ill t > /■ 'm-m M$Mk_ i ) '^ 1 3D i 1 ^ 1 CORNELL UNIVERSITY. THE THE GIFT OF ROSWELL P. FLOWER FOR THE USE OF THE N. Y. STATE VETERINARY COLLEGE. 1897 P 1 f ^ Cornell University Library RB 25.C65 A manual of pathology. 3 1924 000 291 512 Cornell University Library The original of tiiis book is in tine Cornell University Library. There are no known copyright restrictions in the United States on the use of the text. http://www.archive.org/details/cu31924000291512 \- V A A MANUAL OF PATHOLOGY. A MANUAL j<^y^ PATHOLOGY. BY JOSEPH COATS, M.D., >ATHOLOGIST TO THE WESTERN INFIRMARY AND THE SICK CHILDREN'S HOSPITAL, GLASGOW; LECTURER ON PATHOLOGY IN THE WESTERN INFIRMARY; EXAMINER IN PATHOLOGY IN THE UNIVERSITY OF GLASGOW J FOHMEELY PATHOLOGIST TO THE ROYAL INFIRMARY, AND PRESIDENT OF THE PATHOLOGICAL AND CLINICAL SOCIETY OF GLASGOW. WITH THREE HUNDRED AND THIRTY NINE ILLUSTRATIONS. PHILADELPHIA: HENEY C. LEA'S SON & CO., 1883. CG6 DORSTAlSr, PRINTER. TO JOSEPH LISTEE, M.B., F.R.S., WHOSE METHOD OP REGARDING PHYSIOLOGICAL AND PATHOLOGICAL PROCESSES AFFORDED TO THE AUTHOR, DURING THE EARLIER YEARS OF HIS CAREER, AN EXAMPLE OF SCIENTIFIC INSIGHT FOR WHICH HE HAS NEVER CEASED TO BE GRATEFUL, AND TO W. T. GAEDNER, M.D., WHOSE ENTHUSIASM IN THE STUDY OF PATHOLOGY, IN THE POST-MORTEM ROOM AND AT THE BEDSIDE, HAS BEEN TO THE AUTHOR, DURING THESE FOURTEEN YEARS, A PERPETUAL STIMULUS, WHILE HIS GENEROUS FRIENDSHIP HAS BEEN A CONSTANT ENCOURAGEMENT, §his IgarJi is, WITH GREAT RESPECT AND ESTEEM, DEDICATED. PREFACE. The teaching of Pathology in the British schools of medicine has, of late years, assumed greatly enlarged proportions, while the publication of native text-books has by no means kept pace with it. Since the publication of "Wilks and Moxon's excellent work on Pathological Anatomy in 1875, no complete English work has appeared. Green's "Introduction," though improving both in scope and fulness with successive editions, laying no claim to be a complete systematic treatise. In the paucity of English works we have had several translations of foreign manuals. The Sydenham Society, in 1872, issued a translation of Rindfleisch's Manual of Pathological Histology, and during the last few months we have had the first instalments of translations of Cornil and Ranvier's "Manuel d'Histologie Pathologique," and of Ziegler's "Lehrbuch der Pathologischen Anatomic und Pathogenese." These two latter translations were announced after the author had undertaken the present work. The want of a complete English text-book, felt by the author in the course of teaching, suggested this undertaking. It will be seen from the Contents that the scope of this work is somewhat more extensive than that of most works on the subject. These, for the most part, are limited either to Pathological Anatomy or General Pathology, while in this work an endeavor has been made to include both. It will be acknowledged that the whole aim of pathological anatomy is to elucidate the actual vital pro- ' cesses of disease, and it has been felt by the author in lecturing on Pathology that the subject gains in interest and intelligibility when the etiology, anatomy, and general pathology are all taken into account in forming a general conception of each morbid Viii PREFACE. condition. The author is conscious of many imperfections and omissions now that he contemplates his completed task; he can only ask for the indulgence of the reader, and he may be allowed to hope that an opportunity will be given of improving on the present work. It was in the plan of the author to indicate the literature of the various subjects treated