, and small, varying in frequency with
the temperature range. The bowels are constipated and the abdomen is
retracted. In old people the stage of headache may pass unnoticed, and
the delirium first attract attention. In children general convulsions may
be the initiatory symptom, with marked strabismus from its very onset.
If constipation is not present the discharges are scanty and offensive. In
this class of cases the first stage is always preceded by peevishness and irrita-
bility, which lasts from a few hours to two or three days.
In adults the stage of delirium is ushered in by an increase in restless-
ness, jactitation, irritability, and mental confusion. It is sometimes wild,
simulating acute mania ; at first it may be present only at night, coming on
with the evening rise in temperature. In the aged the delirium is typhoid
in character, or marked by incessant talking. Sometimes the aged are only
lethargic and stupid. In adults muscular twitchings of the extremities
and face are present in this stage ; the eyeballs roll about vaguely, the
flexor muscles are often powerfully contracted in one or both limbs, and
there may be opisthotonos or even hemiplegia. Paresis of the thoracic and
faucial muscles causes dyspnoea, irregular respiration, and dysphagia. In
metastatic meningitis delirium may be the first symptom, and simulate
delirium tremens, or the patient may be absolutely mute. The result, if
death does not occur, is sometimes permanent insanity.' As this stage ad-
vances the temperature rises to 104° F., the pulse becomes more frequent
and irregular ; the abdomen is retracted, the vomiting continues projectile,
and the respirations become sighing in character. During this stage the
pupils are uneven — one may be of normal size while the other is quite
small ; when the delirium is subsiding they dilate and contract by turns,
or oscillate. The tdchs cerebrate may appear, and herpetic eruptions are
not infrequent. This stage lasts from one to three days.
The stage of coma comes on gradually. The delirium subsides, and is
followed by a tendency to stupor, lethargy, and deep sleep. Headache,
jactitation, and hyperasstliesia disappear. The pulse becomes slow, irregu-
lar, and intermittent. The pupils are markedly dilated, the breathing is
superficial and irregular. The patient is insensible to all impressions ; he
rolls his head and grinds his teeth, j)icks stupidly at the bedclothes, and
the face becomes alternately white and red. Gradually the coma becomes
complete, and the urine and fgeces are retained, or the latter are passed in-
voluntarily. Drawing off the urine may temporarily rouse the patient
from the coma. The head is drawn to one side, and as the circulation
is retarded the extremities and face are often of a purple hue. Subsultus
tendinum is marked. The pulse runs up to 160 to 170, or until it cannot
be counted at the wrist ; the Cheyne-8tolces respiration of ascending and
descending rhythm becomes established. The expirations are puffing.
The body is bathed in cold sweat, and death results from central paralysis,
causing asphyxia, or heart-failure and pulmonary oedema. The temperature
may rise very high or fall to a subnormal just before death.
1 Vigla, Actes de la Soc. Med. des Hop. de Paris.
ACUTE MENINGITIS. 939
Differential Diagnosis. — Acute meningitis may be confounded with acute
urcBmia, typhus fever, variola, and delirium tremens.
In urcemia the face will be turgid, and there will be puffiness al>out the
eyelids ; in meningitis the face is pale and anxious, and there is no oede Jia.
In ursemia the urine will contain albumen and blood or exudative casts ; in
meningitis only a small amount of albumen is present and no casts. Con-
vulsions, preceding the coma, are far more common m uraemia than in
meningitis. The pulse, temperature, and the subjective symjotoms of
meningitis are absent in acute uraemia. In some cases only a microscopic
examination of the urine will enable one to make a differential diagnosis.
In typhus fever, although the cerebral symptoms closely resemble those
of meningitis, the temperature range is higher, often reaching 106° to
107° F. The pulse is more rapid and compressible in typhus than in
meningitis. In typhus the countenance has a dull, leaden, or mahogany
hue ; in meningitis it is pale and anxious. Surface sensibility is blunted
in typhus, and is exaggerated in meningitis. Vomiting is infrequent in
typhus, in meningitis it is persistent and projectile in character. The
characteristic typhus eruption appears on or about the fifth day ; there is
no characteristic eruption in meningitis. In typhus the pupils are equal,
in meningitis they are unequal.
In small-pox the face is flushed, the pulse is full and bounding, there is
intense pain in the back and loins, the vomiting is retching in character,
and at the end of the third day the characteristic eruption occurs along
the roots of the hair. These symptoms are all absent in meningitis. In
many cases, however, it is necessary to await the appearance of the eruption
before a diagnosis can be made.
In delirium tremens there is a busy delirium, the patient imagines
persons and animals about him, and is wild in his gestures and utterances ;
in meningitis the delirium is incoherent and milder, but marked by a de-
sire to get out of bed. The surface is bathed in a profuse, clammy sweat
in delirium tremens ; it is hot and dry in meningitis. In delirium tre-
mens the temperature, pulse-rate and pupils are normal ; there is no head-
ache.
Prognosis. — The prognosis in acute meningitis is very unfavorable ; severe
cases terminate fatally, mild cases may recover. The duration varies from
two days to four weeks ; fatal cases rarely last more than eight days. If
recovery takes place convalescence may not be fully established before the
third week. The average duration of the disease is about eight days.
Strabismus, hiccough, and local paralyses are very unfavorable symptoms.
The prognosis is better in children than in adults.
Treatment. — The most important local measures at the onset of the dis-
ease are local blood-letting and the application of cold to the head.
Leeches may be applied to the nuchal region or temples. The best method
of applying cold is by means of the ice-bag or coiled tube, and that it may
be thoroughly applied the head should be shaved. The patient must be
placed in a large, quiet, darkened room, with the head elevated and all
obstruction to the return circulation removed. The bowels must be freely
940 DISEASES OF THE NERVOUS SYSTEM.
acted upon by croton oil, and some drastic purge and saline diuretic are
indicated if the urinary secretion is scanty.
In the stage of coma blisters to the back of the neck are of service. To
relieve the great restlessness which often precedes the stage of delirium,
hydrate of chloral and opium may be given. Iodide of potash and mer-
cury are strongly recommended in all stages of this disease, but I have
never obtained any positive beneficial effects from their use. Strong broths
and alcoholic stimulants, if indicated, may be administered throughout the
whole course of the disease. The condition of the bladder and the bowels
must be carefully looked after during the stage of coma, and especially in
the meningitis of old age.
SUBACUTE MEJSrn^GITIS.
Subacute meningitis differs from acute in that it is always secondary, is
of longer duration, and is attended by less active symptoms.
Morbid Anatomy. — Upon the convexity of the brain there is found a sero-
fibrinous exudation, containing few pus globules, and fibrin only in small
quantities. The effusion will occupy the meshes of the pia and the ven-
tricular cavities. As a result of the effusion the convolutions are flattened
and the sulci are deepened. Flocculi of lymph will be found most abun-
dantly along the line of the vessels of the convexity, and the vessels of the
pia mater will be more or less distended. The pia mater will be lifted
from the /Surface of the brain, will lose its glistening appearance, and in old
cases will be slightly opaque.
Etiology. — This form of meningitis may occur during the course of any
exhausting disease, as chronic diarrhoea, cancer, chronic Bright's disease,
typhoid fever, etc.
Symptoms. — Being subacute and always secondary, its early symptoms are
obscure. The stage of headache is wanting or lasts only a few hours, and
is never severe. The delirium, which is often preceded by extreme jactita-
tion, comes on gradually and is always quiet in character, and is character-
ized by an attempt on the part of the patient to get out of bed and walk
around the room ; the patient in walking staggers and is apt to fall for-
ward. The stage of delirium may last only a few hours. In most cases
headache and delirium are rapidly followed by coma. Thus, if a patient
with chronic Bright's disease, after a short delirium, passes slowly into a
state of coma, there is reason to suspect the development of this form of
meningitis.
When the active delirium of typhus fever becomes muttering in charac-
ter, when the pupils dilate and the pulse becomes slow and irregular, sub-
acute meningitis may be suspected. As the coma begins the respirations
become sighing and puffing in character, and the urine collects in the blad-
der. As it deepens, the pulse, which has been slow, is accelerated and in-
termits ; the expirations are short puffs, and the interval between expira-
tion and inspiration becomes lengthened. The typhoid state is rapidly
developed, deglutition becomes difficult, there is blueness of the finger-
CHRONIC MENINGITIS. 941
nails with cyanosis, and the coma ends in death, or is slowly recovered from
and followed by a long convalescence.
Differential Diagnosis. — The history of the case will aid very much in its
diagnosis. Coma being its prominent symptom, the differential diagnosis
is from other forms of coma.
From coma of acute meningitis, of tumors, compression, concussion, or
cerebral softening, the previous history is sufficient to distinguish it.
From coma of poison and narcotics it is differentiated by examination of
the secretions and excretions and by the state of the pupil ; thus, in lead
poisoning the line on the gums, in alcoholic coma an examination of the
urine, and in ojoium coma the pin-head pupils will at once decide.
Hysteria, eiailepsy, and catalepsy are attended with such distinctive signs
that they cannot be mistaken for sab-acute meningitis.
Prognosis. — The prognosis of sub-acute meningitis is determined by the
disease with which it occurs. When it occurs with Bright's disease it is
usually fatal, but when complicating tyj)hus and other fevers it is fre-
quently recovered from.
Treatment. — The chief indication is to remove the cause. In Bright's
disease, elimination of urea, which is causing the meningitis, should be
attempted. In typhus fever free ventilation, stimulants, and concen-
trated nutrition will remove the cause so far as possible. In most instances
blisters applied to the neck will be followed by marked improvement,
and not infrequently by recovery.
CHEOlSriC MENESTGITIS.
Chronic meningitis is an interstitial inflammation of the pia mater,
which causes thickening and opacity of the membrane. It may be lim-
ited to the convexity.
Morbid Anatomy. — The pia mater is thickened, callous, and opaque, and
maybe infiltrated with serum, pus, and new connective-tissue cells.' There
is thickening of the walls of the blood-vessels of the pia, and of their
branches which enter the brain substance. These last adhere to the sur-
rounding brain substance, so that it is torn when the pia mater is lifted
from the brain.' Attendant upon all forms of chronic meningitis there is
more or less interstitial inflammation of a very low grade of the hrain-
sudstance (diffuse interstitial encephalitis), although meningitis chronica
is not ordinarily diffuse, but limited in extent. When the pia and dura
raater are bound together, pachymeningitis has preceded the development
of adhesions. The ventricles usually contain more or less fluid. The
development along the f alx of glandulm pacchionii is due as much to senil-
ity as to chronic meningitis. ' Atrophy of the cortex results from long-
continued chronic meningitis.
1 Ramskill states osseous plates have been found embedded in the thickened membrane.
«Some authors describe a degenerative change in the vessels resulting from previous peri- or endarter-
itis, which is said to resemble colloid metamorphosis. This change is rare.
a Foster states that he has seen cheesy degeneration of the exudation lying in the sulci, and that a cyst-
wall of connective-tissue has formed.
942 DISEASES OF THE NEEVOUS SYSTEM,
Etiology. — Chronic meningitis is a disease of adult life, especially after
fifty years of age. It is often idiopathic, and is met with among the poor
and badly nourished. It is very frequently a complication of chronic
alcoholismus, syphilis/ rheumatism, gout, and chronic Bright's disease
(small granular kidney.) It is sometimes of traumatic origin, and is fre-
quently found in the general paralysis of the insane.^
Symptoms. — The symptoms of chronic meningitis are always obscure. In
some cases there are no symptoms ; patients die of other diseases and
meningitis is found at the autopsy. In others there are well-marked
symptoms. The patient grows stupid, dull and apathetic, the mental
faculties are blunted, and there is headache and a constant desire to sleep,
or the patient may become morose and fretful. In the old the headache
comes in paroxysms, and is attended by marked flushing of the face, fre-
quent pulse and high arterial tension, occasionally attended by delirium.
In nearly all cases vomiting becomes a prominent symptom, producing
great exhaustion. Muscular weakness attends the decline in mental pow-
ers ; the legs tremble in walking, control of the sphincters is lost, and the
urine and faeces may be passed involuntarily. In many cases, chiefly the
aged, there is paralysis of the bladder. The appetite is good, but diges-
tion is slow and the bowels are constipated. The speech is thick, or the
power to articulate certain words is lost. Vertigo, tinnitus aurium, and
muscse volitantes are present, with localized numbness or hyperaesthesia.
The very aged often lie in a stupor, exhibiting no mental or physical signs
of life except to breathe and take food.
There is no typical temperature range. Indeed, in many cases there is
no pyrexia during the whole period of the disease, in others there will be a
chill and fever resembling in its variations that of malaria. In some forms
of chronic meningitis hemiplegia occurs, both with and without facial pa-
ralysis. When the trigeminus is involved the eyeball may slough.^ Ptosis,
strabismus, and variations in the size of the pupils indicate that the third
nerve is involved. These irregular symptoms may continue with increasing
severity for months or years. Toward the end convulsions may occur, and
death takes place in deep coma.*
Differential Diagnosis. — The diagnosis of chronic meningitis is always dif-
ficult. It may be mistaken for cerebral tumors or softening.
With tumors, the headache is more intense and circumscribed, paralysis
of nerves of special sense or of. certain sets of nerves is common, and the
signs of general decline in mental and physical power are less marked.
Chronic meningitis appears in its whole symptomatology to be of a more
general nature, while tumors produce local symptoms; speech and intellect
are usually unimpaired. When neoplasias excite chronic meningitis in their
vicinity the diagnosis is often impossible.
1 Virchow states that when constitutional syphilis exists in the human body, its localization depends
greatly upon previous states of the system.
2 Calmeil.
» See Effect of cutting fifth cranial nerve, in M. Poster's Physiology, p. 381 to 382.
* Many attribute the symptoms of chronic meningitis occurring in the insane, epileptic, and imbeciles to
a cortical encephalitis frequently found at tlie autopsy, with the changes of meningitis.
TUBERCULAE MENINGITIS. 943
Softening of the drain is also often associated with chronic meningitis.
In softening there may be a history of a previous apoplectic seizure ; mus-
cular contractions are common, and the headache is not so severe as in
chronic meningitis. In chronic meningitis there is more mental excitement
than in cerebral softening, and the hemiplegia is more complete after apo-
plectic seizures.
Prognosis. — The prognosis is bad; the disease is a progressive one. Only
in cases of a syphilitic origin can we offer any hope of recovery. Many be-
come permanently insane, and some die from inanition. Death may also
result from exhaustion, from cerebral pressure, and from complicating dis-
eases, as pneumonia, etc.
Treatment. — The patient is to be kept quiet mentally, and the diet must
be fluid and nutritious ; stimulants being only administered to sustain vi-
tality. The bichloride of mercury and iodide of potassium, in small doses,
are the remedial agents most frequently employed. Blisters may be applied
to the back of the neck, or a seton introduced there. The bowels need
careful attention. The urine, if not passed freely, should be drawn and
the bladder washed out.
TUBEECULAR MENESTGITIS.
{Acute hydrocephalus.)
Tubercular meningitis ' is an inflammation of the basal pia mater,
caused or attended by an eruption of gray, miliary tubercles, and occur-
ring most frequently in children.
Morbid Anatomy. — The dura mater is rarely involved. The pia mater in
some cases is congested, in others pale, and it may be infiltrated with
serum, fibrin, and pus. The vessels along the Sylvian fissure and the an-
terior peduncles of the cerebellum are studded, especially at their bifurca-
tions, with miliary tubercles, which lie in the perivascular lymph-spaces.
The lymph-spaces may become filled, and a covering be thus formed over
the vessel ; or the miliary granules dot the vessel like a string of beads.
As they develop they compress and finally occlude the vessels. These gran-
ules are sometimes met with in small numbers on the convexity and along
the longitudinal fissure, but are always more abundant at, if not confined
to, the base, from which they may extend to the pia mater of the cervical
cord. Even at the base they may be few and limited, or so abundant and
extensive as to obstruct the circulation and impair the walls of the vessels,
causing multiple hemorrhages and red softening.
The inflammatory exudation at the base is a turbid, serous effusion, or
more commonly a thick, yellow, semi-plastic layer which extends from
the fossa 8ylvii, where it is most abundant, to the inferior surface of the
cerebellum. When the pia mater of the convexity is involved it may show
no evidences of exudative inflammation, but present a bright, rosy hue.
The ventricles are distended by a serous fluid, usually turbid from admix-
' Is alt^o called by the Germans basilar meningitis ; and by the English acute hydrocephalus. The die
ease was properly named tubercular meningitis by the French.
944 DISEASES 0¥ THE NERVOUS SYSTEM.
ture of cellular elements, which flattens the convolutions and causes cede-
matous softening. The membrane of the ventricles is thick and opaque.
In cases running an acute course, the only lesion except the tubercles may
Fig. 191.
Tubercular Meningitis.
Region of the Sylvian Jismre showing at A, A, miliary tubercles along the line of the blood-vessels.
be a large serous effusion into the ventricles. In most cases tubercular
meningitis is associated with general tuberculosis.
Etiology. — Tubercular meningitis is rare before the first and after the
fifth year. It occurs almost exclusively in children of a scrofulous diathe-
sis, either inherited or acquired. In such children the tuberculous process
is latent, and any debilitating disease may excite it, such as diarrhoea, the
exanthemata, especially measles, whooping-cough, otorrhoea, and skin and
scalp diseases of a chronic nature, dentition, insufiicient or improper
food, and injuries to the head, more particularly at the base of the
brain.
Symptoms. — The symptoms of tubercular meningitis are due not so much
to the tubercular developments, as to the exudative products of the inflam-
matory process, as the pia may be studded with tubercles both at the con-
vexity and base without the slightest symptomatic indications of their pres-
ence. Its advent is generally very insidious ; if convulsions usher it in, its
course is rapid.
The premonitory stage is marked by changes in the nutritive and diges-
tive processes ; the appetite is diminished and capricious ; the breath is
offensive, the tongue coated, constipation and diarrhoea alternate. The
child becomes dull, languid, apathetic, and desires quiet ; its sleep is
restless and troubled. The face assumes a dull, anxious appearance, and
when at play the child will stop suddenly and rest its head on its hands or
TUBERCULAR MENINGITIS.
945
the floor. During the progress of these symptoms a cachexia is developed
and there is progressive emaciation, which in connection with the etiology
gives rise to the suspicion that the disease is developing. These prodro-
mata may last from a few days to a month, and will often attract the
attention of strangers before they are observed by the parents. In most
instances there is a slight evening rise in the temperature and a short
hacking cough at intervals. The symptoms may be divided into three
The first is the irritative stage or period of invasion. In this period the
little patients dislike to be disturbed ; light and noise annoy them ; they
answer questions intelligently, but unwillingly and slowly. The expression
of the countenance is anxious. ' The cheeks will be alternately flushed and
pale. Headache, which is often severe, is paroxysmal and seldom constant.
It is usually frontal and may be accompanied by dizziness. In some cases
the intermissions are short and the pain is diffused. The sufferer will moan
and clasj) the head with his hands. In young children pressure on the fon-
tanelles increases the pain. There is mild delirium alternating with dis-
turbed and fitful sleep, from which the child starts with a piercing Tiydro-
ceplialic cry. They grind their teeth, roll their eyeballs, and the facial
muscles are contorted. The hands will be clenched and the thumbs flexed
on the palms. Muscular tremors pass over the face and body in quick suc-
cession. The abdomen is retracted and hard, due to contraction of the
intestines from central irritation. Projectile vomiting occurs at varying
intervals, independent of the ingestion of
food, and resists all treatment. The bowels
are constipated. The tongue is dry, covered
with a white coating, and the tip is red.
The pupils are contracted, there is photo-
phobia and possibly strabismus ; the con-
junctivae are injected and the brows con-
tracted. On drawing the finger firmly over
the skin, a red line, after a moment, will
follow the removal of the pressure. The
evening temperature is a degree or two
higher than that of the morning, but rarely
rises above 103° F. Sometimes, in cases
where convulsions usher in the disease, the
temperature will reach 104° or 105° F. The
exacerbations and remissions are always
irregular. The pulse is at first full, com-
pressible and regular, or it maybe normal in
character. After the first twenty -four hours
it shows a marked tendency to become accelerated and slightly irregular
upon muscular exertion or excitement. The respirations at times are rapid
and irregular, at others slow and regular, during sleep perfectly natural. At
first drowsiness alternates with periods of excitement, but gradually becomes
more persistent, and the child is disposed to sleep constantly unless aroused.
])ay:
1.
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4.
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EE
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Fig. 193.
Temperature Record in a case of Tuber-
cular Meningitis. The disease was ush-
ered in by convulsions, and terminated
in death on the ninth day.
946 DISEASES OE THE KERVOUS SYSTEM.
After a few days, a week in most cases, these signs of cerebral irri-
tation give place to evidences of depression which attend the second
stage. The pupils are unequal and respond slowly to light. The photo-
phobia and irritability disappear. The muscles at the back of the
neck become rigid ; the head is retracted and rolled slowly from side to
side ; sometimes distinct opisthotonos occurs. This state is irregularly
interrupted by sudden spasms with the hydrocephalic cry, or by parox-
ysms of delirium. The pulse becomes slow, irregular, and intermit-
tent ; the irregularity is very distinctive. It may be doubled in frequency
on slight excitement. There are partial or general convulsions ; ptosis,
strabismus, loss of sight, anesthesia, local paralysis or complete hemiplegia
may occur. There is constipation and retention of urine or involuntary
passages. The projectile vomiting ceases. Deglutition may become dijBB-
cult, and the unparalyzed hand will grasp at the mouth and throat to re-
move supposed obstructions. The respirations are irregular and sighing,
and Cheyne-Stokes' respiration is common. As a rule complete anorexia
exists ; the tongue and mouth are covered with sordes ; and the passages
are unnatural and offensive, often having a slimy, greenish appearance.
The urine is diminished in quantity, of high specific gravity, dark colored,
and contains chlorides, phosphates and albumen in varying proportions.
Facial convulsions are not infrequent. In young children, the temperature
may be subnormal during this stage, even when convulsion follows convul-
sion in quick succession. The ophthalmoscope reveals varicosities' of the
retinal veins, points of hemorrhage, serous peri-papillary infiltration, and
white miliary granulations on the retina and choroid. Optic neuritis is
sometimes present. It is said that ocular disturbances will be present in
this disease only when the cliiasm. is involved.^ They are not present in
tubercular meningitis of the convexity.
At this stage of the disease apparent recovery is of common occurrence.
The child sits up in bed, is free from pain or delirium, eats with avidity,
and will play as though completely convalescent. This is deceptive ; for
.after a few hours he lapses into a deeper stupor than before.
The last stage is indicated by a change in the pulse and by deepening
coma. The pulse runs up to 150 or 170 per mmute, is feeble, small and
irregular. The pupils are widely dilated ; the fontanelles in the very
young may become prominent ; the paralyses — which may have been tran-
sient — are now permanent, and convulsions occur during the development of
the coma. The breathing is sighing or snoring in character. Dysphagia
is marked. The contents of the bladder and rectum are passed involunta-
rily ; the body is covered with a clammy sweat, and one side may be hot, the
other cold. The patient lies, when convulsive movements are absent, on
his back, the head drawn to one side or still rolled from side to side. One
side of the mouth, and one nostril, show that paralysis has occurred. Soon
only reflex movements can be excited. Contractions about the jaw and
neck are frequently observed. The abdomen becomes tympanitic, subsul-
tus tendinum is marked ; the capillary circulation is more and more inter-
1 Cohnheim and Bouchut. 2 jjnvon MediccUe, 1867, GalezowskL
TUBERCULAR MEN-INGITIS. 947
fered with, respirations become less distinct, and death may occur quietly
in deep coma, or from asphyxia at the height of a severe convulsion.
During these last hours the temperature may reach 106° F., is of varying
intensity, and is rarely subnormal. In some severe cases the stage of coma
is reached in a few hours, and death occurs within forty-eight hours ; again
there may be no actual coma throughout. I have occasionally seen cases
begin with paralyses (facial hemijalegia, etc., etc.), and with aphasia.
Differential Diagnosis. — Tubercular meningitis may be mistaken for acute
meningitis, gastro-enteritis, acute Brigltfs disease, spurious hydrocephalus
and infantile remittent fever.
Acute meningitis has none of the prodroraata that in over 80 per cent.
of the cases precede tubercular meningitis ; it is sudden in its onset and
rapid in its progress ; the temperature is higher and has none of the exacer-
bations and remissions that cause the tubercular form to simulate infantile
remittent fever. The ocular symptoms and the boat shaped abdomen
are more prominent in the tubercular than in other forms of meningitis.
The hydrocephalic cry, and the irregular, slow development are character-
istic of the tuberculous variety.
Gastro-enteritis is accompanied by diarrhoea, abdominal pain and tender-
ness. But headache, contracted jDupils, photophobia, the slow, irregular
pulse, reflex movements during sleep, projectile vomiting, and the hydro-
cephalic cry of acute hydrocephalus are wanting.
In Brighfs disease the oedema, the characteristic facial expression, and
the absence of prodromes, taken in connection with the presence of albu-
men and casts in the urine, will establish the diagnosis.
A comatose state following cholera infantum, called spurious hydroceph-
alus, will be recognized by a feeble, rapid pulse, a low (even sub-normal)
temperature, a dilated pupil, a distended abdomen, and the absence of the
characteristic nervous phenomena of meningitis ; the fontanelle is depressed
in spurious hydrocephalus, elevated and strongly pulsating in tubercular
meningitis.
Infantile remittent is attended by a high temperature that remits with
regularity ; the exacerbations and remissions of tubercular meningitis are
irregular, and the fever is rarely over 103° F. In infantile remittent the
vomiting is retching in character, diarrhoea is jDrominent and the discharges
pea-soup in character, the abdomen is distended and tender ; there is great
thirst, rapid pulse, and normal pupils. The photophobia, irregular pulse,
hydrocephalic cry, and the grinding of the teeth so common in acute
hydrocephalus are absent. The severe cerebral symptoms that often attend
the invasion of acute pneumonia, pleurisy, bronchitis, or the exanthematous
fevers in children are to be distinguished by a physical exploration of the
chest or by the appearance of the eruptions and the high fever and pulse-rate.
Prognosis. — Tubercular meningitis is one of the most fatal diseases of
childhood. Many authors state that it is always fatal after its character-
istic symptoms are developed. The duration varies from five days to four
weeks ; from sixteen to twenty-one days after the initial symptoms death
may be expected. If ushered in by convulsions its duration is short.
948 DISEASES OF THE NERYOUS SYSTEM.
Treatment. — It is unnecessary to refer to all the different measures which
have been resorted to for the cure of this disease, for they have all failed.
Prophylaxis alone is effective. A child whose antecedents lead us to fear
the advent of acute hydrocephalus should be given a healthy wet-nurse
from its birth, and the greatest care exercised as to its hygiene and diet for
the first few years of life. Children who exhibit the premonitory symp-
toms, and in whom its development is feared, should be given cod-liver
oil, kept out of doors as much as possible, and placed under the most
favorable hygienic conditions possible ; a frequent change of surroundings
and of climate is important.
The treatment after the disease is established is almost entirely symp-
tomatic. The bowels are to be kept open, and absolute quiet enjoined.
Ice-bags may be placed on the head ; but depletion of all kinds is contra-
indicated. Iodide of potassium (pushed to toxic effects),' the mercury
salts, and soda phosphate have been advocated, but their utility is ques-
tionable. I have obtained the greatest benefit from opium and bromide of
potash during the stage of excitement, to relieve the restlessness and jac-
titation. I have never found that any of the plans of treatment proposed
for this disease have any power to arrest its progress.
Tubercular meningitis in the adult is of rare occurrence, and is found
only in connection with general tuberculosis. The pathological changes
are the same as those found in children, and its etiology is identical with
that of general tubercuiosis. When latent, it may be excited by severe
mental emotions or over-work. Symptom atically, it differs from infantile
hydrocephalus in degree rather than kind, the symptoms being perhaps less
violent. In all other respects the description . just given will apply in all
points to the same disease in adults.
CHEOKIC HYDEOCEPHALUS.
Chronic hydrocephalus is a cerebral dropsy from some cause not well
understood. It is divided into external hydrocephalus, in which the serous
effusion is in the meshes of the pia mater, and internal hydrocephalus,
where the accumulation of fluid is in the ventricular cavities. When both
coexist, it is called mixed hydrocephalus. Chronic hydrocephalus may be
intra-uterine or extra-uterine.
Morbid Anatomy. — The essential lesion of chronic hydrocephalus is a
serous effusion either into the ventricles or upon the surface of the brain.
The fluid consists chiefly of water, containing albumen, sodium chloride,
traces of lime and potash salts, epithelial and blood cells, rarely scanty
lymph-flocculi and urea.^ The ventricles may contain from twenty to
thirty pounds of fluid. ^ The upper wall of the lateral ventricles may be
ruptured ; the brain substance is either softened or abnormally tough and
resistant. The brain will be enlarged, and the convolutions flattened. In
congenital hydrocephalus the bones of the skull are thin, the fontanelles
1 Niemeyer.
2 BrighPs Reports, vol. i., p. 433.
8 Trousseau ( Clin. Med.) mentions a case in which the amount was fifty pounds.
CHEOKIC HTDKOCEPHALUS. 949
and sutures are enlarged ; or, if united, numerous ossa triquetra are found
between them ; and the supra-orbital, temporal, and occipital regions are
distinctly depressed. The head may measure from eighteen to forty inches
in circumference. The large ganglia at the base are pressed downward ;
the yarious septa and commissures are thinned or ruptured ; and finally,
there may be left only a thin layer of brain matter together with the
thalami and corpora striata. The optic chiasm is flattened, and the pons
and cerebellum are compressed. When the lateral ventricles are distended
and the ependyma thickened and granular, the term chronic or granular
ependymitis is given ; in this condition there may be new tissue formation,
and bands of cicatricial tissue join the walls of the ventricles.
Hydrocephalus ex vacuo is the result of defective development of, or
atrophic degenerative changes in, the brain ; the space thus left is filled
hy a serous, sometimes slightly bloody fluid, seldom in great quantity
(hydrocephalus senilis). The membranes (in the very young) are seen
studded with ossific granules. If the bones should unite, there is subse-
quent thickening, and the head is either unsymmetrical, or nearly globu-
lar.' It is not uncommon to find evidences in the membranes of acute or
sub-acute inflammatory processes.
Etiology. — Hydrocephalus may be congenital or acquired. When ac-
quired it usually appears before dentition. A few cases occurring in old
people are mentioned by Watson "^ and Golis, and Dean Swift is said to
have died of it in the seventy-eighth year of his age ; atrophy or imperfect
development of the brain causes it ; and it may arise from chronic passive
hyperemia, weakness of the vascular walls, from compression of the veins,
occlusion of one or both lateral sinuses, or the presence of tubercular
masses in the brain-substance. Eickets and syphilis in children, and
dementia and alcoholismus in adults, are regarded as causes. It is met
with in tubercular and scrofulous subjects, and it is said to have followed
measles and scarlet fever.' Inflammatory changes in the ventricles and
ependyma are accompanied by hydrocephalus. One hydrocephalic child
renders it probable that subsequent children will be hydrocephalic*
Symptoms. — The symptoms vary with the rapidity of its development.
If intra-uterine, hydrocephalus develops rapidly ; the head becomes so
large that its delivery can only be accomplished by operative procedure.
If such children are born alive they die within a few days. In those cases
where the disease is slight, the child at birth appears healthy, but after a
few weeks the head begins to enlarge ; the sutures do not close, and the
fontanelles are persistent ; the forehead bulges so that it overhangs the
face, which is pale, small and weazened, giving a dwarfish expression to
the child. The limbs do not develop ; the abdomen is distended and tym-
panitic, and the skin dry and scaly. Fluctuation * may sometimes be ob-
1 Barthez and Rilliet state that in a few cases of congenital hydroceplialus the bones were normal.
"^ Practice of Phynic : Sir Thomas Watson.
» Tanner's Practice.
* Hoppe, Niemej'er and others regard hydrocephalus arising from nutritive changes in the capillary
Walls as analogous to " skin inflammations that produce blebs,"
* Sir T, Watson ; Dr. Bright.
950 DISEASES OF THE ^^TEEVOUS SYSTEM.
tained between the anterior and posterior fontanelles. Often the child is
unable to hold its head erect even for a few moments ; the pupils are
dilated and the eyes protruded. There are periods of apparent improve-
ment, but after a year of gradual decline death occurs in convulsions, from
starvation or intercurrent disease.
In another class of milder cases the mental faculties are normal, but
nutrition is imperfect ; the limbs are small and the muscles flabby. The
children are irritable, and at times have fever, nausea and vomiting.
After an unusually severe attack of fever they may gain flesh and seem
much improved, but the head still increases in size. After a variable time
of improvement they again become worse, lose strength, and all the active
cerebral symptoms return. When they attempt to walk they totter, stum-
ble and fall. Spasms, epileptiform convulsions and paralysis of certain
groups of muscles follow, and they become idiotic. Such children do not
die from hydrocephalus but from intercurrent disease. Some of these cases
live for four or five years, having periods when they seem to be recover-
ing. When anaemia and asthenia cause death the usual duration is a
year.
A few rare cases are recoi-ded where hydrocephalic subjects have lived
five, ten, and even thirty years.
Differential Diagnosis. — Congenital, or intra-uterine hydrocephalus cannot
well be mistaken for any other malady.
Cranial rachitis does not cause the mental, or even the physical, derange-
ments induced by hydrocephalus ; but it induces an nnsymmetrical en-
largement of the bones.
Prognosis. — The prognosis is always unfavorable. The average duration
is one year. Death may result from any of the complications, from simple
asthenia and anemia, from meningitis, ependymitis, apoplexy, rupture of
the fluid through the brain substance into the epicranial aponeurosis,' or
from general paralysis. The only condition of recovery is a cessation of
increase in the fluid and closing up of sutures ; the cases of absorption of
fluid and return of mental power are doubtful. ^
Treatment. — There is very little to be done for this disease. The treat-
ment which has been employed may be divided into external or mechanical,
and internal or medicinal. Mercurial inunctions and strapping the head
with adhesive plasters have been advised, but are of doubtful utility. Sud-
den compression of the head may cause death. Pale, flabby children bear
it best.
Tapping can be advocated only in external hydrocephalus and where no
inflammatory or organic changes coexist. The anterior fontanelle is the
proper point to insert the aspirating needle ; only a few ounces should be
drawn at a time, the child being carefully watched during and after the
operation. Subsequently the head should be lightly bandaged. Langen-
beck passes behind the upper lid through the superior wall of the orbit and
1 Rokitansky's case.
* Otto states, however, " that new cerebral matter may be deposited in place of re-absorbed fluid."—
Rokitansky's Pathological Anatomy.
PACHYMENINGITIS EXTERNA. 951
enters the anterior horn of the lateral ventricle. But inflammatory action
is apt to be excited by any such procedure.
Internally cod-liver oil and the syrup of the iodide of iron and potash
should be given throughout the disease Calomel (gr. ^^-l) daily has
been recommended, until purging becomes severe. The food, the hygienic
surroundings and the clotliing should also receive careful attention.
Change of air is also highly beneficial. If rickets coexist phosphatic salts
are indicated.
PACHYMEN^ESTGITIS EXTERNA.
Pachymeningitis is an inflammation of the dura mater which may be
acute, chronic, or syphilitic. The inflammation may involve either the
external, internal, or both layers of the dura mater. When the external
layer is primarily involved, it is called external pachymeningitis ; when the
internal layer is the primary seat of the inflammatory process, it is called
pachymeningitis interna. External pachymeningitis is almost always a
secondary inflammation.
Morbid Anatomy. — In the non-suppurative form of pachymeningitis ex-
terna the dura is injected, softer than normal, and covered with ecchymo-
tic spots. New connective-tissue formations occur, which lead to thicken-
ing and induration of the dura and adhesions between it and the cranial
bones. Numerous pigment granules stud the thickened membrane. Os-
teophytes form and the appearance closely resembles periostitis with exos-
tosis. In many cases bony flakes can be detached from the tough, pale,
leathery dara mater.
In purulent pachymeningitis externa suppurative processes are early
established and the external layer is softened, disintegrated, thinned, and
rendered very friable. A thick layer of new connective-tissue separates
the pus from the i7iternal layer of the dura mater. These purulent collec-
tions are usually of traumatic origin and circumscribed, as inflammation of
the dura is rarely diffuse, and the pus detaches the dura from the bone and
may lead to necrosis. When the sinuses are involved in pachymeningitis
their walls undergo thickening, the intima is roughened, and thrombi form
at the seat of the lesion, which may break down and be absorbed or give
rise to emboli or pulmonary infarctions.
In old age it is physiological for the dura to be thick, leathery, cartilagi-
nous and of a dull white color. The sheaths of the arteries are thickened.
Etiology. — Idiopathic pachymeningitis externa is of doubtful occurrence.
Secondary pachymeningitis may result from injuries to, and caries of the
cranial bones or upper cervical vertebrae. Hemorrhage of traumatic ori-
gin may separate the dura from the bone and be followed by inflammation.
Chronic internal otitis and suppurative inflammation of the orbit may lead
to it. An external periostitis maybe followed by external pachymeningitis
without apparent intervening bone-changes. Inflammation in the venous'
sinuses, especially the transverse and petrous, may lead to it, especially
when the thrombus formed undergoes suppurative changes.
953 DISEASES or THE IS-ERVOUS SYSTEM.
Symptoms. — The symptoms of pachymeningitis are generally very ob-
Bcnre. After an injury of the skull or a chronic otorrhoea, we may sus-
pect external pachymeningitis when there is somnolence, headache, dizzi-
ness, photophobia followed by delirium, and perhaps conyulsions and
coma. In cases attended by thrombosis of a sinus there will be hectic
fever and rigors and symptoms simulating an attack of intermittent fever.
When metastatic abscesses develop in the joints and internal organs, the
headache will be severe and localized, and possibly attended by nausea and
vomiting. If there is cerebral pressure, the pulse becomes slow and irregu-
lar, rarely /regwew^ and feeble ; the pupils are unequal; the headache,
apathy, and somnolence increase and are attended by facial paralysis. Just
before death the pulse slows and coma is developed. Circumscribed pain-
ful oedema behind the ear* and less fulness of the jugular of that side are
indicative of thrombosis in the transverse sinus. ^
Differential Diagnosis. — In one who has received an injury of the skull,
with possibly fracture of the base, if the signs of cerebral compression per-
sist, pachymeningitis externa may be suspected. With caries of the cranial
bones or otitis interna, the diagnosis can be made from the complicating
cerebral symptoms. But in chronic cases the symptoms are often so obscure
that a positive diagnosis is impossible.
Prognosis. — Recovery is possible and depends largely upon the cause.
Alcoholic pachymeningitis is almost invariably fatal. That due to otorrhoea
may end favorably if the pus is evacuated either spontaneously or by opera-
tion. The great danger is in extension of the inflammation to the internal
layer of the dura mater and to the pia mater.
Treatment. — The treatment is mainly surgical. Trephining may some-
times save life. Rest, a mild diet, a free evacuation of the bowels, cold to
the head and warmth to the extremities are the principal means of treat-
ment. Disease of the ear demands immediate attention. I recall a case
where, after a deep coma of five days' duration, recovery unexpectedly oc-
curred after a copious discharge of pus from the ear. Should symptoms of
suppuration be well marked, alcoholic stimulants, quinine, and opium are
indicated and the question of surgical interference will present itself.
PACHYMENINGITIS BSTTERNA.
Pachymeningitis interna may be acute or chronic. ^
Morbid Anatomy. — In acute pachymeningitis interna the inner surface of
the dura mater is intensely hypersemic and covered with a layer of iibrin
and pus which may be circumscribed or diffused. The substance of the
membrane may be thickened by new connective-tissue developments ; but
the larger part of the inflammatory exudation is upon its free surface. This
form of pachymeningitis is apt to be complicated by inflammation of the
pia mater. In chronic pachymeningitis interna the dura is covered with a
layer of organized tissue. This thin, filmy new membrane is very rich in
^ Oriesinger calls this phlegmasia alba dolens en miniature. 2 Gerborett.
^ Vircbow was the first to interpret and classily the changes which take place in this inflammation.
PACHYMENINGITIS INTEENA.
953
large capillaries with tkiii walls. It is composed mainly of cells, having
very little basement substance, and is usually most abundant at ^-he con-
vexity of the brain.
Some pathologists claim that before these changes occur, a thin layer of
compact jfibrin, which can readily be stripped off, occupies the site where
Fig. 193.
Pachymeningitis Interna.
Vertical Section of the Skull and Cerebral Meninges.
^ SsctzoTh of tJhB skull
B. Dura mater thicTcened and connected intimately with C, the first layer of the inflammatory deposit.
D. Deposit of pigrnent.
E. Svperftcial layer of exudation containing an hematoma F, caused by rupture of the capillaries m trie
highly vascular tissue.
O. A second and superposed hmmatoma appearing in a new layer of exudation, x 250.
subsequently a hsematoma is developed. The capillaries in the new tissue
are easily ruptured and hemorrhages are liable to occur, forming hsema-
tomata, ranging in size from small clots to large blood sacs covering
the whole convexity.' After a time the v^^alls of the new vessels become
thicker. In rare instances the blood extravasates in small amounts and
is absorbed, and only a thin, transparent well-defined membrane marks the
spot where the pachymeningitis existed.
The hsematoma may become encysted (Virchow's hygroma of the dura
mater), or its contents may undergo caseous and calcareous changes.^ In
some cases the blood has either dissected between the layers of the wall
of the hagmatoma, or else, after one hemorrhage, a new layer of pseudo-
membrane forms, and a second extravasation is followed by a second tis-
' In oppopition to the above description, Huguenin states that a thick (one-twelfth inch) layer of fibrin
forms on an intact dura. This, he says, is rarely demonstrable ; the new, yellow-stained membranes, in
which are colorless masses (? white blood corpuscles) of protoplasm, form later.
"^ Rokitaneky and Forster.
954 DISEASES OE THE NERVOUS SYSTEM.
sue formation. The ventricular cavities are sometimes filled with a sero-
sanguinolent fluid.
Etiology. — Both acute and chronic pachymeningitis interna are usually
secondary, but in rare instances are of. idiopathic origin. The acute form
may be secondary to pachymeningitis externa, pyaemia, Bright's disease,
or the acute infectious diseases. Chronic pachymeningitis interna is a
disease of advanced life, rare before forty, and most frequent between sixty
and eighty. Chronic alcoholismus is its most frequent cause. Atrophy
of the brain, hydrocephalus, cerebral tumors, and general paralysis and
dementia are often followed by pachymeningitis interna. In progressive
pernicious anaemia, hematoma appears in thirty-three per cent, of all
cases.' Leucocytheemia, the hemorrhagic diathesis, scorbutus, and splenic
anaemia are blood states especially liable to be accompanied by pachymen-
ingitis. Valvular diseases of the heart impairing venous return and athe-
roma are important factors in its causation.
Symptoms. — The symptoms vary with its extent and the amount of the
new tissue formation. When the disease is slight, there are no symptoms ;
when extensive, most of the symptoms are due to cerebral pressure. At
first there is constant headache, dizziness, vertigo, tinnitus aurium, mus-
cse volitantes, photophobia, constipation, anorexia and insomnia, with
slight febrile movements. The intellect is impaired, memory fails, and
sometimes there will be a temporary loss of consciousness and partial loss
of sjieech. The symptoms of slight extravasation simulate very closely
those of a small cerebral apoplexy. The pupils will be contracted, one
more than the other. There may be slight wandering, and when the attack
is partially recovered from the mental and bodily conditions are palpably
impaired. The temperature may be slightly raised and attended by irreg-
ular exacerbations and remissions. The pulse is slow, becoming irregular
upon excitement.
Paralysis comes on gradually, as one hemorrhage follows another. Be-
tween the attacks localized headache is the prominent symptom. Some-
times slight epileptiform convulsions occur, followed by temporary loss of
consciousness.^ If the hemorrhage in the new tissue is rapid and exten-
sive, patients may die suddenly from cerebral compression ; or one slight
hemorrhage which gives rise to few symptoms may be followed by a second
more extensive bleeding, attended by the ordinary symptoms of apoplexy.
Recovery after slight hemorrhage not infrequently occurs : but the patient
afterward will be troubled with more or less constant headache, insomnia,
and perhaps by localized paralysis. Moderate-sized htematomata have
been found at autopsies, where, during life, no signs existed.
During the course of acute and chronic pachymeningitis the venous
sinuses may become involved in the inflammatory process, causing thrombi
which give rise to pulmonary or other infarctions, attended by the usual
symptoms : rigors, followed by a temperature of 103° or 104° F,, with ir-
1 Huguenln.
* Pon states that pachymeningitis interna begins, often, with the symptoms of the general paralysis
of the insane upon one side of the body.
PACHVMKJSIKGITIS SYPHILITICA. 955
regular yariations. The pulse at first is rapid, but after a few days it
becomes slow. As the case approaches a fatal termination the pulse runs
up to 120 or 140, and is small and feeble. The patient becomes delirious
and rapidly passes into coma, preceded or followed by convulsions.
DiiFerential Diagnosis. — The diagnosis of pachymeningitis interna is
always difficult ; it may be confounded with acute meningitis of the con-
vexity with which it is frequently associated, with chronic vieningitis, and
softening of the irain. The diagnosis of a haematoma is based on the fol-
lowing conditions, viz. : continued, vertical, localized headache, contracted
pupils, strabismus or ptosis, very slight fever, slow pulse, a history of one
or more apoplectic seizures, or of periods of loss of consciousness followed
by dysphagia, facial paralysis or hemiplegia. The diagnosis is always
problematical, complicating, as it does, so many cerebral affections, and
its symptoms are masked and indefinite.
Prognosis. — The prognosis is bad, although the course of the disease is
usually slow. The cerebral symptoms often intermit. Some die from the
extension of the inflammation ; others from rapid and extensive blood ex-
travasation ; some become insane or demented ; the larger number die from
intercurrent disease. When the venous sinuses are involved patients may
die from the effects of the inflammation or from infarctions. The disease
lasts, in most cases, from one to three weeks, yet one day and one year are
given in a few recorded cases as the limits of this affection.
Treatment. — There is no cure for pachymeningitis interna : all that can
be done is to treat symptoms. Absolute rest in a cool, quiet room is to be
enjoined. Irritative or inflammatory symptoms demand cold to the head,
mild counter-irritation, and heat to the extremities. The bowels are to be-
kept freely opened, and, at the onset, a brisk purge may be given. As the
disease progresses stimulants and a highly nutritious diet are the best
means to combat the affection ; and anodynes may be necessary to induce
sleep and relieve headache. Ergot is indicated on the ground of its
physiological action on the vascular system, to prevent or diminish future
hemorrhages. Eamskill advocates iodide of potash as the chief remedy, but
this and mercury are rarely employed at the present day.
PACHYMENINGITIS SYPHILITICA.
Pachymeningitis syphilitica is a form of meningitis which is met with in
the advanced stage of syphilis.
Morbid Anatomy. — Its lesions differ from the other forms of meningitis,
in that the inflammatory product is circumscribed in the form of gum-
matous tumors, which are composed of small round, oval, and pyriform
cells with basement substance. Tiiese gummatous masses may degenerate
and become cheesy, or be converted into a purulent-looking fluid consisting
of serum, degenerated cells, and granular matter. They may be developed
either on the external or internal surface of the dura mater, and are usually
multiple. Accompanying this form of meningitis, gummatous masses may
develop in the substance of the cranial bones and cause more or less de-
956 DISEASES OF THE IITERVOFS SYSTEM.
struction of them, or it may be complicated by inflammation of the pia
mater, and then gummy masses may develop beneath the pia mater.
Symptoms. — As in the other varieties of pachymeningitis, persistent local-
ized headache is the most constant and prominent symptom ; convulsions
and temporary loss of consciousness not infrequently accompany the
headache. The intellect is impaired, and the patient lapses into a dull,
stupid, apathetic condition. They may be wildly delirious. In some in-
stances there is loss of sight and hearing. If the gummatous masses attain
a large size, facial paralysis and hemiplegia may occur. I have known a
patient with syphilitic pachymeningitis to become hemiplegic, pass into a
state of complete unconsciousness, with stertorous breathing, relaxed
sphincters, and dilated pupils, remain in this condition for ten days, and
finally completely recover.
Differential Diagnosis. — The diagnosis rests entirely on the syphilitic his-
tory in one who has any of the external manifestations of syphilis asso-
ciated with the cerebral symptoms of pachymeningitis.
Prognosis. — The natural termination of this disease is in death. If these
patients are subjected to proper treatment before the gummatous masses'
have become too large or are too far advanced in degenerative changes, re-
covery is almost certain. Eecovery, however, in these cases is rarely per-
manent, for after the treatment has been abandoned, the disease is apt to
return. In one who is addicted to the use of alcohol the prognosis is very
unfavorable.
Treatment. — The treatment is that of advanced sypliilis. Mercury and
iodide of potassium, either together or alternately, are the means to be re-
lied upon. The mercury is best employed by inunctions and baths. My
rule is to apply each day a drachm of strong mercurial ointment in the ax-
illa and flexures of the joints until its specific effects are produced. Iodide
of potassium must always be given in large doses ; from thirty to sixty grains
may be given in from four to six ounces of water, three or four times daily
until the desired effect is reached, which is the disappearance of the cerebral
symptoms. Tonics and cod-liver oil are always indicated, and of service
between the periods of the administration of the mercurials and the iodide.
Under no circumstances should this class of patients be allowed to use stim-
ulants habitually in any form.
CEREBEAL THROMBOSIS AND EMBOLISM.
The cerebral arteries may be obstructed by emboli or thrombi, the cere-
bral veins and sinuses by thrombi only. The changes in, and effects pro-
duced by a plug in the cerebral vessels, whether embolic or thrombotic in
its origin, are identical with similar changes in other parts of the body.
The walls of a cerebral artery which is the seat of thrombosis are usually
thickened. The thrombosis may be the result of slowing of the blood cur-
I'ent from any cause. The results and symptoms of cerebral thrombosis are
essentially the same as those of cerebral embolism.
Cerebral emboli may be bilateral ; several may coexist ; and they have
CEREBRAL THROMBOSIS AND EMBOLISM. 957
been found in all of the cerebral arteries. The left middle cerebral is their
most frequent seat (forty-six in one hundred cases) ; next the internal ca-
rotid, the basilar, and vertebral. Ninety per cent, are in vessels that sup-
ply the ganglia at the base. The artery of the corpus callosum is rarely
implicated.' Embolism in the cortex is rarely attended by serious results,
on account of the free anastomoses between the cerebral capillaries and
those of the pia matei".
When the left middle cerebral artery is plugged, it being a terminal ar-
tery with no anastomoses, well-marked symptoms occur and destructive
lesions follow. This artery has the most direct communication of any of
the cerebral arteries with the left ventricular cavity. This anatomical fact
readily explains the frequent occurrence of embolism in it. The result of
cerebral embolism or thrombosis is to deprive the portion of the brain sup-
plied by the obstructed vessel of its nutrition, in consequence of which it
degenerates and softens. Softening of the brain is the usual result of embo-
lism ; the name embolic softening has been applied to it, to distinguish it
from inflammatory softening.^ Niemeyer describes the initial result of em-
bolism and thrombosis as partial anaemia of the brain,' and states that the
subsequent softening is analogous to gangrene in the extremities induced
by obstruction or obliteration of the vessels. But the difference is, that
within the skull the" absence of exposure to air precludes decomposition.
If a large cerebral vessel, or a large number are obstructed suddenly, it
may cause sudden death, and there will be no time for cerebral softening.
Many writers include in the signs of cerebral embolism those of the first
stage of softening.
Symptoms. — The symptoms produced by the plugging of cerebral vessels,
either by emboli or thrombi, are sudden in their advent. When an artery
of considerable size is obstructed there is temporary loss of consciousness,
the patient passing rapidly into coma, from which he gradually recovers
•with complete hemiplegia. If only a small branch of a cerebral artei'y is
plugged there may be only a slight and transient loss of consciousness or
confusion of mind, or there may be nothing to indicate its occurrence
except sudden loss of speech. During the period of loss of consciousness,
if it occur, the face is pale and cold.
Aphasia is common, but not a constant attendant. It may be complete
or partial, the patient may be able to use only one or two words, as ''no"
or '"table," and employs them to answer all questions. Again, his vocab-
ulary may consist of a number of words, but he cannot use them aright ;
he calls for his boots when he intends to call for bread.
Aphasia may be of two kinds, amnesic or ataxic. Amnesic aphasia is
where the memory of words is lost, though the capability of uttering them
may exist. Ataxic aphasia is where the muscles and parts that produce
1 It is interesting to note that the vertebral was oftenest involved in the large number of cases seen by
Nothnagel.
2 Nothing can be definitely stated concerning embolism and thrombosi-: of the capillaries from pigment
(in malaria), leucocytes (in leukaemia), and from fatty granules or salts. They are more pathological curi-
oaities than well-defined diseases.
' The only other form of partial cerebral anicmia is from collateral oedema about spots of extravasa-
tion.
958 DISEASES OF THE JSTEEVOUS SYSTEM.
articulate speech cannot be co-ordinated ; the patient knows just the word
he wants to speak but he cannot utter it. The ataxic form is commonly
associated with hemiplegia of the right side.' In ataxic aphasia a patient
can read, write^ and listen intelligently to the speech of others. In amne-
sic he only reads and understands what others say. After repeated attacks
of embolism a patient may have both amnesic and ataxic aphasia.
Within twenty-four hours after the occurrence of a cerebral embolism
there may be conyulsive movements in the muscles which are afterward to
be paralyzed ; epileptiform convulsions frequently occur. If the patient
pass into coma he may continue in a comatose state and die within a few
days ; or he may recover from the coma with permanent hemiplegia
and aphasia. There may be temporary improvement in the hemiplegia,
but after the degenerative changes take place in the brain the hemi-
plegia becomes permanent. In most of the cases where the hemiplegia is
permanent the paralyzed muscles become contracted. When the hemi-
plegia and aphasia are partial, and there has been no loss of consciousness,
complete recovery generally takes place. A cerebral embolism may be so
slight that there may be aphasia for a few days, and then the patient will
completely recover without any other symptom.
Hemiopia and unilateral amaurosis with alternate hemiplegia are symp-
toms of cerebral embolism ; they are due to extravasations into the optic
nerve and to embolism of the arteria centralis retinae on the corresponding
side. Embolic amaurosis may precede cerebral embolism for a few days.
The ophthalmoscope shows pallor of the papilla and absence of pulsation
in the retinal arteries. Even when the middle cerebral is alone occluded
collateral fluxion may cause arterial and venous hyj)er8emia of the reti-
nal vessels and congestion of the optic disc. If the patient does not begin
to improve in twenty-four or forty-eight hours after embolism occurs, a
fatal issue may be expected. In such cases the temperature rises to 104°
E., remains at that point for a couple of days, and then rapidly declines.'
There are often evidences of embolism in other j)arts of the body, as the
spleen, kidneys, extremities, etc., etc., which will aid in the diagnosis.
Bilateral embolism usually results from separate attacks. These cases
are marked by epileptiform convulsions, temporary aphasia, l>emiplegia, or
rarely double hemiplegia, accelerated and irregular — perhaps difficult — res-
piration, unilateral anaesthesia of the conjunctiva, and normal sensibilty
of the cornea.
Differential Diagnosis. — Cerebral embolism and thrombosis often cannot
be positively distinguished from cerehral hemorrhage. The symptoms in
some cases are the same. If the hemiplegia is upon the right side and
there is aphasia the probabilities are in favor of embolism. If there is
no aphasia, and the loss of consciousness is prolonged and the facial paraly-
sis is marked, cerebral apoplexy has occurred. If the paralysis is rapidly
recovered from, it indicates embolism and not apoplexy.
Cerehral thromhi form in old age without cardiac or pulmonary disease,
> Ogle states that in left-lianded individuals the centre for language is in the right island of Eeil.
* Boumeville.
CEEEBEAL SOFTENTTTG. 959
on account of rigid, calcified and atheromatous arteries ; the paralysis is
less marked, and aphasia is usually incomplete. If the j^aralysis improves
after a day or two and then gets worse, it indicates embolism.
Prognosis. — The prognosis will depend upon the size of the artery plug-
ged ; complete recovery is always possible, partial recovery is not inf i-equent.
Still, cerebral embolism and thrombosis are serious conditions, on account
of the danger that they will lead to cerebral softening. The prognosis is
usually better in those cases where the hemiplegia is partial than when it is
comjolete. In cases wliere the symptoms at first are mild, but gradually
grow worse, the prognosis is unfavorable. It is impossible to determine the
extent and duration of the paralysis which sometimes continues after its
occurrence. Chronic visceral diseases, senility, and debility or anasmia ren-
der the prognosis unfavorable. The occurrence of coma is very unfavorable.
Even after rapid disappearance of the paralysis and aphasia there is great
danger of another attack.
Treatment. — The plan of treatment in cerebral embolism and thrombosis
is a tonic and stimulant one. No depletory or revulsive measures are
ever admissible. The action of the heart, and the constitutional appear-
ance of the patient must determine whether alcoholic stimulation is to be
resorted to or not. In cases of coexistent cerebral hyperaemia, local de-
pletion may be of service. The hemiplegia is to be treated the same as in
cerebral apoplexy. Iron, cod-liver oil, and a tonic plan of treatment
should follow the disappearance of the paralysis.
CEREBEAL SOFTEKING.
Embolism and thrombosis are undoubtedly the most frequent causes of
cerebral softening. But I shall adopt the view that there are several
varieties of very different causation and anatomical changes, and shall
follow the usual classification of red, yelloio, and loliite softening, although
this division is somewhat arbitrary and unsatisfactory.