of; this, however, has been necessarily left over. In the mean time it may be stated that the author has been much indebted to the works of Virchow, Wagner, Eind- fLEiscH, CoHNHEiM, Pagbt, Wilks and MoxoN, Payne, Klebs, CoRNiL and Ranvier, Forstbr, Eokitansky, Birch-Hirschfeld, Billroth and Ziegler for general guidance in the preparation of the work. As the author for the last fourteen years has been constantly engaged as a practical Pathologist and in teaching large classes of students, the work in most of its departments rests upon his own observation and experience. In the preparation of the work for the press, and in arranging the index, the author has been under great obligation to Dr. Geo. 8. Middleton and Dr. J. Lindsay Steven, the former of whom has also supplied, in the index, the derivations of words. Glasgow, March, 1883. CONTENTS. PAET FIRST.— GENERAL DISEASES. IKTRODUCTION. Pathology is the study of diseases in their essential nature, 17 ; The relation of morbid and healthy conditions, of Pathology and Physiology, 17 ; Pathology elucidated by means of Experimental Pathology, 18 ; Pathological Anatomy, 18 (including Pathological Histology, 20) ; and Clinical Observation, 20. APFECTIOlSrS OF THE CIECULATION AND OF THE BLOOD. Phtsioloqical Cqitsidbkatioh-s. — Arrangements for regulating the distribution of the blood, 23; Tonicity of arteries, 24; Regulation of arteries by peripheral centres, 24. Hyperemia and Anemia, 25 ; (1) Gbnbral HYPBKiBMiA, Plethora an equivalent term, 25 ; Artificial Plethora produced by Teansexj-sion, 25 ; Quantity of blood transfusible, 26 ; Disposal of excess, 26 ; Effects of blood containing free ferment, 26 ; Effects of alien blood, 27. Plbthoka in man, 27. (2) Genbral Ak^mia.— a true general antemia or oligsemia produced by hemorrhage, 27 ; the resulting conditions, Hydraemia, Leucooytosis, 27 ; Re- plenishment of the red corpuscles a slow process, 29. Spontanbotjs Anemias. — Chlorosis, 29 ; Pernicious Ansmia, 30 ; Secondary anaemia, 31 ; Secondary organic changes in anaemia, 31. (3) Local Hyperemia. — Its two forms : (n) Active HYPBKiEMiA or Active Congestion, 82 ; rarely from increase of blood-pressure, 32 ; collateral hyperaemia in relation to blood-pressure, 32. Dilatation of arteries the essential cause of active hyperaemia, 33 ; from application of warmth, from removal of pressure, from vaso-motor paralysis, 33 ; Results and signs, 34. (5) Passive HYPEEiEMiA produced by weakness of the heart with gravitation (hypostasis) , 34 ; obstruction of arteries and veins, 35 ; and valvular disease, 35 ; Results are the consequence of increased blood-pressure, 35 ; chiefly hemorrhage by diapedesis, 36 ; and cedema, 36. (4) Local Anjbmia produced by obstruction of capillaries or arteries, 38 ; its results, 38. Thrombosis and Embolism. — Thrombosis is the coagulation of blood inside the vascular system, 39 ; Conditions of coagulation, 39 ; the part taken by the leuco- cytes, 39 ; red thrombi, 40 ; white and mixed, 40. The two main elements in thrombosis : stagnation of blood, 41 (illustrations, 41) ; injury to v,rall, 41 (illus- trations, 41). Growth of thrombi, 42. [Post-mortem coagula, 43.] Changes in thrombi : softening, 43 ; (vein stones, 44) ; organization, 44. Capillaries in relation to thrombosis, 45. Effects of thrombosis : Hyperaemia and cedema, 46 ; rarely gangrene, 46. X CONTENTS. Embolism. — In anastomosing arteries and capillaries, 46 ; in end-arteries, 47 ; Cohn- heim's experiments, 47 ; the hemorrhagic infarction, 48. Illustrations in man : emholism in lungs, 49 ; spleen, 50; kidneys, 50; brain, 50; portal vein, 51. Peculiar case of the superior mesenteric artery, 52. Case of arteries rendered end-arteries, 53. Further consequences of embolism : necrosis, 53 ; absorption, 54. Oil embolism, 54. Air embolism, 54. Hemorrhage. — Hemorrhage by rupture or by diapedesis, 55 (illustrations, 56). Stilling of hemorrhage, 57 ; by thrombosis and other aids, 57 ; disposal of the extravasated blood, the fibrine and red corpuscles, 58 ; cells containing red cor- puscles, 59 ; pigmentation, 59. The HiEMATOMA, of the scalp, 60 ; ear, 60 ; dura mater, heart, uterus, 60. OEDEMA AND Dropsy. — The lymphatic circulation, 61. Causes of oedema and dropsy, 61 ; obstruction of lymphatics, 61 ; increased transudation from capillaries, 63 ; the latter the essential cause, 63. Illustrations : venous hyperaemia, 63 ; hydriemia, 64. The oedema of Bright's disease and hydrjemic plethora, 64. Leukemia. — Condition of the blood, an anasmia with increase of leucocytes, 66 ; nature of the change, 67. Association with lesions in supposed blood-forming organs : Spleen, 67 ; Bone-marrow, 68 ; Lymphatic glands, 68. Secondary changes in other organs: liver, kidney, 69; intestine, etc., 70; PsEUDO-LEr- KiEMIA, 70. Melan^mia. — Solid pigment in blood after agues, 70; Its origin from red corpuscles, 71 ; Deposition in spleen, liver, brain, kidneys, etc., 72. Uremia. — Supposed to be a poisoning with urinary constituents, 72 ; Various other views, 72 ; Eeasons for adhering to original one, 73. Diabetes Mellittts. — The normal sugar in blood and urine has no relation to the food, 73 ; In diabetes the relation marked, 73 ; An excessive demand for sugar, 74 ; The liver forms glycogen, not sugar, 74 ; Pathological conversion of glycogen into sugar, 75; Explanation of diabetes on this basis, 76; In artificial diabetes circulation in liver deranged, 76; also in some cases in man, 77. A hyperaemia of abdominal viscera generally, 78. Lesions in coeliac plexus, 78 ; in brain, 78. INFLAMMATION. Etiology. — Irritants damage the tissues, 80. Internal inflammations also produced by irritants, 80. Eelation of the nervous system, 81. Path of conduction of irritants, 82. The Principal Phenomena. — Experiment giving a summary view of these, 82. 1. The State oe the Vessels. — Dilatation of the arteries with active hyper- semia (Determination of blood), 84. This a local process from paralysis of mus- cular coat, 85 ; irritants paralyze the tissues, 85 ; evidence from pigment cells of frog, etc. , 85. Retardation of current and pavementing of veins from acquired adhesiveness of coipuscles, 86. Temperature of inflamed parts — the rise due to determination of blood, 87. 2. The Inflammatory Exudation. — The exudation cells, their source in the blood, 89 ; emigration of leucocytes, 90 ; diapedesis of red corpuscles, 90. The serous exudation, shed from surface or causing oedema, 91 ; greatly increased transudation, 91. The fibrinous exudation, its manifestations, 91 ; not usually in serous spaces, 91. Mode of production of inflammatory exudation, 92 ; the damage to the vessels the cause of escape of corpuscles, 92 ; and increased trans- udation, 93 ; the formation of fibrine, 93. Mixed exudations — ^Variations as to site, etc., 94. Pinal disposal of exudation, 95. CONTENTS. XI 3. The Changes in the Tissues and Ne"w Pokmation. — At flrat retrograde changes, 95. New formation — Its type in the gbanitlatino -wound, 95. Character of inflammations leading to granulation, 96. Two kinds of cells, 97. The formative cells and their changes, 97. New formation of bloodvessels, 98. The origin of the formative cells, 99. Connective tissue and the lymphatic system, 