Morbid Anatomy. — Red softening is marked by punctate redness or by
numerous minute capillary apoplectic foci, with fatty degeneration of the
nerve cells and fibres. The pultaceous spot is deep red, shading off into
the neighboring brain-tissue with no distinct limit. There may be several
of these red foci ; as many as twenty have been found in different stages
of discoloration and softening. In all cases the centres show most marked
changes. There is more or less oedematous swelling of the adjacent brain-
tissue, so that upon cutting into it the softened spot will rise above the plane
of the section. The vessels are enlarged, often from proliferation of the en-
dothelium, forming masses of varying sizes, frequently within the vascular
lymph-sheaths, making a white rim visible on cross-section. There is pro-
liferation of the cellular elements of the neuroglia, and the nerve-elements
simultaneously undergo fatty changes. Few pathologists claim that any in-
flammatory exudation accompanies these changes. There is a debris in and
about the focus, consisting of fat granules, altered blood corpuscles, and free
nuclei, a few pigment-granules, shreds of brain-tissue, and large granular
960
DISEASES OF THE NERVOUS SYSTEM.
corpuscles. ^ The nerve fibres become macerated, and their white substance
is coagulated and broken up into large masses. There is varicose hypertrophy
of the axis-cylinders.
This condition is called,
by Hayem, the cloudy
swelling of VircJioio.
A spot of red soften-
ing may become dry
and shrunken, or cica-
trization may occur.
The phenomena of ab-
sorjotion consist in fatty
degeneration and casea-
tion, or the formation
of a cyst by a process
analogous to that de-
scribed under the head
of Apoplexy.
Yellow softening is
usually the result of
partial cerebral ansemia
'from obstruction of the
cerebral vessels. It may
occur in any portion of
the brain, but most fre-
quently has its seat in
the middle or posterior
lobes, and in the cortex
or corpus striatum. Stasis is accompanied by all the changes described
as occurring with an infarction which is followed by fatty degeneration,
and it may proceed very slowly or with great rapidity should hemorrhage
fail to occur. The coagulated blood in the vessels undergoes a retrogres-
sive change, the fibrin becoming granular. Fatty and granular matter
in large quantities surrounds the infarction, which becomes dry and slowly
contracts. Corpora amylacea, blood-pigment, and crystals from the al-
tered fatty material are found. A soft, yellow-white mass — often of a sul-
phur color — is thus formed, varying in size from a hazel-nut to an orange.
The consistence is variable, but in typical cases it is a gelatinous, moist,
and tremulous pulp. A stream of water will readily wash out the focus of
softening. These degenerative changes proceed until the focus of softening
becomes changed into a mass of reticulated fibres, in whose meshes is a
milky fluid. The vessels in the wall of this cyst are covered by fat granules,
and are empty or contain a yellowish clot ; but their lymph-sheaths are
irregularly dilated with pigment, fatty, granular and detached endothelial
^ Gluge's corpuscles are large spherical cells, filled with fat ; they are abundant, dark by transmitted
and bright by reflected light. The origin of Gluge's corpuscle, so prominent in yellow softening, is as
various as that of pus-cells.
Fig. 194.
Cerebral Softening. Elements from an Apoplectic Focus in Eed
Softening.
A. Shreds of }wrve fibres.
B. Altered blood corpuscles.
C. Fat spherules.
B. Masses of myeline-
E. Free nuclei frmn neuroglia.
X 300.
CEREBRAL SOFTENING.
961
cells. In this form of softening there is usually a faint line of demarcation
between the focus and healthy brain-tissue. The color of yellow softening
is due to fatty changes and a deposit of blood-pigment. These foci may
cicatrize similarly to apo-
plectic foci, or result in
the formation of a cyst.
This process may follow
either an obstructive or
hemorrhagic infarction.
Eed softening may also
terminate in yellow soften-
ing.'
White or atrophic soft-
ening is the form met
with so frequently in old
age." It is white or re-
sembles healthy brain-
tissue; the process is a slow
one. Hemorrhage or hy-
persemia is rarely present.
It is usually met with
in the white matter of the
hemispheres, and the de-
gree of change may be •
BO slight as to render its
detection difficult, or it
may be soft and diffluent
The specific gravity of the softened mass is less than normal brain sub-
stance. White softening is never distinctly limited, but shades off into the
adjacent tissue. In chronic softening of the convolutions their form ia
preserved, but they are markedly atrophied ; over them the pia mater is
more or less oedematous, and fills up to a certain degree the space caused
by the atrophy. Should the vessels in or near a white softened patch be
examined, they will usually be found atheromatous or the seat of end-
arteritis. Thus it is evident that the color has no relation to the patho-
logical changes. Red softening may come from embolism ; yellow, directly
from thrombosis, embolism, or be a second stage of red ; white may be
primary, or secondary to yellow. In every case the cause is the primary
pathological feature — the color is secondary.
Etiology.— Embolism and thrombosis are most frequently the causes of
cerebral softening, especially in old age. It is essentially a disease of old
age, for nearly all the predisposing causes of thrombosis are met with in
advanced life. Thrombotic softening between thirty and fifty is rare. But
Fig. 195.
Cerebral Softening. Small Blood-vessel from a Focns of
Yellow Softening.
A A. Lumen of the vessel contairdng the remains of a clot.
BBB. Irregmarly dilated lymph-sheath containing granulo-
fatty viatter and detached e.ndothelia. x 300.
' Rokitansky flescribed yellow softening as occurring in well-developed spots. The fluid is acid in re-
action from liberation of fatty and phosphoric acids. He further says the same kind of softening occurs
about adventitious product-^ in the brain, tumors, clots, etc., etc. — Path. Anatomy.
2 Durand-Pardel and Lancereaux both describe mw,oWis.s«wie«i: Wawc as the last stage of red softening.
Charcot speaks of Us frequency in old people with cancer.— jlfa^. des Vieillards.
61
962 DISEASES OF THE NERVOUS SYSTEM.
eirbolic softening may occur at any period of life where the predisposing
causes of emboli exist. Syphilis and chronic alcoholismus must be ranked
next to embolism and age as causes. It has been shown that syphilitic
disease of the arteries leads to softening. Although the embolus that in-
duces cerebral softening is usually cardiac in origin, it may spring from an
aneurismal clot, from thrombosis in the large arterial trunks, or originate
in gangrenous or carcinomatous foci in the lungs. Cerebral hemorrhage
is a frequent cause of softening, and it may follow blows on the head or ex-
posure to intense cold or heat (sun-stroke).
It is well established that any new growth in the brain is accompanied
by a zone of peripheral yellow softening. Fevers, the exanthematous
especially, ulcerative endocarditis, necrotic and ulcerative diseases in the
lungs and bronchi and osteo-myelitis have led to softening, but are more
frequently the cause of abscess. ' Glanders, puerperal diseases, and the
toxic action of mercury and lead are regarded by some as causes.^
Symptoms. — Inflammatory red softening is usually attended by well
marked febrile symptoms ; the temperature may reach 102° or 103° F.
The pulse is accelerated at first, but afterward it becomes slowed. The
face is flushed and the pupils irregular. There is intense and persistent
cephalalgia, accompanied by dizziness, vertigo, and somnolence, and fol-
lowed by confusion of mind, delirium, convulsions and stupor or coma.
The gait is tottering and speech embarrassed. At first there is hyperses-
thesia, formication, itching, and neuralgic pains. Latex — with the paral-
ysis — there is anaesthesia. Vomiting is often severe and obstinate. Mus-
cular twitchings, contractions, clonic convulsions, and hemiplegic symp-
toms are present and precede coma. Aphasia may accompany these symp-
toms. If meningitis complicate the softening, its diagnosis is difiicult.
The softening may take place rapidly and be accompanied by hemorrhage.
In such a case apoplectic symptoms will be prominent. Sudden and deep
coma, however, may occur in acute softening without hemorrhage. Death
may result in from two to eight days ; or, recovery may rarely occur with
more or less permanent paralysis.
White softening is oftenest met with in old age, and is usually preceded
by despondency, physical weakness, loss of memory, and inability for pro-
longed mental labor. ^ It may come on with acute symptoms, or insid-
iously. Even when sudden in its development prodromata may have, ex-
isted very like those of apoplexy. Diminution in the motor |)ower is often
an important precursor of softening. When such premonitions occur, the
symptoms either gradually increase or advance by sudden exacerbations,
with intervals of apparent improvement. The affected side becomes
feeble, the hands, feet and fingers are moved awkwardly, there is an un-
steady tottering gait, and finally complete paralysis. Death may result
from implication of the respiratory centres.
Many cases are ushered in by the symptoms of cerebral thromiosis or
1 Reynolds and Bastian state that red softening may be caused by " prolonged mental exertion or ex-
citement."
2 M. Rosenthal, Dis. of Nervous System, vol. 1.
' Durand-Fardel lay stress upon monotony of word or gesture as a valuable diagnostic sign.
CEREBRAL SOFTENING. 963
embolism, and subsequently, as softening slowly progresses, its characteris-
tic symptoms are developed. In tlie aged, prodromata may not be promi-
nent, and with momentary or without loss of consciousness the joatient
becomes suddenly paralyzed and aphasic. This resembles an apoplectic
seizure, and is accompanied by headache and vertigo. The features are
symmetrical until attempts at exj^ression are made. Again, conviiUions
may occur instead of an apoplectiform seizure, or delirium may be promi-
nent with muscular rigidity, spasmodic twitchings, dysphagia, and suffu-
sion of the eye. Stupor and paralysis seem to alternate. The urine and
fasces are passed involuntarily, and the patient dies from exhaustion. Bed-
sores are apt to form about the buttocks.
In all forms of softening there is more or less complete hemiplegia at-
tended either by ansesthesia or hypersesthesia. When convulsions occur
they are followed by increasing stupor and paralysis. If the paralysis
begins at the fingers or toes and extends toward the trunk (creeping
palsy), it is the chief symptom aside from the failure of mind and mem-
ory. After a time these patients have to be fed and watched like children ;
after eating they sleep until they are aroused again, and they often in their
actions and in their mental capacity appear like very young children.
Differential Diagnosis. — Eed softening may be mistaken for acute men-
ingitis. Acute meningitis is, however, attended by a higher temperature, a
peculiar pulse, more intense headache and vomiting, and is marked by dis-
tinct stages — headache, delirium and coma.'
Yellow and white softening may be confounded with chronic meningitis
a,nd cerebral tumor.
In softening there is usually a history of cardiac valvular disease or of
senile atheroma. There is well-defined local pain in cerebral tumor,
while the headache in softening is dull and diffused. Speech and intel-
lect are less affected in tumors; they are both markedly implicated in
softening. Permanent facial paralysis is usually present with cerebral tu-
mors, and absent in softening. The limbs are principally involved in soft-
ening. Epileptiform convulsions occur far more frequently with tumors.
The symptoms of softening are usually steadily progressive ; while those
of tumors are irregular and of longer duration.
The diagnosis between the varieties of softening can only be made by
the previous history of the patient.
Prognosis. — Acute red softening may lead to abscess, or be a rapidly
fatal complication of a pre-existing cerebral disease ; death is rarely de-
layed beyond the tenth day. Chronic softening is a slowly fatal disease.
Death may be due to the softening, to meningitis, asphyxia, pulmonary
complications, diarrhoea, acute bed-sores, hemorrhage into the softened
spot, or to exhaustion and anaemia.
Treatment. — In all varieties of cerebral softening the most important
thing to be accomplished is to improve nutrition. In the acute variety the
patient must be kept quietly in bed ; cold may be applied to the head, and
mild revulsives to the extremities.
In threatened chronic softening — in the aged especially — attention is to
964
DISEASES OF THE NERVOUS SYSTEM.
be paid to the diet. The food must be simple, supporting, and very easy
of digestion ; the best article of diet is milk. Excitement, active and
prolonged mental or physical exertion must be carefully guarded against,
and the bowels gently moved each day. Zinc, phosphorus, and strychnia
may be given in combination with iron and quinine. The constant current
alternating with the Faradic should be employed on the paralyzed limbs.
For the relief of insomnia and the nervous phenomena cannabis indica
combined with the bromides and chloral may be given. Bed-sores demand
prompt treatment, for they frequently hasten the fatal issue. Alcoholic
stimulants are indicated in the feeble and aged. '
CEEEBEAL APOPLEXY.
The term cerebral apoplexy, although often applied to a somewhat uni-
form combination of symptoms of varied causation, will be confined to non-
traumatic hemorrhage into the cerebral substance or meninges and the re-
sulting symptomatic conditions.
Fig. 196.
Cerebral Apoplexy.
Horizontal Section of the Cerebrum through a Clot in the Left Optic Tract.
A, A. Clots from hemorrhaqe.
B, B. Area of tissue stained with blood pigment. Lebert.
Morbid Anatomy. — Cerebral hemorrhages are of all sizes, from minute
capillary extravasations^ to large clots containing several ounces of blood,
1 Cautery, blisters, etc., have often been tried. In none of the cases did benefit ensue ; in some, actual
increase in the severity of the symptoms followed. Dr. Reynolds regards cod-liver oil as " the most valu-
able agent in the treatment of chronic cerebral softening." Reynolds' System, art. Softening, by Reynolds
and Bastian.
* Capillary apoplexy of Cruveilhier.
CEREBEAL APOPLEXY. 965
the so-called hemorrhagic foci. Preceding the hemorrhage the ruptured
vessel is the seat of miliary aneurisms due' to arterio-capillary fibrosis, which
commences in the perivascular lymph-spaces, and extends to the tunica in-
tima. Globular, saculated, or fusiform dilatations are developed in vary-
ing numbers, which are generally microscopic in size, but may be as large
as a pin-head, and through their ruptured walls hemorrhage occurs. Mi-
nute extravasations, however, play an important part in the development
of apoplexy. Such foci are sometimes the result of venous thrombosis, and
are probably soon absorbed, or they may accompany cerebral softening, as
well as occur in the neighborhood of large aj^oplectic spots. More rarely
an aggregation of these pin-head extravasations forms an apoplectic focus.
In capillary hemorrhage, the lymph-sheath may remain intact, or be filled
and more or less distended with blood. Fatty degeneration of the walls of
the central vessel usually follows. In the other form (hemorrhagic focus),
there is found, on autopsy, a clot, varying in size from a pea to a hen's
Gg^, imbedded in the cerebral substance, which is irregularly spherical in
the hemispheres, but in the motor tracts it is elliptical or irregular. In
some cases an entire hemisphere is ploughed ujd by a large irregular hem-
orrhage, which when near the cortex may break through the brain sub-
stance, dissecting up or even rupturing the pia mater.
The most frequent locations of these extravasations are the intraven-
tricular nucleus of the corpus striatum, the extraventricular nucleus, optic
thalamus, cerebellum, and pons— in the order named. The corpus stria-
tum is sometimes pushed up and surrounded by the extravasation ; this is
made out most distinctly by looking into the ventricles. The ventricles
themselves may also be filled by a hemorrhage, or their septa torn and blood
escape upon the surface of the brain. In the aged, apoplectic foci are not
infrequently found between the membranes, in the meshes of the pia, or
even superficially. When extravasations are extensive the cerebral convo-
lutions are flattened, the sulci more or less obliterated, the dura is tense,
and sometimes there is visible bulging when the hemorrhages are super-
ficial. The adjacent pia mater and uninjured brain substance are anaemic
from pressure.
A recent clot is a soft, grumous mass, composed of coagulated blood and
brain substance in varying proportions, at whose centre is the opening into
the ruptured vessel.^ It has a ragged wall of cerebral pulp, more or less
deeply stained, and covered with fibrinous material, the result of the hem-
orrhage. Surrounding this is a zone of discolored oedematous brain sub-
stance, studded, in many cases, with capillary hemorrhages.
When the apoplectic stroke is not immediately fatal, the following changes
may take place in the clot : (1) the fluid parts may be absorbed, leaving the
solid elements to undergo secondary changes ; (2) the clot and the lacerated
cerebral tissue surrounding it may undergo fatty metamorphosis and be
absorbed ; (3) inflammation may occur in the surrounding brain substance.
1 Charcot et Bouchard ; Kouvelles recherches sur V hemorrliaiie cerebrate. Arch, de Phys.
2 Rokifansky states that in one form of apoplectic clot the fibrin collects near the centre, and in another
toward the periphery of the mass. Path. Anatumy.
966 DISEASES OF THE NEEVOUS SYSTEM.
The subsequent changes which follow the absorption of the fluid portion of
the clot are a granular and fatty degeneration of its solid constituents. It may
then go on to caseation and subsequent calcareous change, or it may become
encysted by the development of new connective-tissue from the neuroglia",
forming a firm, smooth, pigmented cyst wall, 'in which granular and fatty
corpuscles are mingled with hsematoidin crystals. The contents of this
cyst are at first a milky or dark chocolate fluid, according to the amount of
red globules present, which later becomes thick and creamy, and finally
forms a firm, hard caseous mass, or if entirely absorbed there remains a firm,
or friable, pigmented cicatrix. Around spots of capillary hemorrhage, the
brain is softened and stained ; the medullary substance of the nerve fibref
is broken up and intermingled with pigment granules and red and white
blood corpuscles.
Whether a cyst must have existed previous to the formation of a cicatrix
is a question still in dispute. It requires from six months to two years fo^
the cyst to be absorbed and cicatrix to form. There may be a number ol
these in the same brain, corresponding to the number of apoplexies.^ G-ran-
ules and crystals of hsematoidin are found between the adjacent nerve ele-
ments and in the perivascular lymph-spaces, when the deep layers of the
cortex are involved. The nerves connected with the motor tracts undergo
degeneration, and connective-tissue increase takes place between the
atrophied nerve fibres. These degenerative changes after a time extend
into the spinal cord, and general atrophy of the brain may follow.^
Etiology. — Apoplexy is rare before forty years of age ; and after this the
tendency steadily increases. Thus age is the most powerful predisposing
cause. When it is stated that after seventy the tendency ceases, the small
number of those who live after seventy is not taken into account.
It is now generally believed that miliary aneurism is the antecedent state
of every vessel that spontaneously ruptures within the cranial cavity. Peri-
arteritis is thus a powerful predisposing factor, causing arterio-sclerosis.
Fatty, atheromatous, and fibroid degenerations of the walls of the vessels
also predispose to apoplexy. Hence the importance of gout, rheumatism,
syphilis, chronic Bright's, and chronic alcoholismus as predisposing causes.
Aortic insufficiency, pulmonary emphysema, and left ventricular hyper-
trophy are important etiological factors.*
I have already spoken of the liability to hemorrhage in leukasmia and
progressive pernicious anaemia. Scorbutus, typhus, pyaemia, malignant
jaundice and chlorosis are conditions in which the blood does not afford
adequate nutrition to the vascular walls, and they are then easily ruptured.
Men are more liable to apoplexy than women, on account of their active
mode of life and greater liability to excitement. Apoplexy occurs more in
winter than in summer. The so-called plethoric habit which causes so
much anxiety has little significance, for the emaciated valetudinarian is
' Forster states that a connective-tissue wall is not always found, even when death does not occur. Path,
Anatomy.
"^ Cruveilhier states that he found fifteen in one brain. They cause thickening of the brain.
* Diseases of Old Age ; Charcot and Loomis, N. Y. Wm. Wood & Co., 1881.
* Simple ventricular hypertrophy is a physiological condition in old age. .
CEREBEAL APOPLEXY. 967
Just as liable to apoplexy as he of the o]oposite condition.' "Whether
atrophy of the brain can produce sufficient dilatation of the cerebral ves-
sels to cause rupture is uncertain. Cerebral softening may, by affording
less support to the vessels, predispose to hemorrhage ; but is far more fre-
quently a result than a cause of apoplexy.
The exciting cause of cerebral hemorrhage is usually sudden increase in
the blood pressure, although apoplexy may occur without any such in-
crease. Coughing, running, a fall, sudden mental excitement, straining at
stool or in passing urine, bending the head far over near the feet, a cold
bath, the sexual act (especially in advanced life), large ingestions of alcohol,
sudden stopping of bleeding piles, use of opium, and a too hearty and
indigestible meal may all induce a stroke in one whose arteries or arterioles
are diseased.
Symptoms. — Preceding an apoplectic seizure there may be premonitory
symptoms. Vertigo, dizziness, muscse volitantes, double vision, temporary
blindness due to retinal hemorrhages, tinnitus aurium, flushing or pallor of
the face, nausea, an abnormally keen sense of smell, or a total loss of it, are,
some of them, present in a certain proportion of cases. Epistaxis in one
past middle life is an important and dangerous larodromal symptom. These,
however, are unimportant compared with loss of memory, tremor, or neu-
ralgic pains, irregular or retarded heart action, difficulty and thickness of
speech, lethargy, stupor, change in temper and sense of weight, numbness
or formication, which very often are present before an apoplectic seizure,
and must always excite alarm whenever they occur in one past middle life.
Partial facial palsy is, by some, regarded as a noteworthy precursor. '■^ In
many cases none of these premonitory symptoms are present, but the seiz-
ure is sudden, the patient rapidly passing into a state of coma. In others
the comatose state comes on gradually, and is preceded by pains in the head
and a feeling of faintness. In rare instances hemiplegia and aphasia are
the primary symptoms. Convulsions usher in the attack when large hemor-
rhages occur into the meninges. With very small hemorrhages there may
be only momentary insensibility ; the patient recollects everything, though
not clearly, and those about him pronounce it a fainting fit, or bad attack
of indigestion, as it frequently comes on after over-indulgence at the
table.
Usually the coma is sudden and complete, and lasts from a few hours to
two or three days.^ During this coma the respirations are deep, slow,
stertorous, and accompanied by a puffing sound ; sometimes the face is pale,
but more commonly it is red, swollen, and turgid, and as the coma deepens
it assumes a dusky, livid hue. Pallor may continue throughout the attack
when the hemorrhages are gradual. If the coma lasts from forty-eight to
seventy-two hours the temperature is lowered on the second day in some
1 If, as H. Jackson supposes, there Is an hereditary tendency to apoplexy, it must be transmitted through
arterial disease.
* Trousseau and Hughlings .Jackson.
3 Apoplectic 'coma, according to Niemeyer, Hutchinson, and others, is due to anaemia produced by
presi^ure upon the capillary vessels. This only holds good for large hemorrhages ; and small hemorrhages
sometimes produce coma.
968 DISEASES OF THE NERVOUS SYSTEM.
instances to 96° F. The third day it not infrequently rises. The pulse,
at the onset of the attack, is slow and irregular ; later it becomes frequent
and more regular. The pupils are seldom normal ; they may be dilated,
or, in meningeal apoplexy, contracted. Inequality of the pupils is of much
more serious import than equal dilatation or contraction. Sometimes when
the pupils are small, they quickly enlarge upon rousing or disturbing the
patient. The patient may be unable to swallow, the features become dis-
torted, and, as the paralysis deepens, the pupils dilate ; the skin becomes
cold and clammy, and the urine and fseces are passed involuntarily. An
apoplectic patient may lie apparently dead,' yet even in such cases sudden
death is rare.^ Eeflex movements, except at the very onset, may nearly
always be excited, often more readily than during health. Convulsive
movements during the coma are rare. Hemorrhages into the pons and me-
dulla, implicating the roots of the pneumogastrics, are generally followed
by death in a few hours. The side that is subsequently paralyzed may show
convulsive movements from the commencement, and tetanic spasms in
sets of muscles or in single muscles occasionally occur. In many cases
the head and both eyes are turned toward the healthy side for a short
time.
After the coma, consciousness returns slowly ; and in from forty-eight to
seventy-two hours headache, restlessness, wandering or delirium may come
on. A slight febrile movement, increase of the pulse-rate and respiration,
confusion of the mental faculties, and contraction of the flexor muscles,
indicate the occurrence of inflammatory changes in and about the clot.
Hemiplegia upon the side opposite to the hemorrhage is one of the most
constant attendants of apoplexy, especially in the aged. It may be accom-
panied by anaesthesia, but it is rarely present without hemiplegia. The hem-
iplegia is permanent or temporary, according to the extent and location of
the clot. As recovery takes place the thick speech, retracted mouth,
deviation of the tongue, and other evidences of facial paralysis gradually
disappear. The leg also gains more or less in strength, but the arm is
permanently paralyzed. This is more favorable,' however, than when the
arm recovers and the leg remains- paralyzed. Sometimes the face remains
semi-paralyzed after the other signs of paralysis have disappeared. * Mus-
cular contractures, which relax during sleep, of varying intensity, are
rarely absent.
Diminution of electrical excitability is the rule ; and the temperature
of the paralyzed limb is below normal. The muscles are either hard and
rigid, or weak and flaccid. They always show reflex excitability. An-
aesthesia soon passes away ; but it is claimed that sensation is never as
perfect on the paralyzed as on the non-paralyzed side. Though anaes-
thesia and paralysis are commonly distributed over the same region, the
> Nothnagel.
2 Wilks : Gm/s Hosp. Beiioris, 178, 1866.
3 Trousseau.
* Total loss of motor power is called paralysis ; partial loss is called paresis. Gubler describes some
interesting cases of crossed or alternate paralysis, where a left arm and a right leg, etc., were paralyzed.
A few cases of paralysis of the facial alone and of the musculo-spiral alone have been recorded. — Union
Medicate, 1854.
CEREBKAL APOPLEXY.
969
former is usually confined to the track of certain nerves.' Sometimes the
paralyzed parts are hypereesthetic, the pain being diffused.'" The organs
of special sense are rarely involved. Sight and hearing may be altered,
upon increase of intracranial pressure. Hemiopia is not uncommon.
Paralysis of the olfactory is rare ; but when the chorda tympaui is aifected
taste may be abolished on the fore part of one side of the tongue.
On the second or fourth day after the apoplectic seizure erythematous
patches may appear in the sacral region on the paralyzed side. Excoria-
tion then occurs, and the acute bed-sore, the most important of the trophic
changes, appears as a dry brown crust. The eschar may slowly extend to
the sound side.^ The intellect rarely remains as clear as before seizure,
and the disposition changes. The memory, especially for recent events,
is markedly impaired, and the will-power is greatly diminished. Some-
Fig. 197.
Vertical Transverse Section of the Brain through the Optic Thalamus.
A, A. Motor tracts of the cortex ce7'eb7'i.
B. Optic thalamus. ^ ^ ^,
C. Radiation of internal capsule to tlie motor tracts of the cortex.
D. Lenticular nucl£us.
E. Claustrum.
F. Caudate nucleus. Charcot.
times complete imbecility follows an apoplexy. In the very aged there is
a form of apoplexy that is seemingly associated with hemorrhage into, or
rupture of, the walls of the ventricles ; it is accompanied by a general
> Tiirck states that anaesthesia is permanent when the inner part of the lenticular nucleus, tlie super-
ficial portions of the thalamus opticus and the ad.ioiniu- portions of the corona radiata are involved. The
anaesthesia is also permanent in lesions of the pons and peduncles.
2 Charcot has laid stress on the arthritic pains that occur in the paralyzed limhs (spontaneous), and
Brown-Sequard on the neuralgic pains that are so troublesome during damp, cold weather. The joints
are swollen, hot and moist, and there is pain on motion. _
3 Some claim that these eschars depend upon trophic iniluences due to local hyperaemia. Charcot
states that they are due to irritation of trophic centres in the brain. Most authorities, including Charcot
and Nothnagel. ascribe little influence to vaeo-motorial changes.- CAarcoC, Legons sur les Maladies du
System Nerveux. Paris, 1872.
970 DISEASES OF THE NERVOUS SYSTEM.
epileptiform attack, lasting from fifteen to thirty minutes, during which
the tongue is bitten and frothing at the mouth occurs. This is followed,
apparently, by no serious results, other than the gradual development of
extreme debility. Death, however, usually occurs after a longer or shorter
period, which varies with the age and constitution of the patient.
Localization of cerebral lesions.
I. Hemorrhage into the motor ganglia — corpus striatum^ and lenticular
nucleus — occurs in nearly seventy per cent, of all apoplexies. It is attended
by hemiplegia, partial paralysis of the face, some ansesthesia, and slight
ocular disorders and perversions of the special senses. Intelligence is modi-
fied, memory chiefly, and there may follow hemi-chorea and athetosis.''
The head is turned from the paralyzed side. To say whether the lenticu-
lar nucleus or the nucleus caudatus is alone involved is impossible.
II. When the thalamus opticus is alone involved there is angesthesia
and no motor paralysis. No points (yet) known are' indicative of exclu-
sive implication of this ganglion.'
III. Lesions of the cortex are most interesting from their diverse mani-
festations, and from the study and experimentation that have been ex-
pended upon this subject." The motor zone of the cortex, however, em-
braces the anterior and posterior central convolutions and the lobulus
paracentralis. Hemiplegia, in nowise differing from that due to lesions
of the nucleus lenticularis, may arise from hemorrhage into this part.
Aphasia, both ataxic and amnesic, follows destruction of the island of Reil,
or of the third left frontal convolution. Hemorrhage into \hQ paracentral
lohule is followed by paralysis of the arm and leg of the opposite side.*
Following cortical lesions there appear convulsive epileptiform movements
in certain groups of muscles, or in single muscles called " partial epilepsy
of cortical origin."
IV. Extensive cortical hemorrhage is usually associated with more or
less meningeal apoplexy, and is to be distinguished from pachymeningitis.
The seat of meningeal hemorrhage may be at the base or convexity, or
spread over both hemispheres. The symptoms in children are somno-
lence, spasms and tremor. Death usually occurs rapidly with convulsions,
dyspnoea and sudden attacks of vomiting.'' In the adult death often oc-
curs very suddenly, and most cases of sudden death from apoplexy are at-
tended by meningeal hemorrhage. Eupture of the posterior communica-
ting artery is preceded by signs of compression of the third, fifth and
sixth cranial nerves.''
V. Hemorrhage into the pons is commonly followed by coma and
speedy death. Convulsions attend the passage of blood into the fourth
' The caudate nuclevs.
2 Top. Diagnos. d. Gehirnkt. Nothnagel, 1879.
s Hammond and Luys alone state that aberrations of the special senses follow lesions of this part of the
brain.
* Charcot and Pietres state that destruction of the infr. parietal lobe, angular gyrus, of the anterior
portion of the first, second and third frontal convolutions produces no motor paralysis.
'• M. Rosenthal states that psychical disturbances play the chief part in cortical (hemorrhagic) lesions.
* Wiirt. Med. Corblatt Elsasser.
'' Gougoucnheim.
CEKEBRAL APOPLEXY. 971
ventricle. Incomplete parajolegia, facial paralysis, at times on the same,
at others on the opposite side to the lesion, contracted pupils that do not
respond to light, disorders of taste, smell, or hearing, indicate ajooplexy in
the median portion of the jDons. Sometimes hemorrhage into the pons
attended by slight spasms is followed by partial hemiplegia,' or by irregu-
lar and difficult breathing. Besides crossed paralysis, we may find hemi-
plegia, paraplegia and paralysis of all the extremities, with or without
facial paralysis ; or double facial ]3aralysis with hemiplegic phenomena.^
The mental symptoms are few, if any. Angesthesia is common ; and may
be crossed also. All authorities note that articulation is more difficult
and paralysis of the abducens is more likely to occur with this than with
any other brain lesion.
yi. Hemorrhages into the anterior lobe are commonly attended by hemi-
plegia, incomplete paralysis of the face, and when on the left side by
aphasia.
VII. Hemorrhage into the middle lobe is attended by amblyopia, con-
gestion of the retinal veins, and injection of the optic papilla.^ Nausea,
dizziness and headache often occur.
VIII. Hemorrhage into ihe posterior lobe is marked by intellectual dis-
turbances, and usually by the absence of motor and sensory disturbances.
When hemiplegia occurs its tendency is to gradually disappear. Frequently
no symptoms attend a hemorrhage into the substance of the cerebral
lobes.
IX. In hemorrhage into the cerebeUur)i vomiting is a prominent symp-
tom.* Although it is W\q, great co-ordinating ganglion, clots in the cerebel-
lum rarely produce disturbance of co-ordination. Sensibility is never dis-
turbed, but there is pain in the hach of the head. Sometimes the eyes are
rolled about incoordinately, and amaurosis and amblyopia occur. In
hemiplegia^ from hemorrhage into the cerebellum there is no lingual or
facial paralysis, though there is loss of facial expression. The patients
can, and do, lie only in one position ; when they are moved they immedi-
ately return to it.
X. Hemorrhage into the lateral cerelellar loies is attended by obstinate
headache, vertigo, vomiting, amblyopia, amaurosis, dilatation of the pupils,
thick and difficult speech, and by hemiplegia on the opposite side." Should
the hemorrhage encroach upon any of the great centres, the symptoms will
be more pronounced. Injury of the cardio-inhibitory centre would be in-
dicated by irregular heart action, a condition that frequently occurs.
XI. When the crura of the cerebellum are involved, the symptoms resem-
ble those of hemorrhage into the cerebellum ; most modern pathologists,
ascribe all the symptoms of cerebellar hemorrhage to lesions of the crura.
1 Gubler and Luys state that crossed paralysis is always attended by apoplexy in the pons. Exceptions
have occurred, however. — TrovMeau, Clin. Med.
* Brown-Seqnard.
3 White spots in its centre were noted, in addition to the amaurosis, in Hughlings- Jackson's cases.
— ReyrKjldn' System of Med.
* Berliner Klinische Wochenschrift.—Renvak. 1865.
* iMndon Lancet, Nov. 2, 1861.
8 Rosenthal, Dis. of Nervous Sys. vol. i., p, 50-60.
072 DISEASES OP THE NERVOUS SYSTEM.
The patients are sometimes forced to rotate about the long axis of the body,
in some cases toward, in others from, the paralyzed side.
XII. Hemorrhage into the cerebral peduncle is attended by hemiplegia
and alternating facial paralysis, and by ptosis, mydriasis, and diyerging
strabismus on the same side.
XIII. Destruction of the corpora quadrigemina leads to blindness and
the pupils become fixed.
XIV. When the medulla oblongata is 'involved, the symptoms are the
same as those due to injury of the pons. In addition there is diabetes and
albuminuria in many cases. Grlosso-pharyngeal and hypoglossal paralysis
cause dysphagia and loss of power to protrude the tongue ; dyspnoea, ir-
regular heart action, and gastric derangements arise from implication of the
pneumogastric.
XV. Finally, when hemorrhage occurs into the ventricles, death is usu-
ally rapid. Eecovery is possible, however.' Spasms and contractions of the
paralyzed extremities occur in many of these cases.
Differential Diagnosis. — Apoplexy may be mistaken for cerebral congestion,
urmmia, alcoliolic coma, cerebral embolism, opium poisoning, epileptic and
hysterical coma.
Stertorous breathing — a common symptom in apoplexy — is absent in cere-
bral congestion. The pupils are alike in congestion; in apoplexy they are
unequal. The coma is of short duration in congestion ; in apoplexy it
persists for some time. Congestion has a long prodromal period; in apo-
plexy this is short or absent. Should paralysis be present from congestion,
it is usually bilateral; while in apoplexy hemiplegia is more or less complete.
The mental faculties are rapidly and completely restored after an attack
of apoplectiform congestion, while the reverse is the case in apoplexy.
In urmmia the previous history of the patient is important, and there is
more or less oedema. Hemiplegia is never present in ursemia ; it is rarely
absent in apoplexy. Ursemic coma comes on gradually and is usually pre-
ceded by convulsions; while the coma of apoplexy is more sudden in its ad-
vent, and is followed rather than preceded by convulsions. Casts and al-
bumen in the urine are strong presumptive evidences of ur^emic coma.
Profound alcoholic intoxication is often mistaken for apoplexy. A pa-
tient can be roused from alcoholic coma, but not from apoplectic. There is
no stertorous breathing in alcoholic coma ; while this is rarely absent in apo-
plexy. The pulse, in alcoholic coma is feeble ; in apoplexy it is full, strong
and slow. There is no hemiplegia in alcoholismus, and the urine as well
as the contents of the stomach will contain alcohol.
The diagnosis between apoplexy and cerebral embolism is often difficult.
Both may be preceded by rheumatic endocarditis and valvular disease of
the heart, although they are more frequent in embolism than in apo-
plexy. In embolism there is rarely complete loss of consciousness ; and if
it occur it is of short duration ; while loss of consciousness is the rule in
apoplexy, and it usually continues for two or three days. The pulse in em-
bolism is feeble and frequent, and the face is pallid ; while in apoplexy the
1 Diseases of Old Age ; Charcot and Loomis, New York, 1881.
CEREBKAL APOPLEXY. 973
pulse is slow and full, and the face is suffused. Aphasia is the rule in em-
bolism and the exception in apoplexy. The pupils are unchanged in em-
bolism ; while in apoplexy they may be dilated, contracted, or unequal.
The respiration is normal in embolism and stertorous in apoplexy. There
is usually right-side hemiplegia in embolism; if left side hemiplegia exist,
it is probably due to cerebral hemorrhage. Arterial degeneration is always
present in apoplexy ; while in embolism the arteries may be normal. The
paralysis is temporary in embolism and recovery is comj)lete ; while in
apoplexy it is delayed, and recovery is partial. Vomiting is a far more
prominent symptom of apoplexy than of embolism. Embolism is probable
when hemiplegia occurs suddenly in the young; apojDlexy is a disease of
middle and advanced life. Premonitory cerebral symj)toms are never pres-
ent in embolism ; they may be in apoplexy.
Opium poisoning gives many of the symptoms of apoplexy. Apoplexy
is usually accompanied by dilated or irregular pupils ; opium always pro-
duces regular and generally pin-head pupils. Convulsions may attend
apoplexy ; they are absent in opium i3oisoning. The coma comes on more
gradually, and is not usually as deep in opium poisoning as in aj)oplexy.
An exceedingly slow pulse and respiration indicate narcotic poisoning.
Stertor and liemiijlegia attend apoplexy, and the pulse may be irregular.
The coma of epilepsy may be confounded with that of ajjoplexy ; but
the blood-stained frothing at the mouth, the imprint of the teeth on the
tongue, the history of previous convulsions, the rapid recovery, and the
age of the patient are sufBcient to distinguish epileptic from apo]3lectic
coma.
In hysteria the coma is not deep, and cold will restore to consciousness.
Stertor is absent, the pupils are mobile or unchanged. In hysterical hemi-
plegia the patient drags the limb like an inert mass, contractions develop
more rapidly than in apoplexy, and the electro-muscular contractility
diminishes after it has lasted for a short time. Hysteria is j)receded by
characteristic hysterical attacks which have been followed by abundant
limpid urine. In spinal hemiplegia sensation is preserved. The electro-
muscular contractility is diminished, and reflex excitability is increased.
Sensation is lost on the opposite side, but motion and contractility are in-
tact.
Prognosis. — The prognosis of apoplexy is always grave. The greater the
age the more unfavorable it is.' Death rarely occurs at the onset of the
seizure ; but the hemiplegia, the loss of mental power, and the liability to
recurring attacks render it, even when not at once fatal, a dreaded con-
dition. It is a favorable sign if the hemiplegia begins to improve very soon
after the attack ; but if the period of unconsciousness is prolonged, if the
coma deepens, if reflex excitability is wholly lost, the sphincters relaxed,
the breathing irregular, puffy, and noisy, if the pupils enlarge, or the
temperature after having fallen rises rapidly, a fatal termination is in-
dicated. Convulsions in the aged always indicate great danger.
1 Diirand-Fardel state that ventricular and meningeal hemorrhages are frequent after sixty ; hence an
apoplexy in one who has passed that age must be regarded as very serious.
974 DISEASES OF THE N"ERVOUS SYSTEM.
The general condition of the patient and the extent and degree of paraly-
sis are always important factors in the prognosis. Epileptic seizures may
follow a partial recovery from apoplexy. Death may occur from- the shock
of a large extravasation, from interference with the medullary centres,
from asphyxia, and sometimes from inanition.
Treatment. — In one who has the prodromal symptoms of apoplexy, or
whose age and condition are such as to favor its occurrence, prophylaxis
may avert an attack.
The principal prophylactic measures are the avoidance of sudden or
violent physical exercise or strain, and of strong mental emotions. The
diet should be most nutritious, but non-stimulating, and sleeping and
living rooms should be large and well ventilated. Great care should be
taken that the functions of the intestines, liver, and kidneys are kept at
their normal standard ; and moderate exercise should be taken daily in the
open air. Sudden extremes of temperature should be avoided ; therefore
hot or cold baths are to be forbidden. The body should always be warmly
clothed in flannels.
In the advent of the premonitory symptoms, free purgation and the
application of blisters to the neck with the bromide of lithium and oxide
of zinc are indicated.
When an apoplectic seizure has occurred, the patient's head is to be
elevated, the clothing about the neck loosened, and he is to be put in bed
in a cool, dark and absolutely quiet apartment, with cold applied to the
head and heat to the feet. If the fit occur after a hearty meal, vomiting
must be induced and a purge given. Blood-letting is to be the exception ;
but if a very robust individual with high arterial tension is seized, and
there is evidence of progressive hemorrhage, then six to eight ounces of
blood may be taken. The condition of the heart and the arterial tension
are the guides as to the propriety of blood-letting. In old age or in the
weak, with a pale face and feeble pulse, venesection is never to be prac-
tised. The condition of the bladder should be carefully examined, and the
urine drawn if necessary. Much of the turgescence of the face is due to
the falling back of the tongue, consequently the patient should be placed
on his side. Sinapisms maybe applied to the nape of the neck, calves, and
over the stomach, when venesection is not practised.
As the patient comes out of the coma the vital powers must be sustained,
the most absolute rest and quiet enjoined, and the bowels kept freely open
by mild salines. Milk and beef juice are to be freely administered, and if
there is very great feebleness stimulants may be given. Stimulation is
demanded very early in old and feeble subjects. Narcotics are indicated
when there is great restlessness and insomnia, especially in the aged.
The clot in the brain is now a foreign body : nothing external or internal
can remove it ; hence blisters, ointments, drugs, etc., etc., are worse than
useless. The galvanic current to the paralyzed limbs is indicated if the
paralysis persists. It may be passed directly through the brain, and though
the absorption of the clot may not be aided by it, it often benefits the
paralyzed limbs. It should not be resorted to until three or four months
ABSCESS OF THE BRAIN. 975
after the seizure ; but passive motion, gentle friction, and the application
of stimulating liniments to the surface may be ])ractised early on the par-
alyzed limb. Massage of the paralyzed limb should always form part of
the treatment. When electricity is used, three or four seances a week, each
lasting from five to eight minutes, are suflBcient.'
ABSCESS OF THE BRAEST.
Abscess of the brain or suppurative encephalitis may occur in any part
of the brain. It may be simple or multiple, and may not differ in charac-
ter from abscesses in the connective-tissue in any part of the body.
Morbid Anatomy. — The white substance of the middle cerebral lobes is
its most frequent site. About 16 per cent, of all cases are located in the
cerebellum, and about 3 per cent, each in the pons, corpus striatum and
thalamus opticus.^ They may vary in size from a walnut to the involve-
ment of an entire hemisphere. Usually they are from one to two inches
in diameter. They are irregularly spherical in shape.
Embolic abscesses are usually multiple. Their walls are irregular and
made up of shreddy, disintegrated brain substance, with projections which
are found to surround blood-vessels. A limiting membrane may or may
not exist. In recent abscesses it is either wanting or incomplete. Some
abscesses have a membrane from their very onset ; they are encapsulated.
Usually a zone of red softening surrounds the abscess, and around this is
an envelope of oedematous brain substance.^
Their contents are usually inodorous and composed of a greenish, creamy
pus, fatty and granular matter, the debris of necrosed brain-tissue. Py-
aemic abscesses may contain fetid pus. The pus is decidedly alkaline ; very
rarely is it acid. When mucin is present the pus is ropy, viscid, or gela-
tinous. As an abscess increases in size it causes pressure on the adjacent
brain substance. In large abscesses the convolutions are compressed, so
that their edges are sharpened and their surfaces flattened. On removing
the brain a bulging with a boggy feel is sometimes noticed.
Cerebral abscesses may rupture into the ventricles, or they may make
their way to the surface of the brain and cause diffuse suppurative menin-
gitis. In rare instances they discharge into the cavity of the tympanum,
the nasal fossae, or the orbit of the eye.^ Multiple abscesses are small ;
they are found scattered throughout the brain. The processes by which
the formation of a cyst wall is effected in these abscesses have been de-
scribed by Rindfleisch as follows : a fibrinous wall, sometimes a quarter of
1 The subcutaneous injection of strychnia into the paralyzed limb has been recommended, and hypo-
dermics of ergotin have been advocated during the attack and at the commencement of the subsequent
coma. Dr. Cel borne reports a case where, after an hour and a quarter's persistent practice of artificial
respiration by the Sylvester Method, asphyxia was averted. —Jour. Med. Chirur. Pesth., Dr. Foster, N. Y.
Med. Rec, 1876.
2 Hammond states that the gray matter is involved first, the white secondarily. Gull and Sutton state
just the contrary.
3 Rokitansky states that yellow (chronic) softening surrounds cerebral abscess in a large majority of
cases.
•• Niemeyer states that the pus, after reaching the surface of the brain, may perforate outwardly through
the bones, provided extensive meningitis has not been excited. — Text-Book of Pract. Med., vol. ii., p. 227.
976 DISEASES OF THE IS'EKVOUS SYSTEM.
an inch thick, may envelop tiie abscess. The innermost, lining membrane
of this cyst-wall consists of a yellow, smooth layer of cells. Tortuous
venous vessels traverse it ; it is sometimes called the pyogenic membrane.
Next to it is a layer of germ-tissue, irregular in thickness. Externally is a
stratiform, spindle-celled tissue, that forms a direct transition into the sur-
rounding brain matter ; in spite of which, however, the abscess can be
enucleated. A zone of fatty degeneration surrounds the outermost (fibrous)
layer of the cyst-wall. The pus, Eindfleisch further states, is greasy,
greenish-yellow, acid, and usually odorless. It is to be noted that Grull
and Sutton state the pus to be decidedly alkaline and very fetid in old
abscesses.
Hseraatoidin crystals, margarin, and cholesterin are not infrequently
found mingled with the pus, and the entire capsule is to be regarded as a
neuroglia production. Absorption, cheesy degeneration, and the forma-
tion of chalky masses are said to occur in cerebral abscesses. The cyst-
wall retracts and finally disappears.*
Etiology. — Cerebral abscess occurs at all ages. Males are more subject
to it than females. Among its chief causes are suppurative otitis and
traumatism, especially blows on the head. It may result from suppurative
inflammation of the face and scalp, and from suppuration about the orbit
or nose. Syphilitic and other diseases of the bones of the skull, the tem-
poral especially, are not infrequently followed by abscess. Pyaemia and
glanders are among its frequent causes. Eed inflammatory softening is the
first stage of abscess. Ulcerative endocarditis and osteo-myelitis are espe-
cially liable to give rise to it ; the embolus in these cases has a special
character. There are cases in which no cause can be found for their de-
velopment.
Symptoms. — Headache is the most constant and prominent symptom of
abscess of the brain. In some cases it is not severe but is constant, in
others it is so severe that patients are not able to bear it without an anodyne.
It may be so circumscribed as to localize the very site of the abscess. With
the headache there is vomiting and dizziness. Delirium and disturbance
of intellect may be marked but transitory ; it may alternate with stupor.
Epileptiform convulsions, and signs of cerebral pressure may end in coma.
Incontinence of urine and faeces is a prominent symptom in most cases.
It is to be remembered that large abscesses have been found in the brain
of those who during life, gave no cerebral symptoms. Otitic abscesses
of the brain are preceded by all the signs of the (causative) local disease.
Headache, vomiting, delirium, fever and irregular chills, spasmodic move-
ments in the muscles of the face or limbs, then hemiplegia, coma and death
— this is the usual course of such an abscess. But cases are reported where
an artificial or spontaneous exit to the pus has been followed by recovery.^
In some cases optic neuritis has been found. ^ Rapid and progressive
emaciation usually accompanies cerebral abscess. At times there will be
hyperaesthesia and abnormal acuteness of the special senses at the onset ;
1 Rosenthal, Diseases of Nervous System, vol. i.
a Schloz. 3 HughlingB-JackBon.
TUMOES OF THE BHAIIT AND MENINGES. 977
and this will be followed by sopor, ansesthesia, formication^ numbness, etc.,
etc. If the abscess involves the motor tract, hemiplegia or local paralyses
will occur.
When pysemic abscesses occur in the brain, they are chiefly diagnosticated
by the constitutional symptoms. It will begin with rigors and run an.
acute course ; the temperature may reach 1.05° F. Ague-like rigors and
the initial signs of abscess coming on when the conditions of pyaemia exist
must lead to the suspicion of multiple cerebral abscess.
Sometimes in chronic abscess of the brain there is a long latent period.'
During this time epileptiform convulsions, facial paralysis, and hemiplegia
and aphasia accompanied by intermittent chills and headache may occur ;
After which, acute symptoms may be present for a few days and end in
death. The acute symptoms differ widely in diiferent cases ; there may
be localized headache over the abscess, delirium, nausea, vomiting, well-
marked signs of cerebral irritation, ending by a fall in temperature and
pulse, deep coma and death.
Differential Diagnosis. — It is always difficult to distinguish cerebral ab-
scesses from cerebral tumor. Abscess is accompanied by greater emacia-
tion and is of shorter duration than tumor. Local paralyses of long
standing are common in tumors, rare in abscess. Rigors and more or less
fever usually attend abscess. An ozoenal or otorrhoeal discharge, the his-
tory of traumatism, or the fact of a latent period having existed, is in favor
of abscess. Softening may be mistaken for abscess. The age of the
patient, the condition of the blood-vessels, the slow development of the
hemiplegia, the absence of constant or intense localized pains in the head
and the gradual loss of mental power, distinguish softening from abscess.
Prognosis. — Acute abscess of the brain is always fatal in from four to
twenty days. Chronic abscess terminates fatally from its complications,
the commonest of which are meningitis, cerebral hemorrhage, oedema,
softening, thrombosis of the cerebral sinuses, serous effusions into the
meshes of the pia mater and the ventricles, and pulmonary hypostasis.
When abscesses are situated away from the motor tract and surface of the
brain, they may exist for years and give rise to no symptoms.
Treatment. — The treatment of cerebral abscess is altogether surgical.
The operation of trephining for traumatic abscess, and the treatment of
chronic aural disease, are found in modern surgery and in special works
upon diseases of the ear. Recently the withdrawal of pus from the brain
has received much attention, and marked success has attended surgical
operations for the accomplishment of this end. Anodynes are always indi-
cated for the relief of the intense headache.
TUMORS OF THE BEAIN AND MEISTHSTGES.
The most frequent intracranial growths are tubercle, cancer, gummata
and gliomata. Apoplexy and abscess, which have much in common with
tumors of the brain, are elsewhere described. Some intracranial growths
' Lebert says from one to two mouths.
62
978
DISEASES OE THE NEEVOUS SYSTEM.
are peculiar to the brain, e. g., psammomata ; but the majority (cancer,
tubercle, gummata, etc.)- do not differ, in their anatomical characteristics
from similar growths elsewhere in the body.
Intracranial tumors may have their origin in the meninges, as sarcomata.
Fig. 198.
Cerebral Tumors.
Sketch showing at A a Fibroma of the Cerehdlum^frmn Lebert.
myxomata, lipomata, cholesteatomata and psammomata ; in the Hood-ves-
sels as angiomata, aneurisms, and a peculiar tumor in rare instances found
in the third yentricle — the epithelioma myxomatodes psammomum ;* and
in the neuroglia, as gliomata, gummata and fibromata.
Morbid Anatomy. — The commonest form of cerebral tumor is the tuter-
culous. These growths yary in size from a pea to an orange. They are hard
and compact, their exterior being gray, semi-transparent, and intimately
blended with the surrounding brain-tissue. Their centres are soft and yel-
low. They develop slowly and may calcify. The vessels going to them are
dilated, and at the centre of the growth they are indistinguishable. Tu-
bercular tumors occur in the hemispheres, cerebellum, optic thalami, cor-
pora striata, peduncles, pons Varolii and ependyma of the ventricles f but
the cerebellum^ is their favorite seat. At times tubercular growths are
encysted.
Cancer of the brain may originate in the cranial bones, the dura mater,
the pia mater, the cerebellum, the cerebrum, the pons, or the medulla oblon-
gata. Encephaloid cancer is the commonest variety. The color depends on,
(1) their vascularity, (2) the kind of softening about them, and (3) on
'» E. Long Fox, in Quain's Dictionary, p. 157.
^ Forster.
3 Jenner.
TUMOES OF THE BRAIK AND MENINGES. 979
the amount of retrogressive degenerative changes that have occurred at
their centres. When more than one tumor is present, they develop sym-
metrically, and are liable to involve homonymous parts of the brain (Eoki-
tansky).
Guminata, or syphilomata, may appear as soft, red-gray, jelly-like
masses, irregular in form, and intimately blended with the adjacent brain
substance. They are chiefly composed of round cells, but spindle and
stellated cells are sometimes found. They may have an alveolar frame-
work. Capillaries are not numerous in their substance. There may, how-
ever, be small points of extravasation. There are rare forms of gummata
which consist of a well-defined homogeneous mass, which is dry, friable
and cheesy. Atrophied neuroglia and round and spindle cells in a state
of fatty degeneration are often found throughout the gummy masses.
Syphilomata are generally found at the circumference, and especially at
the base of the brain. They may have their origin in the membranes, the
vessels, or the neuroglia. The surrounding inflammation joins them to
the meninges. If the latter be joined to the dura mater, granules are de-
yeloped in the pia, which vary in size from a pea to that of a small egg.
Syphilitic tumors in the interior of the brain are very rare. '
So-called syphilis of the brain may appear, (1) as well-defined hard
tumors, (2) as thickenings, adhesions, and contractions or puckerings of
the meninges, (3) as disease of the walls of the vessels, and (4) as sjDots
of softening or diffuse gelatinous accumulations.^
Gliomata ^ may develop either in the brain substance, or in the meninges
along the course of the cephalic nerves, or in the retina. On account of
its vascularity, hemorrhages are liable to take place into its substance. At
times a light brown coagulum causes the tumor to resemble tuberculous or
gummatous growths. It is often difficult to distinguish a glioma from nor-,
mal brain substance. These tumors may be either hard or soft ; soft gli-
omata contain only a small quantity of intercellular substance. Hard
gliomata have bundles of parallel or interlacing fibrillse as their fundamen-
tal substance. They vary in size from minute masses to masses as large
as an orange. They grow slowly and are usually solitary. There are fat
granules, cholesterin crystals, neuroglia nuclei, a debris of nerve-tissue,
and more or less redness and softening in the immediate neighborhood of
gliomata." Diffuse gliomatous masses were once thought to be infiltrated
cancer of the brain.
Psammomata, or Yirchow's sandy tumor, are soft, juiceless sarcomata
whose cells are thin, flat, irregular in outline but very large. The vessels
are in direct connection with the cells. Psammomata usually develop
1 Rindfleisch states that sj'philomata develop in the brain substance along the lymphatic sheaths and
the vessels, and that they produce spots of softening by compression of the vessels and arrest of the cir-
culation.
2 Niemeyer states that gummata are more frequent as diffuse infiltrations. Virchow, Charcot and West-
phal have found gummata in the white substance of the hemispheres, in the thai, opticus, the pituitary
gland, the optic tracts, the cerebral pc^duncles, the pons, and in the cerebellum.
3 The neuroglia-sarcomata of Cornil and Ranvier.
< Ernest Wagner and Obermeier regard hyperplasia of the pineal gland as essentially the same as a glio-
matous neoplasm.
980 DISEASES OF THE JSTEEVOUS SYSTEM.
from the dura. They may reach the size of a pea, and are hard, smooth,
and spherical. These calcareous tumors often have a concentric or lami-
nated structure.
Cholesteatoma (called pearl tumors from their lustre) do not always
contain cholesterin, but consist of concentric layers of epithelial cells
that haye partially undergone fatty degeneration. They may have an in-
distinct fibrous envelope. They rarely exceed one and one-half inch
in diameter. They are aggregations of crystalline, pearly masses, the
size of a mustard-seed ; they grow slowly from the pia at the base of the
brain, or in some depression of it. They are pathologically insignificant.
Cysts (independent of cystic developments from echinococci, etc., etc.)
are rare. They seldom exceed the size of a pin head, and are found on the
walls of the lateral ventricle. They may occur singly or in groups. Trans-
parent serous cysts developing from the vessels of the choroid plexus are
not rare.
Medullary or ganglionic neuromata — tumors of nerve-cells and ganglia
— occur in, and on the brain ; they are seldom larger than a pea, and are
found on the ventricular surface, in the white substance, or in the cor-
pora striata.^ A tumor to be a neuroma must contain a large number of
nerve-cells.
Sarcomata appear as well-defined, round or lobulated tumors, varying in
consistency, and in size from that of a walnut to an apple. They may
originate in the cerebral hemispheres, but more frequently they arise from
the dura, especially at the base of the skull. There are two forms, the
hard sarcoma with compact hard fundamental tissue and small cells, and
the soft sarcoma with loose, scanty intercellular substance and numerous
cells of large size. They are separated from the surrounding brain sub-
stance by a very vascular zone.
Myxomata appear either as well-defined tumors or as infiltrated masses
whose seat and size resemble those of sarcomata. Indeed, to determine
whether a tumor is a sarcoma that has undergone mucous transforma-
tion, or a myxoma with patches of embryonic tissue, is always very diffi-
cult.