100. New formation of epithelium, 101. Other instances of new forma- tion, 101. New formation in connection with foreign bodies and dead tissue, 102, 4. Individual Pokms of inflammation : congestive, exudative, 103 ; infec- tive, phlegmonous, ulcerative, 104 ; degenerative, formative, 104. EETBOGRADE METAMOEPHOSBS. Necrosis ; Gangrene, 105. Conditions producing local death, 105 ; interference with circulation, 105; traumatic agents, 106 ; excessive heat or cold, 106 ; special case of senile gangrene, 107; senile softening of the brain, 107; ergotism, hos- pital gangrene, 107. Changes in the Dead Tissue give the character to the necrosis, so (1) Coagulation necrosis, 108 ; (2) Caseous necrosis. 111 ; (3) Desic- cation or mummification. Ill ; (4) Softening and moist gangrene, 112. Limita- tion of the necrosis, 112. Disposal of the dead tissue, 113. Simple Atrophy, 113. Physiological atrophy of hair, teeth, etc., a vital process, 114. General emaciation, 114 ; local atrophies, 115 ; of muscles from disuse, 115; tropho-neuroses, 115. Albuminous Infiltration, causes and appearances, 116. Patty Degeneration, 118. The free and combined fat of the tissues, 118. Bauer's experiments, 118. Patty degeneration in anaemia, inflammation, etc., 118. Source of the fat, 119. The anatomical changes, 120 ; final disposal of the fat ; absorption, 120; formation of cholestearine, 121 ; caseation (tuberculization), 122. Patty Infiltration, 122. Obesity, 122. Infiltration in structures out of use, 122 ; in muscles, heart, disused glands, 122. Special case of fatty liver, 123. Appear- ance of the fat, 124. Pigmentary Infiltration, 124. Connection with hemori'hage, 124 ; in tumors, 125; in lungs ; uterus; bronzing, etc., 125. Mucous AND Colloid Degeneration, 126. The physiological mucus, 126; colloid ovarian cyst, 126; colloid goitre, etc., 127. Mucous degeneration of connective tissue, bone, cartilage, tumors, 127. Calcareous Infiltration, 128. Lime salts dissolved in tissues and juices, 128. Metastatic calcification, 128. Infiltration of dead or obsolete structures, 128 ; of parasites, inflammatory products, 129; of walls of arteries, etc., 129. Amyloid Degeneration, 131. The amyloid substance, 131. The disease afi"ects connective tissue and walls of vessels, 132. Effects on structure and function, 133. Localized amyloid degeneration, 134. Nature of the process, 134. Corpora amylacea, 135. HTPEETKOPHY, EEPAIE, AND EEGENEEATION. Hypertrophy, 137. Its type in normal growth, 137. Process of division of cells, 137. Hypertrophy from excessive performance of a normal function, 188. (1) In muscle of bladder, heart, etc., 139 ; details of process, 139 ; hyperplasia, 140. (2) In epidermis, 140 ; from intermittent pressure, 140. Hypertrophy from in- creased blood-supply, 140; near inflammations, in bone, etc., 141. XU CONTENTS. Eepaie or Injueies and Eestoration oe Lost Parts, 141. Powers of restora- tion in lower animals, 142. Indication of law governing powers of restoration in adult animal, 142. Eepair of injuries, 142. Healing or wounds : imme- diate union. 143 ; primary adhesion, 143 ; by second intention, 144. Kegenera- tion of lost structures, 144 ; blood, 144 ; epidermis, 144 ; connective tissue, 145 ; bone (transplantation), 146; nerve fibres, 146; muscle, 146. INFECTIVE TUMOES (GEANULATION-TISSUE TUMOES). Due to the action of viruses, 147. In structure analogous to inflammatory new forma- tions, and generally associated with inflammation, 147. Syphilis, 148. The primary chancre, 148. The secondary stage, in which the virus is in the blood, 149 ; blood and secretions contagious, 149. The tertiary stage characterized by unsymmetrical gummata, 150; structure and tendencies of gumma, 151 ; its relations to the virus, 152. Hereditary and congenital syphilis, 153. Tuberculosis. — (a) G-eneeal Tubkeculosis, 154. Case of Acute Miliary Tuber- culosis, 154; a virus in blood, 154; comparable to secondary stage of syphilis, 154. The structure and tendencies of the miliary tubercle, 155. Connection of tuberculosis and inflammation, 157. (b) Local Tuberculosis, 157. Illustra- tions : tubercular peritonitis, 157 ; renal phthisis, 158. Tubercular ulcers, 158. Scrofulous tubercle of brain, 159. Aetieicial peoduction oe Tuberculosis ; by inoculation, 159 ; by inspired air, by food, 170. Nature of the tubercular virus, 150 ; the tubercular bacillus of Koch, 161. Scrofula, etc., included in tuberculosis, 162. Source oe the tubercular virus ; in acute miliary tuber- culosis, 163; in local tuberculosis , 163. Bovine Tubeeculosis or Perlsuoht, 164. Lupus, 166. Leprosy, 166. Glanders and Farcy, 168. TUMOES OE MOEBID GEOWTHS. Definition and general characters, 169. Homologous and heterologous, 169. Origin and development, 169 ; theory that tumors arise from embryonic tissue left over, 170 ; applicability of this view to some tumors, 171. Growth and extension ; of simple tumors, 171; malignancy, local and general, 172; metastasis, 172; malignancy of tumors usually simple, 173. Secondary changes in tumors, 173; cachexia, dyscrasia, etc., 174. Classification, 174. A. — Simple-tissue TumOrs. (1) The connective-tissue tumor, or Fibroma, 176; including Elephantiasis arabum, 176 ; cutaneous outgrowth, 177 ; fibroma molluscum, 178 ; soft and hard fibromas, 178. (2) The fatty tumor or Lipoma, 178. (3) The mucous-tissue tumor or Myxoma, 180 ; including hydatid mole, 182 ; and mucous-tissue tumor proper, 182. (4) The cartilaginous tumor or Chondroma, 184. (5) The bony tumor or Osteoma, 185 ; including the spongy exostosis, 185 ; the ivory exostosis, 186; and other osteomas, 187. (6) The muscular-tissue tumor or Myoma, 187 chiefly the smooth-celled form, 188. (7) The nervous-tissue tumor or Neuroma, 190; the false and true neuromas, 191. The painful subcutaneous tumor, 191 (8) The vascular tumor or Angioma, 193. (9) The glandular tumor or Adenoma 194 ; including the mammary, prostatic, mucous, 194 ; thyroid and hepatic forms 196. (10) The glioma or tumor of nervous connective tissue, 196. (11) The brain sand-tumor or Psammoma, 198. CONTENTS. xm B. — COMPOUND-TISStJB TUMORS. (1) The cystic tumor or Cystoma, 198; mode of formation of cysts, 198. (2) The papillary tumor or Papilloma, 202. (3) The Teratoma, 203 ; sacral tumors, 203 ; dermoid cysts of ovaries, etc., 204. C. — Cbllular Tumors. (1) Sarcomas, 204; definition, structure, mode of growth, 204; relation to bloodvessels, 206 ; Varieties ; the round-celled, 206 ; spindle-celled, 207 ; cystic, 208 ; giant-celled, 208 ; osteoid, 209 ; melanoid, 209 ; alveolar, 210 ; and plexi- form, 210. (2) Cancer or Carcinoma, 210 ; definition and structure, 211. Origin of epithelium from preexisting epithelium, 212; illustrations, 212; mode of growth, 214; relation to lymphatics, 214; secondary changes, 215. Varieties: The epithelial cancers or epitheliomas, 215; the flat-celled, 215 ; and cylinder- celled, 217 ; Carcinoma proper, 217 ; including medullary, 218 ; scirrhous, 219 ; colloid, 221 ; melanotic, 222 ; and mucous cancers, 222. (3) The lymphatic tumor or lymphoma, including chiefly the lymphadenoma, 222 ; and lympho- sarcoma, 222. PAEASITES. A. — Vbgbtabib Parasites. Micro-organisms or Bacteria, 224 ; their occurrence in decomposing matter, 