A true myxoma or sarcoma may result from a glioma i^q. v.), the tran-
sition being gradual ; these various sarcomatous tumors are found in the
hemispheres, the anterior lobes, thalamus opticus, cerebral peduncles, or
they may involve the pons and tubercular quadi-igemina.^
Lii^omata are rare, and are only found at the raph6 of the corpus cal-
losum and fornix.^
Osteomata, new formations of bone, independent of ossification or other
neoplasia, are not frequent. Osteoma of the cerebellum has been found to
follow encephalitis. Osseous new growths must not be confounded with
syphilitic or other exostoses.
1 Cornil and Ranvier, Pathol. Histologiqve.
* Transac. Pathol. Society, Dr. Caylej', vol. xvi., p. 33.
3 Virchow. Benjamin reports a case where ossification had occurred ; Niemeyer describes lipomata as
■" small lobulated tumors starting from the dura."
TUMOKS OF THE BRAIN AND MENINGES. 981
Fapillomata are the rarest form of cerebral tumors. They are cauli-
flower-like, budding growths, with abundant milky Juice, very vascular,
and surrounded by a zone of cerebral softening. A large one — situated on
the ependyma of the third ventricle — is described by Cornil and Ranvier.'
Fibromata appear as hard, fibrillar tumors, small, and rarely peduncula-
ted. In one case seventeen fibrous tumors were found on the ependyma of
the lateral ventricle. The pons and the cerebral peduncle are sometimes
implicated by this tumor.
Angiomata, or erectile tumors, are masses composed of vessels of new
formation. They are found in the cerebral substance, corpus striatum,
cerebellum, and floor of the fourth ventricle. They may be multiple.'^
Aneurisms are not uncommon ; they do not attain a large size. They
involve the basilar artery, the vessels in the Sylvian fossa and corpus cal-
losum, the anterior communicating — rarely other than basic vessels ; from
their position they are liable to compress some of the nerves at the base of
the brain. Miliary aneurisms have been considered in the history of apo-
plexy.
Hydatids or ecMnococcus cysts usually exist as solitary tumors Avhich may
attain any size. They are generally located at the centre of the white matter
of a hemisphere. The cyst-wall is always absent when the hydatid is in the
ventricle. Some claim that it is absent even when located elsewhere in the
brain. They grow slowly, producing atrophy of the brain. Five large hy-
datid cysts have been found in various parts of the same brain.
Cysticerci in the brain form small serous cysts that may occur in any part
of the organ, and are rarely solitary. Cruveilhier describes a case where
one hundred were found. When the cysticercus is lodged in cavities, it is
Don-encysted and tends to grow easily into the form of a tape-worm. These
parasites may be found dead and changed to a chalky mass in which some
of the booklets are embedded.
Etiology. — Tumors of the brain are twice as frequent in males as in fe-
males. Tuberculous tumors are most frequent in children ; they usually
do not develop until after the second year. Cancer is rare before forty ; it
is primary in fifty per cent, of the cases. Syphilitic growths are a mani-
festation of tertiary syphilis. Hydatids occur between the ages of ten and
thirty-five ; while cysticerci are rarely found before forty. Aneurisms oc-
cur in middle life, and are associated with evidences of arterial degenera-
tion.
Symptoms. — Cerebral tumors of large size may give rise to no symptoms,
but in most cases their development is attended by more or less marked gen-
eral or local symptoms. These, however, cannot be stated in any order
that is applicable to all cases. I shall only consider the more important
and constant of the general symptoms. The most characteristic are head-
ache and disturbance of the intellectual faculties. The most constant local
symptom is local paralysis. Headache is generally a prominent and per.
> Path. Hist., p. 378.
2 Obermeier gives the name pachymeningitis hemorrhagica bregmatica to angiomatous growths upon the
Inner surface of the dura.
982 DISEASES OF THE NERVOUS SYSTEM.
sistent symptom. It is more severe than in any other cerebral disease, ex-
cept meningitis ; it is constant, and is increased by light, sound, or move-
ments of the head. With the headache there are tinnitus aurium, morbid
acuteness of hearing, disturbance of vision, strabismus, with more or less
perversion of the special' senses, local hypersesthesia, anaesthesia, and im-
pairment of the mental faculties. Vertigo, when the patient assumes the
upright position, is almost always associated with the headache, and vom-
iting occurs at irregular intervals without any apparent cause. There are
rarely any febrile symptoms, except when injlammation occurs about the
tumors. A slow irregular pulse is of frequent occurrence during the early
stage of their development, and the respirations are often irregular and
slowed. Spasm of single muscles or groups of muscles and general epilep-
tiform or choreic seizures often follow severe attacks of vertigo.
Hemiplegia is entirely absent in a large number of cases. If present it
may come on slowly, or suddenly after an epileptiform seizure ; facial paral-
ysis on the same side as the hemiplegia, is present in some cases, and rigid-
ity of the affected muscles is common. Double hemiplegia is not infrequent ;
one side being implicated some time after the other. If paraplegia exists
it indicates a median tumor, usually at the base or in the cerebellum.
If the tumor involves the island of Eeil or the posterior portion of the
third convolution there will be aphasia. The intellectual disturbances are
varied. Melancholia and paroxysms of grief or Joy are frequent. Incoher-
ence of speech, failure of memory, temporary loss of consciousness, and a
gradual passage into a condition of imbecility and helplessness are a part of
its history. This is especially liable to occur in cases where the tumors are
rapidly developed.
The choked disc or congested papilla, and the neuro-retinitis as revealed
by the ophthalmoscope, are regarded by some as important in the diagnosis
of cerebral tumors. Such conditions may cause amaurosis and amblyopia/
If there is loss of sight from involvement of the optic nerves, the pupils
will be dilated and they will not contract under the influence of light. If
the tumor is situated above the corpora geniculata, although there is loss of
sight, the pupils will respond to light. As the tumor increases in size, the
paralysis advances from one set or group of muscles to another, and this ad-
vancing paralysis is a most important diagnostic sign. Its course is usual-
ly from above downward.
On account of the local disturbances which result from the complicating
encephalitis, abscess, softening, or oedema may occur and give rise to their
own peculiar symptoms. The bowels are usually obstinately constipated.
Clinically there may be recognized three classes of cases : (1) those which are
attended by no symptoms, (2) those in which the symptoms are slowly de-
veloped and intermittent and extend over a number of years, (3) those in
which the symptoms come on suddenly and are rapidly fatal.
Differential Diagnosis. — Tumors of the brain may be mistaken tor abscess ,
> Annnske (in v. Graefe's Archiv) states that optic neuritis occupies the first rank among the symptoms of
intracranial neoplasia.
TUMOES OF THE BKAIN AND MENINGES. 983
cerebral softening, epilepsy and chronic meningitis. The points of diagnosis
between the first two have already been considered.
An apoplectic or hysterical seizure will hardly ever be mistaken for a cere-
bral tumor.
Epilepsy is a paroxysmal disease ; it usually occurs early in life and is
rarely accompanied by any of the local phenomena of tumor.
In chronic meningitis the pain is not so severe or as constant as in cere-
bral tumor, the mind is perverted and weakened, epileptiform convulsions
are rare, and the special senses and facial nerves are not implicated.
The differential diagnosis of the different varieties of cerebral tumor
may be briefly summarized as follows : — tubercular growths are met with
in early life ; they are accompanied by fever, have a tubercular history, or
have the evidences of tuberculosis in other parts of the body. They are
usually located either in the cerebellum or pons.* Cancer of the brain
may be suspected when the patient is over forty, when there is a marked
cachexia with progressive emaciation, when there is an hereditary cancerous
history, or when cancer exists in other organs, and when the development
of the cerebral symptoms has been rapid. Implication of the cranial bones
by the tumor always indicates cancer.
Syphilomata are attended by nocturnal headache, by the constitutional
signs of syphilis or evidences of previous syphilitic disease. Their symp-
toms remit and sometimes disappear under anti-syphilitic measures. Ptosis
and dilatation of the pupil are more often met with in syphilitic tumors
than with any other.
Gliomata follow traumatic injuries to the skull, and progress slowly with-
out any interference with the general health.
Aneurism may be suspected in the aged, with the signs of general arterial
degeneration.
Cysticerci occur after forty, and produce, at first, subacute epileptiform
attacks, which become very frequent. One hundred epileptic seizures have
occurred in a day with cysticerci in the brain. Paralysis of the limbs and
hemiplegia are very rare, while the psychical disturbances are marked, and
occur very early.
The diagnosis of hydatids is exceedingly diflBcult. The tumor-symptoms
are inconstant ; the intellect is unaffected, and there may be oedema of
eyelids.
The rules which will aid in the localization of cerebral tumors are as fol-
lows : — tumors of the convexity, even when large, may give rise to no
symptoms. Usually, however, they cause headache, motor disturbances,
delirium, convulsions ; but rarely disturbances of sensation or paralysis.
Tumors of the anterior lobes cause diffuse or circumscribed headache,
convulsions, and epileptiform attacks, hemiplegia, arid aphasia. The
special senses are undisturbed, except the sense of smell.
In tumors of the middle lobes the special senses (especially sight) are
affected, and there is usually anaesthesia of the surface on the side opposite
the tumor.
1 Hirschberg.
984 DISEASES OF THE ITEEVOUS SYSTEM.
Tumors in the posterior lobes cause greater psychical disturbances than
those in any other position. Motion, sensation, and the special senses
(sight excepted) are more or less disturbed. Vertigo and convulsions are
common.
Tumors in the corpus striatum and lenticular nucleus are accompanied
by hemiplegia, convulsions, facial paralysis, difficulty in articulation, dis-
turbance of intelligence ; but the special senses are not impaired. The
symptoms correspond to those of apoplexy, but they are of slower develop-
ment.
Tumors in the tubercula quadrigemina are attended by convulsive spasms,
paralysis of the motor oculi, disorders of vision on loth sides, slight paral-
ysis of the face, and unilateral paralysis of the limbs.
Tumors in the cerebral peduncles induce headache, vertigo, hemiplegia
alternating with sensory disturbances, paralysis of the motor oculi on the
same side, neuro retinitis, difficulty of micturition, but no intellectual dis-
turbances.
Tumors in the pojis Varolii induce crossed paralysis of motion (and
sometimes of sensation also), amblyopia, amaurosis, choked disc, dysphagia,
strabismus, difficulty in articulation, but no convulsions. There is usually
paralysis of the bladder.
When the cerelellar peduncles are involved the gait is tottering and un-
steady ; the patient tends to fall to one side, or rotate around the median
line.
In cerebellar tumors, there will be occipital headache, oscillatory move-
ments, unsteady gait, intense vertigo, strabismus, amblyopia, and amaurosis;
but there are no disturbances of the intellect or sensation.
In tumors of the medulla, the symptoms not infrequently resemble
glosso-labio-laryngeal paralysis. There is dysphagia, disturbances of sensa-
tion, convulsions, occasionally saccharine urine, and difficulty in articula-
tion.
Prognosis. — The character of cerebral tumors varies with their structure.
The prognosis is always unfavorable ; carcinomatous and tuberculous
tumors are progressive and early fatal. In hydatids and aneurism, though
life may be prolonged, death is a certain result. In syphiloma, life may
be prolonged for years by judicious and timely treatment. The average
duration of cancer is about one year.' Echinococci tumors have been
cured.^ In any case of cerebral tumor which is attended by intense pain
and progressive emaciation, the course is rapid, and the prognosis un-
favorable. Death may occur from continued convulsions, paralysis,
cerebral softening, oedema or hemorrhage. Secondary inflammation with
abscess, and meningitis, and pulmonary complication, may be the cause
of death. Anaemia and exhaustion are common modes of death in specific
tumors.
Treatment. — In a case of cerebral tumor where syphilis can even be sus-
1 Lebert states that three months and five years are the extremes.
5 Mouline trephined, and Fletcher incised, a frontal tumor, withdrawing the hydatids. These are
phenomenal cases.
SCLEROSIS OF THE BRAIK.
985
pected, mercury and iodide of potassium in large doses should be admin-
istered. The diet and hygienic surroundings should be carefully regulated,
the patient restricted in exercise, the pain and sleeplessness should be re-
lieved by anodynes.
SCLEROSIS OF THE BRAEST.
Independent of cerebro-spinal ^^erosis, this is a comparatively rare con-
dition. Cerebral sclerosis is a chronic interstitial inflammation, following
hypersemia of the neuroglia.' It may be diffused or multiple.
Pig. 199.
Diagram showing the Connective-tissues of Medallated Nerve Structure.
AA. Two bundles ofmedullated nerves.
BB. Epinevnum.
CC. Penneurivm.
DD. Endonevnum.
E, Axis-cylinders.
F. Neuroglia cells.
Morbid Anatomy. — The medullary substance is the favorite seat of mul-
tiple cerebral sclerosis.
On section, masses of gray, hard, well-defined, transparent sclerotic tissue
are found — sclerotic islands varying in size from one-fourth to one inch.
They may be so numerous and small as to be scarcely discoverable.^
The cut surface of a sclerosed patch is moist with serum ; and usually
shows small blue or gray-red spots.
1 The tissue forming the siteleton framework of the brain is called the neuroglia by Virchow. It is
analogous to the connective-tissue framework between the liver-lobules and kidney tubules.
" Comil and Ranvier describe cerebral sclerosis as almost exclusively involving the convolutions, and
consisting of a first stajje where hyperplasia of the neuroglia produces a vascular, pulpy, gelatinous mass ;
and of a second stage where atrophy of the new elements is accom))anied by development of a vascular
structure, hard and resistant.
086
DISEASES OF THE NERVOUS SYSTEM.
A microscopical examination of the patch in its soft stage shows active
hyperplasia of the neuro-
glia-cells. Later, com-
pression of nerve - sub-
stance occurs from the
pressure of the hyper-
plastic neuroglia tissue,
which, at this period, ex-
ists as fibrillated connec-
tive-tissue, whose fibrils —
extremely fine and inter-
lacing in all directions —
form a network contain-
ing atrophied nerve ele-
ments and small round or
oval nucleated cells. The
axis - cylinders are pre-
served, and are sometimes
markedly hypertrophied
at their periphery. At
the centre of the mass
are found numerous amy-
loid corpuscles, a few
atrophied axis-cylinders,
fat granules, and new
formed fibres that entirely
replace the normal elements. The walls of the vessels are thickened. In
the brain any portion of the white substance may exhibit this lesion.
Etiology. — The causation of cerebral sclerosis is obscure. It unques-
tionably is intimately connected with changes in the vascular system, for
the localities in which it is developed are the terminal arteries, i. e., ar-
teries that do not anastomose, or anastomose slightly. Sclerosis is often
found in epileptics and in the insane. It is occasionally met with in ad-
vanced life.
Symptoms. — The symptoms of cerebral sclerosis are a gradual enfeeble-
ment of the mental powers, especially memory, muscular tremors, headache,
dizziness and vertigo. Accompanying these, one group of muscles after
another becomes paralyzed. There is no regular order in the development
of the paralysis, first a lower, then an upper extremity, then some of the
facial, muscles are involved. Melancholia, pains in the extremities, and a
sense of formication are common. The nutrition is rarely interfered with ;
many patients gain flesh. Convulsions and disturbances of special sense
are rare. Strabismus may be present.
A peculiar symptom is /est ination,— the patient bends forward and trots
along like one trying to run after he is tired out. Late symptoms are
paralyses of the muscles of deglutition, speech and respiration. In rare
instances the first and only symptoms are convulsions of an epileptiform
Pig. 200.
Sclerosis of the Brain.
Section of Cerebrum throvgh a patch of sclerosed tissue.
The normal brain structure has entirely disappeared^ and is re-
placed by interlacing fibrils of connective-tiss^je, in the meshes of
which are shown small nucleated cells, atrophied nerve fibres and
fat granules, x 300.
HYPERTROPHY OF THE BRAIN. 987
character, followed by hemiplegia.' Labio-glosso-pharyngeal paralysis may
exist in sclerosis. Electrical reactions are not changed, when the cord is
uninvolved. Inanition, emaciation, muscular contractures, and, rarely, an
unexplainable rise in temperature, precede death, which occurs in collapse
with loss of consciousness.
Differential Diagnosis. — Sclerosis of the brain may be mistaken for cere-
hral softening, paralysis agitans, or tumors.
Softening occurs in old age ; the j)aralysis is in one set or group of mus-
cles, and if it extends, does so in an orderly manner. There is ancesthesia,
and the symptoms develop more suddenly than in sclerosis.
Paralysis agitans is marked by rhythmic tremor passing from one upper
to the corres23onding lower limb ; there is a peculiar deformity of the fingers
and toes ; the facial muscles are not affected, and the patient inclines to
the paralyzed side in walking. Paralysis agitans occurs only after the fo"-
tieth year, and is accompanied by qio cerebral symptoms.
Cerebral tumors are attended by headache, convulsions, and signs of
brain irritation without loss of mental power.
Prognosis. — Sclerosis of the brain may continue from five to eight years,
but it is progressive and always fatal. Death may occur from inanition, or
complications such as pneumonia, bed-sores, pleurisy, tuberculosis, ma-
rasmus, or cerebral paralysis.
Treatment. — Little can be done for this disease except to improve the
general health. Yet it should be mentioned that Vulpian recommends
chloride of iron, Mitchell the bi-chloride of mercury, Hammond the chlo-
ride of barium, and many the phosphite of zinc. Nitrate of silver and
strychnia are said to relieve tremor.
HTPEETROPHT OF THE BEAIlSr.
Cerebral central hypertrophy is an increase in the neuroglia (the nerve
filaments and ganglia are uninvolved), and may be partial or general. The
term cerebral hypertrophy is really a misnomer.^
Morbid Anatomy. — On removal of the skull-cap the brain protrudes be-
yond the cranial bones. The skull-bones are thinned. If the disease be-
gins very early in life, the head may become as large as in congenital hy-
drocephalus, and the sutures will be separated. The convolutions and sulci
are lessened by pressure, and the membranes are thin and dry. The dura
mater maybe adherent. The ventricular fluid is absent. Intense anaemia
always exists ; the brain matter, both white and gray, is wliite, and tough
and elastic. The brain is heavier than normal. The cerebrum is usually
involved. But hypertrophy of the cerebellum, thalamus opticus, corpus
striatum, pons Varolii, and medulla oblongata may also occur.
Etiology. — Hypertrophy of the brain may be congenital. It appears,
' Charcot states that cerebral sclerosis not infrequently commences with nausea, headache, vertigo, syn-
copal and apoplectiform attacks, followed by diplopia, amblyopia, nystagmus, disturbances of mind and
of speech.
2 Virchow in 1862 and 1867 published his article on hypertrophy of the brain ; his views were based on
the results of autopsies, and to these wc are indebted for our knowledge of this subject.
988 DISEASES OF THE NERVOUS SYSTEM.
when not congenital, in childhood before the third year. It may be hered-
itary, i. e., it may occur in several members of the same family. It may
be the result of traumatism, lead poisoning, chronic alcoholismus, or epi-
lepsy. It not infrequently accompanies idiocy and insanity. In children,
swelling of the lymphatics and thymus gland, and the evidences of rickets
precede or coexist with its development. Dwarfs are often the subjects of
cerebral hypertrophy.
Symptoms. — Virchow makes two forms, acute and chronic. In the former,
headache, epileptiform convulsions, retardation or great acceleration of the
pulse, vertigo, delirium, sympathetic vomiting, dyspnoea, and dysphagia
occur. In children there is weakness, tremor, and a tottering gait, and
the head inclines to one side. Convulsive movements of the eye or arm
occur. There may be permanent strabismus. The child may be very pre-
cocious at first ; later he becomes feeble-minded or idiotic. Periodical lar-
yngeal spasm (thymic asthma) may occur. Bulimia is marked ; and the
child is constantly somnolent. The tongue, often larger than normal, pro-
trudes from the mouth, and children often persistently suck it. Headache
is rarely absent. It is steadily progressive, and e7ids in coma, preceded by
dilated pupils, slowed pulse, vomiting, and repeated convulsive attacks.
DifFerential Diagnosis. — It is very often impossible to differentiate between
chronic hydrocephalus and hypertrophy of the brain. In hypertrophy the
child has been, or is, bright and precocious ; in hydrocephalus he is always
stupid. The fontanelles pulsate in hydrocephalus ; they do not in hyper-
trophy. The cerebral souffle may be heard in hypertrophy but not in hy-
drocephalus.
Prognosis. — It always terminates in death. It may end either by pro-
gressive stupor or from complications.
ATEOPHT OF THE BEAEST.
Atrophy of the brain may be either infantile or senile; it is never met
with in adult life.
Morbid Anatomy. — In children the disease begins in utero. The skull is
oblique ; one-half is thick, smaller than normal, and misshapen. The cor-
responding parts of the brain are atrophied, hard, altered in color, and are
studded with collections of serum. (Rosenthal.) Atrophy, or absence, of
the corpus callosum is the result of defective foetal development. It is
generally accompanied by intra-uterine hydrocephalus. Physiologically,
the brain begins to diminish in R^eight after the sixtieth year; at thai
time it is one-fifteenth lighter than during early adult life. Hence.
slight atrophy is physiological in old age. But in senile atrophy ther^
is more or less marked diminution in the anatomical elements of the
brain, and a loss in the interstitial connective-tissue. The cells of the
cortex are swollen and pigmented ; and pigmentation also occurs in the
walls of the vessels, which often undergo more or less fatty degeneration.
The cortex is thinned, and in it are found corpora amylacea. The fat in
the cerebral substance is lessened, the water increased. Senile atrophy is
ATEOPHY OF THE BRAIN". 989
usually general ; but when partial it affects the left hemisphere. There is
unequal thinning of the convolutions, and the sulci are large and deep.
The meninges are somewhat clouded. The brain is usually tougher than
normal, and the ventricles contain from two to twelve drachms of fluid.
This is a purely conservative process. The ependyma is granular and
nodular. More or less serum distends the meshes of the pia mater. The
medullary substance and the corpora striata are riddled with holes, etat
crihU.^
On section the brain has a leathery toughness ; it may be corrugated. The
cortex is of a dirty gray color; and the medullary substance is a dull white
or drab color. Partial atroj)hy may extend to the cortex, or it may follow
the fibres through the peduncles, pons Varolii, and pyramids. A crossed
lesion may sometimes be met with, due to atrophy of one cerebral and of
the opposite cerebellar hemisphere. There are remarkable instances of
diminution of the cerebellum to one-half its normal size and weight.
The loss in weight of the brain in the general j}aralysis of the insane is
greater than in any other disease. The cerebellum and basal portions of
the cerebrum are unaffected ; the most striking degree of atrophy being in
the frontal lobes, the convolutions exhibiting it most of all. Of all the
changes accompanying this form of atrophy those in the dura are most
marked ; it is adherent to the bone, and hemorrhages into its substance are
frequently met with. Pachymeningitis, hsematoma, ruptures and foldings
of the dura over the brain are often met with. Some regard these as the
specific lesions of general paralysis. The p)ia mater is oedematous and
thickened, either continuously or in patches.
Etiology. — Cerebral atrophy may be congenital or occur as a part of
senile change. It may follow cerebral hemorrhage or softening, and is
occasionally caused by tumors, meningeal inflammation, and internal or
external hydrocephalus. Injury or destruction of the peripheral nerves
may induce secondary cerebral atrophy. Excess in venery, the opium
habit, and alcoholismus are adduced as its causes." It is met with oftenerin
males than in females. Senile marasmus is its chief cause.
Symptoms. — Senile cerebral atrophy is attended by gradual failure of the
mental faculties. Memory is impaired, the special senses 3.re markedly
dulled ; and the movements, at first unsteady, are soon accom|)anied by
tremor. The patient is somnolent ; indeed, he sleeps the greater part of the
time. Soon the condition popularly known as "second childhood" is
reached. There is often more or less complete loss of power over the
sphincters. Atrophic degenerations of that half of the body on the same
side as the atrophied cerebellum, or on the opposite side to the atrophied
cerebrum are apt to occur. Incomplete paralysis accompanies these atrophic
changes. Epileptiform attacks are quite frequent ; choreic attacks occa-
sionally occur.
Only a brief mention can here be made of the symptoms of the extensive
atrophy which occurs in general paralysis of the insane. Headache, dizzi-
ness, irritability of temper, weakness of memory pre-eminently, thickness
> Durand-Fardel and Parchappe.
990 DISEASES OF THE NEEVOUS SYSTEM.
of sjDeech, change in the character of the voice, a feeling of self-importance,
grandeur and great riches, — these are very common. Sudden and uncalled-
for outbursts of rage are common. It is very much like senile dementia.
Atrophy of the brain ultimately involves the medulla, implicates the
great life-centres situate therein, and deglutition or respiration is so much
interfered with that death results. In general paralysis of both sides of the
body there is usually complete imhecility.
Differential Diagnosis. — Senile cerebral atrophy may be mistaken for
cerehral hemorrhage and softening. The history of the case is essential in
its differential diagnosis. Atrophy of the cerehellum may be mistaken for
tabes dorsalis and multijjle sclerosis. From the former it is diagnosticated
by the absence of vesical symptoms and by more intense pains ; the anaes-
thesia about the dorsal vertebrae is a valuable point, as it is always present
in tabes and not in atrophy. The intra-uterine variety of cerebral atrophy
is easily recognized by the paralyses and spasmodic seizures that occur
directly after the birth of the child.
Prognosis. — Congenital atrophies, or those occurring in the early life,
usually terminate during the fourth year. Senile atrophy is steadily pro-
gressive to a fatal termination. No estimate of its duration can be made.
It may be complicated by hypostasis in the lungs, bronchitis, pulmonary
cedema, pneumonia, acute bed-sores, or by disease of the bladder or kidneys.
In the general paralysis of the insane its duration is rarely more than a year.
Death is reached by intercurrent apoplexies, exhaustion from large bed-
sores, ansemia or pulmonary complications.
Treatment. — Improvement of the general health is regarded as the most
important indication. Some advocate exercise and massage of the para-
lyzed limbs. Niemeyer recommends cold douches. In atrophy in general
paralysis, galvanism, iodide of potash, calabar bean, morphia, and chloral,
alone or together, prolonged tepid baths, and attention to the bowels and
bladder have been recommended.
DISEASES OF THE SPINAL COED.
Diseases of the spinal cord and its membranes will be considered under
the following heads :
I. Spinal Ilyijercemia. IX. Acute Spinal Paralysis of Adults,
II. Spinal Meningitis. X. Chronic Anterior Myelitis.
■ HI. Acute Myelitis. XI. Progressive Muscular Atrophy.
IV. Chronic Myelitis. XII. Cerebro- Spinal Sclerosis.
V. JSfon-Inflammatory Soften- XIII. Locomotor Ataxia.
ing. XIV. Spasmodic Tabes Dorsalis.
VI. Acute Bulbar Paralysis. XV. Amyotrophic Lateral Sclerosis.
VII. Progressive Bulbo-Nuclear XVI. Pseudo-Hypertrophic Paralysis.
Paralysis. XVII. Spinal Apoplexy.
VIII. Lnfantile Spinal Paralysis.
HYPEE^MIA OP THE SPINA L COED AND MENINGES. 991
HYPEREMIA OF THE SPINAL CORD AND MENINGES.
Hyperaernia of the spinal cord may be active or passive.
Morbid Anatomy. — The most intense active or passive hyperaemia of the
spinal meninges may disappear between death and the time of a post-mortem,
and a gravitation from position may induce a congestion which is decidedly
misleading. In active hyperasmia the arterioles are injected and the parts
assume a rosy color marked possibly by numerous points of extravasation.
In passive hyperaemia the veins of the cord and membranes are distended
with dark blood. . Chronic congestion results in thickenings, pigmentation
and opacities of the membranes, attended by development of new con-
nective-tissue which may be the starting-point of a general sclerosis.
Etiology. — Active hypermmia may result from muscular exertion, or ex-
cesses in venery, from vaso-motpr paralysis due to exposure to cold and wet,
concussion, and suppression of menstrual or hemorrhoidal fluxes. Hy-
peraemia is always an attendant of general or local myelitis. It occurs with
acute infectious diseases, typhoid, small-pox, scarlet fever, and measles,
with chronic malarial infection, and in some cases of rheumatism and
puerperal fever. It may also result from poisoning by carbonic oxide,
strychnia, nitrite of amyl, alcohol, etc' Intense active hypereemia has
been found in those who have died of spasmodic affections, or who have
worked in compressed air, as in caissons.''
Passive liypercemia is caused by any obtrusive disease of heart, liver or
lungs, and by mechanical pressure uj)on venous trunks, by tumors, fluid
effusion, etc.
Symptoms. — The onset of active hypereemia may be sudden, while pas-
sive hyperaemia generally comes on slowly and often insidiously. In most
instances there is pain along the spine, especially in the lumbar region,
which radiates down the thighs and is increased by movement and pressure.
There is hypersesthesia of the lower limbs associated with itching, burn-
ing, or formication, and reflex irritability is augmented.
Hyperaesthesia, sharp pains, spasms, and symptoms of irritation would
rather point to ac^^/'ve hyperaemia, while numbness, anfesthesia, heaviness of
the limbs and vesical paresis are more commonly associated with congestion.^
In rare cases the disease is so sudden in its onset that the patient may
awake to find himself in a state of incomplete paraplegia. During the
whole course there is no fever and little, if any, change in the pulse.
Dyspnoea occurs when the nerve roots are involved high up in the cord.*
Quite often during attacks of spinal congestion, persistent priapism occurs
and the iron-band sensation about the waist is a frequent symptom.*
1 Magnan has experimented with absinthe on animals, and found it to produce intense hj'perisemia when
given in large doses.
* /S'/. Lovw Med. and Svrg. Jour. — Dr. Clark.
s Ro.senthal states that violent emotions and sometimes the dorsal decubitus increase the rachialagia.
* Steiner reports a case where facial paralysis occwvr Qd.—ArcMv der Heilk. 11, 1870, p. 23.3.
^ Fabra has observed pain, ana3sthesia, hyperajsthesia, slight paresis, and, rarely, convulsive phenom-
ena occurring in tho last stages of heart disease, which seemed to be due to ^awiw hyperasmia of the
cord.— Gaz.disUoi)., 1870, No. 147.
992 DISEASES OF TEE NEEVOUS SYSTEM.
When convulsions occur in sucli diseases as tetanus there is intense hj -
pergemia of the gray matter of the cord. '
Differential Diagnosis. — Hyperaemia of the cord may be mistaken for
spinal ancBmia, meningitis, myelitis or apoplexy.
In anmmia the symptoms are relieved by the recumbent posture, while
they are increased in hypergemia. Anaemia occurs suddenly, as from em-
bolism and thrombosis. Women suffer most frequently from anaemia,
men from hyperaemia. Vesical complications follow congestion, but not
anaemia.
In inflammation of tlie cord there will be fever, paraplegia, paralysis of
the sphincters, loss of electro-contractility, with bed-sores and subsequently
wasting of the muscles.
The onset of spinal apoplexy is sudden, j)araplegia is complete within a
few hours, and accompanied by anaesthesia, paralysis of the bladder and
rectum, the early development of gangrenous bed-sores, and in most cases
by the symptoms of cystitis and myelitis.
Prognosis. — The prognosis is favorable, although the condition is one
which has a marked tendency to become chronic. Complete recovery is
slowly reached, except in those cases where the cause is permanent.
Treatment. — If its cause can be reached, it should at once be removed.
Severe and sudden congestion demands local abstraction of blood by wet
cups along the spine or leeching about the anus. The patient should be
kept quiet on his side. In recent cases ice-bags to the spine, hot foot baths,
and a brisk purge will relieve the pain. Ergot and belladonna and hot
douches along the spine are highly advocated in chronic passive hyperaemia.
In reflex hyperaemia, or hyperaemia due to vaso-motor disturbances, elec-
tricity may afford relief.
SPINAL MENINGITIS.
Spinal meningitis may be acute or chronic.
Morbid Anatomy. — Acute inflammation of the spinal meninges is gener-
ally diffuse, and runs a course similar to acute cerebral meningitis. The
pia mater is hyperaemic, swollen and studded with ecchymoses. The ex-
udation takes place into the meshes of the membrane, and the effusion maj
be sero-fibrinous, or purulent. The pia mater is thickened, opaque, and
cedematous, and a turbid fluid fills more or less completely the spinal
canal. Although the exudation is more abundant upon the posterior sur-
face, it usually envelops more or less completely the whole cord, whose
substance may either be pale and anaemic, or exhibit changes of com-
mencing myelitis and softening. The roots of the nerves are embedded in
the exudation, and present changes similar to those in the cord. The
exudation may be wholly absorbed, and the membranes and the cord return
to their normal condition ; but more frequently the inflammation becomes
chronic.
In chronic spinal meningitis there are found the opacity, thickening,
adhesions, and puckerings so characteristic of chronic interstitial inflam-
1 j?einberg.
SPINAL MENINGITIS. 993
mation in similar membranes. The membrane is tough, dark, bluish -gray
in color, pigmented, and contains calcareous plates. It is adherent at
various points to the thickened dura mater (pachymeningitis spinalis).
The fluid in the spinal canal is always increased in amount ; it may be clear
serum, or contain lymph flocculi,- blood, or pus. The irregular and local-
ized adhesions and retractions produce sclerosis of the cord, and also induce
anaemia, atrophy, and degeneration of the nerve roots.
Etiology. — Spinal meningitis is a disease of youth and early adult life,
and may follow a traumatism, as in a fall, blow, dislocation, fracture, or
other injury to the vertebrae, or concussion, which is thought to be a fre-
quent cause. It may arise from extension of inflammation from the
cerebral meninges, from any disease of the spine, such as caries, cancer,
etc. Prolonged exposure to cold — especially damp cold — or brief exposure
to intense cold when the body is heated, as well as exposure to intense heat,
will induce spinal meningitis. Operations for sjDina bifida have been fol-
lowed by rapid and fatal spinal meningitis.
Eheumatism is said to be an occasional cause, and some authors regard
all febrile and infectious diseases as liable to be complicated by it.' Syph-
ilis, venereal excesses, alcoholismus, chorea, tetanus, and hydrophobia may
each, in rare instances, induce spinal meningitis f and scrofulosis, tuber-
culosis and wasting diseases are very apt to be complicated by it.
The chronic form is often a sequel of the acute, and is very apt to accom-
pany alcoholismus, syphilis, impeded venous return, and diseases of the
cord. The latter are the most frequent of all causes. Chronic or acute
inflammation of the cord, or any neoplasm that encroaches upon the spinal
canal, will lead to localized chronic meningitis. Excessive use of tobacco
or narcotics, and anti-hygienic surroundings are jaredisposing causes.
Symptoms. — When spinal meningitis is associated with cerebral inflamma-
tion its symptoms are less distinct than when it is uncomplicated. Severe
pain in the back is the earliest and most prominent symptom. The pain
at first is localized about the seat of the inflammation, but later becomes
diffused and shoots down the legs and arms. It is constant, and is made
sharp and lancinating by motion, so that the patient holds himself in a
fixed position with rigidly contracted muscles ; pressure along the spine
may increase the pain. A chill or distinct rigor accompanies the pain, and
is followed by rise in temperature, nausea, vomiting, and a sense of general
malaise. The fever is never high and the pulse-rate is frequently below the
normal. The muscles along the spine become rigid, and if the cervical re-
gion is involved there is ojDisthotonos. Convulsive twitching of groups of
muscles is attended by the most excruciating pain. The surface of the body
becomes hyperaesthetic in the area of motor derangement, and reflex activ-
ity is increased. In a few instances all the extremities are involved, but
usually there is only incomplete paraplegia. There is constipation, and
the abdomen has the well-known boat-shaped appearance.
' ('. B. Rndcliffe, in Reynold's SijHtfm,.
'■' Koehler states that any pulmonary or cardiac disease that impedes proper venous return affords a
marked predisposition to spinal meningitis.
63
99-4 DISEASES OF THE NERVOUS SYSTEM.
At the commencement of the attack there is a constant desire to mictu-
rate. Later, paralysis of the bladder and retention of urine accompany the
para-paresis, so that catheterization must be resorted to. If the paralysis
involves the respiratory muscles there will be dyspnoea, and the temperature
will rise to 106° or 107° P., and be followed by coma and death. If the
meningitis is limited to the lower portion of the cord, the case will be pro-
tracted, but marked by periods of slight improvement. In such cases bed-
sores may develop, with incontinence of urine, and death finally occur from
exhaustion. Sudden and profuse sweats may result from vaso-motor impli-
cation.
Glironic spinal meningitis is generally a sequel of acute, although it may
develop without any acute symptoms. When the acute passes into the
chronic form, i)ain and rigidity of the spine remain after the other symp-
toms have subsided. The limbs are hypersesthetic, and the seat of burning,
formication, or itching. There maybe a sensation as of a tight band about
the waist, accompanied by weight and uneasiness in the limbs, which may
develop into incomplete paraplegia. The bowels, at first, are constipated,
but later the passages may be involuntary. The bladder is frequently par-
alyzed, incontinence of urine occurs, bed-sores form, and a well-marked
marasmus is developed. Finally the paralysis will vary in degree with the
posture of the patient — and also from day to day.
Differential Diagnosis. — Acute spinal meningitis may be confounded with
myelitis, tetanus, and muscular rheumatism. In tetanus the locked jaw,
the |)eculiar implication of the facial muscles causing the risus sardonicus,
and the intense cutaneous hypersesthesia, with recurring paroxysms with-
out paralysis, are in marked contrast to the symptoms of spinal meningitis.
In the latter disease there is great pain on motion, little or none on pres-
sure, and muscular spasm is produced by attempts at movement rather than
by irritation. There is, usually, a traumatic history in tetanus.
Rheumatism in the muscles of the hack is accompanied by local pain only
when movements are made : but there is never that rigidity of the spine
which is present in meningitis, nor the cutaneous hyperaesthesia, paralysis,
spasms, or febrile phenomena.
Spinal irritation may be mistaken for meningitis, but the pain on press-
ure confined to one spot, the absence of pain upon ordinary or slight mo-
tion, and the disposition to a sudden transference of the diseased action
from one organ or part to another, with possibly the occurrence of hyster-
ical symptoms, will be sufficient to distinguish between them.
Chronic meningitis may be mistaken for chronic myelitis. In meningitis
pain is a far more prominent symptom than in myelitis ; and it is increased
by motion but not by pressure, the reverse of which occurs in myelitis.
Paralysis is never complete in meningitis, and anaesthesia and muscular
atrophy are rare as compared with myelitis.
Prognosis. — Acute spinal meningitis runs a variable course ; should
death occur within twenty-four or thirty-six hours the case is to be re-
garded as epidemic. The usual duration of the acute form is from seven
to ten days. The majority of cases are fatal, more especially those in which
ACUTE MYELITIS. 995
the membranes of the cervical cord are involved. In these cases, death re-
sults from paralysis of the muscles of respiration, and will be preceded by-
intense dyspncea and cyanosis. Even when recovery occurs, convalescence
is tedious ; and though the general health is restored, pain, paralysis,
and stiffness or atrophy of muscles are apt to continue for many months.
Karely is convalescence rapid. In many acute cases death occurs from
simple asthenia.
. Chronic spinal meningitis runs a very protracted course, and may ter-
minate in death from exhaustion, anaemia or marasmus. It jorogresses by
stages ; and although the prognosis is not so unfavorable as in the acute
form, complete recovery is rare. Both acute and chronic are most severe
in the very young or the very old and enfeebled.
Treatment. — The same principles guide the treatment of acute spinal
meningitis as were advised in acute cerebral meningitis. The patient
should be placed in bed in a cool room and a brisk purge administered.
Ice or counter-irritation may be applied along the spine, and from the on-
set the patient should be kept in a condition of semi-narcotism. Ergotin
and belladonna hypodermically are said to produce contraction of the
arterioles and restrain the inflammatory process. The internal ad-
ministration of the iodide of potash with mercury is advocated. Warm
baths are grateful to the patient, and produce a sedative effect, and have
seemed to me to be of greater service than all other measures. The nour-
ishment should be highly nutritious but never stimulating. When symp-
toms of heart failure or asthenia come on, stimulants are indicated.
Careful attention to the condition of the bladder should never be ne-
glected.
In chronic spinal meningitis counter-irritation over the spine, and de-
rivatives to the surface are to be employed as long as the inflammatory pro-
cesses are in progress.' Warm douches are excellent adjuvants, and in
some cases are followed by marked benefit. Iodide of potash and mercury
— ^the latter both internally and by inunction — are more clearly indicated
in chronic than in acute cases. The galvanic current is often of service
in preventing the muscular atrophy and contractions which are sequelge
of the paralyses.
ACUTE MYELITIS.
Myelitis is an inflammation of the substance of the spinal cord, and
may be limited to the gray or white matter ; it runs an acute or chronic
course, and involves the whole or isolated portions of the cord.
When the gray m.atter alone is involved, it is called central myelitis j
when the white matter and the meninges are involved it is called cortical
myelitis.
When once established the disease may be ascending, descending, or trans-
verse in its extension.
1 Brown-Sequard advises sinapisms, stimulating ointments, and oils, moxa, and in severe cases, white'
not irons to the spine.
996
DISEASES OF THE NERVOUS SYSTEM.
Morbid Anatomy. — In acute myelitis the portion involved is softened and
discolored to an extent
corresponding to the
amount of vascular dila-
tation and transudation
of red blood cells.
Hemorrhage takes place
into the softened spots,
although in many cases
it is doubtful whether
the hemorrhage prece-
ded or followed the soft-
In most cas6s
, and
on section, blood points
and spots of ecchymoses
are seen. The veins
especially are distended
and surrounded by a
layer of red and white
blood corpuscles.
Microscopically there
will be found swelling
of the cells of the neu-
roglia, ampullge-like di-
enmg.
the cord is enlarged,
Fig. 201.
Acute Myelitis.
From a Section through the Dorsal Spinal Cord, including portion of
the Anterior Gray Cornu.
A. Patch of ecchymotic tUsiie.
B. Nerve fibres ivith swollen axis-cylinder.
C , ' Hype.rtrophied and 'pigmented ganglion cells, with ampullar latatioUS of the a\is-CvL
inders
', of nerve fibrils
hypertrophy of
the cells in the anterior horn of the gray substance, and an albuminoid
granular degeneration of the nerve fibres. The nerve cells not infre-
quently show pigment degeneration, and the ganglion cells are clouded
and swollen.
These morbid processes result in entire disappearance of the normal ana-
tomical elements of the cord. The adjacent membranes will be congested,
thickened, opaque, and adherent to the cord, while collections of blood or
pus underneath the membrane may cause it to present a nodulated appear-
ance. These changes are most marked in the gray matter of the dorsal and
lumbar regions. Acute red softening soon becomes yellow from fatty de-
generation, from changes in the coloring matter of the blood, and from
diminution in vascularity. Later, as its consistence diminishes, a pale
yellow or white diffluent mass is left.*
Etiology. — Acute myelitis is a disease of children and young adults. In
children it takes the form of acute anterior polio-myelitis or spinal paral-
ysis. Exposure to excessive heat or cold, intense and prolonged muscular
exertion, and excessive venery are said to predispose to it ; and in children,
dentition is regarded as a predisposing cause. Myelitis may be excited by
1 Erb states that this softening is due to fluid exudation ft'om the vessels and destruction of the nerve
fibres.
ACUTE MlfELlTIS. 997
traumatism, lying on the damp ground, and expos^^re to sudden chilling
of the surface when overheated. Whether suppression of the menses, check-
ing hemorrhoidal fluxes, or profuse perspiration of the feet can cause it is
uncertain. Pressure on the cord, from tumors or displacements of the
bony parts, whether occurring suddenly or developing slowly, will induce
myelitis, or it may be excited by extension of inflammation, especially from
spinal meningitis.
Myelitis also arises during the course of small-pox, measles, scarlet and
typhoid fevers, acute articular rheumatism, malignant pustule, puerperal
fever, and syphilis. Continued jarring of the spine from travel on rail-
ways will induce it. ' Visceral disturbances — especially of the genito-uri-
nary and digestive organs — and diseases of the joints are said to act as
reflex causes. In many cases the myelitis comes on without any assignable
cause.
Symptoms. — Acute myelitis usually commences with slight febrile symp-
toms, pain in the back, a peculiar sensation of an iron band around the waist,
and the pulse is frequently feeble and irregular. Anorexia, headache and
general malaise usually precede the attack. The power of motion in the
lower extremities is rapidly lost, and soon complete paralysis occurs, which
is usually both sensory and motor. Patients will complain of a sense of
numbness in the feet ; they cannot feel the ground under their feet, and
they have a sensation as if something was crawling over their legs. Ee-
tention of urine and fseces, which marks the onset, gives place to inconti-
nence, from paralysis of the sphincters. Tremulous and spasmodic move-
ments often occur in the limbs that are subsequently paralyzed ; and at the
commencement of the paralysis their temperature is elevated. Electro-
muscular contractility is diminished.
The pains in the back are increased by pressure, and localized at certain
vertebra. The application of lieat or cold over the sensitive spot produces
pain ; and a warm or cold sponge at the junction of the normal and anges-
thetic parts produces a burning sensation, felt in a line around the body.
When the paraplegia is sudden and complete, hemorrhage into the softened
focus may be suspected. The paralysis frequently extends rapidly upward,
and when the cervical cord is involved paresis and anaesthesia of the arms,
irregularities of the pupils, dyspnoea and dysphagia will be present ; the
pain in these cases is located in the neck. The itching, burning, or boring
pains in the limbs and the sense of formication that precede the paraplegic
symptoms are rarely influenced either by pressure or motion. Reflex
action is diminished or lost, and its abolition is an indication of the extent
to which the gray matter is involved.
Trophic or vaso-motor disturbances appear early, causing acute bed-sores,
oedema of the paralyzed limbs, effusions into the joints, and more or less
muscular atrophy. The urine becomes alkaline and often bloody. Reten-
tion is of frequent occurrence and results in cystitis and pyelitis ; uraemic
symptoms may appear, and sepsis often occurs from the bed-sores and
gangrenous inflammation. Among the later manifestations are darting
' OUivier, Hine and Leydeii regard mental shock, especially from fright or anj^'er, as a cause.
99.8 DISEASES OP THE NERVOUS SYSTEM.
pains, spasmodic twitchings and contractions, either of isolated groups or
of all the muscles in the paralyzed part/ Tliis marks its passage into the
chronic stage. In some few cases hemi-paraplegia is induced by myelitis.
The disease is always progressive. In some classes the paraplegia may be
so rapidly developed that in forty-eight hours the patient will be unable to
lift or move his legs.
Differential Diagnosis. — Acute myelitis may be confounded with acute
spinal menmgitis, hysterical paraplegia and paraplegia from reflex urinary
irritation.
In meningitis there is acute pain on motion, with rigidity of the muscles
of the back ; in myelitis there is no pain on motion and the muscles are
flaccid and relaxed. Paralysis in spinal meningitis is incomplete, but para-
plegia or liemi-paraplegia is always present in acute myelitis. Cutaneous
and muscular hypersesthesia, with febrile and cerebral symptoms, exists in
meningitis, but is absent in myelitis.
Hysterical paraplegia is diagnosticated by the attendant hysterical symp-
toms, globus hystericus, large flow of limpid urine, Jactitation, etc. It is
not a true paraplegia, and generally occurs in young women.
In paraplegia from reflex irritation, genito-urinary troubles y^'iW precede
the paraplegia ; in myelitis the urinary symptoms follow the paraplegia.
In reflex urinary irritation the paraplegia is incomplete and does not
extend upwards ; in myelitis it is complete and increasing. There is no
paralysis of the sphincters in reflex irritation ; in myelitis it is an early
and marked symptom. There is no girdle sensation, no formication, or
sense of swelling and heat in reflex paraplegia ; while these symptoms are
always present in myelitis. The urine is acid in reflex, and alkaline in
myelitic paraplegia. The muscles are atrophied in myelitis ; and nor-
mal in reflex paraplegia. Myelitis of the cervical portion of the cord is
attended by paralysis of all the extremities, increase in reflex irritability,
dysphagia, dyspnoea, vomiting and impaired speech. When the whole
cervical region is involved the upper extremities are first implicated, and
they lose their reflex irritahility. The pharyngeal, thoracic, and ocular
symptoms are also marked. The pulse is rapid and irregular.
Prognosis. — In acute myelitis death may occur in twelve to thirty hours,
or be delayed two or three weeks. When the disease is protracted a month
it becomes chronic. Complete recovery is rare ; incomplete recovery oc-
curs quite often. Cervical myelitis is the most, dorsal the least unfavor-
able. Bed-sores, cystitis, nephritis, and pyelitis, or high fever and sud-
den and complete paralysis, render the prognosis exceedingly unfavorable.
Treatment. — The most important thing in the treatment of acute mye-
litis is absolute rest. Ergot and belladonna have been highly recommended,
but I have never obtained any positive results from their use. Blisters and
other counter-irritants, electricity and strychnia are contraindicated. Spinal
bags filled with hot water have seemed to me to give the greatest relief to
this class of patients. Diuretics and mild cathartics should be given ; and
' The siiinal epilepsy of Brown-Sequard is a spasm of all the muscles of the lower extremities generally
following transverse myelitis.
CHRONIC MYELITIS. 999
catheterization practised from the outset. If the myelitis is of syphilitic
origin, iodide of potassium may be of service, but not otherwise. A sup-
porting, nourishing plan of treatment is to be adopted from the onset. To
prolong life, complications must be prevented as far as possible. Bed-sores
must be prevented by great cleanliness and the daily use of the galvanic
current ; cystitis may be avoided by the frequent use of the catheter and
the washing out of the bladder.
CHEOlSriC MYELITIS.
Under this term are included a variety of changes in the cord, of which
white softening is perhaps the most frequent.
Morbid Anatomy. — When chronic myelitis is the sequela of acute, the
change to white softening marks the entrance into the chronic stage. In
this stage, by a process precisely similar to that which occurs in the brain,
a cyst is formed. It is divided by numerous septa of connective-tissue, and
contains fluid resembling chalk and water. After absorption the cicatrix
is gray, shrivelled, and pigmented. Less commonly, though by no means
infrequently, there is hyperplasia of the neuroglia, and a dense, gTay, scle-
rosed focus remains. Large cells with numerous processes, called Deiter's
cells, are seen in this sclerosed tissue, and the ganglion cells are found at-
rophied. Large quantities of corpora amylacea are formed. Usually the
cord is hard and gray, but in many cases it appears to the naked eye per-
fectly normal, while the microscope reveals chronic myelitis.' It is slightly
diminished in volume, and the atrophy may be uniform, or irregular, and at
scattered points.
Chronic inflammation of the meninges with progressive atrophy of the
roots and trunks of the peripheral nerves is met with in chronic myelitis.
There is increase in the connective-tissue of the neuroglia, and degeneration
of the nerve fibres. The ganglion cells are hard and pigmented, and large
Deiter's cells are abundant. The axis cylinder remains intact for a long
time.^ Fat cells are everywhere present, and in cases of very long standing
large excavations in the substance of the cord may occur.
It is impossible to distinguish interstitial from parenchymatous my-
elitis.'
Etiology. — All the constitutional causes that were enumerated as causes
of acute may be included under the remote causes of chronic myelitis, and
of these chronic alcoholismus, sexual excesses, and reflex disturbances are
more liable to result in chronic than acute myelitis.
Symptoms.— The symptoms of chronic myelitis are so complex that Char-
cot calls it a " polymorphous " disease. It is usually insidious in its onset ;
' So-called (iray degeneration.
* Charcot and Leyden.
3 Leyden, in the Zeitschr.f. Klin. Med., Berlin, 1879, No. 1, p. 1-26, recites a most interesting case, where
numerous large round nucleated cells were found pushing npart nerve fibres in the posterior dorsal region
of the cord of a man who had been poisoned in a caisson. Recently " systems " have been described in
the cord, and some pathologists huve classified diseases of the cord on this physiological basis. Leyden
describes two forms of system disease of the cord, where chronic myelitis is the sole lesion, i. «., tabes dor-
salifi, and atrophy of the motor parts of the cord. These two combined give a combined system disease. Re-
generation of destroyed nerve fibres in the cord is possible though very rare.
1000 DISEASES OF THE NERVOUS SYSTEM.
and iu its development disorders of sensation precede motor disturbances.
Pains in the limbs simulating rheumatism are gradually associated with
muscular weakness ; and tingling, formication, numbness of the limbs, with
the girdle sensation, are followed by an unsteady gait. ' Local anesthesia
alternates with hypergesthesia. Weakness of the bladder and constiiDation
are both the result of muscular weakness. These symptoms are followed
by paraplegia, muscular atrophy, cystitis, and chronic bed-sores. Slight
tremors and twitchings of the muscles are not uncommon. Patients with
chronic myelitis always complain of cold feet.'
There is usually progressive emaciation and cachexia. Some cases remain
stationary for months and even years ; but the majority reach a fatal ter-
mination through successive exacerbations and remissions.
Differential Diagnosis. — Chronic myelitis may be confounded with spinal
apoplexy, spinal meningitis, or Ioco?notor ataxia.
It is distinguished from hemorrhage by the sudden advent of the hemor-
rhage, and from meningitis by the absence of pain.
In locomotor ataxia the double heel-and-toe tread, the neuralgic pains,
the preservation of motor power, of control of the sphincters and sexual
force, all stand in contrast to the signs of chronic myelitis.
Prognosis. — The prognosis in chronic myelitis is always unfavorable. It
may continue from two to ten years, but in no case can there be complete re-
covery. It may remain stationary also ; but the functions are never restored.
Death results from cystitis and pyelitis, bed-sores, and other complications.
Treatment. — Eest is the most important remedial agent. When a cause — ■
such as lead poisoning, disease of bladder, uterus, etc. — can be reached it
must be removed. Dry cups daily to the spine are usually of service.
Ergot, belladonna, nitrate of silver, iodide of potash, arsenic, phosphorus,
and strychnia have all been recommended and benefit claimed for them,
as may be said of hot or cold baths at natural springs.^ The bladder must
be emptied twice or three times daily and the bowels kept freely open.
The galvanic current is considered beneficial, or at least harmless. Fric-
tion, shampooing, and massage of the paralyzed limbs prevent wasting of
the muscles.
NOlSr-IlSrFLAMMATORY SOFTElSTHsTG.
Our knowledge of this rare condition is vague. Indeed, until recently,
its existence was denied.
Morbid Anatomy. — The site, extent and limitation of non-inflammatory
softening are the same as in myelitic patches. Myeline, broken-down nerve-
tubes, large granulation corpuscles, are all found in the patch. Eadcliffe
describes white softening as non-inflammatory and due to anaemia.
Etiology. — Slowed blood-current, a tendency of the blood to spontaneous
coagulation, and disease of the walls of the blood-vessels are regarded as
causes of non-inflammatory spinal softening/ It is sometimes met with
1 Erb states that catheterization and dressing; the bed-sores produces varied movements in the paralyzed
lii^^o. 2 Erb, Rosenthal and others.
5 Dr. Moxon calls attention to the fact that the blood supply at the lower end of the cord— where soft-
enings are most frequent — is peculiar and easily interfered with..— Bnt. Med. Jour., vol. i. 1881.
ACUTE BULBAK PAEALYSIS. 1001
within the month, after childbirth, in the late stages of syphilis, after great
bodily exertion, sexual excess, and exposure.
Symptoms. — The symptoms of non-inflammatory softening do not differ
essentially from those of chronic myelitis, spinal hemorrhage, and spinal
tumors. Its invasion is generally gradual, and the complexity of symp-
toms varies according as the foci are circumscribed or diffuse, central, lat-
eral, or completely transverse. If the softening extends completely across
the cord, there is complete paralysis of the lower extremities and of the
abdominal muscles. The limbs are cold to the touch and their tempera-
ture is sub-normal. The toes are turned inward, so that as the patient
lies in bed the feet form a cross. The skin becomes dry and rough, and
the muscles are flabby although not wasted. There is almost complete abo-
lition of reflex movement. Early in the disease there is retention of urine,
which is followed by incontinence and partial retention, and the usual
sequelae of cystitis and possibly pyelitis or ammongemia ; the kidney may
become, studded with minute abscesses.
Differential Diagnosis. — Its slow onset and the preyious history enable us
to differentiate between non-inflammatory softening and spinal hemorrhage.
tt is not difficult to determine the extent of the lesion ; but to determine
(vhether it is central or peripheral, anterior or posterior, is always difficult
ftnd often impossible.
Prognosis. — The prognosis is always unfavorable. There is great danger
of intercurrent diseases, especially pneumonia, local or general meningitis,
and inflammation of the genito-urinary tract, or septicaemia. In rare in-
stances the paralysis may gradually disappear and partial recovery take place.
Treatment. — No plan of treatment is successful. The bowels and blad-
der must be attended to, and the latter is best washed out with a one-half
per cent, solution of chlorate of potash. The galvanic and Faradic currents
may be used.
ACUTE BULBAR PAEALYSIS.
While acute bulbar paralysis involves a nervous distribution similar to
that of the chronic form, its morbid anatomy is very different.
Morbid Anatomy. — At the autopsy there will be foci of softening and ex-
travasation from thrombosis and embolism. Erb states that there is an
acute bulbar paralysis not due to these causes, but which is in reality a
primary acute myelitis huTbi.
Etiology. — The etiology of acute bulbar myelitis is unknown, aside from
the causes of apoplexy, embolism, and thrombosis elsewhere in the cerebro-
spinal system.
Symptoms. — Its onset is very sudden; the prominent symptoms are head-
ache, dizziness, and sometimes loss of consciousness (apoplectiform variety).
Cough, dyspnoea, and hiccough are often present, and sometimes there are
convulsions and weakness in the limbs accompanied by tingling sensations.