224 ; their source, in the air, etc., 224; their forms, 225; the cocoo-bacteria, bacillus, spirillum, 226 ; methods of detection, 228. Influence of bacteria on the living tissues, 229. Case of putrefying or septic wounds, 230. Septicaemia, 231. Im- portance of distinguishing its two forms, 231. (1) Putrid or septic poisoning from the products of decomposition, 231. Wound fever, hectic, etc., 232. (2) Putrid or septic infection involving a self-propagating virus, 233 ; experiments of Kock and others, 233 ; septicjemia of mice, 234 ; and of rabbits, 235. Patho- genic BACTERIA, 236 ; cultivation of them, 236. Pyemia a form of putrid in- fection, 237. Its phenomena, 237. Ulcerative endocarditis, 241. Pathogenic bacteria in acute spbcieio diseases, 242. (1) The relation of micro-organisms to zymotic diseases, 242 ; splenic, 242; relapsing, 244 ; typhoid, 245; and other fevers, 246; erysipelas, 246; ulcerative endocarditis, etc., 246. (2) Cultivation of pathogenic bacteria, 248 ; bacillus anthracis, 248 ; tubercular bacillus, etc., 249. (3) The question of immunity, 249; natural, 249; and ac- quired immunity, 251. Pasteur's artificial production of a vaccine for anthrax and chicken cholera, 251. Explanation of immunity, 252. Sarcina Vbutriculi, 253 ; development in blood outside the vessels, 254. Parasitic Fungi, 254. Outline of structure of fungi, 254. Pungi in the blood and tissues, 256. The madura foot, 257. Fungi in the ear, skin, 257 ; hair, 259 ; mucous membranes, etc., 259. Actinomycosis, 798. B. — Animal Parasites. (1) Tkematoda or Flukes, 260. The distomahepaticum, 261; sinense, 261; lanceolatum and h^matobium, etc., 262. (2) Cestoda or Tape- worms, 262. Their structure in general, 262. T«nia solium, 263 ; structure of strobila, 263 ; and cysticercus, 266 ; mode of propaga- tion, 268. Tienia mediocanellata, 268. Taenia eohinococcus, 270. Formation of echinococci or hydatids, 270. Bothriocephalus latus, 278. Rarer tape- worms, 274. xiv CONTENTS. (3) Nbmatoda or Eotjnd-wokms. Trichina spiralis, 275 ; its appearance in muscle, 275 ; development and migration of embryos, 277. Asearis lumbricoides, 278. Oxyuris vermicularis, etc., 279. Pilaria sanguinis, 279; its relations to chylous urine, 282 f lymph-scrotum, etc., 282. Stages of development of filaria, 283. EpIZOA or BXTKKNAL PARASITES, 283. PAET SECOND.— DISEASES OF THE SPECIAL OEGANS AND SYSTEMS. DISEASES OP THE OEGANS OP CIRCULATION. A. — The Heart and Pericardium. Malformations of the Heart, 285. Misplacements, 285. Malformations of the cavities and of their relation to the great vessels, 285 ; mainly dependent on stenosis of the pulmonary artery, 286 ; incomplete closure of septum ventricu- lorum, 286 ; of foramen ovale, 287 ; and of ductus arteriosus, 288. Nature of foetal stenosis of pulmonary artery, 288. Irregularity of primary vessels, 289. Valvular malformations, 290. Eenestrated valves, 291. Cyanosis as a result of malformations, 392; duration of life, 293. Atrophy of the Heart, 294. Hypertrophy; its compensatory nature, 294 ; produced by increased force of con- tractions, in adherent pericardium, 295 ; in valvular disease, 296 ; in Bright's disease, etc., 297. Eorms of hypertrophy, 297 ; general, and of right or left ven- tricle, 297. Congestion of the heart, 299. Patty Infiltration, 299. Patty Degeneration, 300. Calcareous Infil- tration of the muscular substance, 302. Injuries and Eupture, 303. Inflammations of the heart. — (1) Myocarditis, 304 ; mostly interstitial, 304 ; fibroid myocarditis, 305 ; abscess of the heart, mostly septic, 305. (2) Endocarditis, 306 ; acute, 806 ; characters and