In other cases coma and asphyxia precede the rapidly fatal issue. In oc-
clusion of the basilar artery the carotid pulse is unusually full. Eosenthal
states that, in addition to dyspnoea, Oheyne-Stokes' respiration often ap-
1002
DISEASES OF THE NERVOUS SYSTEM.
pears as a characteristic symptom of medullary hemorrhage.' When the
extravasations extend into the fourth ventricle polyuria and albuminuria
are observed.^ In embolism improvement is common, but in hemorrhage
it is rare ; thrombosis of the vertebral arteries pursues a more chronic
course, but with similar results.
Prognosis. — If the patient recovers from the primary effects of the lesion,
the prognosis of the paralysis is better than in the chronic form. The
prognosis is better when the disease is associated with or due to syphilitic
infection. In a few acute cases the paralysis is permanent, although it has
no tendency to increase. In sudden and complete obstruction of the basilar
or both vertebrals the prognosis is exceedingly bad. Limited or capillary
hemorrhages render the prognosis unfavorable.
Treatment. — This does not differ from the treatment of similar conditions
elsewhere in the brain, which has been considered under apoplexy and cere-
bral softening.
CHROETC BULBAR PARALYSIS.
{Olosso-lcMo-laryngeal Paralysis. )
This is a progressive, symmetrical paralysis of the lips, adjacent facial
. muscles, tongue, pharynx,
and sometimes of the
larynx.
Morbid Anatomy. — The
medulla may be atrophied
and show spots of gray
discoloration which have a
sclerotic feel. There is
degenerative atrophy of
the gray nuclei in the floor
of the fourth ventricle ;
with atrophy and gray dis-
coloration of the nerve
roots from the medulla,
especially of the facial and
hypoglossal nerves.^ The
ganglion cells and the
nerve-nuclei lose their stel-
late form and become
shrunken, smaller, and of
Morbid condition on the ^ dull Ochre color. The
prolongations and nuclei
are rudimentary or even
completely atrophied. The
cells are filled with pig-
FiG. 202.
Chronic Bulbar Paralysis.
Transverse section qf the bulbus on a level with the middle of
the nucleus of the hypoglossus.
AA'. Line dividing the section centrally.
left hand.
B. ^Ganglion cells forming nuclevs of hypoglossus.
C. A vessel forming front and inner boundary of B.
D. Floor qf fourth veniricle.
E. Nucleus 'of pnettmogastric.
On the left the nuclei/.s of the hypoglossus is nearly obliterated,
while that of the pneumog astric is 'unaltered. Charcot.
1 See also accounts by Traube in the Berlin. Klin. Wochen., 1869 to 1874.
^ Gazette des Hopitaux, 1862.
3 Recent physiological investigations show that the lower facial nucleus and the hypoglossal nucleus
are closely connected.
CHRONIC BULBAR PARALYSIS.
1003
ment and granulcar matter, the nucleus and nucleolus present a vitreous,
shining appearance,' and are separated from each other by large spaces.
Atrophy and disappearance of the motor ganglion cells is always to be
noted. It may be the sole lesion or be accompanied by increase in the
neurolgia, when fat and granular corpuscles, numerous corpora amylacea,
Gluge's corpuscles, and spider-cells will be found in the newly-developed
tissue. The walls of the vessels are thick, and show more or less fatty
change. The decrease in size of the gray nuclei is a measure of the inten-
sity of the symptoms that existed during life.
Similar bilateral lesions may be found in the nuclei of the pneumogas-
tric, spinal -accessory, glosso-pharyngeal, facial, trifacial, motor oculi, and,
very rarely, of the trigeminus.'^
The muscles are j^ale and the fibres frequently show granular degenera-
tion ; but sometimes fatty tissue is in excess. The fibres may be thin, and
the tissue between them contain the pigment products of degeneration, so
that the muscles, though degenerated, will preserve their normal bulk.
Fig. 203.
Chronic Bulbar Paralysis.
A. Microscojncal appearance of normal viuscle from the tongue,
B. Same m,vscle taken from, a case of Glosno-ldhio-laryngeal
C. Fasciculi of muscular fibres in transverse section.
D. Atrophied fibres seen longitudinally, x 300.
The muscular fibres show increase in their nuclei and changes precisely
similar to those in progressive muscular atrophy.
The nerves going to the muscles exhibit sclerosis of the neurilemma,
slight traces only of the axis-cylinders remaining. The same degenerative
atrophy is found in the nerve roots coming from the bulb. This disease
is rare before the fortieth year of life ; it is essentially a disease of old age.
Males are more subject to it than females.
1 Yellow degeneration of Charcot.
2 Duchenne.
1004 DISEASES OF THE NERVOUS SYSTEM.
Etiology. — Its etiology is always obscure. The neuropathic tendency
seems to exercise some influence in certain cases. It is said to occur with
syphilis and rheumatism. Bad hygiene, exposure to cold, excessive anxi-
ety, close mental application, and prolonged physical exertion are all ad-
duced as causes.
Symptoms. — The earliest symptoms of bulbar paralysis are imperfect move-
ments of the tongue ; the speech is indistinct, and enunciation of the pal-
atal and dental sounds is imperfect. Often the tongue cannot be protruded
as far as normal, nor the lips brought together as perfectly or separated as
promptly as in health. Whistling and whispering are impossible. The
lower part of the face becomes expressionless. The lips remain separated
and the saliva is either tenacious or dribbles from the mouth, which is so
drawn as to give the face a woe-begone expression. Speech may be entirely
lost.
When the palate muscles are involved, deglutition becomes difficult,
and as the soft palate hangs motionless, not closing the posterior nares, the
food regurgitates through the nose, or lodges in the u|)per part of the phar-
ynx and collects between the cheeks and the alveolar arches ; portions are
also apt to fall into the larynx. Another effect of palatal paresis is to give
a nasal twang to the voice.
If the laryngeal muscles become weakened and closure of the glottis im-
perfect, coughing becomes ineffective and phonation is interfered with. The
muscles of mastication are rarely involved until late in the disease, but ex-
haustion and emaciation from insufficient food are developed early. The
muscles atrophy, and tremblings and fibrillar twitchings occur. When the
respiratory centres are involved there is a sense of fulness and constriction
in the chest accompanied by attacks of dyspnoea.
Lesions in the cardio-inhibitory centres are followed by attacks of syn-
cope and a pulse of 140 or 160 per minute. There is an abnormal amount
of saliva secreted, either as paralytic saliva' or from irritation in the me-
dulla.^ The laryngoscope reveals paralysis of the vocal cords. Should
bronchitis occur expectoration is difficult, and if pneumonia or any other
severe pulmonary affection develops it almost always terminates fatally.
The muscles show the reaction of degeneration ; sensibility is unchanged,
but reflex actions are greatly diminished or destroyed. Atrophy of the
muscles at the back of the neck — the trapezii especially — is not infrequent.
In some few cases the paralytic symptoms may be preceded by dull pains
in the back of the head and neck, giddiness, queer sensations in speaking,
and loss of reflex irritability in the pharynx and larynx.'
I See M. Poster's Physiology. Art. Sub-maxillary Gland. ^ Pfliiger's Archiv, Bd. 7.
s Kirchoff reports a case where bulbar paralj'sis was produced by a uniialeral lesion, and from the autop-
sical results in this case the sj'mptoms must be attributed to a lesion of the lenticular nucleus. A new and
peculiar variety of bulbar paralysis has recently been described by Erb. An analysis of the symptoms
shows that the parts chiefly involved are the motor oculi communis, the motor portion of the trigeminus,
the spinal-accessory^, and the upper cervical nerves ; and those more slightly affected are the facial (the
upper branches to the face), the hypoglossal, and probably also the glosso-pharyngeal nerves. The nuclei
of origin of these nerves are all situated in the floor of the fourth ventricle and in its immediate neighbor-
hood in the pons Varolii. Erb supposes that, in the affection under consideration, the lesion is situated in
the upper half of the fourth ventricle and spreads more deeply into the substance of the medulla, affecting
nerve fibres as they pass upward from the nuclei of origin in the fourth ventricle.
CHRONIC BULBAR PARALYSIS. .1005
DiiFerential Diagnosis.— Progressive bulbar paralysis may be mistaken for
tumors in the medulla, double facial palsy , embolism and thrombosis of the
medulla, medullary apoplexy, embolism of one of the vertebral arteries,
progressive muscular atrophy attacking the face, Vind getieral paralysis of
the insane.
In tumors of the medulla, we find neuralgia, clonic convulsions of the
muscles of the face and tongue, disturbarfces of the smell and hearing,
headache, vomiting, dizziness, and epileptiform attacks, the disease being
either unilateral or decidedly marked only on one side.
In double facial palsy , all the branches of the facial nerve are involved ;
movements of the tongue and deglutition are normal.
In embolism or throrhbosis of the medulla, the sudden onset of the symp-
toms with either hemiplegia or paraplegia, taken in connection with the
age of the patient and tlie condition of the arteries, will be the chief points
of diagnosis. In embolism improvement is possible.
In bulbar hemorrhage, loss of consciousness, epileptiform convulsions,
vomiting, prominence of unilateral symptoms are combined with bulbar
paralysis of sudden advent. The previoiis history will aid in the diagnosis.
Embolism of the vertebral arteries is accompanied by sudden (apoplec-
tiform) onset of the symptoms of bulbar paralysis, hemiplegia, anaesthesia,
variations in the paralyses, and co-existing disorders of sight and hearing.
Iw progressive muscular atrophy, paralysis /o/?ows the atrophy ; in bulbar
paralysis it is the reverse. Moreover, the thenar and hypothenar eminences
are involved early, even should muscular atrophy first attack the tongue,
lips and palate.^
In general paralysis of the insane, the cerebral disturbances and the fact
that other muscles are involved besides those in the region of the mouth
and palate, will establish the diagnosis.
Prognosis. — The prognosis is grave ; although a temporary arrest may
occur, genuine bulbar paralysis invariably terminates in death. The
amount of dysphagia and dyspnoea and the rapidity of development will
determine the relative gravity of the case. Its average duration is about
two years. Bulbar j)ara]ysis may be complicated by progressive muscular
atrophy, amyotrophic lateral sclerosis and disseminated sclerosis. Death
occurs from starvation, paralysis of the heart or respiratory organs, or inter-
current pulmonary diseases. Sometimes coma ends the scene, and there
is a slight rise of temperature.
Treatment. — A nutritious diet and the best hygienic surroundings, with
quinine, arsenic and nitrate of silver are the means which have been most
extensively employed. The German physicians condemn, and the English
advocate, the use of strychnine and phosphorus. Ergot, belladonna, and
iodide of potash may be given. Direct galvanic or Faradic currents ap-
plied to the paralyzed parts have been recommended. In some cases a
stomach tube may be used to prolong life, and perhaps gastrostomy may
be demanded.
• Duchenne.
1006
DISEASES OF THE NERVOUS SYSTEM.
INFAISTTILE SPIISTAL PARALYSIS.
Infantile spinal paralysis or acute anterior polio-myelitis is an inflam-
mation of the anterior cornua of gray matter of the cord. It may occur in
adults, hut is almost always exclusively confined to children. '
Morbid Anatomy. — The early changes are those of inflammatory soften-
FiG. 204.
Anterior Gray Cornu of Spinal Cord in
Eaily stage of Infantile Spinal Paral-
ysis.
A. Large mriltlpol'ir ganglion cdls.
B. Neuroglia cells in a state of active pro-
liferation. X 300.
Fig. 205.
Anterior Gray Cornu of Spina Cord
after establishment of the Sclerotic
Process in Infantile Spinal Paralysis.
A. Dense nucleated connective-tisfoie.
B. Large masses of pigment— the re-
mains of ganglion cells.
C. Corpora dm'ylacea. x 300.
ing ; medullary hypergemia and vascular exudations are the incidental
occurrences.^ Extensive changes may exist, and yet the gross appearance
of the cord be unchanged.
Microscopically there will be seen, in its early stage, all the changes of acute
interstitial inflammation, and the neuroglia nuclei are in active prolifera-
tion. Later a sclerotic process is established, and new connective-tissue
developed, in which are multitudes of nuclei and corpora amylacea. Pig-
mentation is more or less marked, and the ganglion cells, that have lost
their processes, may remain only as irregular spherical masses of pigment.
Thickening and increase of neuroglia in the anterior columns result in
more or less atrophy of the nerve fibres. The antero-lateral columns of the
cord may be invaded, but the posterior usually escape.^ The anterior roots
1 Niemeyer calls it essential palsy. Erb describes it as a more or less diffuse myelitis of the anterior
gray substance, which reaches its greatest intensity in the lumbar and cervical enlargements of the cord,
and, as a rule, leaves no permanent and irremediable alteration except at those two points.
2 Rosenthal.
3 The most careful microscopical examination fails to decide what modern pathology is still earnestly
discussing, viz. : whether acute polio-myelitis is an interstitial or a parenchj'matous inflammation. The
majority favor the latter view, the ganglion cells being its supposed starting-point.
INFANTILE SPINAL PARALYSIS. 1007
of the spinal nerve are shrunken, atrophied, and degenerated. They are
gray and transhicent. The vessels undergo considerable enlargement, and
their walls are thickened. The motor nerves are involved secondarily to
the cord at an advanced period of the disease. The muscles which are im-
plicated rapidly undergo fibroid changes and atrophy. Their transverse
sfcrige are indistinct, and the nuclei become abundant ; the muscular fibres
may wholly disappear.' The muscular fibres do not ahvays suffer this
degeneration, but sometimes they undergo fatty degeneration, or the mus-
cles are so infiltrated with oil globules that they retain their normal size,
and may even exceed it ; this is a pseudo-hypertrophy.'^ The hones are
retarded in development, somewhat flexible, and contain more fat than
usual. The tendons become atrophied, and the joints lose their com-
pactness.
Etiology. — This is essentially a disease of the first three years of life, the
usual time of occurrence being between the sixth and fourteenth months.
It attacks equally children of both sexes, the robust as well as those of
feeble and cachectic constitutions. Cold, dentition, and traumatism are
among its doubtful causes. It has occurred in two or more offspring of the
same parents, and once in twins ' after an attack of measles. Many regard
acute febrile diseases as an important factor in its causation. It is devel-
oped, if at all, during convalescence from such fevers.
Symptoms. — The onset of infantile spinal paralysis is sudden. A child
has well-marked febrile movement attended by dizziness, headache, restless-
ness, nausea, vomiting, and sometimes delirium, convulsions and coma.
Accompanying these symptoms there is more or less pain in the back. In
many cases the febrile symptoms only last a few hours. Following a con-
Tulsion or attack of unconsciousness the child becomes paralyzed, or in
some cases paralysis may come on suddenly without a single premonitory
symptom ; the child goes to bed perfectly well and wakes with paraplegia.
If only one lower limb is involved at first, the other soon becomes so ; and
it is not unusual for all four extremities to be affected simultaneously. The
arms alone are rarely involved. The paralysis is not accompanied by loss
of sensiUlity. It reaches its maximum in from ten hours to six or seven
days, and begins to diminish in about two weeks after its commencement.
The paralyzed muscles become flaccid, relaxed, and attenuated, and if the
paralysis is persistent they atrophy and undergo degeneration. The
surface of the body is cold and of a purplish color. The limbs may pre-
serve their normal contour ; but they are soft and often tender to pressure.
The tendon-reflexes and reflex action in the muscles of the paralyzed part
are entirely lost, and they fail to respond to the Faradic current. These
alterations in electrical excitability are results of the reactions of degener-
ation.
Paralysis at the onset is general, bat later it is localized in one group oi
in single muscles. The muscles on the back of the forearm and front of the
leg, in the foot, and the extensors of the leg, are more apt to be affected,
1 Erb lays great Rtres-s upon the replacement of muscle tissue, in this disease, by fat, so that the
muscleshave tlie faded-leaf appearance of a typhoid heart.
2 Erb. ^ Moritz Meyer.
J.008 DISEASES OF THE NEKVOUS SYSTEM.
but the paralysis may involve only the deltoid, tibialis anticus, sterno-clei-
do-mastoid, or the extensor longus digitorum. The joints are loosened, and
the bones, especially the long ones, are smaller and shorter than those in the
unafEected limb. The temperature of the paralyzed parts is often 5° or 8° F.
lower than normal. The deformities and unnatural attitudes that result
may simulate talipes ; and all varieties of contracture occur as late man-
ifestations. The epiphyses atrophy and subluxations sometimes occur.
The general health of the patient is usually good, and there is nothing that
interferes with long life, except the paralysis and deformity. In severe
cases there is at the onset loss of control of bladder and rectum. In such
cases slight vesical weakness usually continues during life. The normal
sensibility of the skin is preserved throughout.
Differential Diagnosis.— Infantile spinal paralysis may be mistaken for
progressive muscular atrophy, pseudo-muscular hypertrophy, rachitis, tem-
porary infantile paralysis, myelitis, and hemiplegia.
Progressive muscular atrophy begins insidiously and is slowly progres-
sive ; spinal infantile paralysis begins suddenly, and after a time a certain
amount of improvement occurs. Progressive muscular atrophy is rare in
children before the fifth or seventh year of age. It commences by palsy
about the lips and mouth, and the electro-contractility of the affected
muscles is lost only in proportion to their atrophy and degeneration^ the
uninvolved fibres rGspondi7ig to the current. This fact taken in connec-
tion with the age of the patient will usually enable one to make a diag-
nosis.
Pseudo-muscular hypertrophy begins loithout fever ; the motor power at
first is only weakened, and the trunk and extremities are involved late
in the disease. The electro-muscular contractility is preserved, and there
is always increase in the volume of the muscles. In walking the patient
spreads the feet far apart, and there is a peculiar incurvation of the verte-
bral column not seen in infantile spinal paralysis.
Bichets is attended by no change in electro-muscular contractility, is
preceded by no cerebral or pyretic phenomena, and there coexist develop-
mental and other changes that cannot fail to determine the character of the
deformity.
In temporary paralysis there are no signs of softening or atrophy of
muscles, there is no change in electro-muscular contractility, and the pa-
ralysis is recovered from in twenty to thirty days.
In myelitis, trophic disturbances and genito-urinary complications are
sufficient to distinguish it from infantile spinal paralysis.
Hemiplegia from acute cerebral affections in childhood can generally be
distinguished from acute anterior polio-myelitis by loss of intelligence and
speech, strabismus, paralysis of half the face, dilated pupils, and normal
electrical contractility in connection with disturbances in sensation, stiff-
ness of the Joints, spasmodic contractures with absence of fever, and mus-
cular atrophy.
Prognosis. — There is little or no danger to life in acute anterior polio-
myelitis, even when the attack commences with very active symptoms. A
ACUTE SPINAL PAEALYSIS OP ADULTS. 1009
mild, or even a severe, onset may be followed by complete restoration of the
function and power of the paralyzed muscles : — so-called temporary spinal
palsy. Usually the improvement is such that the function of the few mus-
cles that remain permanently paralyzed and atrophied is performed by the
muscles not involved. All the paralyzed muscles in which Faradic irrita-
bility is not completely lost are restored. '
Treatment. — In the acute stage rest in the recumbent posture is the most
important element of treatment. Beyond this the treatment is the same
as for acute myelitis. After the febrile symptoms have subsided — usually
by the fourth week — measures must be adopted to restore the function of
the paralyzed muscles. The early and persistent use of the galvanic current
hastens the recovery in those muscles whose electric contractility is but
slightly diminished, and will often arrest the wasting and restore them to
a normal condition. When electric contractility is entirely lost little bene-
fit can be expected. The longer the use of electricity is delayed the less
the chances of recovery. Even if it fails to cure it has a tendency to pre-
vent deformity. Saline and thermal baths and the water treatment of
various kinds are recommended. Massage, friction, shampooing, inunc-
tions, etc., are to be combmed with the electric and hydropathic plans of
treatment. The diet must be such as to bring nutrition to its highest
point. Minute quantities of strychnia injected hypodermically have been
found beneficial. Iron, arsenic, quinine and phosphorus are indicated —
as tonics — in nearly every case.
ACUTE SPJlfAL PARALYSIS OF ADULTS.
Duchenne and Moritz Meyer first observed that this disease not infre-
quently occurred during adult life, with pathological changes identical
with those of the disease in infancy.
The etiology is obscure ; cold., wet, and the debility found in conva-
lescence from fevers, pneumonia, malarial poisoning, etc., have been sug-
gested as causes.
The symptoms at the onset are modified by the greater stability of the
adult nervous system, and there is less restlessness, delirium, fever, etc.
The cerebral symptoms may be very slight, transient, and easily overlooked
and followed by paralyses, which go on to partial recovery as in the infantile
form. There are no bone deformities or arrested developments ; and the
joints do not become lax. Tingling, numbness, and formication occur in
adults at the onset, and gastric symptoms are more frequent.
Differential Diagnosis. — Absence of spasms and of trophic disturbances,
diminution of reflexes, normal sensibility, non-interference with the sphinc-
ters, the sudden onset and the subsequent improvements suffice to distin-
guish this disease from all other affections of the cord.
Chronic atrophic spinal paralysis resembles it, but the abrupt invasion
J Seeligmiiller records two cases where progressive muscular atrophy occurred late in life In those who
In infancy suffered from acute anterior polio-myelitis.
64
1010 DISEASES OE THE NERVOUS SYSTEM.
of anterior polio-myelitis is absent in the former malady. If this point in
the history be wanting a differential diagnosis may be impossible.
^hQ prognosis and treatment are the same as in children.
CHEONIC ANTEEIOR POLIO-MYELITIS.
Duchenne was the first to describe (1853) this disease under the above
name. It has since been called subacute and chronic inflammation of the
gray anterior horns, chronic atrophic spinal paralysis, and subacute spinal
paralysis.
Morbid Anatomy. — The morbid anatomy of this disease is still obscure.
So far as can be stated from the few recorded autopsies it is simply a
chronic myelitis of the anterior cornua ; the neuroglia is increased ; the
blood-vessels are thickened, the anterior nerve-roots are atrophied, and
there is an abundance of granular and fat cells in the diseased district.
Eecently vacuoles have been found in the ganglion cells of the anterior
horns. Almost entire disappearance of these cells was the chief lesion in
one case.*
Etiology. — ^It is a disease of adult life from thirty to fifty, and excesses of
any kind, or exposure to cold and wet, are said to exert an influence on its
development similar to that in other spinal affections.^
Symptoms. — In some subacute cases slight fever and shooting pains in
the back accompany the development of paralysis of the lower limbs. In
others the patient first notices weakness and heaviness in his legs, followed
by paralysis either of groups of muscles or of the whole limb. The mus-
cles become flabby and progressively waste away. They are sensitive to the
galvanic current, but respond little, if at all, to the Faradic. The irreg-
ular distribution of the paralysis is characteristic. As the muscles are
undergoing atrophy, fibrillary twitchings are often noticed. Tendon-
reflexes and skin-reflexes are both abolished ; but sensibility is unaffected.
There is vaso-motorial disturbance, indicated by cold and blue extremities.
The temperature of the affected limbs is lowered. Later, the upper limbs
are involved. The paralysis first attacks the flexors or extensors on the
forearm, and gradually involves isolated groups of muscles, or the whole
limb. The fingers and hand, however, suffer most. When the disease has
reached this stage the wasted muscles will no longer respond to the galvanic
current. The rectum, bladder, and sexual power are undisturbed. When
the process extends to the cervical region dyspnoea is present, and if the me-
dulla becomes involved deglutition and articulation are affected, and great
exhaustion is induced, asphyxia closing the scene. The general health re-
mains good, and the mental faculties are unimpaired.
Differential Diagnosis. — Chronic atrophic spinal paralysis may be mis-
taken iox progressive muscular atrophy, amyotropliic lateral sclerosis, acute
ascending paralysis, and the acute spinal paralysis of adults.
In progressive muscular atrophy paralysis follows the wasting ; the re-
1 Arch, de Physiologle, 1876.
2 Erb suggests that its co-esistence with chronic lead poisoning is the result of an inflammatory
action called forth by the saturnismus.
PKOGRESSIVE MUSCtJLAE ATROPHY. 1011
verse is the case in polio-myelitis. Portions of the muscles only are in-
volved in progressive muscular atrophy, and it begins in the muscles of the
thumb. Reflex action is retained, and the progress is much slower than in
chronic polio-myelitis. Moreover, the susceptibility to the electrical cur-
rents is never wholly lost in progressive muscular atrophy.
In amyotrophic lateral sclerosis, though the upper extremities may be
wasted, there is a characteristically different combination of paralysis ivitli-
out wasting, and with more or less rigidity in the lower extremities. The
reaction of degeneration is far more marked in chronic anterior polio-
myelitis. Keflex clonus and exaggerated tendon-reflexes are absent in
chronic polio-myelitis, and present in amyotrophic lateral sclerosis.
In acute ascending paralysis the atrophy is not marked ; electrical re-
actions of nerves and muscles are normal, reflex action is preserved for a
long time, and bulbar symptoms with vesical disturbances are not uncom-
mon. Acute ascending paralysis is of short duration compared with chronic
anterior polio-myelitis.
In acute spinal paralysis of adults the paralysis, which is sudden in its
onset, is more extensive, and after a short time there is improvement in
motor power ; while in chronic atrophic spinal paralysis there is a dis-
tinctly progressive unremitting spread of the disease from part to part.
Prognosis. — In rapidly progressive cases the prognosis is bad, but in those
that are slowly developed and partial the prognosis is better, and sometimes
complete recovery may take place, or certain muscles or groups remain
paralyzed and atrophied while others improve. After a long time the dis-
ease may be spontaneously arrested and the patient remain paralyzed the
remainder of life. The most unfavorable cases are those in which the
cervical region and the medulla become involved, death occurring with
symptoms of bulbar paralysis. The usual duration is from a few months
to three or four years.
Treatment. — Electricity and a nourishing diet, with rest, give the best re-
sults. Dr. Bastian suggests that counter-irritation may do good in the
early stages. Sulphur, mineral, and brine baths and the cold water treat-
ment are advocated. It is a question whether either iodide of potassium
or ergot is beneficial. Modern literature, though extremely rich in theories,
is devoid of facts which can aid in the treatment.
PEOGRESSIVE MUSCULAR ATROPHY.
As the name indicates, this disease is a progressive and chronic wasting
and atrophy of the muscles, and results from trojjhic changes due to a cen-
tral nerve-lesion.
Morbid Anatomy. — The morbid anatomy of this affection differs little
from that in spinal paralysis of children. Its essential lesion is atrophy of
certain groups of nerve- cells in the anterior cornua of the cord. Some-
times atrophy of the anterior horns is associated with a sclerotic condition
of the lateral columns. The general changes are the same as in the late
stage of anterior polio-myelitis. The central canal of the cord is some^
1012
DISEASES OF THE NERVOUS SYSTEM.
times dilated and filled with fluid. On microscopic examination the
ganglion cells show pigmentation to a marked degree, with more or less
atrophy. They are surrounded by indurated tissue. The blood-vessels
are often dilated, and sur-
rounding them is a zone
of granular disintegrated
or diffluent material, the
so-called mixed exuda-
tion. All these changes,
may be found in both
gray and white matter.
The anterior roots of the
spinal nerves are atro-
phied, and show more or
less gray degeneration.
Sometimes all except the
neurilemma has disap-
peared. The muscles over
the body are not equally
involved ; indeed, bundles
of fibrillse in the same
muscle are affected in dif-
ferent degrees. This un-
even character of the atro-
phy is 'peculiar to this
The muscles
Fig. 200.
Teased Fibres from the Abductor Pollicis in a case of Progressive
Muscular Atrophy.
A. Fibres from a normal bundle.
B. Fibres from a fasciculus adjoining A, atrophied and showing dlSCaSC.
fatty degeneration, x 300. . , ^ ,
Simply waste, and become
pale or of a faintly yellow hue. They are harder and firmer than normal.
The strise disappear only after great reduction in size. The interstitial
structure is increased and filled with numerous lymphoid cells. Fatty and
granular degeneration may occur later, with fatty infiltration, and if the
fat-globules are present in large quantity the muscle may not he reduced
in size. Granular disintegration is soon followed by transformation of the
muscular tissue into fine fat-granules.
In some cases progressive muscular atrophy has occurred without ap-
preciable changes in the cord, and given rise to the belief that such changes-
were secondary to the muscular atrophy. It is very generally accepted,
however, that the central lesion is the primary and characteristic change.'
Etiology. — Progressive muscular atrophy is chiefly met with in adult
males in middle life. Heredity and consanguinous influence can no longer
be doubted.^ Excessive physical labor, exposure to cold and wet, are said
to excite it. Those who habitually use one set of muscles are perhaps pre-
disposed to the disease. Injury to the spine is an important causative factor.
1 Virchow calls fat in the fibres parenchymatous, and fat in the interfibrillary tissue the interstitial
form of degeneration.
5 Leyden states that in hereditary cases the lumbar muscles and those of the lower limbs are first at-
tacked ; that it may appear in childhood, and that several members of the same family may be simulta-
neously afEected.
PROGEESSIVE MUSCULAR ATROPHY.
1013
Symptoms. — The invasion of progressive muscular atrophy is irregular
and variable. It usually comes on insidiously, the first indication of its
presence being a wasting and loss of power of some muscles or group of
muscles. When regular in its course the wasting begins in the muscles of
the hand ; first the ball of the thumb of
the right hand, then the hypothenar
eminence and the interossei are at-
tacked, in the order named. Marked
atrojohy of the interossei causes the hand
to have the characteristic bird-claw look.
The left hand is soon involved, and the
wasting then slowly ascends, attacking the
muscles of forearms, arms, shoulders, the
pectorals, and latissimus dorsi, with sym-
metrical alternation. The arms may be
reduced to skeletons of limbs, and the
wing-shoulder is not uncommonly seen.
When the muscles of the trunk are in-
volved, those of respiration and deglu-
tition are very likely to become im]3lica-
ted early. Sometimes the starting-point
is in the thoracic muscles. Although the
legs become extensively involved later,
the wasting seldom begins there. These
atrophic changes advance very slowly,
and the patient will remember that he had for weeks or months a feeling of
slight numbness or formication, and that his fingers have seemed clumsy.
They also may complain — just before atrophy begins— of a sensation of
cold air being blown on them ; the hand and arm are very easily fatigued,
and wandering pains not infrequently precede the wasting of the muscles.
The parts to be attacked or those just involved are colder than normal. A
peculiar fibrillary tremor — transient oscillatory movements in the fibres
of the affected muscles — is present early. It occurs unknown to the
patient, and may be excited by gently blowing or tapping on the skin.
When the atrophy becomes extensive this ceases. The muscles respond
promptly to the Faradic and voltaic currents, with a force in proportion
to their bulk. The wasting in the muscles produces very different ap-
pearances according to the group involved ; should those of the face be-
come implicated, as frequently happens in children, the expression is
stolid, grave, and unchangeable. Often, the head falls forward, and the
saliva dribbles from the mouth. The speech may be faltering ; and the
tongue small and shrivelled. Mastication and deglutition may become
difficult, and as the muscles of respiration are involved dyspnoea is urgent
and asphyxia or pulmonary complications result fatally. Many state that
the pupil on the affected side is much smaller than its fellow, and re-
acts to light but slightly.'
1 Rosenthal, Schneemann, Voisin, Menjaud and Bergmann.
Fig. 20r.
Sketch of a Hand in Progressive Muscn]ar
Atrophy.-
-Charcot.
]014 DISEASES OF THE NEEVOUS SYSTEM.
In a certain number of cases agonizing pain along the nerves leading to
the affected muscles occurs and is a promineat symptom throughout.
Late in the disease atrophy of muscles proceeds so far that absolute im-
mobility of a member is the result. ' The general health is unimpaired,
and the intellect is clear.
Differential Diagnosis. — Progressive muscular atrophy may be mistaken
for acute anterior polio-myelitis, for j)cdsy due to injury of a nerve, lead
palsy, malarial paralysis, post-paralytic atrophy of muscles, and sclerosis
of the lateral columns.
In injury of a nerve the atrophy is confined to the muscles supjalied by
that nerve, and is not progressive. In injuries of mixed nerves, sensation
will also be lost.
In lead palsy the history of exposure, the blue line about the gums, and
the colic, with the fact that the extensor muscles of the hand, rather than
those of the thenar and hypothenar eminences, are first atrophied, caus-
ing the drop-wrist instead of a claw hand, and that their electric con-
tractility is greatly diminished, are sufficient for a differential diagnosis.
In malarial palsy there is no muscular wasting, no tremor, and there
are the attendant well-known malarial symptoms.
Muscular atrophy sometimes ioWow^ paralysis. But this fact alone, when
the muscles do not respond to Faradization, excludes progressive muscular
atrophy.
Symmetrical sclerosis of the lateral columns — amyotrophic lateral
sclerosis — is, according to Charcot, distinguished by its rapid course, the
ultimate affection of all the limbs, and the almost constant extension to the
bulbar nuclei, by the prolonged preservation of electro-muscular contrac-
tility, and by permanent spasmodic contractures of the paralyzed and
atrophied limbs. The symptoms of muscular atrophy are preceded in
amyotrophic sclerosis by paralysis, and accompanied by rigidity ; this does
not occur in muscular atrophy.
Prognosis.— Progressive muscular atrophy is always a grave disease. Its
course is slow and irregular ; it may appear in the muscles of the hand, and
years elapse before it extends. There is little hope of checking its advance,
even if the treatment is commenced at its onset. The disease is arrested
spontaneously in a few instances within two or three years. Complete re-
covery is rare. One year is the average duration, when recovery takes
place. Its average duration is five years.' An hereditary element in the
etiology renders the prognosis unfavorable, and when the disease is pro-
longed several years, or the muscles of respiration and deglutition become
involved, a fatal termination is rarely long delayed. Inanition, bronchitis,
pneumonia, and hypostatic congestion are the causes of death.
Treatment. — In the cases that have come under my observation no plan
of treatment has had any beneficial effect. If an exciting or predisposing
cause can be reached it should at once be removed. Damp, cold, and over-
1 Herpes has been observed along the line of a nerve going to an atrophied muscle, and Rosenthal
mentions hj'pertrophy of the bones with concentric osseous atrophj% arthropathies, and bed-sores as rare
trophic disturbances.
* Roberts, in Reynolds System of Medicine.
CEEEBRO-SPINAL SCLEEOSIS.
1015
exertion should be avoided, and if syphilis be suspected, an anti-syphilitic
treatment is indicated ; and cod-liver oil, phosphorus, arsenic, and the
mineral tonics are to be given with a highly nutritious diet. The body is
to be warmly clothed in flannel ; friction, moderate exercise, shampooing,
massage, and inunctions are undoubtedly beneficial, if persevered in.
Warm baths at natural springs are strongly recommended. Galvanism,
however, is probably the most efficient remedy. The current should be
applied along the spine, especially in the cervical region, and directly to
the affected muscles. Faradization alternating with the constant current
often leads to improvement and a temporary arrest of the disease/ The
cramps and neuralgic pains are best controlled by hypodermic injections of
morphine.^
CEEEBRO-SPIIirAL SCLEEOSIS.
Morbid Anatomy. — On opening the spinal canal the cord is seen to be
studded with well-defined nodules of sclerotic tissue which have given it
the name of nodular sclerosis.
These nodules are distributed ir-
regularly throughout both the
gray and white matter. They
vary in number, and range in size
from minute microscopical objects
to the size of a walnut. They
present a yellowish red, glistening
appearance, are slightly elevated,
semi-transparent, of a jelly-like or
cartilaginous feel, and are marked
by fine white lines. The meninges
over the nodules are thickened and
opaque, but seldom adherent to
the substance of the cord. The
sclerosed patches are well defined
and easily distinguished from the
normal tissue in which they are
imbedded ; still there is no ab-
rupt transition from healthy to
diseased tissue.
A microscopical examination
shows the centre of the nodules to
be a dense mass of very fine fibril-
lated connective-tissue, containing
fat granules, corpora amylacea, Bel-
ter's cells and small axis-cylinders
which are glossy and brittle. The
persistence of the axis-cylinders is regarded by Charcot as peculiar to dissem-
1 Remak recommends galvanization of the fibres of the sympathetic nerve.
2 Loclthart Clarlt hints that blietering and other forms of counter-irritation to the spine, laU in the dis-
ease, deserve further trial.
Fio. 208.
Cerebro-Spinal Sclerosis.
Nodvles of sclerotic tissue on the surface of the cord.
A. Dura mater divided.
B. Pia mater showing sclerotic patches.
C. Pia mater reflected.
D. Sclerotic nodules on the cord.
1016 DISEASES OP THE NEEVOUS SYSTEM.
inated sclerosis. ISTear the periphery the nerve tubes are surrounded by
connective-tissue fibrillae running parallel with the inclosed nerves, and
there is commencing hyperplasia of the neuroglia, proliferation advancing
more or less rapidly according to the age of the nodule. The walls of the
vessels are thickened and infiltrated with numerous fat and lymphoid cells,
but their lumen is notably diminished. ' The nerve cells in the gray cor-
nua are either primarily or secondarily involved and undergo cloudy swell-
ing, followed by pigmentation or granulo-fatty degeneration, — the yellow
degeneration.
Thus it appears that sclerosis is a primary and multilocular chronic in-
terstitial myelitis or encephalitis a secondary condition.
Etiology, — The recognized exciting causes of multiple cerebro-spinal
sclerosis are damp and cold, sudden chilling of the body, traumatism, and
severe, long-continued brain work or physical exercise. Continued jar-
ring of the body is also thought to produce the disease, and it is said to oc-
cur in nervous people, with hysteria and after acute febrile diseases. It is
essentially a disease of earl}^ life, few cases occurring outside the limits of
fifteen and thirty-five. Heredity is said to play an important part in its
etiology. Quite recently cases are reported as occurring in very young chil-
dren.
Symptoms. — Charcot makes three varieties of this disease, according as it
is confined to the brain, or cord, or involves both. The latter is the more
common ; it may come on insidiously or be sudden in its development. If it
is insidious in its advent the patient complains vaguely of headache, ver-
tigo, muscular weakness, mental disturbances, and queer feelings as for-
mications, itchings, burnings, etc., in the limbs. The symptoms which
are referable to the sympathetic system are nausea, vomiting, and cardial-
gia. The patient notices very soon a loss of co-ordinating power ; he can-
not control his hands in writing or his feet and limbs in walking. There
is also impairment of the special senses. If the spinal element is promi-
nent, there is more or less paresis of all the extremities, with contractures
of the muscles. As soon as an attempt is made to use the paretic limbs,
they become tremulous and contracted. This tremor is peculiar in not oc-
curring until an attempt is made at voluntary motions, and at once ceas-
ing when the parts are allowed to rest. It is called the shaking tremor.
The more powerful the mental efPort the more marked is the tremor. Even
tlie head participates in it.
In some cases the patient becomes childish or morose, and the cerebral
symptoms in such cases are identical with those of cerebral softening. Dur-
ing prolonged fits of yawning, sobbing, or laughing the respirations ie-
come stridulous, and in the advanced stages the voice is changed. The
patient talks in a low monotone or whisper, dividing his words into sylla-
bles, and emphasizing them as when scanning a line of poetry. If the
sensory nerves are involved there are pains in the course of the affected
nerves, and a girdle pain is felt about the abdomen. Amblyopia, nys-
1 Charcot, Cornil and Ranvier maintain that in tiie sclerotic islands nerve-elements are always present.
Frommannand Erb hold the reverse.— Ziewi. Cycl., vol. siii.
CEKEB HO- SPINAL SCLEKOSIS. 101?
tagmus, diplojoia, and inequality of the jDupils evidence invasion of the
base of the brain and optic tracts. In the advanced stage vesical symp-
toms, acute bed-sores, and loss of sexual power and control of the sphinc-
ters become marked symptoms. Sometimes a sudden apoplectiform attack
followed by paretic symptoms ushers in the disease. The course of the
disease is peculiar. As its development is by stages, it may gradually
progress for several years, and then remain stationary for a long period.
Differential Diagnosis. — Disseminated sclerosis of the brain and cord may
be mistaken for paralysis agitans, or locomotor ataxia, and when ushered
in by apoplectiform symptoms may be mistaken for cerebral hemorrhage.
In paralysis agitans the fine tremor exists when the patient is at rest,
and is not accompanied by shaking of the head ; while in the shaking of
disseminated sclerosis the head is always involved, the symptom ceasing as
soon as the patient is at rest. Paralysis agitans is rare before forty ; mul-
tiple sclerosis is rare after thirty-five. Changes in the voice and speech and
ocular symptoms are present in disseminated sclerosis and absent in jDaraly-
sis agitans.
In locomotor ataxia the peculiar tremor, impairment of voice and speech,
and nystagmus that belong to disseminated sclerosis are absent. In the
former disease we notice the peculiar iron-band sensation, vesical symptoms,
the Meniere's vertigo, the very slow and late appearance of paretic symp-
toms, the lightning-like and agonizing neuralgic pains, and the peculiar
double beat in walking, the heel being put down first, all of which are in
marked contrast to the symptoms of multiple cerebro-spinal sclerosis.
When disseminated multiple sclerosis is ushered in by loss of conscious-
ness which rapidly deepens into coma, with marked hemiplegic symptoms,,
it may be mistaken iov cerebral hemorrhage ; but in sclerosis the tempera-
ture is very high during these peculiar attacks— 104° or 105° F. — the hemi-
plegia passes off as the patient returns to consciousness or in a few days
after, and the temperature rapidly falls to normal.
Prognosis.— ^This disease is usually of long duration, five to ten years be-
ing its average. It is rare for death to occur in coma. There is no well-
authenticated instance where recovery has occurred. During the stage of
its development and greatest activity deceptive remissions occur ; but after
six or seven years emaciation sets in, a marasmus is developed, and the pa-
tient is apt to die from intei'current disease.
Treatment. — The best method of treatment yet proposed is the restora-
tive ; the object is to improve nutrition. Among the drugs that have been
used, especially by Charcot and his followers, are chloride of gold, phos-
phate of zinc, nitrate of silver, chloride of barium, potassium iodide and
bromide, arsenic, belladonna, calabar bean, and ergot. The galvanic cur-
rent is the best means of administering electricity. Opinion is divided as
to the benefit obtained from hot or cold baths and thermal springs, or in-
unctions and massage. Pain not infrequently becomes so severe as to de-
mand hypodermic injections of morphine. '
' Leyden reports a case of almost complete cure from galvanism and the baths of Kehme. — Beit. z. acute
u. chron. Myelitis. Zeitsch.fiir klin. Med. Berlin, 1879, i., p. 126.
1018
DISEASES OF THE KERVOUS SYSTEM.
LOCOMOTOR ATAXIA,
Locomotor ataxia ' is one of the most frequent diseases of the spinal
cord.
Morbid Anatomy. — Its principal pathological lesion is an increase in the
J>03ierior.
Pig. 209.
Diagram illustrating the Regions of Degenerative Changes in the Spinal Cord.
A. Pyramidal tracts.
B. Anterior columns.
C. Haddon and Goiuer^s lateral sensory tract.
D. Mixed zone of lateral columns.
E. Processus reiic^ilaris.
F. Crossed pyramidal tracts.
G. Bi7'ect cerebellar tracts.
p. Postero-external columns.
I. Postero-internal columns.
Columns of Goll.
After Flechsig.
interstitial connective-tissue of the spinal cord. As the cord is removed
from the spinal canal there will be noticed a grayish discoloration on both
sides of the posterior median fissure. The pia and dura mater will be
more or less firmly adherent to each other ; and the dura mater may be
thickened, pigmented, opaque and studded with osseous plaques ; the pia
mater may be congested and there may be an exudation into its meshes.
The posterior aspect of the cord may appear atrophied, and have a firm,
hard feel. In advanced cases the whole cord is smaller than normal.
A cross section will show an increase in the cephalo-rachidian fluid, and
the posterior columns will be shrunken, gray, cartilaginous and shining in
appearance. Not infrequently the sclerosis will extend to the lateral
columns and forward to the margin of the anterior columns. These
changes usually begin in the lateral part of the posterior column in the
1 Duchenne was the first to give an accurate description of this disease. Trousseau and others have
called it Duchenne's Disease. It is also known as posterior spinal sclerosis, tabes dorsalis, gray degeneration
of the posterior columns and leuJco-myelitis posterior chronica. It is often called progressive locomotor
ataxia.
LOCOMOTOR ATAXIA.
1019
Fig 310
Locomotor Ataxia.
Section of Spinal Cord in tlie Cenical Region.
A A. Sclerosis of the columns of Goll.
upper lumbar and lower dorsal regions, and extend upward and down-
ward. It is possible in long stand-
ing cases for the medulla and the
second, third, sixth and eighth cra-
nial nerves to be involved, and for
the entire cross section of the cord,
at various points, to be shrunken,
hard and gray.
As a rule, the sclerosis ceases at
the restifo7"m bodies.^ If GoU's
columns are involved it is a second-
ary degeneration. The posterior
roots of the spinal nerves show gray
degeneration and atrophy to the
naked eye.^ On microscopical ex-
amination there will be found evi-
dences of a large amount of dense
and delicate connective-tissue con-
taining nuclei, granular and amy-
loid corpuscles, in which are very
few atrophied nerve fibres, which have lost their medullary sheaths.'
Large spider cells are found throughout the sclerotic tissue. The j^os-
terior columns are seen fused together by connective-tissue in the pia
mater which dips down into the fissure. The walls of the capillaries and
small vessels are thickened and rigid, and their calibre is diminished.
Their sheaths are filled with oil globules. They are also markedly pig-
mented.* The sclerosis travels from the cord to the posterior roots of
the spinal nerves, which show atrophy. The sciatic, crural, and brachial
nerves have been found sclerosed and atrophied.*
Etiology. — Locomotor ataxia is more frequently met with in men than in
women, the proportion being six to one. It occurs oftenest between the
ages of twenty and fifty. In a neuropathic predisposition it may be in-
duced by anything that seriously depresses the nervous system. Cold and
wet, bad hygienic surroundings, excessive mental or bodily exertions, —
onanism, excesses in venery, etc., especially, — depression of spirits, an in-
sufficient or improper diet, the impoverished blood states that occur with
or follow wasting acute or chronic maladies, prolonged lactation, syphilis,*
and, according to some, excessive use of tobacco, — are among its predis-
posing causes. Blows on the spine, the suppression of menses or old
1 Charcot describes the external bands :— two bands near the posterior cornua in the outer part of the
posterior columns. They run parallel with the posterior horns of gray matter.
2 Charcot has drawn attention to the condition of the joints in some cases of locomotor ataxia. " Snr
quelques arthropathies," eic.—A7rhiv. de Fhysiologie, i., 1868, p. 161.
3 Cornil and Ranvier insist that the axis-cylinder always exists, but that it requires a peculiar mode of
preparation to demonstrate this.
* Lockhart Clark states that he has sometimes found the extremities of the posterior cornua, and even
the central gray substance, more or less damaged by disintegration. The question has been raised whether
the initial lesion may not be in these cornua.
6 Friedreich. — V>rchoiu''s Archiv., Bde 26, 27.
« Erb found a, syphilitic history in twenty-seven out of forty-four cases.
1030 DISEASES OF THE NERVOUS SYSTEM'.
hemorrhoidal fluxes may excite it. It is a question, when it follows pneu-
monia, rheumatic fever, or diphtheria, if there is any causal relationship
between them.' Its hereditary tendency is shown by its attacking two or
more members of the same family, other members suffering from some
other form of nervous disease. This is an example of the " neuropathic
tendency."* In a large proportion of cases there is no assignable cause.
Symptoms. — The symptoms of locomotor ataxia may be divided into three
periods : a period characterized by disturbances of sensation, a period in
which there is loss of coordinating power, and a period of paralysis. Dur-
ing the first period there are sharp, tearing, lightning pains in the lower
limbs, dysuria, incontinence, spermatorrhoea, nocturnal pollutions, excite-
ment of, or loss of sexual desire, a sense of weariness in the limbs, and nausea
and vomiting attended by severe and paroxysmal aching in the stomach.
A sense of numbness and formication in the limbs is not uncommon in this
period. There maybe a girdle sensation, not only about the waist, but also
in the limbs — chiefly about the knee and ankle. In some cases there will
be evidence of arthropathies and symptoms much resembling those of active
cerebral hypersemia. Eectal and urethral colics, bronchial spasms, and
nephritic symptoms resembling those of renal colic, are not infrequent. The
pains during this period are usually in the feet and legs ; but they may
have their seat in the back, stomach, intestines, or bladder. If they are
situated in the internal viscera, the functions of those viscera are disturbed.
Wherever they may be seated, at first they do not come on often, and are
of short duration ; but as the disease advances, the attacks become more
frequent and are of longer duration. The muscles of the eyes may be af-
fected, causing double vision or strabismus, which may last a few days or
weeks and then disappear ; or changes may occur in other nerves which
lead to loss of sight. There may be temporary or permanent dilatation of
one or both pupils.
The destructions of surface sensation are manifold ; sometimes the pa-
tient will complain of a sense of numbness in the hips, sometimes a prick-
ing sensation, or a sensation of some soft substance between the feet and
the ground ; one portion of the surface may be anaesthetic, another hyper-
aesthetic. After a varying period, the ataxic symptoms appear, and the
muscles are no longer moved in their natural way. The gait becomes un-
steady, the patient walks like one intoxicated ; there is a sense of heaviness
in the limbs, and if the feet are brought close together, and the eyes closed,
the body sways to and fro and sometimes falls. After a time the patient is
compelled to watch his feet while walking. Later on he throws out his
feet and legs in the most grotesque manner ; for when the will acts the
muscles contract far more than the patient intends. If the upper extrem-
ities are involved, he is unable to dress himself ; he cannot pick up a pin,
button his garments, or hold anything in his fingers. The movements of
1 The most recent theory of its causation is that of Kahler and Pick, who regard those cases whicti fol-
low acute infectious diseases as the result of the accumulation of fungi in the central nervous system
producing nutritive disturbances.
2 Carre records eighteen cases of tabes in the same family in three generations.— J/. Carre, These.
Paris, 1862.
LOCOMOTOR ATAXIA. 1021
his liancls and arms are forcible, irregular, and jerking. The gait during
this period is peculiar ; the heel is brought down first, then the toe : there
IS a double beat to the step. Quiet or steady movements are impossible.
At times the loss of coordination is so great that for days the patient is un-
able to walk, and then the coordinating power is partially restored. One
extremity maybe involved after the other, or both be attacked at the same
time. During this period there is a marked loss of sensation, especially in
the feet and legs ; these patients are often unable to tell when their feet
touch the floor. Sensitiveness to pain is diminished, and it may be several
mmiites before the prick of a pin is felt. The sensation disturbances of the
first period are increased, and the sight is more imjDaired. In this period
there is less loss of the reflex action of the muscles of the lower extremi-
ties, especially the muscles of the calf of the leg. The abolition of the pa-
tellar tend on- reflex is one of the diagnostic signs of the disease. Loss of
the sense of temperature, a greater or less loss in electro-muscular contrac-
tility, and, in the irritative forms, increase in galvanic excitability are not
uncommon. During this period there may be developed a peculiar affec-
tion of the joints ; the Joints mpst frequently affected are the knee, hip,
shoulder, and elbow. The joint rapidly swells and the synovial sac fills with
fluid ; after a time disorganization of the articular surfaces takes place and
may be followed by the destruction of the ends of the bones. In some in-
stances the swelling suddenly disappears and the joint is not disabled.' De-
generative changes in the anterior horns are thought to be the cause of
these joint symptoms. In a few cases skin eruptions of various kinds make
their appearance.^ In the last period paralysis occurs, and then are devel-
oped muscular atrophy, bed-sores, and those vesical and renal symptoms that
are so apt to lead to death.
Nearly all the symptoms of locomotor ataxia appear intermittently, and
the progress of the disease is rarely continuous. During the third period
there is always complete impotence. In some cases the face has a pale
yellow color, which is most marked during cold weather.^ During this
last period sensation about the rectum is lost ; hence the patient is apt to
become exceedingly filthy unless great care is exercised. This condition is
accompanied by almost constant dribbling of the urine. Intelligence,
memory, and the higher cerebral functions are rarely, if at all, impaired.
In a few cases of locomotor ataxia the patients become color-blind. Loco-
motor ataxia is a non-febrile disease, but during the initial period febrile
symptoms may occur, and are then especially important as indicating a
rapid progress in the disease." The former is neither an early nor a late
symptom. Pierret says that all possible nervous disturbances of hearing
may precede ataxia. After reaching the second period, the disease may for
* Blum states that the great friability of the bones that results in spontaneous fracture is due to raxeij-
mgostitis.—Des. Arth. iVori. nen. Thhe. Paris, 1875.
* Chfircot says that they follow the track of nerves that have been the seat of pain.
8 Eulenberg attributes dicrotism of the pulse in ataxics to loss of vascular tone of spinal origin.— Ber-
lin. Klin. Wochen.
* Among the most recent contributions to this disease is Erb's paper, wherein he ascribes great im-
portance as a symptom to spinal myosis, i. «., reflex immobility of the pupil.
1022 DISEASES OF THE KERVOUS SYSTEM.
along time remain stationary, or it may temporarily improve, but com-
plete recovery is rarely, if ever, reached. In the long and slowly progres-
sive cases fluctuations always occur, with improvement in summer and
exacerbations 'in winter.
Differential Diagnosis. — Locomotor ataxia may be confounded with joara-
plegia, multiple cerebro-sinnal sclerosis, cerebellar lesions, chronic myelitis,
hysterical ataxia, and chronic spinal meningitis.
Paraplegia is a true paralysis ; ataxia is not, and it is readily proved that
in the latter disease muscular force is not diminished. In paraplegia the
limbs are not thrown about in walking, — they are merely dragged. In
paraplegia there is little or no resistance to artificial movement, while in
ataxia there is great resistance in bending the limbs against the will of the
patient. The nutrition of the muscles is markedly impaired in paraplegia,
and normal in ataxia. Neuralgic pains are absent in paraplegia and present
in ataxia. Strabismus, ptosis, etc., are present in ataxia and absent in
paraplegia.
The diiferential diagnosis between multiple sclerosis and ataxia has been
given.
Cerebellar disease has for its characteristic symptom vertigo ; this is rare
in ataxia. A patient with cerebellar disease can stand and walk better with
his eyes shut than open, has unimpaired cutaneous sensibility, and the
movements, while uncertain, are not so abrupt, vehement, and Jerky as in
ataxia ; they resemble rather the stupid movements of a drunken man.
The absence of neuralgic pains, of vesical and sexual weakness, and the
prominence of headache, vomiting, and convulsions in cerebellar disease
will be sufl&cient for the diagnosis.
In chronic myelitis there are no disorders of coordination. The patient
sufEers paresis, or even complete paralysis of the lower extremities, while
in ataxia there is no paralysis, muscular power being undiminished. The
limbs are dragged simply in chronic myelitis ; they are thrown forcibly
about in ataxia. Ocular symptoms are absent in chronic myelitis, present
in ataxia. Contractures, spasms, paralysis of the bladder, cystitis, and the
early formation of bed-sores, together with the absence of intense neuralgic
pains, will also serve to distinguish chronic myelitis from ataxia.
In hysterical ataxia the history, and the occurrence of the disease in a
female, with the subsequent course of the disease, will enable one to dis-
tinguish it from ataxia.
In meningitis there is pain, — increased on pressure, — slight paralysis but
no incoordination, no flinging of the limbs in walking or moving, no aboli-
tion of tendon reflexes, and no ocular symptoms such as are present in
ataxia.
Prognosis. — The usual course of locomotor ataxia is progressive.
The prognosis as to its duration is uncertain. The disease sometimes
ceases of itself, leaving the patient in a disabled condition, but still giving
him years of life. The slower the development the longer the duration.
The prognosis is more unfavorable when it occurs with a history of nervous
disease in the family, when the early symptoms are serious and constant.
SPASMODIC TABES DOESALIS. 1023
and when constitutional symptoms (especially emaciation) become marked.
Complications -likewise render the prognosis unfavorable. Comi^lete re-
covery is possible but not jjrobable. The duration of the disease varies
from six months to as many years.
Treatment. — The efficacy of treatment depends upon the stage at which it
is commenced. Undoubtedly, if the disease can be early recognized, its
advance can in many cases be cliecked.
Of the drugs recommended, nitrate of silver is perhaps the one most ex-
tensively used. It should be given cautiously ; about one grain a day in
divided doses. The galvanic current is nearly always of service. Some
cases will be benefited by the iodides, others by the bromides. Strychnia,
phosphorus, arsenic, the chlorides of gold, sodium, and bariam, the phos-
phide of zinc, belladonna and ergot all have been recommended.' The
diet and mode of life should be such as to conduce to the highest degree of
health and nutrition. Cod-liver oil and ]ohosphorus may be given as ad-
juvants to a nutiitious diet.
The patient should remain at rest as much as possible. Under no cir-
cumstances should he be allowed to expose himself to cold or wet or to sud-
den changes in temperature. Flannel should be constantly worn next the
skin. Simple thermal baths seem to do harm, but saline thermal baths
sometimes give good results. Sulphur, clialybeate and mud baths have
been recommended. Erb recommends, as better than all, the cold water
cure. He advocates the wet pack for the neuralgic pains. Bleeding or
depletion of any sort is contraindicated, even in the initial stages. For the
gastric derangement bismuth will generally be found efficacious. Consti-
pation must be overcome by mild cathartics. For the vesical weakness or
for incontinence, Faradization of the bladder, bromide of potash, camphor,
and lupulin are advocated. In order to preserve the nerve force and pre-
vent exhaustion, crutches are very useful, as they prevent the muscles from
being constantly overtaxed.
m
SPASMODIC TABES DOESALIS.
Under this name Charcot has described what Erb calls spastic spinal
paralysis. It has also been called tetanoid pseudo-paraplegia.
Morbid Anatomy. — As far as can be stated there is symmetrical sclerosis
of the lateral columns, chiefly of their posterior portions. The induration
shades off imperceptibly into the normal tissue of the columns.
This degeneration does not differ microscopically from that seen in scle-
rosis of the cord ; it often extends in varying degrees the entire length of
the cord. Anterior polio-myelitis and posterior sclerosis are frequently
associated.
Etiology. — Spasmodic spinal paralysis is more common in males than in
females, and is rare except between the ages of twenty and fifty ; it rarely
1 Lockhart Clark recommends morphine, cannabis indicaand belladonna ivitli silver nitrate when the lat
ter irritates the bowels or bladder.
1024 DISEASES OE THE KERVOUS SYSTEM'.
occurs in children. Traumatism and exposure to wet and cold are named
as its causes.
Beyond this its etiology is obscure.
Symptoms. — Beginning very insidiously, the first symptoms noticed are
weakness and paresis of the lower — rarely of the upper— extremities.
These patients drag their limbs. This is followed by twitchings and stiff-
ness of the muscles, and later there is so much muscular rigidity that loco-
motion is embarrassed or rendered impossible. Exaggeration of the tendon-
reflexes is an early and important symptom, and is associated with marked
ankle-clonus, in which the muscles of the calf or the whole limb are put in
a state of tremor when the foot is flexed, or when the patient puts his toes
to the ground. As the muscular rigidity increases these signs diminish.
Later, general muscular tremors or shiverings unaccompanied by tempera-
ture changes may occur, in which all the muscles partake. They may be
excited by cold or follow excitation of ankle-clonus when they do not occur
spontaneously. If the patient is able to walk, he has the typical spastic
gait ; the adductors keep the thighs close together, the toes are dragged,
and as the heel is brought down the extensors of the foot contract spas-
modically and may throw the patient forward, lifting him on his toes.
Sensibility and skin-reflexes remain normal.
Electric reaction of the muscles is unchanged ; while that of the nerves
is lowered to loth currents. In the advanced stage of the disease the
muscles of the abdomen, back, or upper limbs may become involved. In
the latter case the fingers and hand are strongly flexed ; the forearm is pro-
nated and semiflexed, and the arm is fixed to the side. After a varying
period paralysis of the affected parts occurs, and the contractures become
more marked ; the legs are permanently extended, and the foot assumes
an equino-varus position. Pain rarely accompanies the contractures,' and
the nutrition of the affected muscles is not impaired,^
DiiFerential Diagnosis. — Spastic paralysis may be confounded with tabes
dorsalis, chronic anterior jjolio-myelitis, multiple sclerosis, peripheral paral-
ysis, and transverse m.yelitis.
In locomotor ataxia the ataxic symptoms, the double beat and stamp
of the walk, the absence of tendon-reflexes, the general pains, the bladder
symptoms, and the absence of paralysis and contractures are in direct con-
trast to the symptoms of primary lateral sclerosis.
In chronic anterior polio-myelitis atrophy follows the paresis and the
muscles lose electric excitability. Tendon-reflexes are absent. In spastic
paralysis rigidity follows paresis, and tendon-reflex and electric excitability
are exaggerated.
Multi2Jle sclerosis, when it is located in the lateral column at the onset,
is practically spastic tabes. "When the sclerotic process attacks other
portions of the cord, or when cerebral disturbances occur, it assumes its
distinctive characteristics.
1 Erb states that pain in the back and limbs attended by formication and other paraesthesiae not un-
commonly precedes the motor wealiness at the beginning of the disease. — Virchmv''s ArcMv., b. 70. 1877.
^ Recently, Stumpell calls attention to the relaxation of the muscles which occurs in spastic paralysis
when the legs are not irritated by their own weight.
AMYOTROPHIC LATERAL SCLEROSIS. 1025
In peripheral paralysis there are disturbances of sensation and nu-
trition ; the disease develops unsymmetrically , and reflex excitability and
electro-muscular contractility are rapidly lost.
In tranverse myelitis trophic disturbances, vesical derangements, and
alterations in sensation are early and marked symptoms. They do not oc-
cur in spastic paralysis.
Prognosis. — In uncomplicated spastic paralysis the prognosis is good.
Some claim that complete recovery is possible, and in most instances the
symptoms can be ameliorated. The disease may progress slowly for years,
and then remain stationary indefinitely ; or it may become complicated by
bulbar or glosso-labio-laryngeal paralysis, and prove rapidly fatal.
Treatment. — In addition to the treatment proposed for chronic myelitis the
galvanic current is most useful. Iodide of potash, arsenic and cod-liver oil
in small doses, with careful attention to rest and diet, are to be recommended.
Shampooing, rubbing and massage afford great comfort, and calabar beaq
may be given for the cramps. Nerve stretching has also been employed,
AMYOTEOPHIC LATERAL SCLEROSIS.
{Spastic Paralysis.)
Charcot calls this disease the deuteropathic form of progressive muscular
atrophy. Pathologically and clinically it is a complex of progressive mus-
cular atrophy and spasmodic spinal paralysis.
Morbid Anatomy. — The sclerotic process begins in the cervical region,
and although at first it is limited to the lateral columns, it soon attacks the
anterior cornua and leads to destruction and atrophy of the large ganglion
cells. It also extends downwards into the dorsal and lumbar lateral columns,
and almost invariably upwards so as to involve the medulla, when the signs
of bulbar paralysis are induced and followed by a fatal issue. This process
has its seat in the same portions of the cord as the secondary descending
degeneration of Tiirck, and new bands of dense connective-tissue join the
degenerated lateral columns with those portions of the anterior horns that
are involved. ' In the floor of the fourth ventricle the cells of the nucleus
of the spinal-accessory, facial, and hypoglossal nerves are degenerated. The
anterior roots and peripheral nerves are atrophied. Trophic changes in the
muscles are identical with those of progressive muscular atrophy.^
It is stated that interstitial growth of neuroglia is sometimes found with-
out marked degeneration or atrophy of the nerve fibres, but that the whole
system of fibres and ganglion cells which unite the motor centres iji the
cortex with the muscles is involved.^
Etiology.- — Nothing more can be said regarding its etiology than lias al-
ready been stated concerning the origin of the two diseases of which it is;
a compound.
» Archiv. de Phys. Nor. et Path. 1879.
2 Rosenthal states that their inflammatory character is more marlced in amyotrophic lateral sclerosis^.
and that hyperplasia of the perimysium is more pronounced.
3 Flichsig and Pick state that the whole system of nerve fibres and ganglion cells which unite the motot
centres in the centres of the brain with the muscles are affected in amyotrophic lateral sclerosis.
65
1026 DISEASES OF THE IsTERVOUS SYSTEM.
Symptoms. — The disease begins with weakness, paresis, and then actual
paralysis in tho upper extremities, associated with muscular atrophy, which
is usually diffuse and rapidly progressive. Fibrillary spasms and twitch-
ings of the affected muscles are well marked ; but electrical contractility-
is preserved. Sensibility is not impaired, but the muscles become rigid
and contracted with the arms flexed.' In a few months the lower limbs are
involved in the paralysis and rigidity, with exaggerated tendon-reflexes and
contractures. Subsequently the muscles atrophy and show the reaction
of degeneration and fibrillary spasm, while the contractures diminish.
This is followed by the symptoms of bulbar paralysis.
Differential Diagnosis. — Amyotrophic lateral sclerosis maybe mistaken for
progressive muscular atrophy. But in the latter disease the slow course,
absence of bulbar paralysis, and partial affection of certain groups of
muscles, are in marked contrast to the symptoms of the former. More-
over, in amyotrophic lateral sclerosis the atrophy is preceded by paralysis.
Prognosis.— The prognosis is decidedly unfavorable ; death results in
from one to three years from bulbar paralysis. It is not, however, pre-
ceded by paralyzed sphincters, vesical troubles, bed-sores, or other trophic
lesions.
Treatment. — Eesidence in the open air at a high altitude and strict at-
tention to the genera] health are of first importance. Beyond this the
treatment is identical with that of other forms of spinal sclerosis.
Mitchell recommends cod-liver oil, iron, strychnia, and dry cupping
along the spine, with massage.
PSEIJDO-HYPERTEOPHIC PAEALYSIS.
This is a progressive muscular paralysis occurring chiefly in boys.
Morbid Anatomy. — The German pathologists generally regard this dis-
-ease as a chronic myositis with hyperplasia of interstitial connective-tissue.
Gowers, however, in a recent monograph, describes the substance with
which the muscle is filled and its fibres replaced as a new growth. Fat
:accumulates in the new growth to such an extent as to induce atrophy, and
the muscles undergo granular and fatty metamorphosis.
As a final stage Charcot mentions waxy degeneration of the muscular
elements. If a portion of the affected muscle is examined it will be
found of a pale red or yellow color, according to the date of the disease.^
Etiology. — Age and sex are the most constant predisposing causes, over
eighty-eight per cent, of the recorded cases occurring before the tenth
year. Hereditary influence appears most powerfully on the mother's side.
The neuropathic tendency is more marked than in any other nervous dis-
ease. The recognized exciting causes are cold, falls, and convalescence
from acute febrile disorders.
1 Erb states that as atrophy of the muscles progresses they may undergo simultaneous lipomatous
hypertrophy.
2 Charcot, Cohnheim and Eulenberg found no changes in the cord. Others have found spots of sclerosis
and atrophy of the ganglion cells in the anterior horns. Lockhart Clark and Gowers have discovered ex-
tensive disintegration of the gray matter at the centre of each lateral half of the cord and of the anterior
commissui-e.
PSEUDO-HYPERTROPHIC PARALYSIS. 1027
Symptoms, — M. Duclienne makes three stages : first, a stage of weakness
without increase in the size of the muscles ; the muscles chiefly affected are
those of the legs, especially the gastrocnemii, lower part of the back, and
the erectores spinas. Second, a stage in which hypertrophy appears and
weakness extends to the u])per extremities. During this stage for a year
or more the child may evince no symptoms beyond a progressive weakness.
He is easily and quickly tired, raises himself with increasing difficulty, and
when erect does not stand firmly. He soon begins to show a peculiarity of
gait and attitude. He walks with a swaying, unsteady step, and as he
stands the shoulders are thrown backward and the spine is sharply bent in
the lumbar region. The hyperplastic and degenerative changes in this stage
produce the pseudo-hypertrophy of the muscles, which become firm and
hard with increased loss of function. When the child is j)laced in an
erect position the increase in size becomes very marked. In the supine
position the soles of the feet are approximated and the joints of the lower
extremities are flexed. Similar hypertrophy sometimes affects the muscles
of the upper half of the body ; but more commonly they are wasted, and
thus the protuberant belly and the thick, firm calf and thigh afford a strik-
ing contrast to the emaciated muscles above the diaphragm. The children
walk only with the greatest difficulty, or possibly they cannot stand without
support, and the act of sitting or rising becomes difficult. Sometimes it is
impossible for them to maintain even a sitting posture. The antero-pos-
terior curvature of the spine and the displacement of the shoulders are much
exaggerated, and the toes often undergo a claw-like deformity.
Gradually some muscles become soft and fatty while others remain firm
and hard, and the child passes into a stage of complete jaaralysis of the
trunk and upper extremities in which all the muscles that were hypertro-
phied atrophy, and the patient becomes completely helpless. Formication
is not uncommon at first, but neither anaesthesia nor hyperesthesia is pres-
ent at any time. Electro-contractility of the muscles is unimpaired until
the advanced stages of the disease. The upper extremities seldom suffer
pseudo-hypertrophy, but may exhibit true progressive muscular atrophy.
The deltoid and triceps are usually the only muscles enlarged. In nearly
all cases the disease progresses symmetrically. The skin of the affected
parts is sometimes bluish, dry, and thinned. The tongue and the muscles
of the face may become enlarged,, and some consider the cardiac hyper-
trophy that is often present as of similar origin.
In a number of cases the mental faculties have been impaired, but the
general health is usually good, and the sphincters are never involved.
Prognosis. — The prognosis is unfavorable, and when progressive muscular
atrophy is superadded it is especially so. Cases of- recovery have been re-
ported. Its duration varies from a few months to several years. Intercur-
rent disease is generally the direct cause of death.
Treatment. — Duchenne's treatment is regarded as the most efficient. Lo-
cal electricity, shampooing, and massage, if employed before the hyper-
trophic changes occur, may arrest its development.
1028 DISEASES OF THE NERVOUS SYSTEM.
ACUTE ASCENDING PARALYSIS.
This peculiar disease has no well recognized anatomical lesions, but is
regarded by most observers as a purely functional disease,'
Etiology. — Acute ascending paralysis is a disease of adult life, more com-
mon in 'men than in women. Exposure to cold, emotional influences,
venereal excesses, syphilis, acute febrile disease, and poisoning from corro-
sive sublimate' have each been followed by it.
Symptoms, —For the first few days there is possibly a slight fever, accom-
panied by a sense of weariness and numbness and darting pains in the
limbs, chiefly in the feet and in the tips of the fingers. This is followed by
paresis, then actual paralysis of the distal portions of the lower extremities.
The paralysis gradually extends upward, until in a few days paralysis of
the lower extremities is complete. Soon the trunk muscles are implica-
ted ; the patient can neither turn nor sit up in bed. The upper extrem-
ities are then involved, the paralysis extending from the finger tips to the
shoulder joint. Sometimes there is a distinct interval between the paraly-
sis of the trunk and the upper extremities. In about seventy per cent, of
cases the muscles of the neck and the diaphragm are involved, and finally
bulbar paralysis is superadded.
In some cases the disease pursues a reverse course, palsy of the extremities
following the symptoms of bulbar paralysis. The paralyzed limbs are lax
and the muscles flaccid ; but they do not undergo atrophy, and the electri-
cal reactions of nerves and muscles continue perfectly normal. Sensibility
is little if at all affected, the sphincters are not involved, cutaneous nu-
trition is unimpaired, and there are few, if any, vaso-motor or trophic dis-
turbances. Eeflex action diminishes after the first two or three days. There
is usually constipation and difficult defecation, on account of the paralysis
of the abdominal muscles. The intellect is never disturbed. In over thirty
per cent, of the cases, when, or before, the arms are implicated, the disease
is arrested, and soon recovery of power begins to manifest itself, the parts
first paralyzed being last restored. It is said that recovery has taken place
even after the paralysis has reached the nerves of the bulb. As a rule there
are no pains complained of in the paralyzed parts.
DifFerental Diagnosis. — Acute ascending paralysis may be confounded with
acute myelitis, acute spinal paralysis of adults, and, when slowly evolved,
with chronic spinal paralysis.
Acute ascending paralysis is differentiated from acute ascending mye-
litis by the slight disturbances of sensation which attend it, by the preser-
vation of electrical excitability, and by the absence of motor irritation and
trophic disturbances.
Acute ascending paralysis differs from acute spinal paralysis of adults
1 Dejerine claims to have found in two cases an alteration in certain fibres of the anterior roots (parenchy-
matous neuritis;. The myeline was brolien up into fragments. Multiplication of the nuclei in the white
substance of Schwann, and disappearance of the axis-cylinders were noted. The majority of the fibres
were unaltered. The same lesions were found in the intramuscular nerves of the affected members.
2 Ketly in the Pester Med. Chir. Fres. Nos. 8-9. 1878.
SPINAL APOPLEXY.
1029
in the absence of atrophy of the paralyzed muscles ; the electrical reactions
remain normal, and it is more rapidly progressive. The medulla is not
involved in acute spinal jjaralysis, whereas about seventy per cent, of cases
of ascending paralysis end in bulbar symptoms.
Kapid atroj^hy of the muscles and the reaction of degeneration are
prominent symptoms of chronic spinal paralysis, which are absent in acute
ascending paralysis. In the latter disease there is persistence of reflex
actions and a far greater tendency to extend to the medulla.
Prognosis. — Acute ascending paralysis is generally fatal. It may last
several weeks ; but its average duration "is from ten to fifteen days. The
more rapid its progress, and the earlier the medulla is involved, the more
unfavorable the prognosis. Improvement may take place even in the most
acute cases. Death occurs from the same causes as in bulbar paralysis.
Treatment. — All that can be done in this disease is to maintain the
nutrition. Electrical currents may be ajDplied to the affected muscles.
Sulphur baths, iron, arsenic, strychnine, and iodide of potash are recom-
mended for the more slowly progressive forms, but clinical experience
does not sustain the claim of beneficial results which have been obtained
by their use.
SPinSTAL APOPLEXY.
Spinal apoplexy is not of frequent occurrence, except when due to trau-
matism or to some pre-existing disease of the cord.
Morbid Anatomy. — A meningeal hemorrhage may extend the entire
length of the cord ; primary
hemorrhage, however, usually j-
occurs into the gray matter,
and if slight, may only involve
one side. The white matter
is never alone involved, but
about fifty per cent, of spinal
hemorrhages are circumscribed.
In a few cases punctate capil-
lary hemorrhages are found
studding the gray substance.
A clot of varying size, one-
fourth to one inch in diameter,
is found in the central portion
of the cord containing debris of
nerve-tissue, corpora amylacea,
fat' granules, and pigment. This
blood sac commonly lies with
its long axis parallel with the
cord. The centre may have undergone softening, and the wall is formed
of ragged nerve- tissue. About a clot in the white substance, the tissue is
always more or less deeply tinged with blood. When the extravasation in-
volves the periphery of the cord there will be hypersemia of the adjacent
Fie. 211.
Spinal Apoplexy.
Section of the Cervical Spinal Cord, shoiving a small clot in
the region of the anterior cornu of the left side.
A. Clot.
B. Meninges adjacent to the clot shoioing hypercEmia.
1030 DISEASES OE THE NERVOUS SYSTEM.
membranes. Capillary aneurisms have usually been found in the spinal
vessels at the seat of the apoplexy ; and Liouville has found ampullary dila-
tation of the large vessels, thickening of their walls, and proliferation of
their nuclei. Charcot states that there is swelling of the nerve cells and
axis cylinders. The clot may undergo retrogressive changes and result in
softening, abscess, or a cicatrix. Erb describes softening of the gray sub-
stance as a not infrequent sequela of spinal apoplexy. White softening
accompanied by gelatinous oedema surrounds the blood tumor and merges
imperceptibly into healthy cord substance. Ch. Bastian states that inflam-
matory softening may start from the clot and extend up or down the
cord. '
Etiology. — Spinal hemorrhage is most commonly the result of trauma-
tism, and especially of severe concussion." It may result from rupture of
vessels in or near neoplasia, in foci of myelitic or other softening, or in
any chronic spinal disease. Small hemorrhages may occur with scorbutus,
purpura, and in the hemorrhagic diathesis. Atheromatous, fibroid, and
fatty degeneration of the blood-vessels, nuclear proliferation, and minute
aneurismal dilatations predispose to spinal hemorrhage. Age and sex are
also predisposing factors, as it is most frequently met with in men between
the ages of fifteen and forty. Anything that induces or predisposes to ac-
tive hypersemia acts as a predisposing cause. ^
Symptoms. — Sometimes the symptoms of myelitis, spinal irritation, or
active spinal hypersemia precede the extravasation, but usually it com.es on
suddenly and causes complete paralysis of both motion and sensation be-
low the site of the hemorrhage, without loss of consciousness. It is at-
tended by severe pain in the back, that may be localized or extend the
entire length of the spine. This sometimes disappears when the paralysis
becomes complete. Pressure does not increase it. At the onset spasmodic
twitchings may occur in the paralyzed parts ; and all reflex motion is
abolished — the muscles being completely relaxed. Priapism and dyspnoea
may occur when the clot is high up. When hemorrhage occurs in the
dorsal or lower cervical region, the temperature of the paralyzed limb
— which at first is sub-normal — rises 2° to 3° F. higher than the axillary
as a result of vaso-motor paralysis. The bladder is at first paralyzed, but
when the sphincters are also involved the urine passes involuntarily. Cys-
titis is soon developed and pyelitis rapidly follows. The faeces are passed
involuntarily and bed-sores appear early. The paralyzed parts begin to
undergo atrophy, and while so doing exhibit the electrical reaction of
degeneration. If a clot occupies one-half the gray matter at any point,
Jiemi-paraplegia is developed in the limb of the same side as the lesion.
Should it implicate the root of the phrenic nerve, intense dyspnoea and per-
haps instantaneous death may result.
Differential Diagnosis. — Apoplexy of the cord may be confounded with
' Charcot and Hayem regard this lesion as always consecutive to myelitis.
2 Sir William Gull relates a ease where small extravasations were found on the anterior and posterior
comua as well as in the posterior columns of the cord. The case was the result of a fall.
' Erb claims that variola hemorrhagica, typhoid, yellow, and malarial fevers are causes of spinal hemor-
rhage.
TUMOKS OF THE SPINAL CORD. 1031
meningeal apoplexy and tliromhotic soflenlng. In meningeal apoplexy sen-
sory paralysis is absent or but sliglitly marked ; after the initial motor
paralysis, improvement is marked and speedy ; pain, hypergestliesia, and
irritation symptoms are prominent ; and bed-sores, cystitis, and pyelitis
do not occur. All these are in distinct contrast with the symptoms of
spinal or intramedullary apoplexy, Vaso-motor disturbances are absent
in meningeal, but present in spinal hemorrhages.
Thrombotic softening produces incomplete paraplegia, without loss of
sensation. The absence of sensory and motor excitement is regarded as
diagnostic. Hemorrhage not infrequently occurs in a spot of myelitic soft-
ening, but in such cases the paraplegia /oZ/o2^s irritation, pain on pressure,
fever, vesical symptoms, and the girdle sensation. In apoplexy paraplegia
is i\\Q first symptom, the other symptoms coming on at greater or less in-
tervals.
Prognosis. — Charcot states that a true spinal apoplexy is always fatal.
The prognosis is certainly exceedingly unfavorable when the onset is severe
or when the thoracic and respiratory muscles are implicated. Death
may occur in six hours. Incomplete recovery is possible, with paralysis
and atrophy of the muscles of the lower extremities. Septic fever, cystitis,
and pyelitis are its complications ; and death may occur from exhaustion
and marasmus. The chief danger, if life is prolonged a few weeks, is from
myelitis and extensive softening.
Treatment. — Absolute rest in the prone (not supine) position, is most im-
portant. Blood-letting, purgatives, or revulsives are not allowable. Ice-bags
should be applied along the spine. Bromides and oj)iates may be employed
to insure rest. Attention to the bladder is an important element of treat-
ment. The treatment is the same as for cerebral apoplexy with transfer-
ence of local measures from the head to the spine.
TUMOES OF THE SPINAL CORD.
As tumors in the spinal canal arise from the same causes and present the
same anatomical appearances as similar growths in the brain, it is only
necessary to consider their clinical phenomena.
Symptoms. — These will vary greatly in their nature and in the order of
their development, with the seat of the tumor, its extension, and the
amount of intercurrent changes in the adjacent tissues.
I. Tumors which primarily involve the substance of the cord are more
common in the gray matter, and are attended by a gradual abolition of
function. The changes are due more to pressure than inflammation, so
that pain is a less common and prominent accompaniment. The earlier
symptoms are those of paresis., either with hemiplegia or paraplegia of the
parts below the tumor, according as the growth involves a lateral half or
the entire substance of the cord. When the lesion is lateral, the paralysis
may be crossed or mixed ; motor paralysis of one side may be attended
by anesthesia of the other. The paralysis is rarely complete at first, but
is progressive, though liable to remarkable remissions, and eventually be-
1032 DISEASES OF THE NERVOUS SYSTEM.
comes complete. As these tumors extend and involve the meninges and roots
of the nerves and are attended by inflammation, peripheral pains and mus-
cular spasms may develop, while the edematous softening or ascending and
descending degenerative changes may cause atrophy and wasting of the
muscles. Tumors of the substance of the cord may thus resemble muscu-
lar atrophy, tabes dorsalis, or other forms of sclerosis.
II. Meningeal growths and tumors developed exterior to the membranes
pursue a less latent course. They involve the roots of the nerves early, and
are productive of more marked inflammatory changes. Hence the early
symptoms are those of both sensory and motor irritation. There are burn-
ing, lancinating, and crushing pains, which are irregular and liable to
severe exacerbations, which may be attended by hyperaesthesia and cuta-
neous eruptions. There are muscular twitchings and spasms which, as the
nerves are more seriously affected or the cord becomes compressed, pass on
to paresis or complete paralysis with muscular ati'ophy and wasting. The
sensory symptoms at the same time give place to numbness and anaes-
thesia.
Spinal tumors of all forms produce more or less myelitis, and with this
the reflex excitability is greatly increased and may cause contraction and
rigidity.' Trophic changes are late symptoms. In all forms of spinal
growths the symptoms are liable to sudden and marked changes either
favorable or unfavorable. A sudden a3dema or hemorrhage may cause ex-
tensive paralysis, which may be permanent or slowly recovered from. Or
a rapid and marked improvement may be speedily followed by a more com-
plete and widespread paralysis. When the new growth involves the verte-
brae and results in destructive changes, as frequently occurs with cancer,
the early symptoms of pain and hyperaesthesia are usually severe and the
paralysis rapidly becomes complete.
DiiFerential Diagnosis. — Inflam^nation, hemorrhage, and softening of the
cord are excluded by their abrupt onset, and the fact that their symp-
toms are more general and uniform in their development than those of a
tumor.
The nature of a tumor can seldom be determined, and the diagnosis rests
almost entirely upon the history and the presence of some adventitious
growth in other organs.
Prognosis. — Complete or even partial recovery is not to be expected. The
paralysis and muscular atrophy are progressive. No estimate of their
duration can be made.
Treatment. — Every tumor should be treated as syphilitic, as this is the
only kind amenable to treatment. When the vertebras are involved, sup-
porting appliances are indicated. Beyond this the treatment is purely
symptomatic.
• Schiippel claims that the spine is always curved towards the side upon which the tumor is situated,
and that the combination of irritative and paralytic symptoms of striMng inconstancy is diagnostic of
tumor.
SPIHA-BIFIDA. 1033
SPIJSrA-BIFIDA.
Spina-bifida is a congenital malformation due to arrested development
of some portion of the spinal column. It is usually associated with dropsy
of the spinal cord, or hydrorachis. Internal hydrorachis is a collection of
serum in the central canal, causing atrophy or destruction of the spinal
medulla. External hydrorachis is an effusion into the subarachnoid space.
If the spinal canal closes, it is called H. incolumis ; if not, H. deldscens.
Morbid Anatomy. — Usually two or three spinous processes and laminai are
deficient, the rudimentary portions of the vertebral arches are spread out
and irregularly expanded, and the membranes protrude through the aper-
ture as a hernial sac. The tumor, which is oval or spherical and at birth
about one inch in diameter, occurs almost invariably in the lumbar or
lumbo-sacral region. It is tense and fluctuant, being tilled with cerebro-
spinal fluid. Pressure on the tumor increases the tension, and may produce
symptoms of cerebral pressure. The skin over the tumor, although some-
times normal, is usually thin and transparent. The nerve-trunks forming
the Cauda equina often traverse the interior of the sac. The skin at the
apex of the tumor is sometimes destroyed and the sac exposed. The point
is excoriated or covered with pus and granulations, and the ulceration may
go on to perforation. The dura mater always forms one layer of the sac.
Etiology. — Nothing is known concerning the etiology of the hydrorachis
which accompanies spina-bifida.
Symptoms. — The symptoms of hydrorachis are obscure. It may cause
pressure on various parts of the cord and cause paresis or absolute paralysis
and wasting of the muscles. When associated with spina-bifida, the tumor
is the diagnostic symptom. If the effusion is in the central canal and the
cord is thus implicated, the lower limbs are usually paralyzed as well as the
bladder and the lower bowel. Convulsions, spinal inflammation, or rupture
of the sac with escape of its contents, usually precede death, which usually
occurs within a few weeks after birth. When the fluid oozes away gradu-
ally, relief follows ; spontaneous and complete cure may then occur, the
tumor contracting to a small nodule, and the aperture in the canal closing
more or less completely. When the dropsy is external to the cord and the
skin thick, the tumor may increase in size without causing serious disturb-
ance, and may even reach the size of a child's head, and life be prolonged
twenty or thirty years.
Other forms of arrested development often accompany spina-bifida.
Prognosis. — It is very rare for patients with spina-bifida to reach puberty.
The majority of cases terminate fatally a few days or weeks after birth.
The prognosis is favorable when the base of the tumor is narrow, the skin
over it thick and normal, and when it is situated in the sacral region.
Treatment. — The process of spontaneous cure has been successfully imi-
tated by small tappings, frequently repeated, and followed by light com-
pression. Only a small portion of the fluid should be withdrawn at any
operation, and the puncture should always be made at the side of the
1034 DISEASES OF THE NERVOUS SYSTEM.
tumor so as to avoid injury to nerve-trunks. Cases have been successfully
treated by the injection of small quantities of iodine.
Other opersitive measures, such as compression of the neck of the tumor
by means of a clamp or ligature, and excision, have occasionally been em-
ployed with success ; but no such attempt should be made except when the
tumor has a very narrow base, and is situated over the sacrum,
FUN^OTIONAL DISEASES OE THE NEKVOUS SYSTEM.
I shall consider under this head —
I. Epilepsy. XI, Paralysis Agitans.
II, Hysteria. XII. Localized Spasm and Paralysis.
III. Hystero-Epilepsy, XIII, Chronic Lead Poisoning.
IV, Catalepsy. XIV. Chronic Mercurialism.
V, Neurasthenia. XV, Vertigo.
VI. Chorea. XVI, Neuralgia.
VII. Sunstrohe. XVII, Megrim.
VIII. Spinal Irritation. XVIII, Eclampsia and Infantile Coti'
IX. Tetanus. vulsions.
X, Facial Paralysis. XIX, Sea-sickness.
EPILEPSY.
Epilepsy is a chronic functional disease of the nervons centres marked by
sudden signs of temporary loss of consciousness or some other mental dis-
turbance, accompanied by tonic or clonic convulsions,^
In its, typical and fully developed form the disease has received the name
epilepsia gravior, or le haul mal, and when mild and incomplete is called
epilepsia mitior, le petit mal, or epileptic vertigo.
Morbid Anatomy. — Diiferent portions of the nervous system have been re-
garded as the seat of lesions which may cause epileptic seizures. Some have
located these lesions in the convolutions of the hemispheres, the ganglia
at the base, or the pons and medulla oblongata. Others have claimed that
all the nervous centres are involved. Death has occurred in some cases dur-
ing an epileptic seizure in which no change was discovered at the autopsy
except cerebral hypergemia. Many pathologists claim that the vaso-motor
centre in epileptics is so easily excited that slight impressions result in ar-
terial spasm producing angemia of the brain, Brown-Sequard states that
the true seat of epilepsy is in nerve cells having the power of producing
muscular contractions, and that these cells are located chiefly at the base
of the brain. Experiments on animals show that epileptiform convulsions
may be produced by irritation of the skin after the removal of the brain
and cerebellum.
The pathology of epilepsy is still obscure, and no uniform, constantly
1 In ionic convulsions the muscles involved remain in continuous contraction; in clonic the spasmodic
movements are of short duration, alternating with periods of relaxation.
EPILEPSY. 1035
recurring histological changes have as yet been discovered. Russell Rey-
nolds sums up its pathology as follows :
I. The seat of primary derangement is the medulla oblongata, upper por-
tion of the spinal cord, and vaso-motor system of nerves.
II. This derangement consists in an increased and perverted readiness of
action in these organs ;' the result of such action being the induction of
spasm in the contractile fibres of the vessels supplying the brain, and. in
those of the muscles of the face, pharynx, larynx, respiratory apparatus,
and limbs generally. By contraction of the vessels, the brain is deprived
of blood, and. consciousness is arrested ; the face is, or may become, pale by
being deprived of blood. ; from contraction of the muscles mentioned there
is arrest of respiration, the chest walls are fixed, and the other phenomena
of the first stage of the attack are brought about.
III. The arrest of breathing leads to the special convulsions of asphyxia,
which are in direct proportion to the completeness and continuance of the
asphyxia.
IV. The subsequent phenomena are those of poisoned blood, i. c, of
blood poisoned by the retention of carbonic acid, and altered by the absence
of a due amount of oxygen.
V. The primary nutrition change which is the starting-point of epilepsy
may exist alone, and epilepsy be an idiopathic disease.
■VI. This change may be transmitted hereditarily.
VII. It may be induced by conditions acting upon the nervous centres
directly, such as mechanical injuries, overwork, insolation, emotional dis-
turbances, excessive venery, etc.
VIII. The nutrition change of epilepsy may be a part of some general
metamorphosis, such as that present in the several cachexiae, rheumatism,
gout, syphilis, scrofula, and the like ; and further, it may often be asso-
ciated with change in the cortical substance of the cerebral hemispheres.
IX. It may be induced by unknown circumstances determining a rela-
tive excess of change in the medulla during the general excess and per-^
version of organic change occurring at the periods of puberty, pregnancy,
and dentition.
X. It may be due to diseased action extending from contiguous portions-
of the nervous centres or their appendages.
XI. The so-called epileptic aura is a condition of sensation or of motion
dependent upon some change in the central nervous system, and, like the
paroxysm, is a peripheral expression of the disease ; not its cause. Paraly-
sis of the cerebral blood-vessels and resultant hyperasmia of the medulla is
a constant change in a severe epileptic seizure.
Etiology. — Thirty per cent, of epileptics give a history of an inherited
tendency, either to epilepsy or some neurosis ; and children of consanguin-
eous marriages are often epileptics. It most frequently develops between
the ages of ten and twenty. The next most frequent period is between the
' Gowers thinks that loss of inhibitory function of the nerve cell is far more likely than increased irri-
tability. For a complete and exhaustive summary concerning pathology and pathogenesis, vide Hugh-
lings- Jackson, Medical Times and Gazette, 1879, vol. i., p. 233.
1036 DISEASES OF THE NEEVOUS SYSTEM.
second and the tenth year. In a small number of cases it exists at, oi de-
velops immediately after birth.' Sex appears to have no influence, except
in hereditary epilepsy, which develops earlier among girls than boys.^ That
puberty is an exciting cause of epilepsy is a fact accepted by the majority
of authorities. Irritation of some portion of the nervous system is its fre-
quent exciting cause, such as injury to peripheral nerves, the skull or
meninges, and diseases of the brain substance.^ Sunstroke has induced it.
Epileptiform seizures are not infrequent symptoms of disease of different
portions of the nervous system. Among its nervous causes, excesses in
venery and onanism have undoubtedly been over-estimated.
Among its psychical causes are great anxiety, grief, mental overwork,
and long-continued depressing emotions. Sympathetic epilepsy is claimed
to arise in children from dentition and intestinal irritation. It may arise
from irritation of the genitals, anomalies of menstruation, and phimosis.
Blood changes are also enumerated as among its causes.*
Symptoms. — The phenomena of epileptic seizures differ so widely that it
is impossible to give a description which will answer for all cases. Epilep-
sia gravior may or may not be preceded by premonitory symptoms. If
present, these warnings may precede the seizure for a day or only for two
or three minutes. The epileptic aura of Galen, the sense of a mist or va-
por rising from the feet, occurs only in rare instances. Under the head of
prodromata are included changes indisposition, moroseness and irritability,
cold feet, spasm of certain muscles, epistaxis, headache, vertigo, a marked
increase or decrease in the sexual appetite, optical illusions, hallucinations,
involuntary discharge of urine and faeces, great somnolence or insomnia,
darkening of the skin, changes in the appetite, cardiac palpitation, cardi-
algia, vomiting, abundant flow of tears, and excessive secretion of saliva.
Sometimes the attack is preceded by a definite sensation referred to the
head, stomach, or limbs. Drawing the head toward one shoulder is some-
times a warning of an epileptic seizure. In the majority of cases prodro-
mata are absent, and the onset of the fit in a typical attack is sudden and
attended by complete loss of consciousness. Uttering a loud, sharp cry,
the epileptic falls heavily, or sinks to the ground. The face is extremely
pale immediately before and at the time of the seizure, and there may be
tonic spasm of the muscles of the eye and face. The pupil is invariably
dilated at the onset. Tonic spasm of all the muscles immediately occurs ;
the eyes are fixed and staring, and the muscles of the face, trunk, and ex-
tremities are rigid. Opisthotonos or emprosthotonos may occur, or the
body may be bent sidewise. The face soon becomes dark, the veins tur-
gid, and though the carotid pulsates strongly the radial pulse is weak.
Respiration is impeded and asphyxia rapidly develops, until after a few
seconds — rarely over a minute — clonic convulsions succeed the tonic spasms,
1 Reynolds and Echeverria state that hereditary epilepsy does not develop later than the twentieth
year.
2 Brown-Sequard states that after the twenty-fifth year women are attacked oftener than men.
3 Wostphal {Berlin. Kiin. Wochen.) has shown that in guinea-pigs blows on the head may immediately
give rise to epileptiform attacks ; and that on pinching the skin of the epileptogenic zone several weeks
after, convulsions will occur.
■* Gowers states that rickets causes it, through defective nutrition of the nervous system.
EPILEPSY. 1037
which, though general, are usually best marked upon one side. Sensation
is usually wholly lost, and onJy in rare cases can reflex action be excited.
The unconsciousness still continues. The muscles contracting and relaxing
in quick succession induce the most violent contortions. The tongue is
thrust between the teeth, which, closing ujion it, cause deep indentations
or lacerations of its edges. The teeth are sometimes In-oken ; bones may be
fractured or dislocated, and muscles torn- from their attachments. The
patient froths at the mouth, and, from the injuries to the tongue, the sal-
iva is often bloody. The body is bathed in a profuse (sometimes very
fetid) sweat, and frequently the contents of the bladder, bowels and vesic-
ulaB seminales are forcibly ejected. All secretions are abnormally increased.
The breathing is forcible, irregular, and rapid, and the auxiliary muscles
are called into play ; the face is turgid and distorted, the eyes protrude,
the pupils are alternately dilated and contracted, inspiration is accompanied
by loud gurgling noises, the pulse becomes full and labored, and when the
cyanosis reaches its maximum the paroxysm, which seldom lasts longer
than one or two minutes, begins to abate.
The fit may terminate suddenly or gradually. If it subsides gradually
the spasms become less violent and frequent, the respiration quieter and more
regular, and the jDatient passes into a comatose state. Consciousness grad-
ually returns, and the patient appears as if waked out of a deep sleep. He
recovers rapidly or remains confused, delirious, or maniacal for hours. A
day may elapse before complete recovery is reached. The patient has no
recollection of the attack. The degree and duration of stupor after an at-
tack have no relation to the duration of the convulsive period. A_ slight
seizure may be followed by great mental disturbance, and vice versa.
Marked dicrotism of the pulse often occurs as the patient is recovering c-on-
sciousness ; and for twenty-four hours the ophthalmoscope shows hyperse-
mia of the fundus oculi. The urine after the' attack is increased in quan-
tity and contains an excess of urea and phosphates.
Brown-S6quard gives the accompanying table of the causes and effects of
an epileptic attack:
Cause. Effect.
T. Excitation of certain parts of I. Contraction of blood-vessels of
the excito-motor organs of the nerv- the brain and face ; tonic spasm of
ous centre. the muscles of the eye and face.
II. Contraction of the facial blood- II. Facial paleness,
vessels.
III. Contraction of the blood-ves- III. Loss of consciousness, con-
sels of the cerebral lobes. gestion of the base of the brain and
the spinal cord.
IV. Extension of the excitation IV. Tonic contraction of the
in the excito-motory organs of the laryngeal, cervical and some respira-
nervous centre. tory muscles (laryngismus and trach-
elismus).
1038
DISEASES OF THE iSERVOUS SYSTEM.
Cause.
Y. Tonic contraction of some re-
spiratory and vocal muscles.
VI. Further extension of the ex-
citation in the excito-motory organs.
VII. Loss of consciousness alone,
or with tonic spasm in trunk and
limbs.
VIII. Laryngismus, trachelismus
and rigid spasm of some respiratory
muscles.
IX. InsuflBcient breathing, rapid
consumption of oxygen, and deten-
tion of venous blood in the encepha-
lon.
X. Asphyxia and perhaps pressure
by accumulated venous blood in the
base of the brain.
XI. Exhaustion of the nervous
power generally, and of the reflex
excitability, especially return of reg-
ular respiratory movements.
Effect.
V. Epileptic cry.
VI. Tonic contraction reaching
most muscles of trunk and limbs.
VII. Fall or precipitation, forward
or backward, to the ground.
VIII. Insufficient breathing ; ob-
stacle to entrance of blood into the
chest and to its issue from the cra-
nio-spinal cavity.
IX. Increasing asphyxia.
X. Clonic convulsions everywhere:
contractions of the bowels, the blad-
der, the womb, increase of secretions,
efforts to inspire.
XI. Cessation of the fit, coma, or
fatigue, headache and sleep.
Le petit mal, or epilepsia mitior, is a momentary loss of consciousness; the
patient while about his usual avocations suddenly stops, or drops whatever
he may hold, has a fixed gaze for a second or two, and upon coming out of
such a faint or blank proceeds as if nothing had happened. Sometimes
these blanks may be accompanied by vertigo, and then the patient will
stagger slightly. In rare cases he proceeds mechanically with what-
ever is occupying him during the paroxysm. He often pales for a
few minutes and then grows red in the face. The pupils are somewhat
dilated. The mind may be distinctly confused for a long period after such
an attack. Sometimes momentary spasmodic contractions occur in the
muscles of the face, tongue, throat, eyes and neck. The head is turned
slightly to one side and the face is pale. Clonic spasms never occur.
There may be slight cyanosis when the diaphragm and respiratory muscles
are involved. Sometimes certain fingers, or part of one extremity, suffer
transient spasm.
The variations from the typical phenomena of an epileptic seizure are so
numerous that it is impossible to give them in detail ; I shall only refer to
those which are of common occurrence.
Sudden tonic spasm of the facial and thoracic muscles may be followed
by a clonic convulsion without any loss of consciousness. An attack may
be marked by such motor activity that the patient runs or walks rapidly
EPILEPSY. 1039
during a period of complete unconsciousness. Sometimes maniacal excite-
ment talies the })]ace of the fit.' In this delirium lu epileptic may be
haroiless and wanders around in a dazed condition ; or be exceedingly-
dangerous to those about him. Kleptomania and dipsomania are said to
be exhibitions of epileptic delirium. Brown-Sequard describes nocturnal
attacks of epilepsy that not infrequently occur without the knowledge of
the person so affected. In such cases the individual on wakmg is tired
and exhausted; he has pains in the limbs, back and head, his mind is con-
fused and his memory enfeebled ; he is disinclined to exert himself, and
remains during the day in a confused state. His tongue shows the indents
of the teeth, and the pillow may be blood-stained. More rarely it is found
that an involuntary discharge of urine has occurred. Such attacks, al-
though frequent and violent, may remain altogether unknown and unsus-
pected by the patient or his friends.
Between the paroxysms the condition of epileptics varies greatly. In
the majority there is no impairment of mental or physical condition ; not
infrequently, however, there is depression of nervous vitality and mental
activity. Of all the abnormalities met with, sub-normal temperature is the
most common.'^ Of the mental faculties, memory is most often impaired.
Women show mental disturbances more frequently than men. The earlier
epilepsy commences the less liable are mental changes to occur ; and the
mental deterioration is in inverse ratio to that of muscular disturbance.
The most remarkable mental phenomena are those which constitute the
so-called epileptic mania. Epileptics are frequently gloomy, capricious
and irritable, all the finer psychical functions are dull, acquisition of new
ideas is difficult, and hypochondria, melancholia and imbecility may occur
as late exhibitions of the disease. Motor disturbances, such as tremors
and clonic or tonic spasms, ai'e not infrequent between the paroxysms.
Epilepsia major is more common than epilepsia mitior, and hereditary ten-
dencies seem to predispose more to the former than to the latter.
As regards frequency of attack there is the widest range : the first fit may
also be the last ; they may occur once a year, or two or three times in the
twenty-four hours. In "women it sometimes seems to be connected with the
menstrual epoch. Eighty per cent, of all epileptics are attacked oftener
than once a month ; sometimes paroxysms occur on days that are multi-
ples of seven. Often three or four fits occur in a day, and then ensues a
period of immunity. When the seizures follow one another so closely as
to leave no rest,^ we have the status epilepticus, in which the temperature
may rise to 108° F., or higher as death approaches. If the patient re-
covers, bed-sores are liable to be formed. Pneumonia and pulmonary
oidema are apt to occur in this condition. Seizures of petit mal are usually
verj xVtr^fUtJkt. All the different forms may occur in the same individual.
Differential Diagnosis. — An epileptic seizure may be confounded with
1 Delirium epilepticum.
2 Brown-Sequard, in Quairi's Dictionary, states that the health is very poor, an. opinion antagonistic to
all other anthorities.
3 In Delasianre's case there were twenty-five hundred attacks in one month in a.boy of fifteen. — Traite
de V Ejnlepsie, Paris, 1854.
1040 DISEASES OF THE NERVOUS SYSTEM.
cerebral apoplexy and hysteria. It is often difficult to distinguish le petit
mal from an attack of syncope.
Convulsions from urmmia, opium poisoning, or alcohoUsmus are at-
tended by coma as the chief event, and are, each of them, accompanied
by such peculiar signs, or urinary conditions, and give such a definite
previous history, that they will not long be mistaken for an epileptic
seizure.
In the convulsions of children caused by dentition, falls, and gastric
disturbances there is not complete loss of consciousness ; the fit is of
shorter duration than an epileptic paroxysm, is longer in coming on, and
IS not followed by stupor. The discovery of a cause of the seizure is an
argument against epilepsy.
Convulsions from organic brain-disease, tumors, chronic softening, men-
ingitis, and sclerotic processes are distinguished by the attendant inter-
paroxysmal symptoms, viz. : pain, mental aberration of various kinds,
paresis or paralysis, and disorders of special senses. In other words, a con-
vulsion is a part only, and not the chief part, of the symptoms ; whereas a
paroxysm is the prime event in epilepsy. Moreover, the previous history,
the slowness of invasion, and the absence of subsequent stupor in organic
brain disease will confirm the diagnosis.
Hysterical convulsions are always preceded by hysterical symptoms ; voli-
tional power is diminished, the fits come on gradually, the pupils are not
dilated, there is no frothing at the mouth, loss of consciousness is not com-
plete, tonic and clonic spasms alternate, stupor does not follow, and the
subsequent hysterical mania has its own peculiarities. The attack is always
followed by a profuse flow of pale, limpid urine.
Syncope differs from le petit mal in that the loss of consciousness is not
sudden, is always preceded by a weak, faint, sickening sensation, recovery
is slow, and the patient recollects the details of the syncope. Loss of con-
sciousness is usually longer in syncope than in epilepsia mitior.
Malingerers overact their part, the conjunctivae retain their sensibility,
and the size of the pupils and the color of the face are both normal.
Prognosis. — Epilepsy rarely directly causes death. But its long duration
and the suddenness of its onset make it a dreaded disease. About two to
five per cent, undergo spontaneous cure.' The curability of the disease
diminishes with its duration. Inherited epilepsy is rarely recovered from.
Epilepsy beginning before the twentieth and after the fiftieth year fur-
nishes the best prognosis. Reynolds states that the more obscure the
origin the worse the outlook. Alcoholismus always renders the prognosis
worse.
Treatment. ^The two things to be accomplished in the treatment of
epilepsy are, if possible, to remove the cause or render it inoperative ; and
to diminish the number, length and severity of the paroxysms.
When aurcB exist it may be possible to abort the fit by tying a hand-
kerchief around a limb, pinching or rubbing the surface, irritating it by
means of cold or galvanism, and pricking it with needles. When muscular
i Nothnagel.
EPILEPSY. 1041
contraction precedes a Qt, forciblt/ axcitmg the contracting muscles or a
blow on them will sometimes prevent the convulsions. When disturbances
of respiration precede a paroxysm, inhalation of ether, chloroform, or amyl
nitrite may abort it. An emetic, purge, a hypodermic of morphia and.
atropia, ice to the nape of the neck, hot water to the extremities, valerian,
belladonna, a large dose of chloral hydrate, breathing very fast, running,
reading very rapidly and loudly have all been found in some instances to
abort epileptic paroxysms. Reynolds advocates the administration of dif-
fusible stimulants. When an epileptic fit is once established there is little
to be done but to prevent the patient from injuring himself. The chest
and neck should be freed from close-fitting garments, and if possible a
piece of rubber or cloth should be inserted between the teeth.
The measures employed for the cure of epilepsy are innumerable. Tre-
phining over cranial depressions, operations for phimosis, excisions of
cicatrices, removal of neuromata, opening of abscesses, ligating the caro-
tids, application of caustics to the throat, and tracheotomy have all been
undertaken for its cure. Since epilepsy is a neurosis, different drugs must
not only be employed with different individuals, but the doses must be
varied in different cases. The bromides have the most extensive reputa-
tion, and at the present time are more used than any other remedy. They
should be given in large doses and continuously for a long period, and only
discontinued temporarily when the symptoms of bromism appear. Sixty
grains of bromide of potassium a day in divided doses is the usual amount
to commence with; it may be gradually increased until one hundred grains
a day is administered. It is best to commence with the bromide of potash,
the bromide of ammonium, iodide and bicarbonate of potash in a strong,
bitter infusion — I prefer hops. With the bromides the oxide of zinc,
strychnine, arsenic or atropia may be given.' Oxide of zinc (one and
one-half grains a day at first, increasing to five grains per diem), especially
with valerian root, or belladonna, or hyoscyamus, is regarded as next in
efficacy to the bromides. Atropine and ammoniated sulphate of copper
are regarded by Brown-Sequard as forming a most powerful comjDOund in
idiopathic epilepsy. The same authority ranks next in order the cotyledon
umMlicus, silver nitrate and bromide of zinc. Whenever there is a weak
pulse, the sesquicarbonate of ammonia must be substituted for the bromide
of the same salt in the combination treatment."
In mild epilepsy, or le petit mal, large doses of bromide of ammonium
should be administered until a condition of bromism is reached. Cod-liver
oil is especially useful in this form of epilepsy. Iron is only to be used — and
then as the citrate — in the anaemic or cholorotic. Manganese is often ser-
viceable here. External applications such as setons, issues, inunctions,
croton oil, blisters, or the actual cautery to the nuchal region, have been
extensively used without satisfactory results. Galvanization of the sympa-
1 Echeverria recommends conium, and Clonston the Indian hemp.
2 Belladonna Is recommended by Trousseau is one-fifth grain of the extract daily for the first month
to be gradually increased until from one to two grains are taken daily.
1042 DISEASES OF THE NERVOUS SYSTEM.
thetic is strongly recommended by some.' Epileptics should lead a life
free from mental excitement or physical excess. '^
HYSTEEIA.
Hysteria is a functional disorder of the nervous centres, affecting pri-
marily the psychical faculties, especially the will, reason, imagination and
the emotions ; and secondarily both the motor and sensory tracts, in which
the protean manifestations at different times indicate abolition, exaltation,
and perversion of functional activity of the nervous centres.
Morbid Anatomy. — Hysteria has no pathological changes or morbid
anatomy. The special functional disturbance is generally considered to be
an exalted irritability of sensory centres and peripheral expansion, which
results in an acquired, or is associated with a congenital, neurasthenia,
most marked in the higher centres, but extending to those controliing auto-
matic movements, and characterized by partial or complete suspension of
inhibitory influence.^ It is quite possible that in many cases the centric
neurasthenia may be the primary condition and the cause of the exalted
irritability.*
Etiology. — Hysteria affects females principally ; usually making its ap-
pearance between the ages of puberty and thirty years. Over one-fourth
of the cases occur between the ages of twenty and thirty ; a little less than
one-fourth between the ages of fifteen and twenty ; and about one-sixth be-
tween the ages of ten and fifteen. It is rarely developed after the meno-
pause, although it frequently occurs jast at the climacteric. It is most
liable to occur in women of a neuropathic tendency and in members of
families in which epilepsy, chorea, catalepsy, and insanity have occurred.
Anything which affects the emotions powerfully, such as fright, anger,
jealousy, grief, and disappointment, predisposes to its development, and
secret nursing of imagined wrong or anxiety is especially liable to induce it.
Sexual abuse, masturbation, onanism and premature cessation of ovulation
;are at times exciting causes of hysteria. Its relation to uterine and ovarian
disease is direct and well established,^ but is by no means constant, as many
patients with severe ovarian disturbances remain entirely exempt from hys-
terical phenomena. Hysteria is undoubtedly oftener met with in the single
than in the married, and is intensified by the menstrual epoch. Occupa-
tion and position in life have much to do with its production. Women
who lead a life of continual excitement are more prone to hysteria than any
1 Nothnagel recommends methodical hydrotherapeia for three or four months, especially in cases that
are not inveterate.
2 Reynolds advocates quinine, but Brown-Sequard considers it' highly injurious, stating that malarial
disease in epileptics is better treated by arsenic. Recently Lepine has had success from bleeding and
depletion. Kunze reports radical cures from subcutaneous injection of curare ; Vallender from apomor-
phia. Govcers, in Gulstonian Lectures., says borax deserves a trial when bromide fails. Very recently
picrotoxine and cocculus indicus have been tried and found to produce — especially the former — most bene-
ficial effects.
3 Jolly and Buzzard.
* Rosenthal states that the vaso-motor system is also involved, and that spasm of the cerebral arteriee
and consequent anaemia are often present in hysterical paroxysms.
fi Charcot claims that hysterical fits can be produced by firm pressure over the ovaries.
HYSTERIA. 1043
other class. Among savage nations and hard-working women it is unknown
or rare. It is said that since the blacks have been freed and their education
and condition bettered, hysteria, previously unknown, has appeared among
them.
It not infrequently becomes epidemic, and is apparently contagious.
Symptoms. — The symptoms of hysteria are manifest through all the
nervous phenomena, and may be grouped as psychical, motor, sensory and
sympathetic.
I. In many cases mental and moral disturbances appear only during the
attack, and the patient has full control of the mental powers in the inter-
vals. More frequently, and when the condition has become chronic, the
patients are constantly irritable and excessively emotional. As a rule their
judgment, energy, and concentration are enfeebled, and although their
memory is not aHected the will-power is greatly impaired. During their hys-
terical paroxysms they always want an audience ; they crave attention and
sympathy, and will at all times deceive and practise most dishonest meas-
ures to obtain them. Their emotions pass beyond their control, tears and
laughter being apparently always at their command. Hallucinations and
various kinds of fancies and delusions are common.
After a violent fit of hysteria, patients often become dangerously un-
manageable, mischievous, and highly abusive or blasphemous. The coma
that follows an attack is like a deep sleep, and may last for hours or days.
More or less analgesia is present, but complete unconsciousness never oc-
curs. Probably a so-called ''trance" is but prolonged hysterical coma.
Ecstasy and somnambulism, temporary catalejDsy and trance, are all
reckoned by some among chronic hysterical psychoses.'
II. The motor symptoms of hysteria are very varied. Globus hysteri-
cus is the most common ; the patient imagines that a lump rises from the
epigastric region into the throat and remains there causing a sensation of
choking. Spasm of the respiratory muscles produces peculiar, harsh,
rasping, expiratory sounds, and the inspirations are prolonged, rapid, and
whooping in character, accompanied by yawning, hiccough, laughing,
crying, and sneezing. There is a loud, barking, brassy cough (the hyster-
ical cough), but no expectoration. The patients claim that all voluntary
movements are impossible ; they cannot rise or move from their beds — yet
they gesticulate wildly and perform irrational movements in excess. The
facial muscles are in constant action. Reflex action is so exaggerated that
the slightest irritation produces spasms. Clonic spasms of muscles of the
face and cervical region and of the muscles of the thigh are common.*
Tonic muscular spasms in the limbs are frequent, often lasting for months;
they may suddenly disappear, but these contractions resist the influence
of chloroform and persist during sleep. Abdominal phantom tumors are
thus produced, but long-continued Faradization will reduce them. When
the tonic spasms affect, as they may, portions of the alimentary canal,
1 Griesinger and Briquet.
' Rhythmical contraction of the thigh muscles induces an apparent pulsation which may be mistaken for
that of aneurism.
1044 DISEASES OF THE NERVOUS SYSTEM.
vomiting, griping pains, borborygmi, eructations, diarrlicea or constipa-
tion, and dysphagia occur. Ketention of urine and great distention of the
bladder may happen. In rare instances the secretion of urine is almost
entirely suppressed. ' In hysterical hemiplegia the face and tongue are not
involved. While walking, hysterical patients look about, whereas a true
paralytic keeps his eye on his feet. The paraplegia may be complete and
the patients unable to walk, but their limbs are perfectly well nourished
and they can regain the upright position loithout assistance. Hysterical
is distinguished from organic aphasia by the fact that the patient is able
to write his wishes with the greatest readiness. Hysterical aphonia comes
on abruptly, and as abruptly disappears. When an hysterical patient has
a convulsive seizure the globus hystericus precedes the fall, which always
takes place where there is no chance of injury. The patients often talk
continuously and incoherently during their convulsive seizure, and throw
themselves into the most grotesque attitudes. Complete loss of conscious-
ness rarely if ever occurs. The pupils are not dilated, and no respiratory
symptoms are present sufficient to cause asphyxia.^
III. Derangements of sensibility form one of the most common exhibi-
tions of this disease. Local or general hypersesthesia is never entirely
absent ; it is sometimes evinced by increased acuteness of the senses.