localization of lesions, 306 ; chronic, 308 ; effects on valvular structures, 308 ; relation in some cases to atheroma, 310. Ulcerative endocarditis, its specific characters, 310. (3) Pericarditis, 313;. acute, 313; usual appearances, 313 ; and results, 315 ; adhesion of the pericardium, 315. Tubercular pericarditis, 316. White or milk spots, 316. Aneurisms. — (1) Of the heart, appearances and mode of formation, 317. (2) Of the valves, their relation to acute endocarditis, 318. Valvular Disease, 319. Insufficiency of mitral, 319 ; characters, 319 ; and effects, 320. Stenosis of mitral, 321 ; the funnel-shaped malformation, 322 ; effects, 322. Aortic insufficiency, 323 ; conditions, 323 ; and effects, 324. Aortic stenosis, 325, Valvular diseases of the right heart, 326. CoAGULA IN this Hbart.— Simple clots, 327 ; thrombi, 327 ; warty, globular, poly- poid, 327. Tumors of the heart, 329. B. — The Bloodvessels. Inflammation, 330 ; acute, rare except as part of a septic process, 3-SO. Chronic Endarteritis — Atheroma, 332 ; a disease of advanced life, 332. Ana- tomical changes, the patch, 332.; the abscess. 334; the ulcer, 334; calcareous in- filtration, 334; changes in middle and external coats, 335. Effects on circula- tion, 335. CONTENTS. XV Endarteritis Obliterans, 337. Patty degeneration of intima of arteries, 888. Cal- careous infiltration of arteries, 838. Syphilitic Disease or Arteries, 340. Aneurism, 342; forms, 842; causation — weakening of wall, 843; increase of blood- pressure, 344. Condition of the coats of the artery, middle, internal, and ex- ternal, 344. Thrombi in aneurisms, 346. Condition of branches arising at site of aneurism, 346. Effects on heart, 347 ; and on parts around, 347. Termina- tions, 348. Varieties op Aneurisms, 849 ; cirsoid and aneurism by anasto- mosis, 849 ; traumatic and spurious aneurism, 349 ; dissecting aneurism, 850 ; varicose aneurism and aneurismal varix, 351. Varix, 352 ; causation in increased blood-pressure, 352. Condition according to site : in lower extremities, 353; hemorrhoids, 854; varicocele, etc., 355. C. — The Lymphatic System, Spleen, and Bone-marrow. The Lymphatic Vessels, 355. Inflammation ; lymphangeitis, 355 ; erysipelas, 356. Dilatation of lymphatics, 356. The Lymphatic Glands. — Structure and function, 857. Pigmentation, 859. In- flammation, acute, 859 ; and chronic, 360. Scrofulous disease, a true tuberculosis, 360. Syphilitic disease, 363. Degenerative changes, 363. Tumors, 368. The Spleen. — Structure, 364. Malformations, 865. Active congestion and inflam- mation : the acute splenic tumor, 365. Chronic inflammation, the chronic splenic tumor, 367. Passive hypersemia, 367. Embolic infarction, 368. Rupture of the spleen, 869. Amyloid disease, 369 ; the sago spleen, 369 ; the diffuse amyloid spleen, 870. Tuberculosis, etc., 371. The Bone-maerow, 371. DISEASES OF THE NERVOUS SYSTEM. Introductory, 872. The general plan of the nervous system, 372 ; lower and higher centres in cord, medulla, middle brain, 373 ; basal ganglia, cerebral convolutions, 374. Lesions irritate or destroy, 374. Coarse and fine lesions, 374. A.— The Peripheral Nerves. Introductory Considerations as to structure and function, 375. Eeeects of Division of nerves, 377; degeneration and restoration, 377. Hypbr- iEMiA and ACUTE inflammation, 378. Chronic neuritis, 379. Tumors. Leprosy, neuroma, etc., 379. B.