Photophobia is common. The sense of touch is so exaggerated that hys-
terical women will recognize individuals by the touch ; the olfactory sense
is also exceedingly acute, and patients are disturbed by the slightest noise
and can recognize friends by their step at a long distance. Muscse voli-
tantes, tinnitus aurium, pains and neuralgias in various parts are all com-
mon. The pains complained of are greatly in excess of any discoverable
cause, and cease when the attention of the patient is diverted. The pain
often simulates left intercostal neuralgia or is situated over the vertebral
spines or stomach, in the Joints, mammae, skull or the iliac regions. Pain in
the skull, as if a nail were being driven into the bead, or a kettle were
simmering on top of it, called by the ancient physicians clavus hystericus,
is by many regarded as pathognomonic. The whole cutaneous surface
may be hypersesthetic, or only parts of it. Sometimes there are ob-
served hysterical angina pectoris and hysterical peritonitis. All the
senses in an hysterical patient are abnormally acute. The genital organs
are often so sensitive that sexual intercourse is impossible. On the other
hand, anassthesia is of frequent occurrence in hysterical persons ; it may ap-
pear in any part of the body and be limited to a distinct portion of a single
nerve. The anassthetic parts are usually pale and their temperature sub-
normal. Anaesthesia may be superficial or so deep that pins can be thrust
into the deep tissues without any expression of pain. The conjunctiva
loses its sensitiveness and may be rubbed or touched without causing con-
tractures of the lids. There may be coexistent loss of sensibility in the mus-
cles, bones, and joints.^
* T. Buzzard in Qiiain's Diction, of Med.
2 Hnghlings- Jackson advances the hypothesis that inhihitory control of the spinal cord over reflex action
is temporarily suspended, the cerebellar influence having full play.
3 Jolly.
HYSTEEIA. 1045
In some instances the pharynx and epiglottis may be tickled or pinched,
or irritating vapors inhaled without producing the customary results.
Large faecal accumulation in the rectum is presumably due to similar
anaesthesia of its mucous membranes. There may be hemiopia in one or
both eyes, accompanied by loss of smell, taste and hearing. Sensations as
if a limb or part were greatly enlarged or attenuated, as if the feet were
being buoyed up or loaded with lead, or as if pins and needles were being
thrust into the waist are of common occurrence.'
IV. Of the circulatory changes, cardiac palpitation is perhaps the most
common. Feeble heart action, with a small and hard, or a full and soft
pulse, is frequently noticed during hysterical fits. The abdominal aorta,
and sometimes other arteries, pulsate so strongly as to suggest aneurism. Ac-
cording as there is stimulation or paralysis of the vaso-motor nerves there
will be a cold, pale surface or hypersemia, redness, and consequent profuse
sweating. Coldness of the extremities is one of the most common evidences
of vaso-motor change. The dilatation of the vessels may become so great
that hemorrhages will occur in the skin, internal organs, genitals, and
stomach. It is often difficult to diagnosticate hysterical bsematemesis from
that due to ulcer. A single observation is rarely sufficient for a diagnosis.*
The following hysterical phenomena are all undoubtedly due to vaso-motor
disturbances, viz. : fever and chill, flashes of heat alternating with rigors,
hyperesthesia, enlargement and oedema of the joints,'-' an abundant flow of
pale, clear urine deficient in salts, excessive salivation, abnormal dryness
of the mouth, increased flow of gastric juice, an abundant secretion of
milk, lasting for years,* and profuse uterine and vaginal secretions.*
Differential Diagnosis. — Hysteria may be mistaken for epilepsy, multiple
sclerosis of the hrain and spinal cord, hypochondria, neuralgia, and urcemic
coma. It is distinguished from ejnlepsy by its slow onset, by incomplete
coma, a normal pupil, sobbing and crying, and absence of subsequent
stupor. The tongue is not bitten in hysteria. An epileptic seizure is short
and the convulsions are not symmetrical.
Multiple sclerosis of the train and cord is often accompanied by parox-
ysms like those of hysteria ; but between the attacks the psychical symptoms
and emotional disturbances are absent.
In hypochondria the patient is always morose ; there are not those varia-
tions in temper that are so characteristic of hysteria. Hypochondria is rare
before the thirtieth year, is more common in men than in women, and is
geldom marked by convulsions. The two diseases may be conjoined.
J Charcot notices that with hemi-ansesthesia there is usually ovarian hyperesthesia of the opposite
side.
2 Astley Cooper and Parrot record cases where hemorrhages have occurred from the breast and con-
junctivfe.
= Brodie.
* Briquet.
* Lasegue has described, under the name of hysteria peripherique, a group of cases of considerable in-
terest, in which, although the patients do not exhibit the general hysterical temperament, the slightest
peripheral irritation causes obstinate muscular spasms. Such are certain cases of rheumatic torticollis
and of blepharospasm from slight and passing irritation of the conjunctiva. Lasegue says : "The tran-
sition from the typical hysteria to the other (functional) diseases of the nervous system is not abrupt, but
by imperceptible gradations."
1046 DISEASES OF THE NERVOUS SYSTEM.
The comatose state following an hysterical seizure is distinguished from
urcemia by an examination of the urine, by the fact that dropsy is ab-
sent ; and the coma is preceded by sobbing, crying, and other hysterical
phenomena.
Neuralgia, if of hysterical origin, ceases when the patient's attention is
diverted. In genuine neuralgia the pain follows the distribution of a nerve,
and there are certain recognizable painful spots ; in so-called hysterical
neuralgige the reverse is the case.
Organic paralysis is to be distinguished from hysterical paralysis by the
plumpness of the limb or part m the latter, and the electrical reaction,
which is normal.
Prognosis. — The prognosis in hysteria is always favorable, although re-
covery is rarely permanent, but exacerbations and remissions occur at ir-
regular intervals. Some develop every phase of the disease at different
epochs. Its tendency is to cease after the menopause, but it may continue
to old age. Briquet states that when it commences in youth it is more
persistent than when it occurs later in life. If associated with uterine
diseases and displacements, the prognosis is better than when it is purely
psychical. ' When it is constitutional, hereditary, or -an evidence of the
neuropathic tendency, even temporary recovery is rare.
The hysterical contractures, when prolonged, often cause permanent de-
formities.
Treatment. — Moral treatment is far more efficacious than medicines.
Discipline, exercise in the open air, healthy occupations, early hours, and,
if possible, a change of residence, all exercise a marked influence on
hysterical subjects. Bromide of sodium or potassium, valerian, asafoetida,
belladonna, hyoscyamus, and hydrate of chloral are all at times of service
in controlling the more active manifestations of hysteria. When a cause
can be reached it should, if possible, be immediately removed ; and uterine
diseases and displacements must receive their appropriate treatment. Iron
should be given when anaemia exists. Many authorities state that half
their cases have been cured by the use of o^Dium, and all agree that hys-
terical patients tolerate it in large doses. The attacks may generally be
shortened by dashing cold water over the patient, and sometimes by pres-
sure over the ovaries. Subcutaneous injections of morphine, or inhalation
of ether or chloroform until complete insensibility is reached, are sometimes
advisable when the seizure is very violent.^ In tympanitis and colic,
enemata of asafoetida are useful. Hysterical vomiting, often very ob-
stinate, is best treated by the blandest possible diet. In paralyses of
hysterical origin electricity and the internal use of strychnine are some-
times of service. Hysterical pains are most efficiently relieved by hypo-
dermic injections of morphine. Aphonia may be treated by the elec-
tric current. Sea-baths or a course of hydrotherapy are often highly
• Wunderlich and Rullier describe cases of acute fatal hysteria with high temperature, great dysphagia,
and frequent epileptiform convulsions.
''Reynolds, quoting Dr. Hare, states that forcibly preventing the patient from breathing for a certain
time, by holding the nose and mouth, is followed by a long breath and a relaxation of the spasm.
HTSTERO- EPILEPSY. 1047
advantageous to hysterical subjects. Phosphorus and strychnine are re-
garded by some as specifics, and may be given in small doses. Children
who are j^eculiar and have a tendency to hysteria, should be subjected to
a firm, gentle discipline during their childhood and period of development.
The manner of the physician, his conversation in the presence of the pa-
tient, the behavior of the friends and family both during and between the
paroxysms, all have a great influence upon the case.
HYSTEEO-EPILEPSY.
This is a very grave form of hysteria, attended by epileptiform convul-
sions and marked by the occurrence of peculiar anaesthesia, paralysis, and
muscular contraction. It has no especial morbid anatomy.
Etiology. — Epilepsy may be the primary disease, and some strong psy-
chical disease superinduce hysteria ; or epilepsy may slowly develop after
long-continued hysteria. The etiology is the same as that of hysteria ; but
puberty, the menopause, and extreme fright' are among its most frequent
causes.
Symptoms. — An hysterical aura, usually abdominal, precedes the convul-
sion, which at first is identical with an epileptic seizure. Following the
clonic convulsions is a short period of muscular relaxation, during which
the patient appears comatose, but which is soon followed by contortions of
the most violent character. The motions may intentionally indicate any
or all of the vilest passions or fears, or there may be simply irrational twist-
ings. Opisthotonos usually occurs after the attack, the patient usually
suffering from hysterical excitement, laughing or crying immoderately, and
has hallucinations and delusions resembling those of delirium tremens.
Contractures, either paraplegic or hemiplegic, subsequently occur in one
or more limbs, which may be persistent, and yield only to deep chloroform
narcosis. It is to be remembered that these hysterical contractures may oc-
cur without any other symptoms of hysteria ever having existed, or may
follow burns.^ After a long duration they sometimes relax from a great
moral shock. During such a fit the temperature may rise to 105° F.' Ova-
rian hypersesthesia almost invariably precedes these attacks.^ Anaesthesia
and analgesia are common, but usually affect only one half of the body.
The special senses may all be affected, and color-blindness is not uncom-
mon.
DijBferential Diagnosis. — The diagnosis of hystero-epilepsy in a well-marked
case is easily made. The salient points of hysteria and epilepsy are com-
bined, and the picture of a patient in the fit is one that will not be con-
founded with any other condition.
Prognosis. — The prognosis is the same as in hysteria, and far more favor-
able than in epilepsy.
» The tragedies of the Commune in Paris during the Franco-Prussian war are said to have produced many
severe attacks in hysterical females.
^- Progres Medical, Feb. and March, 188.3.
'^ Charcot.
* Charcot states that ovarialgia is an important part of the seizure.
1048 DISEASES OF THE NERYOUS SYSTEM.
Treatment. — The treatment will require a combination of the remedies
proposed for hysteria and epilepsy in the proportion that each enters as an
element of the disease. Metallo-therapeutics have been extensively em-
ployed in the treatment of this affection. A fevi^ discs of metal are bound
at intervals around an anaesthetic limb ; in ten to twenty minutes sensation
returns to the skin around the discs, and then to the whole limb, but, un-
fortunately, m the mean time corresponding parts on the other limb grad-
ually lose their sensibility, and the results are not permanent. The slight-
est electrical currents produce the same results. Contractures of years'
duration often can be cured or transferred in like manner. Metals, mag-
nets, bits of wood — all have produced the same effect. Different metals
act on different subjects. Gold, silver, iron, tin and copper have all been
used. Long-continued blistering and Faradization have removed contrac-
tures of long standing.
CATALEPSY.
Catalepsy is a functional disease of the nervous system, closely allied to
hysteria and epilepsy. It is characterized by loss of consciousness, sensa-
tion and volition, accompanied by a peculiar muscular rigidity in which
the limbs remain for some time in whatever position they are placed.
There are no appreciable pathological changes, but the muscular rigidity
is generally considered to be of centric origin.
Etiology. — Catalepsy may occur at any age, but is rarely met with except
in females about the age of puberty, and is usually associated with hys-
terical phenomena. It may precede melancholia and epilepsy. Trau-
matism, strong emotions, fright, shock, and, in many instances, religious
excitement may induce an attack. Hereditary influence is frequently
marked, and it occurs in families where insanity, mania, epilepsy, etc., have
occurred. '
Symptoms. — Catalepsy occurs in paroxysms which are either regular or
irregular. Headache, vertigo, hiccough, etc., may precede the attack.
Consciousness is suddenly lost, and the limbs — remaining in the position
occupied at the onset — are as rigid as if petrified, soon relax a little, how-
ever, and can be moved, but will remain in whatever position they are
placed. They resist passive movement as if made of wax, hence the name
flexihilitas cerea. The rigidity slowly yields to the force of gravity. Sen-
sibility and reflex movement may be totally or partially lost ; rarely is
there paroxysmal hypersesthesia. The respiration and heart movements
are weak ; the face is expressionless, and often has a death-like appearance.
The skin is cold, and the temperature is commonly lowered perhaps 2° or
3° below normal. Substances placed in the back of the mouth are slowly
swallowed. In a few cases there is only partial loss of consciousness, the
patient being able to appreciate strong sensorial or emotional impressions.
When the attack is of short duration it vanishes as quickly as it appeared ;
and an impression upon the patient remains like that following a confused
dream. When the attack lasts for many hours or days several paroxysms
1 Eulenburg inclines to the view that malarial infection may cause it.
NEURASTHENIA, 1049
go to make up the whole attack. Between the attacks there are no symp-
toms as a rule. ' The attacks may occur at regular intervals ; tlie slightest
mental disturbance or excitement may bring on a paroxysm.
Differential Diagnosis. — True catalepsy cannot be mistaken ; but it may
be, and often has been, successfully simulated.
Prognosis. — The prognosis is favorable, except in those cases where there
is a marked nervous tendency in the family. The prognosis is best where
there are no symptoms between the attacks.
Treatment. — Treatment should be directed more especially to the accom-
panying hysterical diathesis, but we may endeavor to rouse the patient by
the use of ammonia, snuflp, or the Faradic current. An emetic will gener-
ally cut short an attack. ° The wet pack and the cold douche have been
used. Between the attacks iron, quinine and antispasmodics — valerian
especially — are indicated.
iraUEASTHElSnA.
Neurasthenia spinalis is a functional weakness of the spinal cord; or, as
Eosenthal calls it, a depressed form of spinal irritation.' It is commonly
known as nervous debility. Eolando, Luys and others have advanced views
concerning the cerebellum that may lead to this organ being regarded as
the seat of the disorder. Some authors claim that it is an augemic condition
of the spinal cord, but its morbid anatomy is not as yet determined.
Etiology. — Men are far more liable to this condition than women. It
often develops at puberty, but is common in adult and middle life. It is
most frequent in those of a neuropathic tendency. Sexual excesses, mas-
turbation and onanism are said to induce it. Excessive mental labor, late
hours, long-continued emotional disturbances of any kind, insomnia, insuf-
ficient or improper food, and excessive use of tobacco or alcohol may excite
it in those who are predisposed to neuroses. Rosenthal claims that the pro-
longed action of these causes in the young produces irritability of the med-
ullary and vaso-motor centres, and thus the vascular equilibrium of the cord
is lost.
Symptoms. — These patients are weak, easily fatigued and prostrated by
slight muscular exertion. They are languid and despondent. There is
aching in the limbs, the sleep is broken, or there is actual insomnia, and
they complain that they are always tired and the subjects of nervous debil-
ity. They suffer constantly from dorsal and. lumbar pains and nocturnal
emissions, and the passage of a urethral sound produces excessive pain and
sometimes convulsions. The sexual powers are enfeebled. During excite-
ment or after the use of alcoholic stimulants, neurasthenic patients are able
to perform a large amount of mental labor, but afterwards they are greatly
prostrated. The emotions are easily excited, and. they often imagine that
they are the subjects of some grave organic disease. There is a tendency
1 Eulenburg states that cataleptic children are often remarkably bright. — Ziemsseti's Encyc.
' Gowers advocates the subcutaneous injection of apomorphia — one-twentieth to one-twelfth grain.
' Erb claims that it is not a manifestation of hypochondria, and that, although often combined with It,
it is to be regarded as distinctly of spinal origin.
1050 DISEASES OF THE NERVOUS SYSTEM.
to melancholia and hypochondriasis. Neurasthenia is not at first accom,
panied by anaemia, but later the insomnia and anorexia induce it. The
tongue is coated. Flatulence, dyspepsia, and dilatation of the stomach
are usually ]3resent.
Often the patients have a healthful appearance, which leads one to suspect
that they are feigning disease.
Differential Diagnosis. — Neurasthenia may be mistaken for incipient ataxia,
incipient myelitis, or commencing vertebral caries.
In ataxia the lancinating pains, disorders of sensation, the iron band sen-
sation, the ocular symptoms and the increased galvanic excitability will
enable one to reach a diagnosis. The paralysis which occurs in myelitis
distinguishes it from neurasthenia.
In spinal caries the pain on motion and the angular curvature, in con-
nection with the traumatic history of the case, will establish the diagnosis.
Prognosis. — The prognosis in neurasthenia is always good. It may con-
tinue for months, or relapses occur ; but complete recovery may always
finally be reached under proper treatment.
Treatment. — The most important indication in this condition is to secure
absolute rest. Change of scene, nutritious diet, outdoor life, and especially
sound sleep at night tend to produce a cure. Sea bathing is highly rec-
ommended, and a light wine or beer with meals is frequently of service. The
functions of the skin should be carefully attended to. Iron, strychnine and
some form of the hypophosphites are indicated.
CHOREA.
{St. Vitus's Dance.)
Chorea is a disease of the nervous system marked by clonic muscular con-
tractions without order or rhythm, which tend to subside spontaneously
after a few weeks' duration.
Morbid Anatomy. — Chorea has usually been regarded as a purely func-
tional disease, but recent investigations, although leaving the pathology
still somewhat obscure, seem to indicate that active hyperaemia of the
brain and cord is always present, if not the exciting morbid condition, and
is due to vaso-motor disturbance, which may be associated with the rheu-
matic diathesis or result from various mental and reflex irritations.
The occasional occurrence in chorea of capillary emboli and thrombi,
with consequent minute points of softening in the gray matter of the
brain, corpora striata, optic thalami and cord, together with the fact that
in nearly all fatal cases endocarditis, with valvular vegetations, is present,
has given rise to the supposition that these conditions represent the
pathology. The commonly unilateral nature of the disease, its cessation
during sleep, the absence of large emboli with consequent paralysis, and
finally the fact that it is only in a small proportion of cases that the
capillaries are found obstructed, are serious and fatal objections to this
theory.
C'HOKEA. 1051
Whatever the morbid condition, it probably affects more especially the
corpus striatum, thalamus, or a single hemisphere primarily, but in severe
cases, when the muscles of deglutition and plionation are affected, extends
to the medulla. An ataxic gait occasionally indicates disturbance of the
cord.
Etiology. — Chorea is most frequently met with between the ages of six
and sixteen, i.e., from second dentition until puberty, in children whose
parents have suffered from hysteria, epilepsy, and other forms of func-
tional nervous disease ; from two-thirds to three-fourths of all cases occur
in girls. Feebleness of constitution, and the injurious system of forcing
the education of children, as well as the conditions which tend to the
premature development of the sexual instincts, predispose to chorea.
Anaemia, chlorosis, onanism, and anomalies of menstruation are also pre-
disposing causes.
Acute articular rheumatism and its cardiac complications bear such an
intimate relationship to chorea that many authorities regard them as one
and the same affection under different forms. The rheumatic diathesis
and the resulting cardiac disease must certainly be accepted as among the
most important causes of chorea. The more directly exciting causes are
fright, shock, and extreme mental labor or any form of severe nervous
disturbance.
Symptoms. — The onset is seldom well marked, although cases are record-
ed where, after a fall or shock, not more than four hours have elapsed before
distinct choreiform movements occurred. It may be said that in these
cases recovery is also rapid. As a rule, the child's disposition becomes
irritable or moody, and although choreic subjects are very excitable, there
is decided mental weakening, indicated by loss of memory and interest in
things that have before interested them. The sleep is disturbed and hal-
lucinations are common, and actual mania may be a precursor of chorea.
The first direct indications of the disease are a restlessness of movement
and clumsy handling of the limbs. There will usually for awhile be inter-
vals when these children act naturally for a short time, but, if observed care-
fully, and especially when they are conscious of being watched, they are
seen to drag a foot, fidget with their fingers, twitch the shoulders, or jerk
the head in a peculiar manner. As they gradually lose control of their
movements they stumble in walking, spill their food or drink, and fre-
quently drop articles they may be holding. The choreic movements are
usually unilateral, at first confined to one hand, leg, or side of the face,
and in a small per cent, of cases the manifestations remain limited to one
side, but more commonly extend to the other side within a few days.^
In the fully developed disease the symptoms vary in degree rather than
kind. In the mildest cases a child simply seems awkward, breaking dishes,
stumbling about the room, hurting himself with knife and fork, or, in the
case of older children, never being able to correctly perform tasks where
> Broadbent considers the parallelism between hemichorea and hemiplegia so perfect as to suggest at
once that the two affections represent different conditions of the same nerve-centres, and that it is
made more complete by the very discrepancies as they may at first sight appear.
1052 DISEASES OF THE NEEVOUS SYSTEM.
slight dexterity is required. Irregular action of the muscles of speech
may occur, and words may be uttered against the will of the patient.
Spontaneous jDain is often complained of in the affected side.
In the worst form of the disease every feature and limb may be hideously
contorted, the teeth ground together or snapped off, and bones may be
broken. A patient will turn somersaults without rest, rush around in a
circle, colliding with nearly everything in the room ; or, if in bed, may be
suddenly contorted and thrown therefrom with violence enough to produce
a fracture or dislocation. Between these two extremes are cases of every
degree, but in all the convulsions are made up of irregular, sudden, im-
pulsive movements, which are entirely involuntary and aggravated by every
attempt at voluntary movements. After the muscles involved have been
in incessant action and violent contraction for hours, muscular exhaustion
does not occur. In most instances, however, the muscles enjoy complete
repose during sleep. When this is not the case rapid and intense anaemia
occurs. As in these cases movement is almost continuous, and the patient
can neither eat nor be comfortably fed, death from exhaustion may result.
Chorea of the laryngeal muscles is marked by a monotonous voice having
a deep pitch, and deglutition is often greatly interfered with. The pupils
are commonly dilated and the special senses may be slightly blunted, but
the cutaneous sensibility is rarely affected. The bowels are constipated as
a rule, although sometimes the fseces are involuntarily discharged.' After
chorea has lasted for a long time the heart's action is disturbed ; ansemia is
marked, and the mental condition of the child approaches that of the idiot.
In girls who are old enough the menstrual functions will usually be de-
ranged. The skin is harsh and dry, and in this class of patients hysteria
often develops as a sequel.
Chorea is almost invariably accompanied by some paresis and often by
complete paralysis during or preceding the development of the con-
vulsions.
Differential Diagnosis. — Disseminated sclerosis of the nerve centres is
accompanied by tremor and jactitation that may be mistaken for chorea,
especially as it is a disease occurring in children. But ankle-clonus, paresis
of both lower extremities, and the occurrence of tremor on voluntary ex-
citation of the muscles, will decide the case. Hysteria and epilepsy are
readily distinguished from it, as is also the tremor of old age.
Prognosis. — Chorea is a chronic disease of varying duration, but in most
cases lasting for two or three months. Eelapses frequently occur dur-
ing puberty; but may occur after intervals of twenty or thirty years.
Complete recovery is the rule ; the patient fully recovers his intelligence
and muscular strength. Among children the mortality is about five per
cent., and death is usually preceded by delirium, and is due usually to
asthenia or some complication. Hemiplegia, aphasia, hemiansesthesia,
anaemia, heart disease, rheumatism, and erysipelas or abscesses originating
in wounds which the sufferer inflicts on himself, may be reckoned among
the complications. Abortion or premature delivery may occur when a
1 Bence-Jones states that the amount of urea excreted is increased.
SUNSTROKE. 1053
mother is choreic. Very rarely does jiermanent mental derangement
follow.
Treatment. — Should an exciting cause be discovered (constipation or in-
testinal worms), it must be immediately removed. In all cases mental and
bodily rest, a generous but bland diet, and pleasant, and, if possible, rural
surroundings should be ordered. Children with chorea should not go to
school. Many authorities advocate a generous wine in connection witli
iron. Sleep should be secured by the use of hydrate of chloral if necessary ;
Harley advocates conium. The most useful drugs are arsenic, zinc, the
bromides, and hydrate of chloral. Arsenic has given me better results than
any other drug ; it must be given in proportionately increasing doses until
its specific physiological effect is produced. Copper, the silver salts, and
strychnia are much used by the French.' Weir Mitchell has successfully
used salicylate of soda, probably in rheumatic cases. In extreme cases
chloroform and other anassthetics may be needed. The hypodermic injec-
tion of curare, friction-electricity, and galvanism are recommended. Baths,
wet packs, or a thorough rubbing often act beneficially, and the ether
spray along the spine seems to induce sleep and diminish violence of the
choreic movements *
SUNSTROKE.
{Insolation.)
Insolation is that complex of symptoms occurring in persons exposed to
extreme heat under unfavorable circumstances.
Morbid Anatomy. — The heart is usually firmly contracted, but it may be
flaccid. The left heart is empty, while the right side and the venous tracts
are filled with dark, often fluid blood. The blood is seldom coagulated ;
its corpuscles are crenated and do not tend to form rouleaux, and contain
less oxygen than normal. The lungs are intensely congested, oedematous,
and sometimes exhibit spots of hemorrhage. The spleen is swollen
and soft, and, with the kidney and liver, exhibits cloudy swelling or paren-
chymatous degeneration. The meninges are intensely hypergemic, and there
may be evidences of incipient meningitis. The ventricles of the brain con-
tain more or less serum, and the brain substance itself is congested or hem-
orrhage has occurred into it. The cord is sometimes abnormally soft. In
severe cases the body is covered with ecchymoses, and sub-serous hemor-
rhages are common. In the neck the sympathetic ganglia, the vagi, and
the connective-tissue are surrounded by, or infiltrated with blood. Eigor
mortis comes on very rapidly.^
Insolation generally results from exposure to heat, in persons who are
exhausted by either mental or physical labor.
' Gaz. Medical, Paris, Oct., 1846. Jour, de VAnat. et de Phys., 1874 ; also Trousseau.
''In the Children's Hospital at Paris much reliance is placed on gymnastic exercise, performed with
pleasant surroundings and music.
3 Very recently Arndt states that in his autopsies there was anasmia of the brain and its membranes ;
and that observers must have been misled by the blood escaping from large congested vessels, and running
over an anaemic brain. By him all the viscera are described as pale and oedematous. Virchow's Archiv.,
vol.64, pp. 15-39. See also Koster in Berlin. Klin. Wochen., No. 34, 1875. Also for July 17th, 1876.
1054 DISEASES OF THE KERVOUS SYSTEM.
Etiology. — Workmen, soldiers on the march, stokers and cab-drivers, or
brain-workers and those who are suffering anxiety or mental distress are
more liable to be overcome by the heat. Hot, wet, muggy days — our Au-
gust dog-days — are the most favorable for its occurrence. Acclimatization
has very much to do with its development. Nearly all new arrivals in India
at first suffer more or less severely from the heat. Nevertheless, when a
certain temperature of the air is reached all alike succumb.' Dry, hot
winds are not prejudicial. In Dakota men can work all day exposed to the
sun when the temperature of the air is at least 140'^ to 160" F., while in
New York on a cloudy, wet day in August, with the temperature at only
93° F., large numbers of men and animals are prostrated. The vigorous,
thin, healthy individual who leads a temperate and regular life seldom
suffers from the heat; while those who drink freely of alcoholic beverages
and dissipate during the summer months are those that most commonly
suffer. Large immbers are affected just after eating a hearty meal.^
Symptoms. — The majority of cases occur in the middle of the day. In
mild cases the patient suddenly becomes exhausted, and probably faints or
becomes semi-comatose. He is utterly prostrated ; the skin is pale, cold, and
moist, the pulse is quick and feeble, various colored spots appear before the
eyes, and all kinds of symptoms are referred to the head — floating, swim-
ming, vertigo, fulness, neuralgic pains, etc. These cases may recover, or
collapse may terminate fatally from heart failure.
In the foudroyante form a man may be struck down suddenly, or there
may be prodromata, which are generally depression of spirits, muscular
weakness, dyspnoea, epigastric oppression, and perhaps nausea and vomit-
ing. Unconsciousness suddenly follows ; the skin is cold, the pulse is fee-
ble, respiration and circulation are markedly interfered with, and death
may result from heart-failure due to injury of the nerve centres from sud-
den elevation of temperature. Reaction may set in, but it is, at best, te-
dious and imperfect. This form is a true coup cle soleil.
In another form called tliermic fever the temperature rises to 108° oi
110° F., or even higher. This is due to the influence of heat on the
nerve centres and subsequent action upon the vaso-motor system. It often
occurs at night and in those who are dissipated or worn out, or are in the
midst of anti-hygienic surroundings. There is great restlessness, thirst,
and dyspnoea. The skin is burning hot, and either dry or moist. The
upper part of the body is congested and livid ; the pulse may be full and
labored or quick and jerking, and the carotids pulsate forcibly. The
pupils are at first contracted but later widely dilated, and the frequent
micturition of the early stages gives place to urinary suppression. De-
lirium and epileptiform convulsions are common. Toward the end the
pulse becomes extremely rapid and feeble, the patient passes into a com-
plete coma, the breathing is sighing or stertorous, sometimes peculiarly
moaning, and the urine and faeces are passed involuntarily. Some of these
> The East Indian loomarna, or hot wind stroke.
^ J. Fayrer states that the most frequent cases are those that come on in houses, ships, tents, laundries,
cook-rooms, etc., during the night, or in the day, away from the direct solar rays.
SPINAL lERITATIOK. 1055
cases are marked by persistent vomiting and purging ; sucla cases rarely
recover.
Differential Diagnosis. — Severe cases attended by hyperpyrexia cannot be
confounded with any other disease. Moderately severe cases, however,
may be mistaken for acute meningitis. In the latter the projectile vomit-
ing, the boat-belly, the pale face, the tdche cereirale, and the tense, hard,
wiry pulse are in striking contrast to the symptoms of the former. Tlie
history of the case is always important. Under the head of acute alco-
holismus, are given the symptoms of alcoholic coma, which may be con-
founded with sunstroke.
Prognosis. — The prognosis, except in mild cases, is very bad ; nearly one-
half die. Many who recover are invalids for life. Among the sequelaD
are a sub-acute or chronic meningitis, epilepsy, insanity (in every degree),
partial paraplegia or hemiplegia, loss of memory, blindness, extreme in-
tolerance of heat, almost constant headache and, in many cases, great irri-
tability of temper.
Treatment. — In all cases the patient must have absolute rest and plenty
of cool, fresh air. The more these i^atients are carried about the worse
their chances. All tight or needless clothing should be at once removed.
Stimulants are often necessary ; if they excite vomiting they should be
given hypodermically or as enemata. Ether, mnsk, carbonate of ammonia,
turpentine, etc., are recommended.
In most cases the cold water treatment is the best. The patient should
be taken to the nearest pumj:), stream, or water-tank and immersed for a
considerable time, or a stream of cold water Should be poured over the
head, neck and back. Between the baths dry cnps may be applied, and
during the baths stimulants may be given if the pulse demands them. A
patient should always be removed from the bath before the temperature
falls to normal. Purgative enemata and cardiac stimulation, with the
cold water treatment, are all that is required in those moderately severe
cases where the temperature does not rise above 105° F.
In thermic fever, venesection is contra-indicated. Ice water should be
applied to the surface, the bowels should be moved by a brisk saline, and
morphine and quinine given hypodermically. Blisters about the nuchal
region are often beneficial. The severe cerebral symptoms in this form
are often relieved by the inhalation of ether or chloroform. These patients
need careful watching during convalescence, and should remove to a cool
climate, and engage in no business that demands active brain work. It is
in this last-named variety that rapid lowering of the temperature by the
application of cold to the surface is of the greatest importance.
sphntal iekitation.
This is always functional. Strictly speaking, it has no morbid anatomy,
but in most cases is associated with congestion or ansemia.
Etiology. — It occurs chiefly in women between the ages of fifteen and
twenty-five. Spinal shock, or concussion from any cause, and all those
1056 DISEASES OF THE NEEVOUS SYSTEM.
practices and habits which cause nervous strain and result in nervous ex-
haustion, may also produce spinal irritation. Chronic alcoholism and the
opium habit may also induce it. All severe diseases where there is a pro-
longed drain ' on the system will be followed by spinal irritation. A neu-
ropathic tendency or hysteria often accompanies or causes spinal irrita-
tion.
Symptoms. — The one constant and special symptom of spinal irritation is
tenderness, which may be excited either by pressure or motion. It may
extend along the entire spine, or be localized over a single vertebra. This
tenderness, which varies greatly in degree, becomes marked on the ap-
plication of heat, cold, electricity, and other irritants. The spinous proc-
ess is the place where pressure causes greatest pain, and if severe it
may excite convulsions and paraplegic or cataleptic symptoms. Tactile
hypersesthesia is very marked, but anesthesia is rare, and myalgia may co-
exist with pains in internal organs. In about half the cases it is spon-
taneous ; its character is very variable, but its seat is generally at the
point of exit of the nerves from the spinal column.
Motor disturbances are common. Weariness, heaviness, and pseudo-
paraplegia of the lower limbs follow the slightest exertion. Contraction
occurs in some muscles, especially those of the forearm, and twitchings,
spasms, and choreic movements may be present. Cardiac palpitation is
very common ; and nausea and vomiting, nervous cough, embarrassed
phonation, deglutition, and breathing, or attacks of fainting are not un-
common.
Patients with spinal irritation are depressed, melancholy, and irritable,
and subject to insomnia, headache, dizziness, and disturbances of the
special senses. Yaso-motor changes are marked. The extremities are cold,
sometimes blue, and the face alternately pales and flushes.
When the point of tenderness is in the cervical region the pains are re-
ferred to the head, pharynx, and chest, and are associated with psychical
disturbances. When it is lower there are respiratory and cardiac symptoms,
and if in the dorsal region it is accompanied by pain in the stomach, with
dyspepsia, nausea, and vomiting. This last is the most frequent seat of
the disease. Lumbar spinal irritation is less common and is indicated by
neuralgic pains and weakness in the lower limbs, myalgia in the abdomi-
nal and lumbar regions, spasm of the vesical and anal sphincters, uterine
and ovarian pains, and disorders of menstruation.
In many cases there is dysuria and vesical spasm, increased desire to
urinate, and the discharge of a large amount of pale, limpid urine may
occur. Sometimes the liver, kidneys, or bowels are the seat of functional
derangements. The disease may progress slowly or it may be of short du-
ration, and rapidly become severe or as rapidly improve.
The symptoms are always variable and inconstant, and the pains often
shift from one part to another. No true paralysis of limbs or of the sphinc-
ters ever occurs. Sometimes spinal irritation will suddenly pass into neu-
rasthenia.
» Hammoud calls spinal irritation anoBmia of the posterior columns of the cord.
TETAKUS. 1057
Differential Diagnosis. — Spinal irritation may be mistaken for spinal con-
gestion, meningitis, myelitis, tumors, and tetany.
In spinal congestion there is no tenderness. Paralytic symptoms are
frequently present, and gastric and cardiac derangements are never prom-
inent. In spinal congestion the symptoms are aggravated by the supine
position, in spinal irritation the reverse is the case. It is claimed that the
subcutaneous injection of one-thirtieth grain of strychnine will aggravate
the symptoms in spinal congestion, while in spinal irritation its adminis-
tration affords relief. Spinal irritation is of much longer duration than
congestion.
Spinal meningitis is accompanied by pyrexia, and the pain in the spine
is increased by motion, so that the patient assumes, and remains in a fixed
position. The pain is violent and diffused in meningitis, and muscular
spasms occur in the back and neck, which are never present in spinal irri-
tation.
The presence of the iron-band sensation about the waist, paralyses, vesi-
cal irritation, and relaxation of the sphincters, and anaesthesia, especially
in the early part of the disease, are almost diagnostic of myelitis, and are
never met with in spinal irritation.
Spinal irritation is differentiated from spinal tumors by the fact that in
the latter the symptoms are localized, permanent, and unaccompanied by
visceral derangements, which in irritation assume such a variety of forms.
The rare disease called tetany by Trousseau is differentiated from spinal
irritation by the muscular contractions, which are accompanied by trem-
bling, ansesthesia, and a feeling of intense fatigue.
Prognosis. — The prognosis is favorable, although after apparent recovery
the disease is apt to return. Very frequently it resists treatment, especially
if gout, rheumatism, scrofula or syphilis exist.
Treatment. — The remedies which are employed in the treatment of anae-
mia are always indicated in spinal irritation. Alcoholic stimulants are
usually of service and in many cases must be given freely, combined with
a meat diet and exposure to sunlight and fresh air. Injections of morphia
or atropia combined with strychnine should be given over the site of ten-
derness, the dose at first being small and gradually increased to the point
of relieving pain. Aconite and veratria may be applied locally in the form
of an ointment. The galvanic current and the Faradic current in some
cases will give immediate relief. The daily application of the ice-poultice
or the actual cautery is highly recommended. Absolute rest in the coun-
try with a highly nutritious diet often does more for this class of patients
than any other treatment.
TETAIfUS.
Tetanus or loch-jaw is a tonic spasm with paroxysmal exacerbations of
the voluntary muscles ; those of the lower jaw, neck, and pharynx are usu-
ally first affected. Acute and chronic varieties are recognized ; the latter
ia called tetanus mitis.
67
1058 DISEASES OF THE NERVOUS SYSTEM.
Morbid Anatomy. — There are bo constant lesions in tetanus, and those
which are commonly present are quite as possibly secondary as primary.
In traumatic tetanus the nerves supplying the affected parts are some-
times inflamed, but even this condition is not invariably present. In the
cord there is often more or less hypersemia, with slight effusion, and per-
haps extravasation. This is frequently attended by some cedematous soften-
ing and interstitial exudation of finely granular or structureless matter,
especially in the gray substance, in the fissures, and on the surface of the
cord. Notwithstanding the frequent occurrence of such lesions the pecu-
liar etiological relation which injuries bear to the disease renders it probable
that the primary disturbances are purely functional and reflex in their
nature, or due to some peculiar blood-poison.' Tetanus is usually traumat-
ic and may follow the most trivial injury, as a splinter in the finger, but
is more apt to develop after compound or complex fractures, lacerated,
crusbed, and punctured wounds, and wounds comjDlicated by the presence
of foreign bodies. It may occur after abortion or normal delivery, and
trismus nascentium is ascribed to the wound at the navel.
Climatic conditions have a distinctly exciting influence in the production
of tetanus. It is much more common in hot than in temperate climates,
and rapid changes of temperature, cold and wet, are especially favorable to
its development. It is said that fright, anxiety, or depression markedly
predisposes to its occurrence, as in armies it prevails most extensively among
the defeated.
Clinically, tetanus can be excited by strychnine, ergotin, brucine, picro-
toxin, and caffein. Occasionally tetanus arises from unknown influences,
when no wound or abrasion is present and when the only possible assignable
cause is exposure to wet and cold.
Tetanus may occur at any age and in either sex, but is most frequent in
adult males.
Symptoms. — Tetanus generally comes on in from six to twelve days after
the injury, but may be delayed three or four weeks or appear within a few
hours. In the largest number of cases it begins with stiffness of the mus-
cles of the neck and jaw. This quickly extends to the muscles of mastica-
tion and facial expression ; the patient's jaw becomes locked and the head
fixed, and the face wears a peculiar frown. The tonic stiffness is aggra-
vated by every attempt to use the muscles. Deglutition is difficult, and
later becomes almost impossible. By degrees the other muscles are in-
volved, the trunk is stiff and more or less curved, the abdomen tense and
hard, and the limbs extended and rigid. When the diaphragm is moved,
a sharp, sudden pain shoots through the body from the ensiform cartilage,
which is considered diagnostic. It is accomjDanied by intense dyspnoea.
This general rigidity of the muscles is continuous and progressive, but is
marked by paroxysmal attacks in which all the symptoms are immensely
exaggerated. They are excited by any muscular action, by jars and other
slight causes, or may occur spontaneously. During a spasm all the muscles
become powerfully contracted. The limbs are extended, the back arched,
1 Sir T. Watson.
FACIAL PARALYSIS. 1059
and the face assumes the risus sardonicus. The head is retracted, and
the patient may rest only on his head and heels. The respiratory muscles
suffer also, and respiration may be entirely arrested, and the face become
cyanotic. As the paroxysm passes away it is only a remission ; the muscles
are still hard and stiff, the jaw closed, and the respiration rapid and shal-
low. The intense cramping pain of the paroxysm gives place to a heavy
ache and soreness.
Notwithstanding the severity of the disease, consciousness and intelli-
gence are rarely impaired, and the temperature and pulse-rate are only
elevated on account of the muscular action. Just before death, however,
in many instances, there is a rapid and enormous rise in the temperature,
which may reach 112'^ or 114° F. The urine is scanty, the bowels are con-
stipated, and the body is bathed in a profuse sweat. Reflex irritability is
increased to a high degree throughout.
Differential Diagnosis. — The absence of headache, delirium, and coma,
and a normal temperature in the intervals between tlie attacks, will suffice
to distinguish tetanus from any cerebral or cerehro-^pinal inflammation.
Hysteria, hystero-epilepsy, and sometimes ejjilepsy may simulate it, but
the development of the disease quickly affords a diagnosis.
Strychnia poisoning is to be differentiated by the history of the case and
the examination of voided matter. In strychnia poisoning, consciousness
is lost, and the muscles of the jaw, head, and neck are last and least
affected.
Prognosis. — Tetanus usually terminates fatally before the tenth day ; but
if the twelfth day be passed and the temperature does not pass 102° F.,
and the respiratory muscles are not involved ; or if the disease has occurred
at a remote period from the reception of the wound, the outlook is quite
hopeful. When the patient is young, when strabismus occurs, or the
wound is very recent, and when rigidity appears early the case is nearly
always fatal.
Treatment. — So far as is known, no treatment has any controlling effect
upon tetanus. Innumerable remedies have been tried, with equally bad
results. A highly nutritious diet, with alcoholic stimulants, is, perhaps,
the best treatment. Alimentation must be carried on by a stomach-tube
or by the rectum. Recently, curare, nitrite of amyl, and hydrate of chloral
(in forty-grain doses) seem to be the favorite drugs. Locally, ice and cold
effusions to the spine prove beneficial, although hot applications are more
grateful to the patient.
The utmost care should be taken to avoid all irritation and to Keep the
patient in the most absolute quiet.
FACIAL PARALYSIS.
{Bell's Paralysis.)
Bell's paralysis is a paralysis of the muscles of the face due to any lesion
implicating the nucleus or fibres of the seventh pair of nerves.
Etiology. — It may be caused within the skull by blood extravasations.
1060 DISEASES OF THE NERVOUS SYSTEM.
tumors, and inflammatory products, which give rise to pressure. Fracture
and morbid growths may cause pressure on the nerve, in its passage
through the cranial bones, sufficient to produce the paralysis. It may
occur in connection with disease of the internal or middle ear and from
local neuritis. Outside the skull, blows, wounds, swellings of the parotid
gland or other tumors may cause it. It is most frequently the result of a
draught of cold air on the side of the face, especially while sleeping.
Symptoms. — Its onset is usually gradual ; but when fully developed its
symptoms are striking and characteristic. All the muscles supjolied by the
seventh nerve on one side of the face are paralyzed. The forehead is smooth
and motionless on the paralyzed side, the corner of the mouth is drawn to
the opposite side, and the paralyzed side closes less perfectly than the other.
The patient cannot close the eye on the affected side. As soon as the face
is moved the paralysis is unmistakable. Whistling and drinking are im-
possible. Certain letters, as P and B, cannot be jDronounced; food collects
between the cheek and teeth on the palsied side. The tears run down over
the cheek, and, if the chorda tympani is involved, the sense of taste is per-
verted or destroyed on one-half of the anterior portion of the tongue. At
the same time the salivary secretion is diminished. The uvula is usually
deflected; the alaof the nose becomes flaccid, and the nostril on the affect-
ed side is narrowed and loses its rotundity. Imperfect closure of the eye
exposes the organ to all sorts of injuries, hence disease of the cornea and
conjunctiva is very common. During the first two or three days the mus-
cles show increased irritability to the electrical current ; but they gradually
lose their Faradic, while they retain their galvanic irritability.
DiiFerential Diagnosis. — When otorrhoea, disturbances of hearing, obliquity
of the uvula, diminished salivary secretion, and loss of taste occur, the origin
of the paralysis is within the aquseductus Fallopii. When the taste is nor-
mal and the uvula straight the cause is usually peripheral, e. g., cold. In
these cases also electro-muscular contractility is rapidly lost. The origin
may be supposed to be central when other nerves are involved. Bell's palsy
is usually associated with paralysis of the sixth nerve.
Prognosis. — In organic disease of the brain or with lesions of bone the
prognosis is unfavorable. When arising from cold, slight injuries, or syph-
ilis the prognosis is favorable. Complete recovery is usually reached in two
or three months. There is no rule by which one can estimate its duration.
The more the electro-muscular contractility is diminished the less the
chances of complete recovery.
Treatment. — When due to cold, apply a few leeches to the mastoid proc-
ess, followed by hot fomentations ; subsequently blisters behind the ear and
other counter-irritants may be resorted to, and the alternate Faradic and
voltaic currents are to be relied upon. Massage and shampooing may be
tried. Cowers recommends inunctions of oleate of morphia. When due
to syphilis, anti-syphilitics are indicated. Niemeyer recommends mercu-
rial ointment.
PAKALYSIS AGITAK8. lOGl
PAEALTSI8 AGITANS.
Shaking palsy, or the trembles, is a disease of advanced life characterized
by motor weakness and tremors of the voluntary muscles, especially of the
limbs, occurring independently of muscular exertion, which are finally fol-
lowed by paralytic symptoms.
Morbid Anatomy. — As yet no constant changes have been discovered.
Some authorities consider it of spinal, others of cerebral origin. Among
the former are Charcot, Lebert, Marshall Hall, and Rosenthal. Among
the latter are Oppolzer and Skoda. Senile changes in the brain and cord
are found in a certain number of cases. There may be sclerotic jiatches in
the pons, the medulla oblongata, the optic thalamus, and hippocampus
major, and Charcot has found increase of the ei3ithelium of the central
canal in the cord with pigmentation of the cells in the j)osterior columns
of Clark. Diseased arteries and slight sanguineous exudations have also
been noticed.
Etiology. — Earely occurring before forty, the liability to it is increased
every year thereafter. It is more common in men than women, and occurs
chiefly in the lower classes. Violent emotions, as grief, fear, anger or dis-
tress of mind, degeneration of the heart and vessels, and great bodily
fatigue and exposure, are among its exciting causes. There are no indica-
tions that the disease is hereditary.
Symptoms. — In nearly all cases paralysis agitans is insidious in its' ap-
proach, and begins in one foot, hand, or possibly a single finger or the
thumb, as a slight oscillating motion, which is quite rhythmical and charac-
teristic. For a time this trembling may be intermittent, but appears with-
out any apparent cause and unexpectedly. In this early stage it can possi-
bly be arrested by an effort of the will, a condition in marked contrast
with the very decided increase in the tremor which late in the disease
follows every effort to control the muscles. As the disease advances simi-
lar oscillating movements affect the muscles of the forearm, arms and
shoulder, and the entire limb is in a continuous tremble. The remaining
limb of the affected side usually becomes involved before the disease crosses
the median line. Pain, weariness and stiffness in the affected muscles pre-
cede, in some cases, the development of the characteristic tremors ; or the
disease may attain its full development through a series of increasingly fre-
quent sudden attacks of tremor lasting only a few days each.
At the height of the disease nearly all the limbs are involved in an inces-
sant motion which is liable to severe exacerbation upon muscular exertion
or during mental disturbance, and which ceases only during sleep or anses-
thesia.
Later on, rigidity, painful cramps, and contractions affect not only the
muscles of the limbs but also those of the trunk, neck and face, giving the
patient quite a characteristic appearance. The countenance assumes a
fixed, staring look of distress, the head is drawn forward and the trunk
flexed ; the lower limbs and arms, which are drawn away from the side.
1062 TSEASES OF THE NEEVOUS SYSTEM.
are rigid, and all the joints are flexed, often causing marked deformity of
the hands. Altliough the rigidity of the limbs does not prevent walking,
the patient's gait is characteristic. As he rises, or when he stands, there
is great unsteadiness and difl&cnlty in maintaining equilibrium, which, as
he starts to walk, causes him to run forward to avoid falling. This dis-
turbance of equilibrium is not associa.ted with vertigo.
The muscles of respiration and deglutition are not involved, but the voice
is often tremulous and speech is slow, hesitating and laborious, so that
words are distinctly broken up into syllables. Although muscular move-
ments are attended with extreme fatigue, the force of the contractions is
but slightly diminished until late in the disease, when, from increase in the
rigidity, the patient takes to his bed, and the muscles suffer in their nutri-
tion or become distinctly fatty.
As the end approaches, the memory and intelligence fail in connection
with the generally defective nutrition. Although the disease may last for
twenty or thirty years, death most commonly results from some intercur-
rent disease.
DiiFerential Diagnosis. — In disseminated sclerosis tremors occur only
when the muscles are in use ; the disease begins in the lower limbs, affects
younger persons, and paralysis occurs early. The patient has no tendency
to run forward, and does not present the peculiar physiognomy of shaking
palsy. Senile, alcoholic, lead and mercurial trembling are readily diagnos-
ticated by the previous history and concomitant symptoms.
Prognosis. — Paralysis agitans is a very chronic disease, and the outlook is
never favorable. It may last twenty-five years. After a few years the
muscles waste, the patient is confined to his bed, there is physical and
mental exhaustion, bed-sores form, and death results from asthenia or
complications. The more common complications are acute lobar pneu-
monia and pleurisy. Paralysis agitans has been recovered from in the
early stages, but Eulenberg says that there is reason to doubt the diagno-
sis in such cases. ^
Treatment. — No definite results have been attained by the use of any
remedy. All the nerve stimulants, tonics, and sedatives have been em-
ployed, of which Charcot considers hyoscyamus the only useful one, and
the effects of this are temporary. The constant current has seemed to
have some value as a distinctly curative agent. Beyond this, general tonic
treatment is the most that can be attempted, and this should never be
omitted.
LOCALIZED SPASM AOT3 PAEALYSIS.
{Scrivener's Palsy, etc.)
Writer's cramp is one of the more common varieties of anomalous mus-
cular movements, or of those diseases which Duchenne calls " functional
1 Handfield Jones thinks that there are two forms : one, entirely incurable, occuring in old persons and
depending upon organic changes in the central nervous system ; the other, in younger persons, curable
and probably not dependent upon organic changes.
LOCALIZED SPASM AND PARALYSIS. 1063
impotences." Of essentially the same nature are piano-players' cramp and
the inability of tailors, dairymen, bricklayers, or telegraphers to execute
movements to which they have long been accustomed.
Morbid Anatomy. — It has been thought that degenerative changes occur
in the spinal cord, but according to Dr. Eeynolds these diseases are due to
a perverted nutrition of these parts.
Duchenne believes that the primary change is in the nei-ve centres, and
gives as a strong argument in favor of this view the fact that the malady very
quickly affects the left hand, when this is used to supply the right in one
who has writer's cramp. Dr. Poore, however, suggests that the lesion in
typical cases is at the periphery, either in the muscles themselves, or in their
terminal motor nerves. He attributes the disease to over-use and over-
fatigue, not to central changes ; and states that muscles which are
trained to worlc in order together no longer do so when even one of them
fails.
Etiology. — Writer's cramp, like other similar conditions, as from violin or
piano-playing, telegraphing, mili^ing, etc., is for the most part induced
by long-continued use of the affected muscles.
Symptoms. — It will be sufficient to describe writer's cramp as a type of
all this class of spasms, since they differ only in the muscles involved. It
generally commences with a sense of weight or stiffness in the affected
muscles, together with discomfort and indefinite pain, which is perhaps
relieved by strong contractions or stretching the muscles. This uneasi-
ness slowly increases, and there is added a tendency to spasmodic movements
which renders the handwriting irregular and covered with unnecessary
lines.
The pain and spasm at first follow only prolonged use of the pen, but
soon are induced very readily, until at length all attempts at writing are
abandoned. In the earlier stages the patient is able to control the spasms
somewhat and to relieve them by holding his pen in an unusual way or
by some other device. For a time also after more delicate manipulations
are impossible, he can still perform coarser operations, but the disease al-
most invariably extends so long as the muscles are kept in use, and may
result in severe spasm whenever any attempt is made to use the hand in
writing. Occasionally it assumes a paralytic form and the patient is un-
able to hold a pen at all, or pain may be a prominent symptom, radiating
up the arm as a severe neuralgia.
The disease may affect any or all the muscles of the hand or arm, and it
rarely extends to the shoulder and trunk. More commonly the extensors
and flexors of the thumb or index finger are affected, but though there is
generally a distinct loss of power the muscles act perfectly in any motions
save those which induced the disease.
In the other forms of local spasm the general history will be the same,
and the deformities and disturbances will depend entirely upon the action
of the muscles implicated. It is more likely to occur in those who merely
copy than those who write an equal amount, but think at the same time —
as authors and journalists.
1064 DISEASES OF THE NERVOUS STrriTEM.
Differential Diagnosis. — The history of the case is all-important, and will
generally be sufficient for a diagnosis.
Lead palsy, with which scrivener's palsy maybe confounded, is generally
preceded by several attacks of lead colic ; there is the peculiar blue line at
the margin of the teeth, the skin assumes an earthy hue, and the " drop-
wrist" exists, conditions which do not occur in writer's cramp.
Paralysis agitans, disseminated sclerosis, and the trembling due to old
age or to chronic alcoJiolisinus will be readily differentiated by the bistory.
Prognosis. — The prognosis is favorable. The shorter the duration of the
condition, and the greater the opportunity the patient has to give the part
rest, the better the outlook. Writer's cramp is much more easily relieved
in the weak and nervous than in the strong and robust.
Treatment. — Absolute rest is essential, and will sometimes alone be suffi-
cient for a cure. The mild galvanic current, blistering along the nerve-
trunks, should they be tender, and rhythmical exercise of the affected mus-
cles short of fatigue, is otten of marked service. Morphine hypodermically
may relieve, but does not effect a cure. The mind and body must have rest
as well as the muscles. Hypodermic injections of atropia, strychnia, and
Fowler's solution have been used with success. Massage to the part is rec-
ommended by Beard. In my experience the only course which has been
followed by markedly beneficial results has been absolute rest of the affected
muscles, with sea bathing and the internal use of iron.
CHEOlSriC LEAD poiso]snKa.
(Lead Palsy.)
This is a morbid condition produced by the introduction of tbe salts of
lead into the system, either through the mucous surfaces or the skin.
Morbid Anatomy. — After the salts of lead have been received into the
system, they become deposited in various tissues or are discharged by the
emunctories. They have been found in all the tissues of the body. They
are eliminated mainly by the kidneys. In the paralysis caused by lead
poisoning the muscles and nerves are early affected ; later the nerve-
centres become implicated. It is probable that the lead deposited in the
affected tissues impairs their function and leads to their degeneration when
the paralysis has existed for a long time.
Etiology. — The sources of lead poisoning are numerous : painters and
workers in lead are those most frequently affected. Drinking-water, wines,
and ales frequently become impregnated with it, and then become a source
of infection. The application of lead powder as a cosmetic to the face and
neck has caused lead-poisoning. Some persons are much more susceptible
to its poisonous influences than others ; I have known a few doses of lead
taken as a medicine to give rise to pronounced symptoms of lead poisoning.
Symptoms. — The general health of those who are the subjects of chronic
lead poisoning is always more or less impaired. Their skin becomes sallow,
dry and harsh, they suffer from dyspeptic symptoms, loss of appetite, and
CHRO]SriC LEAD POISO]SriN"G. 1065
constipation. A blue line forms along the edge of the gums immediately
adjoining the teeth, which is regarded by some as diagnostic of lead poison-
ing — it is often present in those working in lead who are free from other
symptoms.
The most important and characteristic symptoms are intestinal colic,
and affections of the nervous system. Lead colic has been considered in
the list of Intestinal Diseases. The most frequent of the nervous affections
is drop- wrist from paralysis of the extensors of the fore-arm. It generally
comes on gradually after one or two attacks of colic. Sometimes its ad-
vent is sudden. In painters the right hand is first affected, but after a
time both hands are involved. The signs of lead palsy are loss of power
over the extensor muscles of the fore-arm ; first the patient is unable to ab-
duct the thumb, then to extend the finger, then to extend the hand on the
fore-arm, and the hand drops when the arm is held in a prone position.
The paralysis is generally limited to the muscles supplied by the radial
nerve.
The paralyzed muscles waste rapidly and lose to a greater or less degree
their electro-contractility ; there is no loss of sensation in the paralyzed
limb, and not infrequently it is the seat of severe joains and tenderness.
In some instances other muscles besides those of the fore-arm are affected,
as the deltoid and triceps, and the palsy may involve the muscles of the
lower extremity, especially the extensors of the foot and leg. In rare in-
stances all the voluntary muscles are involved. G-outy subjects are pe-
culiarly susceptible to lead poisoning, and in such cases the cirrhotic kidney
almost always exists, giving rise to albuminuria and the other phenomena
of the cirrhotic form of Bright's disease.
This condition is often accompanied by amaurosis and other grave ner-
vous symptoms.
Differential Diagnosis. — The diagnosis of lead colic has been considered
under the head of Intestinal Colic. Lead palsy may be distinguished from
other forms of palsy, by the history of the case, by the absence of cerebro-
spinal disturbance, and by the blue line on the gums. When the muscles
of a paralyzed limb respond to the influence of the electric current lead
poisoning may be excluded.
Prognosis. — Chronic lead poisoning is rarely a direct cause of death,
although it may exist for years, the longer its duration the less pvosjDCct
there is of complete recovery. Extreme wasting of the paralyzed muscles
with loss of electric contractility renders the prognosis unfavorable. In
some instances the muscular power may be regained when the excitability
does not return.
In most cases the general health is not seriously impaired, and the re-
covery from the paralysis, if not complete, is partial. The fatal cases are
those which have been a long time exposed to the jjoisonous influence of
lead, and who have been intemperate.
Treatment. — The first thing to be accomplished is to remove the patient
from all sources of lead poisoning. Extreme personal cleanliness is im-
portant for those who cannot avoid such exposure. The habitual use of
1066 DISEASES OF THE NERVOUS SYSTEM.
lemonade made with sulphuric acid is regarded, to some extent, as pro-
tective ; it acts by converting the carbonate and other salts of lead in the
stomach into the insohible sulphate. Various methods have been proposed
for removing the lead from the system, the most effective of which is baths
containing some soluble sulphide.'
Iodide of potassium is recommended on the ground that the iodide
makes, with the insoluble salts of lead deposited in the tissue, a new soluble
salt, which can be eliminated by the kidneys. Its administration should
begin with fifteen grains a day, and be gradually increased to thirty grains
a day ; it may, in anaemic subjects, be combined with chloride of iron. The
bowels should always be kept freely open.
The only effectual remedy for restoring the paralyzed muscle is electric-
ity in the form of Faradization. Its application should not be continued
more than ten or fifteen minutes three times a day for two or three months.
Severe shocks should be carefully avoided, although a current of high
tension causes no movement in the paralyzed muscles. It is important that
each paralyzed muscle should be treated separately.
CHEONIO MEECIJEIALISM.
{Mercurial Tremor.)
Chronic mercurial poisoning may result from the long-continued intro-
duction of mercury into the system, either through the stomach, respiratory
organs, or skin.
Morbid Anatomy. — ISTo characteristic lesions have been discovered in those
who have died of chronic mercurialism, except the deposit of mercury in
the tissues, especially the brain, liver and kidneys.
Etiology. — Workers in mercury, as gilders, looking-glass manufacturers,
and those engaged in quicksilver mining, are those who chiefly suffer from
chronic mercurialism, although it may result from its long-continued
medicinal use. Those who are exposed to its fumes are especially liable
to its poisonous effects.
Symptoms. — The manifestations of chronic mercurialization are mainly
confined to the nervous and muscular system, and may be designated as
mercurial tremors. Its first indication is a tremulousness of the hands
and arms, accompanied by numbness and tingling, with pain in the
joints. These symptoms may continue for years without interfering
materially with the general health of the individual ; but sooner or later
the entire muscular system becomes invaded, and speech, deglutition, and
respiration are more or less interfered with. Choreic movements occur,
the patient is unable to walk or stand without assistance, and the face \h
contorted by muscular spasms ; while the patient is in the recumbent pos-
ture and makes no muscular efforts, the muscular spasms cease, but as
soon as he attempts to stand or move, the choreic movements commence.
In an advanced stage of the disease the convulsive movements do not
1 Dr. Pereira recommends baths medicated by dissolving sulphide of potassium in the proportion of
two ounces in fifteen gallons of water.
VEETIGO. 10G7
entirely cease wlien the joatient is in the recumbent posture. After the
tremors have continued for a long time and have been severe, the patient
loses appetite, becomes sallow and emaciated, and cerebral symptoms de-
velop, the most constant of which are headache, vertigo, delirium, and
epileptic convulsions.
LifFerential Diagnosis. — Mercurial tremor may be confounded with mul-
tiple sclerosis, paralysis agitans, and chorea. But a history of exposure
to mercurial poisoning, and the fact that the nervous symptoms were pre-
ceded by ptyalism, ulcerated gums, mercurial fetor of the breath, nausea,
colicky pains and diarrhcBa, are generally sufficient to establish a diagnosis.
It is also to be remembered that in paralysis agitans the muscles of the
head and neck are not involved in the convulsive movements, and that the
position of the patient does not influence the spasms.
Prognosis. — Mercurial tremor does not often directly cause death, but if
exposures to the causes of mercurial poisoning are continued, death may
result from exhaustion, intestinal or cerebral complications, or from in-
tercurrent disease.
Treatment. — As soon as any of the symptoms of mercurial poisoning are
present, the individuals must immediately be removed from all chance of
exposure to the poison. If this cannot be effected, and they are compelled
to continue occupations where they are exposed to the fumes of mercury,
they must wear a protection over their face, and exercise the greatest per-
sonal cleanliness.
Drugs are of little service, the treatment is altogether prophylactic.
VERTIGO.
Vertigo has been well defined as the consciousness of disordered equili-
bration. It may vary from an uncomfortable sensation to one in which the
patient is unable to maintain his equilibrium. It may be momentary or of
long duration.
Morbid Anatomy. — Lesions are only found in labyrinthine or apoplecti-
form vertigo, called Meniere's disease ; all other varieties are purely func-
tional. In aural vertigo there may be found hemorrhage, congestion, or
inflammation of the labyrinth ; or there may be evidences of otitis media,
obstruction of the Eustachian tube, or the presence of foreign bodies which
press upon the tympanic membrane.
Etiology. — Vertigo has been divided into ocular, aural, stomachic, ner-
vous, epileptic, and gouty.
I. Paralysis of a single muscle may cause ocular vertigo.
II. Meniere's disease may be caused by disease of the semicircular
canals and cochlea, tympanic catarrh, or spasm of the tensor tympani,
paralysis of the stapedius, or by syringing the ears, esi^ecially when the
tympanic membrane is perforated. Wax and foreign bodies in the meatus
externus may also induce it. '
' Knapp believes that there is always either a hemorrhage or serous or purulent; exudation ii>to the semi-
circular canals. — Archiv. Ophth. and Otol., vol. ii., No. 1.
1068 DISEASES OE THE NERVOUS SYSTEM.
III. Gastric vertigo is the most common, and is an almost invariable
attendant on dyspepsia. Hepatic disorders, perhaps cholsemia, or choles-
tersemia may induce it.
IV. Nervous vertigo is induced by physical or nervous excesses, and
Eamskill ranks vertigo from overwork as next to gastric in frequency.
Those who are ill-fed and overworked are predisposed to it. It is also
caused by excessive use of tea, coffee, tobacco, and alcohol. Vertigo is
commonly present in megrim or sick or nervous headache.
V. Epileptic vertigo precedes an epileptic seizure, and usually does not
occur without a well-marked paroxysm. Vertigo is also a common symp-
tom in many diseases of the nervous system, such as cerebral tumors, cere-
bral apoplexy, sclerosis, tabes, and cerebellar disease.
VI. Gouty vertigo is due to the blood-changes which characterize the
gouty diathesis. The vertigo of the aged is a result of disordered cerebral
circulation, produced by the senile condition of the heart and vessels.
Chronic malarial infection frequently induces " cachsemic " vertigo.
Symptoms. — The sensation may be that of objects moving around the pa-
tient, or of the patient moving around objects which remain stationary.
There may be a feeling of confusion or instability, or the movements may
be uncertain and unsteady. More or less suddenly a giddy sensation comes
on, objects become indistinct, the patient staggers, and perhaps falls, un-
less he grasps something to steady himself. There is no loss of conscious-
ness. Nausea and vomiting are not infrequent, and there is ringing in the
ears, fluttering in the heart, and external sounds are greatly magnified.
The first symptoms in ocular vertigo will be running together of the
letters on the page, headache, nausea, and pains in the eyes. In Meniere^ s
disease slight or serious tinnitus aurium accompanies the vertigo. Sud-
denly it becomes greatly exaggerated, and the patient feels as if he were in
motion, or actually moves in a direction opposite to the side on wliich the
ear is affected. The motion may be forwards or backwards, to one side, or
about a vertical axis. These patients may be thrown to the ground, so in-
tense are the movements. The eyes sometimes oscillate. Consciousness is
rarely lost.
After the attack of vertigo passes off deafness remains. The vertigo and
vomiting may continue for some time, and are increased by the uiDright
position. One attack follows another, until a persistent vertiginous state
is reached. When permanent deafness occurs, the vertigo ceases.
Gastric vertigo is accompanied by dyspeptic symptoms, nausea, pyrosis,
heartburn, flatulence, diarrhoea, or constipation with pain and fulness in
the hypogastrium. It is often so severe and sudden in its onset that the
patient thinks he is soon to have a stroke of paralysis. The mental state
is often deplorable, and true melancholia may ensue.
Nervous vertigo is apt to occur after excessive mental effort : the
patient while standing experiences a dizzy, sick sensation, which is rarely
severe ; objects seem to whirl for a moment, and there is a slight tendency
to fall. This form of vertigo not infrequently precedes softening of the
brain in those who are overworked and badly nourished. Irritability^
NEURALGIA. 1069
restlessness and insomnia often accompany it. And though gastric dis-
turbances may be present, their relief is not followed by a relief of the
vertigo. Sick headaches are frequently accompanied by nausea, vomiting
and this form of vertigo.
In epileptic vertigo the vertiginous sensation either replaces the fit or
accompanies it. After a paroxysm of gouty arthritis an attack of vertigo
is not uncommon.
Differential Diagnosis. — The vertigo of Meniere's disease may be distin-
guished from that of epilepsy, apoplexy, gastric dera^igements and the other
causes of vertigo, by the co-existence of tinnitus aurium, deafness, com-
bined with syncope, nausea and vomiting. The movements are in a uni-
form direction and tingling and numbness are absent.'
An otoscopic examination should be made in all cases of continued-
vertigo, and the tuning-fork and watch test should be employed.
Prognosis. — Vertigo in the adult, unaccompanied by visceral diseases, is
not dangerous. In Meniere's disease, when the labyrinthine affection is
due to some remediable defect, the disease will subside on removal of the
cause — such as cerumen, tympanic catarrh, etc. When the lesion is pri-
marily of the labyrinth, a certain degree of deafness and tinnitus always
remains, and recurrence of the attack is to be anticipated. The longer
an attack has existed the better the prognosis.
Treatment. — Gastric vertigo demands the treatment already given under
the head of dyspepsia. When disorders of vision are the cause of vertigo,
rest for the eyes and properly adjusted glasses will remove it. In Me-
niere's disease the patient should be placed in the recumbent jDOsture and
a full dose of bromide of potassium or ammonium given, followed by qui-
nine in full doses. Charcot states that this plan is attended by the best
results. ^
In nervous vertigo, iron, quinine, strychnine, and the removal of the
cause are sufficient. In the overworked and under-fed, wine, hypophos-
phites and a nutritious diet are indicated.
The vertigo of old age is benefited by the bichloride of mercury and the
tincture of iron ; a highly nutritious diet and small doses of Burgundy
wine are also of service in such cases.
NEFEALGIA.
The term neuralgia is applied in a very general way to pain, which is
either of idiopathic origin or constitutes the principal and at times the
only symptom of some obscure lesion of functional disturbance. Neuralgia
is a symptom indicative of direct injury to, or altered nutrition of, a sen-
sory nerve, which in the former case is more or less persistent, but in the
latter is usually paroxysmal.
Morbid Anatomy. — It may be functional or organic ; but in the majority
1 Woakes states that aching of the upper extremities and discoloration of the hands may occur from
irradiation of the irritation from the inferior cervical ganglion to the brachial plexus.
" Gowers and MacKenzie recommend gelsemium, salicylate of soda, counter-irritants, or even the
actual cautery applied to the mastoid region.
1070 DISEASES OF THE NEKVOUS SYSTEM.
of instances no changes can be found after death. ' When neuralgia is a
symptom of acute neuritis or peri-neuritis, the nerve trunk is hyperaemic
and swollen or degenerated and atrophied ; when a symptom of chronic neu-
ritis, the nerve has undergone sclerotic processes, and compression with
degeneration of the nerve-substance follows.
Neuritis may be descending or ascending. When it attacks nerves at
various points it is called disseminated or migrating neuritis. When
neuralgia is a symptom of pressure from tmnors, either in brain, cord or
at any jioint along the nerve trunks, tlie pain will be confined to the single
nerve. Gummata, aneurisms, and osteomata are the tumors which usually
induce such compression.
Etiology. — Neuralgia is often an hereditary disease in those of a neuro-
pathic tendency. Any disease causing general, or local, permanent or
transient ancemia, is a marked predisposing cause.
Among exciting causes are cold (especially dmnp cold), lead, mercurial
and other states of chronic blood poisoning, and traumatism. Disease of
the genito-urinary tract, especially in women, often excites reflex or sym-
pathetic neuralgia in remote nerve-trunks. Reflex neuralgia is also induced
by decayed teeth, dyspepsia, worms, constipation, etc. Neuralgia may
follow or accompany herpes zoster, and occurs very frequently in convales-
cence from relapsing fever.
It is rare before puberty, but just at this epoch there is a marked predis-
position to it. Those between twenty and fifty years of age suffer most
frequently. Women are more liable than men ; but males suffer from
sciatic neuralgia much more frequently than females.^
The theory that neuralgia often depends on dilatation of the venous
plexuses which surround a nerve at its exit from a bony canal, is supported
by the fact that the first branch of the trigeminus suffers far oftener than
either the second or third, or both combined. ^
Symptoms. — Before the actual pain begins in a nerve, there may be
numbness, slight cutaneous hyperaesthesia, or some peculiar skin sensation
which is well-known by the neuralgic individual. The pain is at first in-
termitting, later it is continuous with slight remissions. The character
of the pain varies : it may be dull, boring, stabbing, tearing or darting,
and is confined very distinctly to the course and distribution of the af-
fected nerve. Indeed, many patients trace exactly the course of some
nerve when pointing out the locality of the pain. Sudden movements, as
turning and coughing, often increase the pain.
Increase of pain on pressure is an important point ; the exacerbation is
greatest during a paroxysm, and greater in proportion to the intensity of
the original pain. Certain points are markedly sensitive : these are at the
exit of nerves from bony canals, or foramina, the spot where they pass
1 It is claimed that the acid products of metamorphosis of nerve-tissue acting upon the nervous system
must be neutralized by the blood, before pain ceases. Also, that nutritive lesions of the central sensory
tract within the confines of the gray matter are the essential lesions. Peripheral pain is supposed to
originate in the cord.
2 Ilenle states that the left side is predisposed to intercostal neuralgia on account of the arrangement
of the venous circulation.
3 Allg. Wien. Med. ZeiL, 1876, pp. 24, 36.
NEURALGIA. 1071
through a muscular aponeurosis, at their bifurcation, and where terminal
branches become superficial. These pain-jjoints are better marked the
longer the patient has suffered from neuralgic attacks. In connection
with the j)ain, there is generally associated with it some vaso-motor dis-
turbance, as extreme pallor or vivid redness and reflex movements and
twitchings of the muscles. Sliould the nerves of a gland be attacked, se-
cretion will probably be increased. After cessation of the pain the part
often feels sore and bruised, and there is a general sensation of exhaustion
and weariness.
Actual temporary paralysis, muscular spasm, herpetic eruptions, and
ansesthesia of the skin may complicate or follow an attack of neuralgia,
and later the muscles supplied by the affected nerves may be atrophied
and become abnormally weak. During a prolonged paroxysm the jiain
may extend from one nerve to another of a different origin. ' In a few rare
cases mental effort or excitement will exacerbate, or even excite, a parox-
ysm of neuralgia.
If neuralgia be caused by neuritis the pain is more continuous, and the
nerve may be felt as a hard cord beneath the skin, which latter is red and
cedematous. With neuritis of a mixed nerve, twitching and contractions
occur with the pain. In neuralgia of functional origin, the pain is more
likely to shift and to involve corresponding tracts on the other side of the
body or head.
One of the most common forms of neuralgia is that of the tri-facial
nerve, usually attended with painful spasm, called tic douloureux. One
or two, rarely all the divisions, may be involved. The first branch is its
usual seat, when it is termed hrow-ague ; the third is rarely attacked.
When the ophthalmic division is affected the neuralgia is called hemi-crania
or migraine.
Claris hystericus is a variety of tic in which there is a sensation as of a
nail being driven into the skull. It is usually met with in anaemic females.
The hair on one side of the head or one eyebrow may turn white, or pig-
mentation may occur along the course of the pain, and the tongue on the
side of the pain may exhibit epithelial overgrowth in long standing tic
douloureux.
Acute glaucoma and recurrent iritis are said to result from trophic
changes due to neuralgia.^
Pain on pressure is usually best marked (1) at the exit of the frontal
branch, (2) the exit of the inferior maxillary branch, (3) over the tempo-
ral and parietal bones, or (4) along the supra-orbital ridges (supra-orbital
neuralgia).
Sciatica is a neuralgic affection of the sensory nerves of the sciatic plexus.
It may be caused by the pressure of tumors and inflammatory exudation
within the pelvis, or by caries or carcinomatous vertebrae at the point where
the nerves pass through the intervertebral foramena. Irritation of the pe-
J Epileptiform neural£?ia is that variety of tic doulonreux where the seizures are very abrupt and ac
companied by spasm of the facial muscles.
» Anstie states tliat near the painful parts ihe periosteum and the fibrous tissue are thickened.
1072 DISEASES OF THE ISTERVOUS SYSTEM.
ripheral branches of tlie sciatic, due to pressure along the line of the nerve,
from tun^ors, etc., may cause sciatica, but in the majority of instances the
origin is rheumatic and the direct result of taking cold. Chronic malarial
infection may be the cause of sciatica. It is most frequently met with in
males between the ages of twenty and sixty-
It is usually preceded by tingling or stiffness in the buttock, back of the
thigh, knee and leg. The pain may be continuous or intermittent,
and its most frequent seats are the posterior and outer part of the thigh
(particularly near the tuberosity of the ischium), the outer side of the
ankle, and the dorsum of the foot. It usually comes on gradually, the
pain becoming more intense at night. The patient usually lies with his
legs flexed. In walking he moves the affected leg slowly, as any sudden
motion greatly aggravates the pain. The pain is most markedly increased
by pressure over the posterior iliac spine, at the fold of the buttock and the
head of the fibula. Cramps in the muscles of the leg are common. The
limb maybe atrophied and the patient pass into a semi-paralytic condition,
which is very apt to be chronic. It is a very obstinate affection, lasting
usually from six weeks to two months, though it may last for years. Re-
lapses are not uncommon.
Intercostal neuralgia is an affection of any of the dorsal nerves ; the an-
terior branches of two or three of the nerves upon the left side are those
usually affected. It occurs in women as a rule. Intermittent pain is felt
in the region of the sixth, seventh, eighth and ninth intercostal nerves,
tearing or stabbing in character, increased by coughing or sneezing, and
perhaps accompanied by a dry cough.
There are three diagnostic points of tenderness : (1) at the exit of the
nerves from the spine, (2) at the side of the chest, where they become
subcutaneous, and (3) near the sternum or median line at the terminal
branches. Cardiac palpitation, dyspnoea, nausea and vomiting are fre-
quent symptoms of this ^o-coWq^ false pleurisy . Herpes zoster, intolerable
itching, and attacks of angina pectoris often complicate it.
Cervico-occipital neuralgia is usually attended by pain along the course
of the occipitalis major,' and often resembles that form of muscular rheu-
matism called torticollis, or wry-neck. (See art. Eheumatism.) A branch
of the Iracliial plexus may be involved ; the ulnar, however, is more fre-
quently affected than any other.
Coccyodynia is common in women, and is due to neuralgia of the coc-
cygeal plexus.
Headaclie. — Headache, or cephalalgia, is properly a form of neuralgia, as
it can only be referred to the sensory nerves supplying the meninges and
scalp, and like other neuralgias is of both organic and functional origin.
It is a frequent symptom of cerebral disease, either inflammatory or such
as produces compression of the cranial contents, and is especially severe in
the acute forms of meningitis and some cerebral tumors. It results from
disturbance of the cerebral circulation, which causes either compression of
the cranial nerves or angemia, and consequent disturbance of nutrition. Its
1 Gray's Anatomy, pp. 636-637.
NEUKALGIA. 1073
primary cause, however, is more frequently in other organs, as the stomach
or genito-urinary tract, in which cases the headache is the result of reflex
disturbances, frequently of the circulation, from vaso-motor irritation. Of
a similar nature is the headache resulting from the strain of the ciliary
muscle, consequent upon defects of refraction. Again, headache is fre-
quently a symptom of blood poisons, as in rheumatism, gout and septic
diseases.
In these diseases, as probably also in headache with high temperature, the
condition is presumably one of direct irritation of nerve centres, or of de-
fective nutrition. Headache assumes a great variety of forms. It may be
limited to one half the head, to the forehead, vertex, occiput, temporal re-
gion, or any point on the cranium, or it may be diffuse and extend to the
eye, face and neck. In character and severity it may assume any of the
characteristics of neuralgia. Headache is a symptom of exceedingly diffi-
cult interpretation. In a general way, however, it may be stated that head-
ache of gastric or hepatic origin is commonly frontal and throbbing in
character and associated with cerebral congestion. It may be bilateral or
unilateral. Headache at the vertex is quite constantly symptomatic of cere-
bral disturbances of local origin, or due to reflex irritation starting in the
pelvic organs, especially the genital tract of the female. Pain in the occip-
ital region is mostly an accompaniment of disorders of circulation, and vaso-
motor spasm and anaemia in particular. The pain of cerebral compression
or tumor, although often diffuse, is generally localized, persistent, and very
intense.
All forms of cephalalgia may be attended by hyperaesthesia, especially of
the optic and auditory nerves, with subjective sensations of light and
sound, by vertigo, nausea, drowsiness or wakefulness, and possibly deliri-
um. Visceral neuralgias have been considered in the list of Visceral Dis-
eases.
Differential Diagnosis. — Neuralgia may be mistaken for myalgia, syphi-
litic periostitis, and for cerebral abscess.
Myalgia is distinguished by its non-paroxysmal character, by the pain
being increased by motion, and by the fact that the attachments of the
muscles are the points chiefly involved.
SypMlitic periostitis \'s, to be distinguished from neuralgia by the pres-
ence or absence of other symptoms of constitutional syphilis.
Cerebral abscess often occurs secondarily to caries of the internal ear and
after otitis in childhood ; neuralgia rarely appears before puberty. Cere-
bral abscess frequently follows a blow or injury ; neuralgia comparatively
seldom. In the former there are no true points douloureux ; these are
present early in severe neuralgia. In cerebral abscess the pain does not
completely intermit ; intermissions of pain, complete, and of considerable
length, occur in neuralgia. The pain is at first severe in cerebral abscess ;
in neuralgia it is slight at first and gradually exacerbates. Pain in cere-
bral abscess is often limited in situation, seems deep-seated, though often
it has no relation to the site of the abscess ; in neuralgia pain is superficial,
and follows the distribution of recognizable nerve branches belonging to
1074 DISEASES OF THE NEKVOFS SYSTEM.
the trigeminus or great occipital. In cerebral abscess there are no well
localized vaso-motor or secretory complications, while lachrymation or
congestion of the conjunctiva usually occurs in neuralgia. Cerebral ab-
scess is rare in old age, and then generally traumatic ; neuralgia is most
common at that period.
Prognosis. — Life is rarely compromised by neuralgia, but when it is per-
sistent the general health may be seriously affected. When occurring in
early life and with no hereditary predisposition the prognosis is the most
favorable.
Treatment. — Neuralgia has been well said to be the cry of a nerve for let-
ter blood. Should anasmia be evidenced, a generous diet, cod-liver oil, the
hypophosphites, or small doses of phosphorus and the appetizers, along with
quinine, iron and strychnine should be ordered. Neuralgia due to syphilis
demands iodide of potash ; to rheumatism, the anti-rheumatics ; to gout,
colchicum ; and to malaria, quinine, but in many non-malarial cases also,
especially in tic, quinine is the most effectual remedy. A patient with
neuralgia should be removed from all exposure to cold and irritations of
all kinds.
Locally, blisters, the continuous current, chloroform, opium, belladonna
and veratria liniments, and cold, or very hot water may be applied, and
these sometimes afford permanent, nearly always temporary relief. Aco-
nite enjoys the highest reputation at the present day among local remedies.
Firing, sinapisms and actual cautery are frequently beneficial. Sometimes
prolonged residence in a warm, dry climate is the only means of effecting
a permanent cure.
For immediate relief of pain, morphine is the most effectual. Neuralgic
attacks and headache that are accompanied hj flushing of the face are often
relieved by ergot. But when the face is very pale, nitrite of amyl is to be
preferred. Gelsemium is sometimes especially effectual in the treatment
of trigeminal neuralgia. This and croton chloral are largely employed.
In severe chronic neuralgias a portion of the nerve may be excised (neu-
rectomy), or the nerve may be simply cut (neurotomy).
Nerve-stretching may be practised upon any trunk which can be sur-
gically reached. The sciatic is the nerve which has been stretched with
most success. In headache, cold to the head and heat to the feet, or at
times the persistent application of heat to the head for several hours, will
afford relief. Guarana, caffeine, and similar remedies are often very useful
in sich headache. In these cases a purge or an emetic will also frequently
bring relief.
In all severe cases of sciatica, in addition to the treatment of neuralgia
in general, absolute rest is essential to its successful management. If it is
caused by gout, rheumatism, or syphilis, treatment appropriate to these
conditions must be employed. If there be a chronic malarial taint, quinine
and arsenic must be given in full doses. The hypodermic injection of
morphine gives the most speedy relief. The point of the needle should be
introduced deep into the tissues over the exit of the nerve. In many in-
stances its daily use for some time will cure sciatica, even of long standing.
MEGRIM. 1075
The continuous voltaic current is often palliative and sometimes curative.
The systematic treatment with baths at the Hot Springs of Arkansas and
Virginia, I have found especially efficacious in sciatica that has resisted all
other remedial measures. The apjolication of the hot iron and blisters
along the course of the nerve have, in some instances, acted remedially.
MEGRIM.
{Sick Headache.)
Sick headache, or hemi-crania, is a form of headache attended by marked
gastric and nervous disturbances.
Morbid Anatomy. — Megrim is probably due to disordered cerebral circu-
lation, the exciting cause of which is vaso-motor disturbance. Changes
similar to those of epilepsy are generally considered to be the pathological
condition, that is, vaso-motor irritation with arterial sjoasm and consequent
anaemia of the cerebral ganglia, followed by relaxation and congestion.
This condition, however, still demands an ultimate cause, which is prob-
ably nervous (cerebro-spinal) exhaustion, following prolonged irritation, as
indicated in its etiology.
Etiology. — Megrim is often hereditary, or, more exactly, the nervous
weakness and instability which predispose to the affection are hereditary.
Whether inherited or acquired, it commonly develops before thirty, and
subsides in later life. Digestive disturbances are frequent exciting causes,
but a much larger proportion of cases are due to nervous irritation and
exhaustion. It is an almost unfailing symptom of chronic uterine irrita-
tion or sexual excesses, and is frequently due directly to mental labor,
worry, or excitement. In neurasthenic patients, it is often excited by
over-exertion, or the lack of it, by too much or too little sleep, and by
irritation of the nerves of special sense — flickering light or loud noises —
and in some cases the slight disturbance of co-ordination attendant upon
the use of the stereoscope or opera-glass is sufficient to excite an attack.
Symptoms. — As the term indicates, hemi-crania is almost invariably
confined to one side of the head, and is generally distinctly localized in the
frontal, temporal, or occipital region, and even when it attacks all three
places, or becomes diffuse, the pain is still most intense and persistent at a
small circumscribed point in each region. In such cases there is often a
sensation of an intra-cranial cord joining the painful points.
Frequently, and esjDecially in cases due to ocular strain, the eye becomes
the seat of pain and is tender and hypersesthetic. Early in the attack the
face may be pale and the cardiac action slow and weak. Very soon, how-
ever, the head becomes hot and the pulse slow, and with each heavy heart-
beat the carotids pulsate strongly and the pain is greatly increased. Gen-
erally within a few hours nausea supervenes, and may be attended by dis-
tinct recurring chills and paleness of the surface. The patient is greatly
depressed and is wretchedly sick. If the pain is not too severe he may fall
asleep, to wake in tlie morning with only a soreness about the scalp and
stiffness of the muscles of the neck remaining. More frequently the nausea
1076 DISEASES OF THE 2TERV0US SYSTEM.
increases until relieved by an attack of vomiting. A few hours of sleep
then restores the patient to his usual condition.
Quite characteristic premonitory symptoms are present in many cases.
The most common are disorders of vision in the form of retinal anaes-
thesia or irritation. The anesthetic spot may be located in any part of the
retina, but generally affects the macula lutea. Eetinal irritation causes the
patient to see variously colored lights and scintillations. The disturbance
in vision may commence with a wavy glimmering at the outside of the
field of vision or by the appearance of a black spot close to its centre. Simi-
lar disturbances of the other nerves of sense, either irritative or paralytic,
may be present, but they are less common than the visual disturbances.
Hemi-crania may last from a few hours to two or three days, but in most
cases is relieved within twenty- four hours. It is very apt to recur at regu-
lar intervals, and become more intractable with each attack.
Treatment. — By way of prophylaxis, the patient should avoid all known
causes of the attack, and pursue a tonic course of living. At the beginning
of the attack full doses of alcoholic or other stimulants may prevent its
development. Later, the bromides, quinine, strychnia, belladonna, canna-
bis indica, caffeine, guarana, and chloral at times afford relief. When
nausea is present, however, an emetic, followed by a few hours' sleep, brings
about the most speedy cure. Morphia hypodermically is the best and
surest means for the relief of pain.
During the interval between the attacks the treatment should be such as
will as far as possible render inoperative its cause. No two cases will re-
quire the same hygienic or therapeutic measures. The main thing is to
overcome the acquired or hereditary neurotic tendencies of the patient by
diet, exercise in the open air, and cheerful surroundings. Drugs accom-
plish very little for this class of sufferers except to give temporary relief.
ECLAMPSIA AND INFANTILE CONVULSIONS.
Epileptiform convulsions are of frequent occurrence in connection with
distinct lesions of the nervous centres as well as with various reflex disturb-
ances. Indeed, they may be symptomatic of any cerebral disease, as com-
pression from fracture, hemorrhage and tumors, or thrombosis, embolism
and inflammatory processes. In those conditions where they can be,
■ascribed to distinct pathological changes they are termed eclampsia. Clini-
cally such convulsions, as well as those from uraemia and other poisons, are
often identical in appearance with epileptic fits, and are to be diagnosticated
by the concomitant symptoms.
When such convulsions occur in children, as they often do from reflex
irritation during teething, in gastro-intestinal disorders, in the early stages
of blood poisoning, and, indeed, in any condition which in the adult pro-
duces a chill, they are then called infantile convulsions. Although fre-
quently indistinguishable from epilepsy, the convulsions of eclampsia, and
more particularly infantile convulsions, may present only a portion of the
true epileptic fit or even be very slight. They are, moreover, less regular
SEASICKNESS. 1077
in their occurrence and, until the cause is removed, tend to increase in fre-
quency and intensity. They are less sudden in their development also,
and, although much more fatal, owing to their frequent dependence upon
an irremediable cause, generally cease permanently when the cause is re-
moved. Infantile convulsions present the widest range of intensity, but are
always a cause of anxiety, especially when the respiratory muscles are in-
volved, as is frequently the case.
The indications for treatment are,of course,f ound in the cause. In syphi-
lis, uraemia, ansemia, gastro-enteritis, etc., the treatment will in most cases
be under way before the occurrence of convulsions. When, however, they
are the initiatory symptoms, all possible causes must be carefully sought.
The discovery of a cause will indicate the treatment. Infantile convulsions
often arise from slight causes that frequently escape detection. In such
cases the general health must be improved, the alimentary canal freed from
a possible hidden cause, and the clothing carefully inspected and made
loose and unirritating. The usual anti-spasmodics, belladonna, the bro-
mides, etc., may then properly be used. Hot baths, counter-irritants to
the back and neck, or cold to the head, are often of service. Chloroform
is the most appropriate agent for controlling the spasms temporarily.
SEASICKNESS.
The term seasickness is applied to a peculiar form of functional disturb-
ance of the nervous system characterized by severe depression and persistent
nausea and vomiting.
Morbid Anatomy. — The only organic changes which have been found,
which are probably secondary, are slight hyperemia of the gastric mucous
membrane, due to the prolonged efforts at vomiting and the presence of
abnormal quantities of gastric juice, and cerebral anaemia with congestion
of the spinal centres. The primary irritation may properly be considered
as a form of shock arising from the unusual combination of nervous im-
pressions calling for unaccustomed action on the part of the nerve centres.
In other words, the nerve centres are embarrassed, and the resulting nervous
irritation manifests itself through vaso-motor disturbances in precisely the
same manner as is seen when persons blush under embarrassing circum-
stances or pale when startled. In the present instance this disturbance,
though general, is most marked in gastro-intestinal and cardiac derange-
ments. Paleness of the surface from vaso-motor irritation is probably asso-
ciated with anaemia of the brain and congestion of the spinal centres.' As
a consequence there is irritation of those centres, manifested by severe gas-
tric irritability, with nausea and vomiting of centric origin.
Etiology. — As indicated in the name, seasickness is most commonly the
result of the motion of a ship. It may, however, be the result of any un-
usual motions to which the person is unaccustomed, and especially such as
' Dr. Clapham reports an autoi)sy made four hours after death upon a man accidentally killed while
vomiting, in which there was intense congestion of the spina! cord and distention of the vessels, closely
resembling the condition found in an epileptic who had died during an epileptic seizure —London Lancet,
1864.
1078 DISEASES OP THE JSTERVOUS SYSTEM.
raise the body rapidly or suddenly allow it to fall, as the motion of a swing
or an elevator. Waltzing, riding backwards, turning a somersault, or the
sudden jerk of a railroad train as it starts or stops or goes rapidly around
curves in the track, may each produce a precisely similar condition. They
are not usually followed by the full development of the disease, solely be-
cause they are not repeated or continued sufficiently long.
Moreover, it is not always necessary that the patient himself should be
moved. Frequently, simply watching oscillating objects is sufficient to
produce a mild form of sickness. Personal idiosyncrasy is a very impor-
tant factor in predisposing to seasickness.' Some persons never suffer, even
under the most trying circumstances, while others are unable to endure the
slightest motion on the water or elsewhere. This peculiar susceptibility
varies also in the same person, and an individual who has resisted through
several sea voyages may finally succumb during a sail on some small inland
lake.
Habit and experience are generally suffiicent to do away entirely with the
susceptibility to the disease, but occasionally an individual suffers, it may
be with increasing severity, whenever he is on rough water.
Symptoms. — Seasickness usually presents the two stages of (1) depression
and exhaustion, and (3) reaction.
It begins with a sense of weight and epigastric oppression, often describei?
as a feeling of coldness, which at first may be distinctly intermittent, oc-
curring only during the rapid rise and fall of the vessel. It may, however,
be continuous from the start, and even at first be a distinct nausea. In any
event it speedily becomes so, and is accompanied by vertigo and headache.
INausea is quickly followed by vomiting, which partakes of the nature of both
gastric and cerebral vomiting. N'ausea is always most intense, and at the
same time the vomiting is often sudden and projectile, as from a central
cause. As the vomiting continues the ejected matter is composed of in-
tensely acid gastro-biliary secretions. Constipation is the rule, and all the
secretions except the saliva are decreased. The appetite is entirely lost, and
there is a marked repugnance to food, and especially to all forms of fat. In
many cases the simple smell or thought of food is sufficient to excite a
paroxysm of vomiting. In this stage the mental depression is very charac-
teristic, the patients almost exulting in the thought of shipwreck as afford-
ing relief from their sufferings. In the majority of cases this condition con-
tinues from three to five days, provided the voyage is of that length, during
which time the nausea, vomiting and mental depression continue with vary-
ing intensity, and is then followed by reaction and a more or less rapid dis-
appearance of the vomiting, with return to the normal condition.
In such cases, owing to the enforced abstinence, there is for a time a rav-
enous appetite and a feeling of special well being.
In other cases, however, the stage of depression continues until the pa-
tient is again on terra firma, lasting it may be for weeks, or it may in a few
days pass into a stage of partial collapse. The patient is sleepy and apa-
1 Tn some instances naval officers of many years' experience have been led to leave their profession from
their inability to accustom themselves to the sea.
SEASICKNESS. 1079
tLetic, the surface is cold, and he suffers from neuralgic pains or general
numbness. Finally, a partial coma may supervene and the case assume a
very grave aspect.
Convalescence is generally rapid, and the patient passes from a state of
the greatest depression to one of comfort and entire recovery within a few
hours ; but when the case has been prolonged, convalescence may be de-
layed and be attended by rise in temperature and other febrile conditions.
Other forms of seasickness present differences of degree rather than of
kind.
Diagnosis. — Owing to the peculiar circumstances under which it is devel-
oped, seasickness can rarely be mistaken for any other condition. It may
simulate an attack of gastro-enteritis in the early stages. In seasickness
constipation is the rule, and the intense nausea, the persistent violent vom-
iting, and the loathing of food are much more marked. Gastro-enteritis is
most common in children, while they seldom suffer severely from seasickness.
Prognosis. — It is very rarely fatal, but occasionally a condition of collapse
develops which, if not assiduously treated, may pass into coma and death.
A general irritability of the gastro-intestinal mucous membrane often re-
mains for some time after a prolonged sickness.
Treatment. — The remedies proposed and tried for seasickness are innu-
merable, but as most of them are only palliative or worse than useless it is
unnecessary to enumerate them. Two general plans of treatment have been
adopted, based upon the accepted pathology of vaso-motor disturbance and
spinal congestion, (1) the sedative, and (2) the stimulant. Among the
remedies of the first class counter-irritation to the spine, or ice bags, the
bromides and nitrite of amyl have proved the most useful. The applica-
tion of ice to the spine was advocated by Dr. Chapman as being the best
means for controlling spinal congestion. It is of decided value, but is un-
comfortable and hardly available for a large number of cases. The bro-
mides are often used successfully, but their use must be begun some time
before the voyage and continued in large doses until the patient is fully ac-
customed to the motion of the sea. Amyl nitrite, both from the rapidity
with which it acts and the certainty of its results, seems to be the most de-
sirable and efficacious remedy yet proposed. It should be given in full
doses upon the first appearance of epigastric distress, and repeated as nec-
essary. '
Under the class of stimulant remedies the various forms of alcohol and
the diffusible stimulants are most used, but the results, though good in some
cases, are generally far from satisfactory.
In some cases of slight disturbance, any device which controls the move-
ments of the diaphragm may be sufficient to prevent the development of vom-
iting. Among the most successful of these is a prolonged even inspiration
as the vessel rises, followed by a similar expiration during descent. It
must be confessed, however, that in many instances all remedies are un-
availing, and only time and experience can effect a cure.
J Dr. Clapham (Lancet, vol. ii., 1875, p. 376) reports 121 successful cases out of a total of 124 in which amyl
nitrite was used.
INDEX.
Abdominal aneurism, difEerential diagnosis, 528.
etiology, 527.
morbid anatomy, 527.
physical signs, 528.
prognosis, 528.
symptoms, 527.
treatment, 538.
Abdominal dropsy. See Ascites, 333.
Abortive form of typhoid fever, 630.
Abortive typhus, 730.
Abscess, 3.
Abscess, bronchial, 129.
Abscess of the bralu. See Brain, abscess of, 975.
Abscess of tlie liver. See Hepatitis, suppurative, 349.
Abscess, pericsecal. See Perityphlitis, 281.
Abscess, perinephritic. See Perinephritis, 600.
Abscess, retropharyngeal. See Ketropharyngeal ab-
scess, 223.
Acholia. See Catarrh of the bile-ducts, 397.
Active hypersemia of the liver. See Liver, hyperae-
mia of, 337.
Acute anterior polio-myelitis. See Infantile spinal
paralysis, 1006.
Acute aortitis, 511.
Acute articular rheumatism. See Kheumatism, artic-
ular, 858.
Acute ascending paralysis. See Paralysis, acute
ascending, 1028.
Acute Bright's disease of the kidney. See Kidney,
acute Bright's disease of, 552.
Acute bulbar paralysis. See Paralysis, acute bulbar,
1001.
Acute capillary bronchitis, 46.
Acute catarrhal bronchitis, 42.
Acute catarrhal laryngitis, 17.
Acute coryza, 9.
Acute croupous laryngitis, 27.
Acute endarteritis. See Endarteritis, acute, 511.
Acute exudative endocarditis. See Endocarditis,
acute exudative, 431.
Acute gastric catarrh. See Sub-acute gastritis, 229.
Acute general diseases, classification of, 610.
definition of, 609.
theories regarding the nature of, 610.
Acute hydrocephalus. See Meningitis, tubercular,
943.
Acute intestinal catarrh. See Enteritis, 257.
Acute meningitis. See Meningitis, acute, 935.
Acute miliary tuberculosis. See Tuberculosis, acute
miliary, 706
Acute myelitis. See Myelitis, acute, 996.
Acute pancreatitis. See Pancreatitis, acute, 410.
Acute parenchymatous nephritis. See Kidney, acute
Bright's disease of, .552.
Acute pericarditis. See Pericarditis, acute, 420.
Acute phthisis. See Phthisis, 172.
Acute spinal paralysis of adults. See Paralysis,
acute spinal of adults, 1009-
Acute ulcerative endocarditis. See Endocarditis,
acute ulcei'ative, 433.
Acute uraemia. See Uraemia, acute, 537.
Acute yellow atrophy of liver. See Parenchymatous
hepatitis, 356.
Addison, 888.
Addison's disea-e, difEerential diagnosis, 899.
etiology, 897.
morbid anatomy, 897.
prognosis, 899.
syra'ptoms, 899.
treatment, 900.
Adhesive pleurisy. See Pleurisy, 162.
Adhesive pylephlebitis. See Pylephlebitis, adhesive,
362. , ,
Adults, acute spinal paralysis of. See Paralysis,
acute spinal of adults, 1009.
Albrecht, 740.
Alcoholism, differential diagnosis, 915.
etiology, 914.
morbid anatomy, 913.
prognosis, 915.
sj'mptoms, 914.
ti eatment, 915.
" Alcoholismus." See Alcoholism, 913.
Allbutt, 445.
Althaus, 867.
Ammonaemia, difEerential diagnosis, 907.
etiology, 900.
morljid anatomy, 900.
prognosis, 907.
symptoms, 900.
treatment, 907.
Amyloid degeneratiim of artories, 513.
Amyloid degeneration of the heart. See Heart,
amyloid degeneration of, 494.
Amyloid degeneration of the intestines. See Intes-
tines, waxy degeneration of, 297.
Amyloid degeneration of the spleen. See Spleen,
waxy degeneration of, 417.
Amyloid form of Bright's disease. See Waxy kid-
ney, 575.
Amyotrophic lateral sclerosis, difEerential diagnosis,
1026.
etiology, 1025.
morbid anatomy, 1025.
prognosis, 1026.
symptoms, 1026.
treatment, 1026.
Anaemia, difEerential diagnosis, 884.
etiology, 883.
morbid anatomy, 883.
prognosis, 885.
symptoms, 884.
treatment, 885.
Anaemia, cerebral. See Cerebral anaemia, 933.
Anajmia of the brain. See Cerebral anaemia, 933.
Anaemia of the lungs, 129.
Anagmia, proL'ressive pernicious. See Progressive
pernicious anaemia, 888.
Anaemia, pulmonary, 129.
morbid anatomy of, 129.
svmptoms of, 129.
Anse'^tliesia, 928.
Anchylostomnm duodenale, 309.
Andejvoii, Dr. McCall, 178.
Andral. 8S8.
Aneurism of the brain. See Cerebral tumors, 977.
Aneurism of the heart. See Heart, aneurism of, 500.
Aneurism, valvular, 434.
Angina pectoris, differential diagnosis, 505.
etiology, 504.
prognosis, 505.
symptoms, 504, 505.
treatment, 506.
Angiomata of the brain. See Cerebral tumors, 977.
Aniniske, 982.
Anstie, 171, 1071.
Anterior polio-myelitis, acute. See Infantile spinal
paralysis, 1006.
Anterior polio-myelitis, chronic. /See Polio-myelitis,
chronic anterior, 1010.
1082
INDEX.
A.ntbracosi8, 182.
Antiseptic treatment of phthisis, 203.
Aortic insufflciencj'. See Aortic regurgitation, 448.
Aortic obstruction. See Aortic stenosis, 444.
Aortic regurgitation, differential diagnosis, 452.
etiology. 449.
morbid anatomy, 448.
physical signs, 450.
symptoms, 449.
Aortic stenosis, differential diagnosis, 447.
etiolog3% 445.
morbid anatomy, 444.
physical signs, 446, 447.
symptoms, 444.
Aortitis, 511.
Aphasia. See Cerebral thrombosis and embolism, 9.56.
Apoplexy, cerebral. See Cerebral apoplexy, 964.
Apoplexy, circumscribed pulmonarj', 120.
Apoplexy, diffuse pulmonary, etiology of, 125.
morbid anatomy of, 124.
physical signs of, 125.
prognosis of, 125.
symptoms of, 125.
treatment of, 12.5.
Apoplexy, nodular pulmonary, 120.
Apoplexy, spinal. See Spinal apoplexy, 1029.
Aphthous stomatitis. See Follicular stomatitis, SIO.
Arndt, 1053.
Arteries, cnncer of, 513.
classification of diseases of, 513.
fatty degeneration of, 513.
guneral dilatation of, 514.
syphilis of, 513, 514.
tuberculous granules in, 513.
waxy degeneration of, 5.13.
Arterio-capillary filn-osis with contracted kidney,
diagnosis, 587.
morbid anatomy, 584, 585.
symptoms, 586.
Arterloma, 514.
Arthritis deformans, differential diagnosis, 867.
etiology, 86").
morbid anat< >my, 865.
prognosis, 867.
symptoms, 866, 867.
treatment, 8R7.
Arthritis rlieuiuatoid. See Arthritis deformans, 865.
Articular rlicumatism, acute. See Rheumatism,
acute articular, 858.
chronic. See Rheumatism, chronic articular.
Ascaris Inmbricoides, 308.
Ascending paralysis, acute. See Paralysis, acute
ascending, 1028.
Ascites, differential diagnosis, 335.
etiology, 3.33.
morbid anatomy, 333.
physical signs, 334.
prognosis, 336.
symptoms, 334. ■
treatment, 336.
Asthma, bronchial, 59.
differential diagnosis, 62.
etiology, 59.
pliysical signs, 61.
prognosis, 62.
symptoms, 60.
treatment, 63.
Ataxia, locomotor. See Locomotor ataxia, 1018.
Atelectasis, 129.
Atelectasis, congenital, 129.
Atelectasis, pulmonary, differential diagnosis, 131.
etiology of. 130.
morbid anatomy of, 129.
physical signs, 1.30.
prognosis of, 131.
symotoms, 130.
treatment, 131.
Atheroma. See Chronic endarteritis, 511.
Atonic dyspepsia and chronic gastritis, 235.
Atrophic iiasal catarrh, 13.
difl rential diagnosis, 14.
etiology, 13.
niorb'd anatomy, 13.
prognosis, 14.
symptoms, 14.
treatment, 14.
Atrophy of the brain. See Brain, atmptiy of, 988.
Atrophy of the heart. See Heart, atrophy of, 496.
Atrophy of the liver. See Liver, chronic atrophy
of, 370.
Atrophy of the lung, 144.
Atrophy, progressive muscular. See Progressive
muscular atrophy, 1011.
Autumnal fever, i'ee Typhoid lever, 611,
Bacillus, the tubercle, 172, 174 175.
Balfour, 455, 457.
Bamberrier, 82, 434, 460.
Bard, 669.
Barloive, 471.
Bartel, 557.
Barthez, 913, 949.
Barlholoiv. 578.
Barton, f,?A.
Bar well. 863. 866.
Basedow's disease, differential diagnosis, 510>
etiology, 509.
morbid anatomy, 508, 509.
prognosis, 510.
symptoms, 509.
treatment, 510.
Bastian, 962, 964, 1011, 1030.
Beard, 1064.
Reck, 588.
Beduar, 936.
Begbie, 466. 467.
Bellingham, 453, 467, 528.
Bell's palsy. See Facial paralysis, 1059.
Bell's paralysis. See Facial paralysis, 1059.
Bence-.Join-». 1052.
Benedict, 803.
Beneke, 205.
Benjamin, 980.
Bennet, 95,891.
Bergnumn, 1013.
Berlin, 462, 466.
Bernard, 265.
Biermer, 889.
Bile-ducts, catarrh of, differential diagnosis, 397,
eti()loi;T,396.
morbid"^ anatomy, 395.
physical signs. 397.
prognosis, 397.
symptoms, 396.
treatment, 397.
Biliary calculi. See Gall-stones, 401.
Biliiiry colic, 404.
Biliary passages, exudative inflammation of, differ*
ential diagnosis, 399.
etiology, 398.
morbid aniitomy. 398.
phy^ical signs, 398.
prognosis, 399.
symptoms, 398.
treatment, 399
Bilious remittent fever, 822.
Biliousness. See Functional derangements of livei^
406.
Billroth, 696, 699, 701, 739.
Binz, 802.
Birch- Hirschf eld, 417, 910.
Bii-d, 802.
Black measles. See Measles
"Bleeders.'" See Haemophilia, 902.
Bleeding piles. See Hiemorrhoids, 304.
Blood-vessels, classification of diseases of, 511.
Bloody flux. See Dysentery, 272.
Bhrin. 821.
Bothriocephalus latus, 808.
Bouchard, 965.
Bouchut, 946.
Bouillard, 85.
Bouillaud, 441.
Bourneville, 958.
Brain, abscess of, differential diagnosis, 977.
etiology, 976.
morbid anatomy, 975.
prognosis, 977.
symptoms, 976.
treatment, 977.
Brain, aniemin of. See Cerebral anasmia, 933.
Brain and meninges, tumors of, differential diagno-
sis, 982-984.
etiology. 981.
morbid anatomy, 978-981.
prognosis, 984.
INDEX.
1083
Brain find meningps, tumors of, sj'mptoms, 981.
treatment, 984, 985.
varieties, 977.
Brain, aneurisms of. See Cerebral tumors, 977.
Brain, angiomata of. See Cerebral tumors, 977.
Brain, atropliy of, differential diagnosis, 990.
etiology, 989.
morbid anatomy, 988.
prognosis, 990.
symptoms, 989.
treatment, 990.
Brain, cholesteatoma of. See Cerebral tumors, 977.
Brain, cysticerci of. See Cerebral tumors, 977.
Brain, cysts of. See Cerebral tumors, 977.
Brain, diseases of, 930.
Brain, embolism and tlirombosis of. See Cerebral
thrombosis and embolism, 956.
Brain, fibromata of. See Cc'rebral tumors, 977.
gliomata of. See Cerebral tumors, 977.
hydatids of. *(? Cerebral tumors, 977.
hyperajmia of. See Cerebral hypersemia, 930.
Brain, hypertrophy of, differential diagnosis, 988.
etiology, 987, 988.
morbid anatomy, 987.
prognosis, 988.
symptoms, 988.
Brain, lipomata of. See Cerebral tumors, 977.
Brain, localization of lesions within, 970-972.
Brain, myxomata of. See Cerebral tumors, 977.
osteomataof. See Cerebral tumors, 977.
pa))illomata of. See Cerebral tumors, 977.
psammomata of. See Cerebral tumors, 977.
sarcomata of. See Cerebral tumors, 977.
Brain, sclerosis of. See Sclerosis of the brain, 985.
Brain, softening of. See Cerebral softening, 959.
Brain, thrombosis and embolism of. See Cerebral
thrombosis and embolism, 956.
Bramwell, 890.
Brif/hf, 265, 551, 584,949.
Bright's disease, amyloid form of. See Waxy kid-
ney, 575.
Bright's disease, cirrhotic. See Kidney, cirrhotic,
Bright's disease of, 568.
Bright's diseases of the kidneys. See Kidney,
Bright's diseases of, 551.
BHgidi. 889.
Brimer, 798.
Brinton, 293.
Briquet, 1045.
Bristowe, 294.
Broadhent, 1051.
Brodie, 1045.
Bronchial abscess, 129.
Bronchial a-thma, 59.
Bronchial hemorrhage, 65.
differential diagnosis, 68.
etiology, 66.
morbid anatomy, 66.
prognosis, 69.
symptoms, 67.
treatment, 69.
Bronchiectasis, 55.
differential diagnosis, 57.
etiology, 56.
morbid anatomy, 55.
physical signs, 56.
symptoms, ,56.
treatment, 57.
Bronchitis, acute capillary, 46.
differential diagnosis, 47.
etiology, 46.
morbid anatomy, 46.
physical signs, 47.
prognosis, 48.
symptoms, 46.
treatment, 48.
Bronchitis, acute catarrhal, 42.
differential diagnosis, 45.
etiology, 4.3.
morbid anatomy, 42.
prognosis, 45.
symptoms, 44.
treatment, 45.
Bronchitis, chronic catarrhal, 49.
differential diagnosis, 53.
etiology, 51.
morbid anatomy, ,50.
physical signs, 53.
Bronchitis, chronic catarrhal, prognosis, 54.
symptoms, 52.
treatment, .54.
Bronchitis, clar-siflcation of, 42.
Bronchitis, croupous, ,57,
■ differential diagnosis, 58.
etiology, 57.
morbid anatomy, 57.
physical signs, 58.
prognosis, 59.
symptoms, 57.
treatment, 59.
Broncliitis, fetid. See Chronic bronchitis, 51,
Bronchitis, vesicular, 129.
Broncho-phthisis, pulmonalis. See Chronic phthisis,
184.
Broncho-pneumonia. See Lobular pneumonia, 101.
Brown induration of the lungs, 11.3.
Brown oedema of lungs, Vircnow's, 115.
Brown- Sequard, 897, 969, 995, 1036, 1039, 1043.
Bi'undes, 95.
Brunei, 654.
Brvnton, 557.
Buck, 751.
Buhl, 144, 672, 800, 910.
Bulbar paralysis, acute. See Paralysis, acute bulbar,
1001.
chronic. /Sfee Paralysis, chronic bulbar, 1002.
Burns, 441.
Buzzard, 1042-1044.
Cascitis. See Typhlitis, 279.
Calcification of arteries, 513. -
Calculi, biliary. See Gall stones, 401.
Calculi of the pancreas. See Pancreas, calculi of, 413.
Calculi, renal. See Eenal calculi, 593.
CalineU, 942.
Cancani, 881.
Cancer of arteries, 513.
of brain. See Cerebral tumors, 977.
of gall-bliidder. See Gall-bladder, cancer of,
399.
of heart, 501.
of intestine. See Intestine, cancer of, 298.
of kidney. See Renal cancer, 596.
of larynx, 40.
of liver. See Liver, cancer of, 377.
of lungs. 140.
of oesophagus. See (Esophagus, cancer of,
226.
of pancreas. See Pancreas, cancer of, 411.
of perioardinm, 502.
of pleura. See Pleura, cancer of, 164.
of ^pleen, 418.
of siomnch. See Stomach, cancer of, 241.
of tongue. See Tongue, cancer of, 216.
pulmo'naiy, 140.
Cancrum oris. See Gangrenous stomatitis, 211.
Camtatf, 558, 910.
Capillary bronchitis, acute, 46.
Caput MedusiB. 345.
Cardiac dilatation, differential diagnosis, 484.
etiology, 4hl.
morbid anatomy, 480.
physical signs, 483.
prognosis, 485.
symptoms, 482.
treatment, 486.
varieties of, 480.
Cardiac hypertrophy, differential diagnosis, 478.
etiology, 474.
morbid anatomy, 473.
physical signs, 476.
symptoms, 475.
trcitment, 479.
varieties of, 472.
Cardiac murmurs and their relation to valvular dis>
ease of the heart, 441.
murmurs. /See Murmur, cardiac, 441.
Cardiac neuroses, varieties ol, 502.
Cardiac p.Upitation. nervous, differential diagnosis,
.503.
etiology, ,502.
lU'OLTiiosis, .504.
symptoms, .503.
_ treatmi-nt, 504.
Cardiac thromliosis, differential diagnosis, 499.
etiology, 498.
1084
INDEX.
Cardiac thrombo-'is, morbid anatomy, 497, 498.
physical signs, 499.
prognosis, 499.
symptoms, 499.
tieaiment. 500.
•' Carditis." See Myocarditis, 487.
Camificatioii of lung, 114.
Carre, 1020.
Carter, 740.
Cary, 891.
Casts in the urine, 536.
Catalepsy, differential diagnosis, 1049.
etiology, 1048.
prognosis, 1049.
symptoms, 1048.
treatment, 1049.
Csre, 904.
Pat embolism of the lungs, 122.
Fate of pus, 8.
Fatty degeneration of arteries, 513.
Fatty degeneration of the heart. See Heart, fatty de-
generation of, 491.
Fatty degeneration of the pancreas. See Pancreas,
fatty degeneration of, 411.
Fatty hypertrophic cirrhosis' of the liver, i'49.
Fatty infiltration of liver. See Fatty liver, 372.
Fatty liver, differential diagnosis, 374.
etiolosy, 373.
morbid anatomy, 372.
physical signs. 374.
prognosis, 374.
symptoms, 373.
treatment, .374. 375.
Fatty metamorphosis of the liver. See Fatty liver,
372.
Eaulkner, 65.
Eay?r,r, 1056.
Eede, 888.
FeMing's test for sugar in the urine, 879.
Eeinberg, 992.
Fermentation test for sugar in the urine, 879.
F«>tid bronchitis. 5de Chronic bronchitis, 57.
Fetid nasal catarrh. See Ozsena, 15.
Fever, continued malarial. See Continued malarial
fever, 827.
dengue. See Dengue fever, 849.
enteric. See Typhoid lever, 611.
infantile remittent, 260.
intermittent. See Intermittent fever, 810.
malarial. See Malarial fever, 810.
milinry. See Miliary fever, 794.
peniicious malarial. See Pernicious malarial
fever, 839.
relapsing. See Relnpsing fever, 7-38.
remittent. See Remittent fever, 818.
rheumatic. See Rheumatism, acute articular,
857.
Fever, scarlet. See Scarlet fever, 765.
spotted. ,S'«« Cerebro-spinal meningitis, bai.
typhoid. See Typhoid fever, 611.
typho-malarial. See Continued malaria! fever,
827
typhus. See Tyi^hns lever, 710.
tongue in, and catarrhal stomatitis, 209.
Fibroid disease of the heart. See Heart, fibroid dis-
ease of, 490.
Fibroid induration of the lung and cancer of the
lung, 142.
Fibroid pneumonia, 108.
Fibromata in lungs, 142.
Fibromata of the brain. See Cerebral tumors, 977.
Fibromata of the heart, 501.
Fibromata of the kidney, 598.
Fibrous phthisis. See Phthisis, chronic fibrous, 181.
Eitz, 803.
Eletchei', 984.
Eliclisiq, 1025.
Flint, loo, 899. „ ,.
Floating or movable kidney. See Kidney, floating or
movable, 601.
Flux, the bloody. See Dysentery, 272.
Follicular enteritis. See Intestinal ulcers, 285.
Follicular pharyngitis. See Catarrhal pharyngitis,
221.
Follicular stomatitis. See Stomatitis, follicular,
210.
Follicular ulcers of the intestine. See Intestinal
ulcers, 285.
Forster. 953. 966, 978.
Foster, 557, 882, 892, 941, 942, 975, 1004.
Fotherqili. 885
Fox, 79, 95, 108, 109, 174, 190, 978.
Frank, 878.
Frankel, 175.
Franklin, 207.
Free surfaces, mflammation of, 4.
Freiich, 538.
Friedreich, 887, 1019.
Eriedrich, 510.
Enedrichs, 441.
Frarmnann. 1016.
Functional derangements of the liver, 406.
Functional diseases of the intestines, 314.
Functional diseases of the nervous system, 1034.
Ocdezoivski, 946.
Gall-bladder, cancer of, etiology, 399.
morbid anatomy, 399.
physical signs, 399.
symptoms, 399.
Gall-bladder, diseases of, 395.
Gall-bladder, dropsy of. See Enlarged gall-bladder,
399.
Gall-bladder, enlarged, differential diagnosis, 400.
etiology, 400.
morbid anatomy, 400.
physical signs, 400.
prognosis, 401.
symptoms, 400.
treatment, 401.
Gall-ducts, diseases of, 395.
Gall-stone colic, 404.
Gall-stones, differential diagnosis, 405.
etiology, 403.
morbid anatomy, 401,
prognosis, 405.
symptoms, 403.
treatment, 406.
Gangrene, 125.
Gangrene, circumscribed pulmonary, 125.
Gangrene, diffuse pulmonary, 125.
Gangrene of the lungs, 125.
Gangrene, pulmonary, differential diagnosis of,
127.
etiology of, 126.
morbid anatomy of, 126.
physical signs, 127.
])rognosis of, 128.
symptimis of, 126.
treatment of, 128.
Gangrenous stomatitis. See Stomatitis, gangrenous,
211.
Crctrdner. 888.
aarrod. 858, 860, 874.
Gastric catarrh, acute. See Sub-acute gastritis, 229.
1088
ISTDEX.
Gastritis, ncnto, 228.
dilieieulial diagnosis, 229.
etiol()c;y, S-^8.
morljid anatomy, 228.
\>v t'liosis, 229.
tiymptoms, 2a8, 229.
tieatmi'iit, 2;Jil.
Gastritis, chronic, 231.
ditt'ereuuiil diagnosis, 235.
.•tioiosy, 233.
morbid iuiatomy, 231.
prognosis, ■i'io.
sympioms, 233.
treatment, 235.
Gastritis, piilegmonous, differential diagnosis, 237.
etiology. 237.
morbid anatomy, 236.
symptom^, 237'.
prognosis, 237.
treatment, 237.
Gastritis, sub-acuie, differential diagnosis, 231.
etiology, 230.
morbid anatomy, 229.
prognosis, 231.
symptoms, 230.
treatment, 231.
Gastritis, toxic. See Acute gastritis, 228.
Geigel, 457.
Gelatiniform infiltration. See Chronic phthisis, 179.
Getulrin, 441, 978.
General dilatation of arteries, 514.
General pnralysis, 925.
GerboreU, 952.
Qerhnrdt, 124.
German measles, differential diagnosis, 793.
etiology, 729.
morbid anatomy, 791 .
prognosis, 793.
symptoms, 792.
treatment, 793.
Gihh, 829.
Gibney, 601.
Gill, 100.
Gliomata of the brain. See Cerebral tumors, 977.
Glossitis, 214.
differential diagnosis, 215.
etiology, 215.
morbid anatomy, 214.
pro'jnosis. 216.
symptoms, 214.
treatment, 216.
vsirieties of, 214.
Glosso-labio-laryngeal paralysis. /Sije Chronic bulbar
paralysis, 1002.
Glottis, dropsy of, 25.
Glottis, oedema of, 25.
Glucosnria. See Diabetes mellitus, 877.
Glycohfemia. See Diabetes mellitus, 877.
Glycosuria. See Diabetes mellitiis, 877.
Goitre, exophthalmic. See Basedow's disease, 508.
Golgi, 933.
Golis, 949.
Goodhart, 885.
Good3'ear's atomizer, 10.
Gougoiienheim, 970.
Gout, differential diagnosis, 874.
etiology, 872.
morbid anatomy, 870-873.
prognosis, 875.
symptoms 873.
treatment, 875, 876.
Gouty kidney. See Kidney, cirrhotic Bright's dis-
ease of, .568.
Gonty liver S-'e Interstitial hepatitis, 342.
Gotuers, 1035, 1036, 1042, 1049, 1060, 1069.
(?/««/e,669.
Grariular liver. See Interstitial hepatitis, 342.
Gravel, hepatic, 403.
Graves' disease. See Basedow's disease, 608.
Graves, 735.
Gray. 1072.
Gray infiltration. (S'fg Chronic phthisis, 179.
Greene, 87.
Greenhorv, 900.
Griexinger. 6.52, 727, 931, 952, 1043.
GrlfoJe, 79, 88, 95, 108.
Growitz, 888.
Gubkr, 538, 968, 971.
Gull, 475, 90P, 1030.
Gull and Sutton, 490, 513, 538, 569, 584, 587, 862, 975i
976.
Gummata of spleen, 418.
Gummata of the br.dn. See Cerebral tumors, 977.
Gummata of the heart, ,508.
Gummy rumor ot the liver. See Liver, gummata of,
Gusferoa , 889.
Guttmuii, 457, 465.
Hsematemesis and bEeniopty.«is, 254.
Hsematemesis, differential diagnosis, 254
etiology, 2.53.
prognosi.'^, 254.
symptoms, 2,53.
treatment, 254.
Hsemntinuria, 604.
Usemntomata in the lungs, 142.
Hsematiiria, differential diagnosis, 604.
etiology, 602.
sj'uipioms, 603.
Hsematnriii, endemic, 603.
Haemoglobinuria, 604.
HEemopericardium. 507.
Hsemopliilia, differential diagnosis, 903.
etiol. gy, 902.
morbid anatomy, 903.
prognosis, 903.
symptoms, 902.
treatment, 903.
Haemoptysis and hsematemesis, 254.
Haemoptysis, f^pnnou:^, 69.
Hsemothorax, 171.
etiology, 171.
symptoms, 171.
treatment, 171.
TToimsch, 650.
Hall, 1041.
Hamilton, 183.
Hammond. 970, 975, 987, 1056.
Hanof, 349.
Hardie, 654.
Hare, 1046.
Harkin, 903.
Harley, 603 1053.
Harvard, 122.
Hay den, 454, 460, 462, 471, 528.
Hayem, 960.
Headache, sick. See Megrim, 1075.
Heart, amyloid degeneration of, etiology, 495.
morbid anatomy, 494.
sympfoms, 495.
treatment, 495.
Heart, aneurism of, 440.
etiology, 500.
morbid anatomy, 500.
physical signs, 501.
prognosis, 501.
symptoms, ,500.
treatment, 501.
Heart, atrophy of, etiology, 496.
morbid anatomy, 496.
prognosis, 497.
symptoms, 496.
treatment. 497.
Heart, cancer of, 501.
Heart-clots. See Cardiac thrombosis, 497.
Heart, cysts of, 502.
Heart, dilata'ion of. See Cardiac dilatation, 480.
Heart disease, pneumonia, 114.
Heart, diseases of. 420.
Heart, fatty degeneration of, differential diagnosis,
494.
etiology, 493.
morbid anatomy, 491.
physical signs, 493.
prognosis, 494.
symptoms, 493.
treatment, 494.
varieties, 491.
Heart, tibroid disease of, differential diagnosis, 491.
etiology. 490.
morbtd anatomy, 490.
prognosis, 491.
symptoms, 490.
treatment, 491.
Heart, flbrou.a of, 501.
INDEX.
1089
Heart, gummata of, 508. „ „ ,. , . ,
Heart, hypertrophy of. See Cardiac hypertrophy,
273.
Heart, lipoma of, .501.
Heart, lymphoma of, 501.
Heart, myoma of, 501. _ .
Heart, new formations in, varieties, 501.
Heart, parasites of, 501.
Heart, parenchymatous degeneration of, diiEerential
diagnosis, 495.
etiology, 49.i.
morbid anatomy, 495.
prognosis, 495.
symptoms, 495.
treatment, 495.
Heart, rupture of, etiology, 497.
morbid anatomy, 497.
prognosis of, 497.
symptoms, 497.
treatment, 497.
Heart, sarcoma of, 501.
Heart, syphilitic disease of, etiology, 508.
morl)id anatomy, 508.
symptoms, 508.
Heart, tubercle in, 501. .
Heart, valvular disease of, prognosis of, 467.
valvular diseases of, treatment, 470.
Heart-burn, 333.
Heidenham, 78.
Heller, 865.
Helmholtz, 65. -r -,.
Hematogenous jaundice. See Jaundice, 393.
Hemiplei;ia. causes of, 936.
definition of, 936.
Hemorrhage from the kidney. See Kenal hemor-
rhage, 54S.
Hemorrha"-e, intestinal, differential diagnosis, 289.
etioloay, 288.
morbid anatomy, 288.
prounosis, 289.
symptoms, 288.
treatment, 289.
Hemorrhagic diathesis. See Haemophilia, 903.
Hemorrhagic nodular infarction, 120.
Hemorrhagic variola. See Small-pox, 745.
Hemorrhoids, differential diagnosis, 306.
etiology, 305.
morbid anatomy, 304, 305.
prognosis, 306.
symptoms, 305.
treatment, 306.
varieties of, 304.
Eenle, 898, 1070.
Hepatic gravel. 403.
Hepatitis, circumscribed suppurative, differential
diagnosis, 353.
etiology, 351.
morbid anatomy, 349.
physical signs, 353.
prognosis, 354.
symptoms, 351, 352.
treatuient, 355.
Hepatitis, diffuse parenchymatous, differential diag-
nosis, 359
etiology, 357.
morbid anatomy, 356.
physical signs, 358.
prognosis, 360.
symptoms, 3,57.
treatment, 360.
Hepatitis, interstitial, diagnosis, 346.
etiologv, .344.
morbid anatomy, 342.
physical signs, 346.
prognosis, 347.
symptoms, 344.
treatment, 348.
Hepatization, white, 143.
Hepatogenous jaundice. See Jaundice, 393.
Hernia, internal. See Intestinal obstruction, 294.
Hertz, 125.
Him, 997.
Hirgch, 78, 686.
Hirschberrj, 9a3.
Hob-nailed liver. See Hepatitis, 342.
Hodgkin's disease, differential diagnosis, 896.
etiology, 896.
morbid anatomy, 895.
69
Hodgkin's disease, prognosis, 897.
symptoms, 896.
treatment, 897.
Holmes, 698.
Hoppe, 949.
Hoppe-Seyler, 605.
Hubner, 766.
Hugwian, 9.36, 953, 954.
Huidenlanrj, 429.
Hunter, 44.
Huss, 79.
Hutchinson, 967.
Hater, 800.
Hydatids of the brain. See Cerebral tumors, 797.
Hydatids of the kidney. See Kidney, hydatids of,
599.
Hydatids of the liver. See Liver, hydatids of, 385.
Hydatids of the lung, 144.
Hydatids of the spleen, 418.
Hydremia. See Anaemia, 883.
Hydrocephalus, acute. See Meningitis, tubercular,
943.
Hydrocephalus, chronic, differential prognosis, 950.
etiology, 949.
morbid anatomy, 948.
prognosis, 950.
symptoms, 949.
treatment, 950, 951.
Hydronephrosis, differential diagnosis, 590.
etiology, 590.
morbid anatomy, 589.
prognosis, 591.
symptoms, 590.
treatment, 591.
Hydropericardium, etiology, 506, 507.
morbid anatomy, 506.
prognosis, 507.
symptoms, 507.
treatment, 507.
Hydro-peritoneum. See Ascites, 333.
Hydrophobia and (Esophagitis, 226.
Hydrophobia, differential diagnosis, 805.
etiology, 803.
morbid anatomy, 803.
prognosis, 805.
symptoms, 804.
treatment, 805.
Hydrops cystidis fellae. See Enlarged gall-bladder,
399.
Hydrothorax, 169.
differential diagnosis, 170.
etiology, 170.
morbid anatomy, 169, 170.
prognosis, iTO.
symptoms, 170.
treatment, 170.
Hygroma of the dura mater, 953.
Hypersemia, cerebral. See Cerebral hj^persemia, 930.
Hyperaemia, inflammatory, 1.
Hypersemia of the kidneys. See Renal hyperaemia,
543.
HyperEemia of the liver, acute. See Liver, hyperae-
mia of, 337.
Hyperaemia of the lungs, 113.
Hyperaemia of the spinal cord and meninges. See
Spinal cord and meninges, hyperaemia of,
991.
Hypertemia of the spleen. See Spleen, hyperaemia of,
413.
Hyperaesthesia, 928.
Hypertrophic cirrhosis of the liver, 343.
Hypertrophic cirrhosis of the liver, fatty, 349.
Hypertropliic nasjil catarrh, differential diagnosis, 13.
etiology, 12.
morbid anatomy, 11.
prognosis, 12.
symptoms, 13.
treatment, 13.
Hypertrophy of the brain. See Brain, hypertrophy of,
987.
Hypertrophy of the heart. See Cardiac hypertrophy,
472.
Hypertrophy of the spleen. See Spleen, hypertrophy
of, 416.
Hypostatic congestion, 113.
Hypostatic pneumonia, 114.
Hysteria, differential diagnosis, 1045, 1046.
etiology, 1042.
1090
INDEX.
Hysteria, morbid anatomy, 1042.
prognosis, 1046.
symptoms, 1043-1045.
treatment, 104fi, 1047.
Hystero-epilepsy, difEerential diagnosis, 1047.
etiology, 1047.
prognosis, 1047.
symptoms, 1047.
treatment, 1048.
Icterus. See Jaundice, 393.
Beitis. See'Eu teritis, 357.
Jmmerman, 886.
"India liver," 341.
Induration, brown, 113.
Induration, inflammatory, 4.
Induration of lung, brown, 114,
Induration, pigment, 114.
Infantile convulsions and eclampsia, 1076.
Infantile remittent fever. 260, 823.
Infantile spinal paralysis. See Paralysis, infantile
spinal, 10U6.
Infarction, liemorrhagic nodular, 120.
Infarction of the kidney. See Kenal hemorrhage,
.548.
Infarction of tlie lungs, 120.
Infarction, pulmonary, differential diagnosis, 123.
etiology, 122.
morbid anatomy, 120.
physical signs, 123.
prognosis, 123.
symptoms, 123.
treatment, 124.
Inflammation, adhesions in, 5.
cellular elements in, 3.
cicatrization in, 2.
croupous, 6.
definition of, 1.
diphtheritic, 7.
exudation in, 2.
fate of pus in, 8.
hypersemia in, 1.
interstitial, 4, 8.
mucous, 5.
of free surfaces, 4.
of mucous surfaces, 5.
of serous membranes, 4.
parenchymatous, 8.
resohttion in, 3.
Inflammation, scrofulous. See Chronic phthisis, 179.
serous, 4.
suppuration in, 2.
ulceration in, 7.
Inflammation of the spleen. See Spleen, inflamma-
tion of, 414.
Influenza, differential diagnosis, 799.
etiology, 798.
morbid anatomy, 797.
prognosis, 79!t.
symptoms, 798.
treatment, 799.
Inherit ed syphilis. See Syphilis, 918.
Inoculation, 759.
Insolation. /S«e Sunstroke, 1053.
Insufficiency at the aortic orifice. See Aortic regur-
gitation, 448.
Insufficiency at the mitral orifice. See Mitral re-
gurgitation, 457.
Insufficiency at the pulmonary orifice. /Sfe« Pulmonic
regurgitation, 467.
Insufficiency at the tricuspid orifice. See Tricuspid
regurgitation, 462.
Interlobular emphysema, 131.
Intermittent fever, differential diagnosis, 815.
etiolosy, 811.
morbid anatomy, 810.
prognosis, 815.
symptoms, 811.
treatment, 815.
varieties, 811.
Intermittent fever, masked, 817.
Internal hernia. See Intestinal obstruction, 294.
Interstitial endocarditis. See Endocarditis, inter-
stitial, 439.
Interstitial hepatitis. See Hepatitis, interstitial, 341.
Interstitial inflammation, 8.
Interstitial nephritis, acute. See Surgical kidney,
588.
Interstitial nephritis, chronic. See Gouty kidney,
568.
Interstitial pneumonia, 108.
Intestinal catarrh. (S'ee Enteritis, 257.
Intestinal colic. See Colic, intestinal, 317.
Intestinal dyspepsia. See Dyspepsia, intestinal, 271.
Intestinal hemorrhage. See Hemorrhage, intestinal,
287.
Intestinal obstruction, definition of, 289.
diff'erential diagnosis, 294.
etiology, 290, 291, 292.
morbid anatomy, 290, 291.
prognosis, 295.
symptoms, 292, 293, 294.
treatment, 296, 297.
varieties of, 290.
Intestinal parasites, description of, 306.
differential diagnosis, 312.
etiology, 310.
morbid anatomy, 306-310.
prognosis, 312.
symptoms, 310, 311.
treatment, 312, 313.
varieties of, 306, 307, 308, 309, 310.
Intestinal ulcers, difftise catarrhal, etiology, 285.
morbid anatomy, 285.
Intestinal ulcers, follicular, symptoms, 285.
Intestinal ulcers, tuberctdous, differential diagnosis,
287.
etiologj', 286.
morbid anatomy, 285.
physical signs, 2ti7.
prognosis, 287.
symptoms, 286.
treatment, 287.
Intestinal ulcers, varieties of, 284.
Intestine, cancer of, differential diagnosis of, 30O.
etiology, 299.
morbid anatomy, 298.
prognosis, 301.
symptoms, 299-300.
treatment, 301.
Intestines, classification of diseases of, 257.
Intestines, functional diseases of, 314.
Intestines, waxy degeneration of, differential diag-
nosis, 298.
etiology, 297.
morbid anatomy, 297.
prognosis, 298.
symptoms, 297.
treatment, 298.
Intra-thoracic tumors and sub-acute pleurisy, 155.
Intussusception. See Intestinal obstruction, 290.
Irritability, electrical, 925.
Irritation, spinal. See Spinal irritation, 1055.
Jaccoiid, 85, 433, 529.
Jackson, 654. 967, 971, 976, 1035, 1044.
Jacobsori, 538.
Jarvis' ecraseur, 13.
Jaundice, differential diagnosis, 394.
etiology, 394.
morbid anatomy of, 398.
varieties of, 393.
Jaundice, malignant. ^S'ee Parenchj'matous hepatitis,
356.
Jeiunitis. See Enteritis, 257.
Jenner, 191, 490, 759, 978.
Johnson, 569.
Jolhj, 1042, 1044.
Jones, 915, 1062.
Jurgensen, 97, 101, 104, 107, 134.
Kahler, 1020.
Kdsch, 5.53
Ketley, 1028.
Key, 475. , ,._ i_. . ji
Kidney, acute Bright's disease of, dmerential olag.
nosis, 559.
etiology, 554, 555.
morbid anatomy, 552.
prognosis, 559.
symptoms, 555-559.
treatment, 560-562.
Kidney, amyloid form of Bright's disease of. See
Waxy kidney, 575.
Kidney, amyloid. See Waxy kidney, 575.
Kidney, Bright's diseases of, classification of, 552.
INDEX.
1091
Kidney, Bright' s diseases of, varieties of, 551.
Kidney, calculi in. See Renal calculi, 592.
Kidney, cancer of. 8ee Renal cancer, 596.
Kidney, chronic Bright's diseases of, 562.
Kidney, chronic parenchymatous inflammation of.
See Nephritiri, chronic parenchymatous, 562.
Kidney, cirrhotic Brighi's diseases of, differential
diagnosis, 573.
etiology, 571.
morbid anatomy, 568.
prognosis, 573.
symptoms, 571.
treatment, 574.
Kidney, classification of diseases of, 543.
Kidney, congestion of. See Renal hypermmia, 543.
Kidney, contracted and arterio-capillary fibrosis. See
Arterio-capillary fibrosis, 584.
Kidney, cystic. See Cystic kidney, 591.
Kidney, cy.sts in. See Cystic kidney, 591.
Kidney, diseases of, 529.
Kidney, dropsy of. See Hydronephrosis, 589.
Kidney, embolism of. See Renal hemorrhage, 548.
fibromata of, 598.
Kidney, floating or movable, differential diagnosis,
602.
etiology, 601.
morbid anatomy, 601.
prognosis, 602.
syniptoms, 602.
treatment, 602.
Kidney, gummaia of, 597.
Kidney, hemorrhage of. See Renal hemorrhage, 548.
Kidney, hydatids of, morbid anatomy, 599.
prognosis, 599
symptoms, 599.
treatment, 600.
Kidney, hyperaemia of. See Renal hyperisemia, 543.
Kidney, infarction of. See Renal hemorrhage, 548.
Kidney, lar^e white, 564.
Kidney, leukaemic tumors in, 597.
Kidney, lipomata of, 598.
Kidney, lymphadenomata of, 597.
Kidney, new growths in, 596.
Kidney, parasites in, 599.
Kidney, sarcomata of, 598.
Kidney, small granular, fatty, 564.
Kidney, surgical. See Nephritis, suppurative inter-
stitial, 588.
Kidney, tuberculosis of, differential diagnosis, 599.
etiology, 598.
morbid anatomy, 598.
prognosis, 599.
symptoms, 598.
treatment, 599.
Kidney, waxy degeneration of, dtfEerential diagno-
sis, 578.
prognosis, 578.
treatment, 578, 579.
Kidney, waxy. See Waxy kidney ,'575.
Kirchof, 1004.
Klebs, 101, 483,581, 588, 809, 853.
Klein, 767.
Klob, 936.
Knapp, 1067.
Knecht, 751.
Koch, 174, 175.
Koehler, 993.
Kolliher, 897.
KoBter, 1053.
Kreizlnrj, 439.
Kuhn, 79.
Kuvze, 1042.
KuUner, 121.
Kuasmaul, 513.
LaMnnec, 55, 179, 203, 204, 441.
Laennec's rale, i,37.
Lancereaux, .349, 961.
Lardaceous degeneration of the intestines. See In-
testines, waxy degeneration of, 297.
Lardaceous degeneration of the liver. See Amyloid
degeneration of liver, .366.
Large white kidney. See Nephritis, chronic paren-
chymatous, 562.
La Roche, 6.50.
Laryngeal paralysis. See Neuroses of the larynx, .34.
spasm hysterical and acute catarrhal laryngi-
tis, 19.
Laryngisums stridulus, .37.
Laryngitis, acute catarrhal, 17.
differential diagnosis, 19.
etiology, 18.
morbid anatomy, 17.
prognosis, 19.
symptoms, 18.
treatment, 20.
Laryngitis, acute croupous, 27.
differential diagnosis of, 30.
etiology of, 28.
morbid anatomy of, 27.
prognosis of, 30.
symptoms ol, 28.
treatment of, 31.
Laryngitis, chronic catarrhal, differential diagnosis
of, 22.
etiology of, 21.
morbid anatomy, 21.
prognosis, 22.
symptoms, 21.
treatment, 22.
Laryngitis, chronic catarrhal in phthisis, 23, 24.
Laryngitis, chronic catarrhal in syphilis, 25.
Larynx, cancer of, 40.
catarrhal ulcer of, 32,
chronic catarrh of, in phthisis, 23.
classification of diseases of, 17.
cystic tumors of, 40.
diseases of, 17.
fibro cellular growths of, 40.
fibromata of, 40.
follicular ulcer of, 32.
glandular growths of, 40.
Larynx, neuroses of, differential diagnosis, 96.
etiolog}'', 35.
morbid anatomy, 34.
prognosis, 36.
symptoms, 35.
treatment, 37.
Larynx, oedema of, 25.
papilloma of, 39.
phthisical ulcers of, 32.
Larynx, spasmodic affections of, 37.
differential diagnosis, 38.
etiology, 37.
morbid anatomy, 37.
prognosis, .38.
syniptoms, 38.
treatment, 38.
Larynx, syphilitic ulcers of, 33.
LarynXj tumors of, 39.
differential diagnosis,'41.
etiology, 40.
morbid anatomy, 39.
prognosis, 41.
symptoms, 40.
treatment, 41.
LarjTix, typhous ulcers of, 32.
Larynx, ulcers of, differential diagnosis, 34.
etiology, 33.
morbid anatomy,' 32.
prognosis, 34.
symptoms, 33.
treatment, 34.
varieties of, 32.
Larynx, variolus ulcer of, 32.
Lasegue, 1045.
Lateral sclerosis, amyotrophic. /Stee Amyotrophic lat-
eral sclerosis, 1025.
Laycock, 883.
Lead colic. See Intestinal colic, 317, 319.
Lead palsy. See Chronic lead poisoning, 1064.
Lead poisoning, 319.
Lead poisoning, chronic, differential diagnosis, 1065.
etiology, 1064.
morbid anatomy, 1064.
prognosis, 1065.
symptoms, 1064.
treatment, 1065.
Lebert, 79, 95, 437, .529, 712, 713, 715, 716, 740, 863, 888,
977, 984, 1061.
Lego, 902.
Leicblenstem. 195.
Lenitis. See Phlegmonous gastritis, 236
Leo, 7'51.
Leptothrix buccalis. See Thrush, 213.
Leiulle, 898.
1092
IlifDEX.
Letzreich, 800.
Leucocythsemia, differential diagnosis, 895.
etiology, 893.
morbid anatomy, 891.
prognosis, 894.
symptoms, iS93.
treatment, 895.
Leulcaemiii, pseudo. See Hodgliin's disease, 894,
•'Leukismia." See Leucocytlisemia, 891.
Leiiksemic tumors of the kidney, 597.
Lewinsky, 475.
Ley den, 461), 997, 1012.
Lichtheim, 130.
Liebermeister, 100.
Lientery. See Diarrtioea, 264.
Lipomaita in the lungs, 142.
Lipomata of the brain. See Cerebral tumors, 977.
Lipomata of the heart, 501.
Lipomata of the kidney, 598.
LiouvUle, 10.30.
Litten, 518, 888.
Liver, abscess of. See Suppurative hepatitis, 349.
Liver, active hyperemia of, difEerential diagnosis,
338.
etiology, 338.
morbid anatomy, 337.
physical signs, 338.
prognosis, 339.
symptoms, 338.
treatment, 339.
Liver, acute yellow atrophy of. See Parenchyma-
tous hepatitis, 356.
Liver, amyloid degeneration of, differential diag-
nosis, 369.
etiology. 368
morbid" anatomy, 366.
physical signs, 369.
prognosis, 369.
symptoms, 368.
treatment, 369.
Liver, cancer of, differential diagnosis, 381.
etiology, 380.
morbid anatomy, 378.
physical signs, 381.
prognosis, 382.
symptoms, 380.
treatment, 382.
varieties, 377.
Liver, chronic atrophy of, differential diagnosis, 371.
etiology, 371.
moi'bid anatomy, 370.
physical signs, 371.
prognosis, 371.
symptoms, 371.
treatment, 372.
Liver, cirrhosis of. See Interstitital hepatitis, 342.
Liver, congestion of. See Passive hyperemia of the
liver, .339.
Liver, diseases of, 337.
Liver, fatty degeneration of. See Fatty liver, 372.
Liver, fatty hypertrophic cirrhosis of, 349.
etiology, 349.
morbid anatomy, 349.
symptoms, 349.
Liver, fatty infiltration of. See Patty liver, 372.
Liver, fatty metamorphosis of. See Patty liver, 372.
Liver, functional derangements of, differential diag-
nosis, 409.
etiology, 406.
prognosis, 409.
symptoms, 407, 408.
treatment, 409.
Liver, gouty. See Interstitial hepatitis, 342.
Liver, granular. See Interstitial hepatitis, 342.
Liver, gummata of, differential diagnosis, 384.
etiology, 384.
morbid anatomy, 383.
physical signs, 384.
prognosis, 384.
symptoms, 384.
treatment, 384.
Liver, hydatids of, differential diagnosis, 388.
etiology, 387.
morbid anatomy, 385.
physical signs, 388.
prognosis, 389.
symptoms, .387.
treatment, 389.
Liver, hypertrophic cirrhosis of, 343.
Liver, melanotic sarcoma of, 378.
Liver, multilocular hydatids of, differential diagno>
sis, 391.
etiology, 391.
morbid anatomy, 390.
physical signs, 391.
prognosis, 392.
symptoms, .391.
treatment, 392.
Liver, passive hyperemia of, differential dia^osis,
341.
etiology, 340.
morbid anatomy, 339.
physical signs, 341.
prognosis, 341.
symptoms, 341.
treatment, 341.
Liver, pigment degeneration of, differential diagnO'
sis, 377.
etiology, 376.
morbid anatomy, 375.
physical signs. 377.
prognosis, 377.
symptoms, 376.
treatment, 377.
Liver, rare tumors of, 393.
Liver, torpid. See Punciional derangements of liver»
406.
Liver, tuberculosis of, etiology, 393.
morbid anatomy, 39:2.
symptoms, 393.
Liver, waxy. See Amyloid degeneration of, 366.
Livingstone, 825.
Lobular pneumonia. See Pneumonia, lobular, 101.
Localization of cerebral lesions, 970, 971, 972.
Localized spasm and paralysis, differential diagno-
sis, 1064.
etiology, 1063.
morbid anatomy, 1063.
prognosis, 1064.
symptoms, 1063.
treatment, 1064.
Lock-jaw. See Tetanus, 1058.
Locomotor ataxia, differential diagnosis, 1022.
etiology, 1019.
morbid anatomy, 1018.
prognosis, 1022.
symptoms, 1020.
treatment, 1023.
Louis, 79.
Lung, atrophy of, 144.
etiology, 144.
morbid anatomy, 144.
physical signs, 144.
symptoms, 144.
Lungs, active hypersemia of, 113.
Lungs, anaemia of, 129.
Lungs and pleura, diseases of, 70.
Lungs, brown cedema of, 115.
Lungs, cancer of. 140.
differential diagnosis, 141.
etiology, 141.
physical signs, 141.
prognosis, 142.
symptoms, 141.
treatment, 142.
varieties of, 140.
Lungs, carniftcation of, 114.
cirrhosis of, 109.
coal-miner's, 182.
compensatory hypercemia of, 113.
compression of. See Atelectasis, 19.
congestion of, 113.
dermoid cysts in, 142.
echinococci. See Hydatids, 144.
enchondromata in, 142.
epithelioma of, 143.
fat embolism of, 122.
fibromata in, 142.
gangrene of, 125.
hfematomata in, 142.
Lungs, hydatids of j 144.
differential diagnosis, 145,
etiology, 145.
morbid anatomy, 145.
prognosis, 145.
syrnptoms, 145.
INDEX.
1093
Lungs, hydatids of, treatment, 146.
Lungs, hypenieinia of, 113.
ditlerential diagnosis, 116.
etiology, 115.
morbid anatomy, 113.
physical sigus, 116.
prognosis, 116.
symptoms, 115
treatment, 116.
Lungs, infarction of, 120.
Lungs, lipomata in, 143.
melanotic tumors in, 142.
myxomata in, 142.
Lungs, non-malignant growths in, 142.
differential diagnosis, 143.
symptoms, 143.
Lungs, ijeduma of. See (Edema, puhnonary, 117.
osteomata in, 142.
passive hyperasmia of, 113.
sarcomata in, 142.
scirrhus of, 108.
sclerosis of, 103.
splenization of, 113.
Lungs, syphilitic disease of, 143.
morbid anatomy, 143.
symptoms of, 143.
Lumbas^o, 860.
L^l.ys, 970, 971, 1049.
Lymphndenomata of the kidney, 597.
heart, 501.
Mackenzie, 1069.
Mackrill, 659.
Maclean, 349, 828.
Magnan, 991.
Mahomed, 538, 573, 584, 587, 908.
Maiei', 513.
Malarial fever, continued. See Continued malarial
fever, 827.
Malarial fever, introduction, 806-810.
Malarial fever, pernicious. See Pernicious malarial
lever, 839.
Malarial infection, chronic. See Chronic malarial
infection, 853.
Malassez, 192.
Malignant jaundice. See Parenchymatous hepatitis,
356.
Malignant pustule and gangrenous stomatitis,
211.
Manassein, 739.
Mannkopf, 693.
Masked intermittent fever, 817.
Maumene's test for sugar in the urine, 879.
Maw-worm. See Intestinal parasites, 306.
Mayer, 851, 931.
Measles, complications, 787.
differential diagnosis, 788.
etiology, 783.
morbid anatomy, 782.
prognosis, 789.
sequelae, 788.
symptoms, 784.
treatment, 790, 791.
Measles, German. See German measles, 791.
Meckel, 441.
Mediastinal tumors, etiology, 529.
physical signs, 529.
progno^^is, 529.
seat of, 529.
symptoms, 529.
treatment, 529.
varieties of, 528.
Megrim, etioiogy, 1075.
morbid anatomy, 1075.
symptoms, 1075.
treatment, 1076.
Meir/s, 802.
Melanotic liver. See Liver, pigment degeneration
of, 375.
Melanotic timiors in the lungs, 142.
Melasma saprarenalis. See Addison's disease, 897.
Melier, 659.
Mellituria. See Diabetes mellitus, 877.
Membranous croup. See Laryngitis, acute croup-
ous, 27.
Memltraiious fjesophagitis. See (Esophagitis, 224.
Membranous pharyngitis, 223.
Vniere's disease. See Vertigo, 1067.
Meninges, hyperaemia of. See Spinal cord and
meninges, hyperaemia of, 991.
Meninges, tumors, etc. See Brain and meninges
tumors of, 97'8.
Meningitis, acute, differential diagnosis, 939.
etiology, 936.
morbid anatomy, 935.
prognosis, 939.
symptoms, 937.
treatment, 93'.^.
Meningitis, cerebro-spinal. See Cerebro-spinal men-
ingitis, 684.
Meningitis, chronic, differential diagnosis, 942.
etiology, 942.
morbid anatomy, 941.
prognosis, 943.
symptoms, 942.
treatment, 943.
Meningitis, epidemic cerebro-spinal. See Meninglp
tis, epidemic, 684.
Meningitis foudroyante, 690.
Meningitis, spinal, differential diagnosis, 994.
etiology, 993.
morbid anatomy, 992, 993.
prognosis, 994.
symptoms, 9H3.
treatment, 995.
Meningitis, sub-acute, differential diagnosis, 941.
etiology, 940.
morbid anatomy, 940.
prognosis, 941.
symptoms, 940.
treatment, 941.
Meningitis, varieties, 935.
Meningitis, tubercular, differential diagnosis, 947.
etiology, 944.
morbid anatomy, 943.
prognosis, 947.
symptoms, 944.
treatment, 949.
Menjaud, 1013.
Mental disturbances in nervous diseases, 929.
Merbach, 195.
Mercurialism, chronic, differential diagnosis, 1067.
etiology, 1066.
morbid anatomy, 1066.
prognosis, 1067.
symptoms, 1066.
treatment, 1067.
Mercurial tremor. See Chronic mercurialism, 1066.
Merkel, 685, 898.
Meschede, 685.
Meyer, 1007, 1009.
Miasm, definition of, 609.
Miclull, 656.
Miliary fever, differential diagnosis, 796.
etiology, 794.
morbict anatomy, 794.
prognosis, 796.
symptoms, 795.
treatment, 797.
Miliary tuberculosis, acute. See Tuberculosis, acute
miliary, 706.
Mitchell, 987, 1053.
Mitral obstruction. See Mitral stenosis, 453.
Mitral regurgitation, differential diagnosis, 461.
etiology, 459.
morbid anatomy, 457.
physical signs, 460.
symptoms, 459.
Mitral stenosis, differential diagnosis, 457.
etiology, 455.
morbid anatomy, 453.
physical signs. 456.
symptoms, 455.
MOller's oil in chronic phthisis, 200.
Montague, Lady Ma.ry^ 759.
Moore's test for sugar m the urine, 879.
Morbid sensibility of the stomach. See Chronic gas-
tritis, 231.
Morbus Addisonii. See Addison's disease, 897.
Morbus macnlosus Werlhofii. See Purpura, 905.
Moslei; 417, 902.
Motor paralysis, 924.
Movline, 984.
Mouth, diseases of, 208.
Movable or floating U-idney. See Kidney, floating
or movable, 601 .
1094
INDEX.
Moxon, 557, 898, 1000.
Mucous menibiane, croupous inflammation of, 6.
Mucous surfaces, inflammatiou of, 5.
Mucous surfaces, ulceration of, 7.
" Muguet." See Thrush, 213
Multliocular hydatids of )iver. See Liver, multiloc-
ular hydatids of, 390.
Mumps. See Parotitis, ai7.
Murvhison, 407, 40s, 715, 727, 729.
Murmurs, cardiac, liistory of, 441.
mechanism of, 441, 442.
theories of, 441.
Murmurs, endocardial, characteristics of, 443.
classiticaTion of, 444.
combination of, 443.
relative frequency of, 443.
table of, 443.
Muscular atrophy, progressive. See Progressive mus-
cular atropny, 1011.
Muscular uuuition, !)25.
Muscular rheumatism. See Rheumatism, muscular,
868.
Myalgia. See Muscular rheumatism, 868.
"Mycosis endocardii," 433.
Myelitis, acute, differential diagnosis, 998.
etiology, 996.
morbid anatomy, 996.
prognosis, 998.
symptoms, 997.
treatment, 998.
varieties of, 995.
Myelitis, chronic, difEerential diagnosis, 1000.
etiology, 999.
morbid anatomy, 999.
prognosis, 1000.
symptoms, 999.
treatment, 1000.
Myocarditis. difEerential diagnosis, 489,
etiology, 488.
morbid anatomy, 487.
prognosis, 489.
symptoms, 488.
treatment, 489.
varieties of, 487.
Myocarditis, chronic. See Fibroid diseases of the
heart, 490.
Myomata of the heart, 501.
Myxoedema, differential diagnosis, 908.
etiology, 908.
morbid anatomy, 907.
prognosis, 909.
symptoms, 908.
treatment, 909.
Mjrsomata in lungs, 142.
Myxomata of the brain. See Cerebral tumors, 977.
Nasal catarrh, atrophic, 13.
Nasal catarrh, chronic. See Chronic coryza, 10.
Nasal catarrh, dry. See Atrophic nasal catarrh,, 13.
Nasal catarrh, fetid. See Ozasna, 15.
Nasal catarrh, hypertrophic, 11.
Nasal passases, classification of diseases of, 9.
Nasal passages, diseases of, 9.
Naso-pharyngeal catarrh, chronic. See Hypertrophic
nasal catarrli, 11.
Necrosis, 3.
Nephritic colic, 594.
Nephritis, acute suppurative interstitial, differential
diagnosis, 589.
etiology, 588.
morbid anatomy, 588.
prognosis, 589.
symptoms, .588.
treatment, 589.
Nephritis, chronic parenchymatous, differentiaVdiag-
nosis, 566.
etiology, 565.
moibid anatomy, 562.
prognosis, 566. —
symptoms, 565.
treatment, 567.
varieties of, 562.
Nephritis, strumous, 598.
Nervous cardiac palpitation. See Cardiac palpita-
tion, nervous, ,502.
Nervous system, functional diseases of, 1034.
Nervous system, general symptomatology of the
diseasee of, 924.
Neuman, 893.
Neuralgia, differential diagnosis, 1073.
etiology, 1070.
morbid anatomy, 1069.
prognosis, 1074.
symptoms, 1070.
treatment, 1074.
varieties, 1071.
Neurasthenia, differential diagnosis, 1050.
etiology, 1049.
prognosis, 1050.
symptoms, 1049.
treatment, 1050.
Neuroses of the heart, varieties of, 502.
Neuroses of the larynx, 34.
Neuroses of the stomach. See Stomach, neuroses of
252.
New formations in the heart. See Heart, new forma-
tions in, 501.
New growths in the kidney. See Kidney, new
growths in, 596.
Niemeyer, 108, 111, 186, 418, 434, 467, 472, 476, 607,
861, 886, 903, 912, 930, 948, 967, 975, 979, 990,
1060.
Nodular infarction, pulmonary, 120.
Nodular pulmonary apoplexy, 120.
Noma. See Ulcerative stomatitis, 212.
Non-inflammatory softening of the spinal cord. See
Spinal cord, non-inflammatory softening of,
1000.
Non-malignant erowths in the lungs, 141.
Nothnarjel, 930, 931, 934, 957, 968, 1040, 1042.
Nutrition, muscular, 925.
Obenneir, 739, 751, 979, 981.
Obstruction at the pulmonary orifice. See Pulmonic
obstruction. 465.
Obstruction at the tricuspid orifice. See Trictispid
stenosis, 462.
Obstruction, intestinal. See Intestinal obstruction,
289.
Obstruction of the mitral valve. See Mitral stenosis,
453.
(Edema glottidis, 25.
differential diagnosis of, 26.
etiology of, 26.
morbid anatomy of, 26.
prognosis of. 27.
symptoms of, 26.
treatment of, 27.
(Edema of the larynx, 25.
(Edema, pulmonaiy, differential diagnosis, 118.
etiology, 117.
morbid anatomy, 117.
physical signs, 118.
prognosis, 119.
symptoms, 118.
treatment. 119.
(Edema, Virchow's brown, 115.
Oertel, 672, 800.
(Esophagitis, differential diagnosis, 836.
etiology, 224.
membranous, 224.
morbid anatomy, 224.
prognosis, 226.
symptoms, 225.
treatment, 226.
(Esophagus, cancer of, differential diagnosis, 9St
etiology, 226.
morbid anatomy, 226.
prognosis, 227.
symptoms, 227.
treatment, 227.
(Esophagus, diseases of, 224.
(Esophagus, stricture of, 225.
Oqle, 958.
OVdium albicans. See Thrush, 313.
Oinomania, 915.
Oligsemia, 883.
Olhvier, 997.
Oppolzer, 334, 1061.
Ord, 907.
Ormerod, 466.
Osteomata in the lungs, 143.
Osteomata of the brain. See Cerebral tumors, ^f.
Otto, 950.
Oxyuris vermicularis, 309.
Ozsena, 15.
INDEX.
1095
Ozsena, differential diagnosis, 16.
etiology, 15.
morbid anatomy, 15.
progiioi?is, 16.
symptoms, 15.
treatment, Iti.
Pachymeningitis externa, differential diagnosis, 952.
etiology, 951.
morbid anatomy, 951.
prognosis, 953.
symptoms, 9.52.
treutment, 9.52.
Pachymeningitis interna, differential diagnosis, 955.
etiology, 954.
morbid anatomy, 953-954.
prognosis, 955.
symptoms, 954.
treatment, 955.
Pachymeningitis syphilitica, differential diagnosis,
956.
morbid anatomy, 955, 956.
prognosis, 956.
symptoms, 956.
treatment, 956.
Paget, 408.
Palpitation of the heart, nervous. See Cardiac pal-
pitation, nervous, 503.
Pancreas, calculi of, morbid anatomy, 413.
etiology of, 413.
symptoms, 413.
Pancreas, cancer of, differential diagnosis, 413.
etiolOLfy, 412.
morbid anatomy, 411, 413.
prognosis, 413.
symptoms, 412.
Pancreas, cysts of, etiology, 413.
morbid anatomy, 413.
symptoms, 413.
Pancreas, diseases of, 410.
Pancreas, fatty degeneration of, etiology, 411.
morbid anatomy, 411
varieties, 411.
Pancreas, round worms in, 413.
small-celled sarcoma of, 413.
syphilitic gnmmata of, 413.
tuberculosis of, 413.
vi'axy degeneration of, 411.
Pancreatitis, acute, differential diagnosis, 410.
etiology, 410.
morbid anatomy, 410.
prognosis, 410.
symt)toms, 410.
treatment, 410.
Pancreatitis, chronic, etiology, 411.
morbid anatomy, 411.
symptoms, 411.
Panum, 698.
Papillomata of the brain. See Cerebral tumors, 977.
of the larynx, 40.
Paralysis, acute ascending, differential diagnosis,
1028.
etiology, 1028.
prognosis, 1029.
symptoms, 1028.
treatment, 1029.
Paralysis, acute bulbar, etiology, 1001.
morbid anatomy, 1001.
prognosis, 1003.
symptoms, 1001.
treatment, 1003.
Paralysis, acute spinal of adults. drEEerential diag-
nosis, 1009.
etiology, 1003.
morbid anatomy, 1009.
prognosis, 11)10.
symptoms, 1009.
treatment, 1010.
Paralysis agitans, differential diagnosis, 1063.
etiology, 1061.
morbid anatomy, 1061.
prognosis, 1062.
symptoms, 1061.
treatment, 1062.
Paralysis, Bell's. See Facial paralysis.
Paralysis and spasm, localized. See Localized spasm
and paralysis, 1063.
Paralysis, chronic bulbar, differential diagnosis, 1005.
Paralysis, chronic bulbar, etiology, 1004.
morbid anatomy, 1003.
prognosis, 1005.
symptoms, 1U04.
treatment, 1005.
Paralysis, facial, differential diagnosis, 1060.
etiology, 10.59.
prognosis, 1060.
symptoms, 1060.
treatment, 1060.
Paralysis, general, 925.
Paralysis, glosso-labio-laryngeal. See Chronic bulbar
paralysis, 1003.
Paralysis, infantile spinal, differential diagnosis,
1008.
etiology, 1007.
morbid anatomy, 1006, 1006.
prognosis, 1008.
symptoms, 1007.
treatment, 1009.
Paralysis, lead. See Chronic lead-poisoning, 317,
319.
Paralysis, motor, 934.
Paralysis of the abductors of the vocal cords, 34.
of the adductors of the vocal cords, 34.
of the tensors of the vocal cords, 3 1.
Paralysis, pseudo-hypertrophic. Bee Pseudo-hyper-
trophic paralysis, 1026.
Paralysis, recurrent laryngeal, 34.
Paralysis, sensory, 938.
Paralysis, spastic. See Amyotrophic lateral sclero-
sis, 1025.
Paraplegia, causes of, 937.
definition of, 937.
Parasites, intestinal. See Intestinal parasites, 306.
Parasites in the heart, 501.
Parasites in the kidney, 599.
" Parasitic nephritis." See Surgical kidney, 588.
Parchaj^pe, 989.
Parenchymatous degeneration of the heart. See
Heart, parenchymatous degeneration of, 493.
Parenchymatous hepatitis, diffuse. See Hepatitis,
parenchymatous, 356.
Parenchymatous inflammation, 8.
Parenchymatous nephritis, acute. See Kidney, acute
Bi'ight's disease of, 5.52.
nephritis, chronic. See Nephritis, chronic pa-
renchymatous, 563.
Parkes, 860.
Parotitis, differential diagnosis, 219.
etiology, 218.
metastatic, 318.
morbid anatomy, 217.
prognosis, 219.
symptoms, 218.
treatment, 219.
^varieties of, 317.
Parrot, 1045.
Passive hyperemia of the liver. See Liver, passim
hyperemia of, 339.
Pasteur, 804, 900.
Peacock, 445.
Penzoldt, 906.
Pepper, 303, 888.
Periarteritis, etiology, 513.
morbid anatomy, 513.
Pericecal abscess. See Perityphlitis, 281.
Pericarditis, acute, differential diagnosis, 426.
etiologv. 422.
morbid anatom^y, 430.
physical signs, 424.
prognosis, 427.
symptoms, 423.
treatment, 428.
varieties of, 421.
Pericarditis, chronic, differential diagnosis, 430.
etiology, 429.
morbid anatomy, 429, 430.
physical signs, 430.
prognosis, 430.
symptoms, 430.
treatment, 430.
Pericardium, cancer of, 502.
dropsy of. See H ydropericardium, 506.
tuberculosis of, 503.
Pereira, 1066.
Perihepatitis, differential diagnosis, ,361.
etiology, 361.
1096
INDEX.
Perihepatitis, morbid, anatomy, 360.
prognosis, 362.
symptoms, 361.
treatment, 363.
syphilitica, 360.
Peri nephritic abscess. See Perinephritis, 600.
Perinephritis, differential diagnosis, 601.
etiology, 600.
morbid anatomy, 600.
physical signs, 601.
prognosis, 601.
symptoms, 600.
treatment, 601.
Periplilebitis, 515.
Periproctitis, diflferential diagnosis, 304.
etiology, 302.
morbid anatomy, 303.
prognosis, 304.
symptoms, 304.
treatment, 304.
Peritoneal dropsy. See Ascites, 333.
Peritonitis, 321.
difEerential diagnosis, 339.
etiology, 32-1, 325.
morbid anatomy, 331.
prognosis, 330.
symptoms, .326, 327, 328, 829.
treatment, 330, 331, 333, 333.
Peritonitis, cancerous, 334.
Peritonitis, chronic, 333.
Peritonitis, hemorrhagic, 333.
Peritonitis, tubercular, 333.
Peritonitis, varieties of, 331.
Perityplilitis, difEerential diagnosis, 282.
etiology, 283.
morbid anatomy, 281.
physical signs, 382.
prognosis, 283.
symptoms, 233.
treatment, 283.
Pernicious aniemia. /Sfee Progressive pernicious an-
eemia, 888.
Pernicious malarial fever, differential diagnosis,
845.
etiology, 849.
morbid anatomy, 839.
prognosis, 846.
sj^mptoms, 840.
treatment. 847.
Pertussis. See Whooping-cough, 800.
FMger, 1004.
Pharyngitis catarrhal, morbid anatomy, 221.
etiology, 333.
symptoms, 233.
differential diagnosis, 223.
prognosis, 323.
treatment, 233.
Pharyngitis, croupous, 223.
Pharyngitis, diphtheritic, 223.
Pharyngitis, follicular. See Catarrhal pharyngitis,
221.
Pharyngitis, membranous, 233.
Pharyngitis, phlegmonous. See Quinsy, 219.
Pharynx, classification of diseases of, 219.
diseases of, 319.
Phlebitis, difEerential diagnosis, 515.
etiology, 514.
morbid anatomy, 514.
prognosis, 515.
symptoms, 514.
treatment, 515.
Phlegmonous gastritis. See Gastritis, phlegmonous,
236.
Phlegmonous pharyngitis. See Quinsy, 219.
Phthisis, catarrh of larynx in, 23.
cavities in, 180.
classification of, 172.
diiierential diagnosis, 196.
different names of, 172.
etiology of, 185, 186, 187.
antihygienic surroundings in, 185.
climate in, 186.
heredity in, 185.
local causes in, 186, 187.
Koch's experiments concerning, 174, 175.
physical signs of, 193, 196.
prognosis, 197.
quiescent cavities in, 184.
Phthisis, symptoms, 187-193.
cough, 188.
emaciation, 190.
fever, 190.
haemoptysis, 189.
pulse, 191.
respirations, 191.
sputa, 189.
theories of , i71.
treatment, 19S.
antiseptic, 203.
climatic, 203-207.
hygienic, 303.
medicinal, 199, 200.
prophylactic, 198, 199.
Phthisis, acute, 171.
difEerential diagnosis, 177.
etiology, 174, 175.
morbid anatomy, 172, 173, 174.
physical signs, 177.
prognosis, 178.
symptoms, 175.
treatment of, 178.
Phthisis, catarrhal, cavities in, 180.
morbid anatomy, 178-181.
Phthisis, chronic, 178
Phthisis, fibrous, 181.
morbid anatomy, 181, 182, 183, 184.
Phthisis, hemorrhagic, 206.
Phthisis, infective. 187.
Phthisis, stone-cutter's, 182.
Phthisis, tubercular 183,
morbid anatomy, 183, 184
sputa in, 175.
Phthisis, tuberculo-pneumonic, 174.
HcJc, 1020, 1025.
Pietres, 970.
Pigment induration of lungs, 114.
Pigment, liver. See Liver, pigment degeneration itment, 1032.
Spinal irritation, differential diagnosis, 1057.
etiology, 10.55.
prognosis, 1057.
Spinal irritation, symptoms, 1056.
treatment, 1057.
Spinal meningitis. See Meningitis, spinal, 992.
paralysis, infantile. See Paralysit^, infantile
spinal, 1006.
Spinal paralysis of adults, acute. /See Paralysis, acute
spinal of adults, 1009.
Spleen, cancer of, 418.
Spleen, cysts of, 418.
Spleen, diseases of, 413.
Spleen, enlarged. See Spleen, hypertrophy of, 416.
Spleen, gummata of, 418.
Spleen, hydatids of, 418.
Spleen, hyperajmia of, etiology, 413.
morbid anaiomy, 413.
prognosis, 414.
symptoms, 413.
treatment, 414.
Spleen, hypertrophy of, etiology, 417.
morbid anatomy, 416.
symptoms, 417.
treatment, 417.
varieties, 416.
Spleen, inflammation of, differential diagnosis, 415,
416.
etiology, 415.
morbid anatomy, 414.
physical signs, 415.
prognosis, 416.
sj'mptoms, 415.
treatment, 416.
Spleen morbid growths in, 418.
Spleen the sago. &e Spleen, waxy degeneration of,
417.
Spleen, tubercles in, 418.
Spleen, waxy degeneration of, etiology, 417.
morbid anatomy, 417.
symptoms, 418
treatment, 418.
Splenitis. See Spleen, inflammation of, 414.
Splenization of the lungs, 113, 129.
pulmonary, 129.
Sporadic cholera. See Cholera morbus, 266.
Spotted fever. See Cerebro-spinal meningitis, 684.
" Sprue." See Thrush, 213.
Squire, 802.
Stasis, inflammatory, 3.
Sleiner, 991.
Stenosis at the mitral orifice. See Mitral stenosis,
453.
at the pulmonary orifice. See Pulmonic ob-
struction, 465.
at the tricuspid orifice. See Tricuspid steno-
sis, 462.
of aortic valve. See Aortic stenosis, 444.
Stewart, 601.
Stiemer, 757.
Stokes, 4,50, 613. 735.
Stomach, acidity of, from hypersecretion, and from
fermentation, 240.
Stomach, cancer of, 300.
differential diagnosis, 345.
etiology, 243.
morbid anatomy, 241.
physical signs, 245.
prognosis, 246.
symptoms, 244.
treatment, 246.
varieties, 241.
Stomach, dilatation of, differential diagnosis, 356.
etiology, 255.
morbid anatomy, 254.
physical signs, 256.
prognosis, 256.
symptoms, 255.
treatment, 256.
Stomach, diseases of, 228.
Stomach, erythism of. See Stomach, neuroses of,
252.
Stomach, hemorrhagic erosion in, 234.
Stomach, morbid sensibility of. See Chronic gastri-
tis. 231.
Stomach, neuroses of, differential diagnosis, 253.
etiology, 252.
prognosis, 2.53.
symptoms, 252.
treatment, 253.
Stomach, ulcer of, differential diagnosis, 250.
1100
IlfDEX.
Stomadi, ulcer of, etiology, 248.
morbid anatomy, 247.
prognosis, 250.
symptoms, 249.
treatment, 251.
varieties, 246.
Stomatitis, aplitboiis. See Follicular stomatitis,
210.
Stomatitis, catarrhal, 208.
differential diagnosis, 209.
etiology, 208.
morbid anatomy, 208.
prognosis, 209.
symptoms, 209.
treatment, 209.
Stomatitis, croupous. See Follicular stomatitis, 210.
Stomatitis, foihcular, difiereutial diagnosis, 210.
etiology, 210.
morbid anatomy, 210.
prognosis, 210.
symptoms, 210.
treatment, 210.
Stomatitis, gangrenous, differential diagnosis, Sll.
etiology, 211.
morbid anatomy, 211.
prognosis, 211.
symptoms, 211.
treatment, 211.
Stomatitis, ulcerative, differential diagnosis, 212.
etiology, 312.
morbid anatomy, 212.
prognosis, 213.
symptoms, 212.
treatment, 213.
Stone-cutter's phthisis, 182.
" Stony kidney." See Renal hypersemia, 543.
SiracMns, 79.
Strieker. 876, 935.
Stricture of the oesophagus, 225.
Strumous enteritis. See Intestinal ulcers, 285.
Strumous nephritis, 598.
Stumpell, 1024.
Siurges, 78.
Sub-acute meningitis. See Meningitis, sub-acute, 940.
rheumatism . Set Rheumatism, sub-acute, 863.
Summer complaints. See Cholera infantum, 268.
Sunstroke, differential diagnosis, 1055.
etiology, 1054.
morbid anatomy, 1053.
prognosis, 1055.
symptoms, 1054.
treatment, 1055.
Suppuration, 2.
Suppurative hepatitis, circumscribed. /i'7<' y ^
^7
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