— The Spinal Cord and Medulla Oblongata. Introductory, 380. The gray substance, with its groups of ganglion cells, 380. The white substance, with its various tracts, 381. Separate development of fibres and centres, 382. Fibres and centres in medulla oblongata, 388. Secondary Degenerations of the Cord, 384. Characters of gray degeneration (sclerosis), 385. Descending degeneration, 886 ; its locality, 387 ; its relation to late rigidity, 387 ; and increased tendon reflex, 388. Ascending degeneration, 388. Degeneration after amputation, 389. Inflammations of the Cord. — Transverse myelitis: acute, 390; chronic, 391. Systematic myelitis, 892. Reasons of systematization, 892. (1) Sclerosis of posterior columns, 893 ; special localization in these, 393 ; physiology of the disease, 894; trophic lesions, 396. Eriedrich's hereditary ataxia, 396. (2) Spon- taneous lateral sclerosis, 396. (3) Poliomyelitis anterior acuta, 397 ; anatomical condition, etc., 397; its occurrence in adults, 399. (4) Poliomyelitis anterior XVI CONTENTS. chronica, 399. (5) Progressive muscular atrophy, 400; changes in muscles, and in cord, 400. (6) Bulhar paralysis, 401 ; its locality and relation to nuclei of nerves, 402. (7) Pseudo-hypertrophic paralysis, 403 ; condition in muscles, 403 ; and cord, 403. TUMOKS OT THE CoRD AND MbDTJLLA, 406. C. — The Bncbphalon-. Introdtjctoky. — Course of fibres and position of centres in basal parts, 406 ; in hemispheres, 409 ; and in cerebellum, 412. The arteries of the brain, 412. Secondakt Degeneration, chiefly of pyramidal tract, 414. Embolism and Thrombosis in cerebral vessels, 415. Causes and localities of em- bolism and thrombosis in arteries, 415. Effects of occlusion of arteries, 416. Embolism in chorea, 418. Thrombosis of the cerebral sinuses, 418 ; localities, effects, etc., 418. Cerebral Hemorrhage, 419. (1) From the larger cerebral arteries, 420 ; connec- tion with aneurisms, 420; atheroma, 421; increase of blood-pressure, 421. (2) Prom the nutritive arteries, 421 ; miliary aneurisms, 422. (3) From the capil- laries, 423. Appearances in the brain after hemorrhage, 423. Organization of the clot, 424. The apoplectic cyst, 424. Softening of the Brain, 425. Anatomical conditions and appearances, 426. Inflammations, 427. (1) Acute localized encephalitis, 427 ; usually traumatic, 427 ; abscesses, 428. (2) Chronic localized encephalitis, 428 ; disseminated sclerosis, 429. (3) Diffused encephalitis, 429 ; deliriumof fevers, 429 ; general paralysis of the insane, 430 ; (atrophy of the brain, 430 ;) hydrophobia, 432 ; lesions in nervous system and elsewhere, 433 ; tetanus, 434. Atrophy and Degenerations, 434. Congenital atrophy, 434. Atrophy of white substance, 435 ; and ganglion cells, 435. Syphilis of the Brain and its Membranes, 485. The gumma in brain and membranes, 435. Disease of the arteries, 437. Inflammations of the membranes, 438. Localization in relation to symptoms, 438. Tumors OP the Brain, 438. Solitary tubercle, 439 ; glioma, 439; sarcoma, etc., 440. Parasites, 440. D. — Membranes and Cavities of Brain and Cord. Introductory, 451. Meningeal Hemorrhage, 442. Hsematoma of dura mater, 442 ; its relation to pachymeningitis, 442. Hemorrhage in the soft membranes, 443. Inflammations, 444. (1) Pachymeningitis, 444. (2) Simple acute meningitis, 444. (3) Simple chronic meningitis, 444. (4) Epidemic cerebro-spinal menin- gitis, 445. (5) Tubercular meningitis, 445 ; appearances of brain, 446 ; situation of tubercles, 447. Accumulation of Cerebro-spinal Fluid, 447. Accumulations ex vacuo, 448. Hydrocephalus, 448 ; congenital and acquired, 448 ; chronic hydrocephalus, 449. Hydrencephalocele, 450. Spina bifida, 451 ; condition of cord, 452. Tumors of Meninges, 452. Parasites, 453. DISEASES OF THE ORGANS OF RESPIRATION. A. — The Air-passages. The Nasal Passages.— Congenital malformations, 454. Acute catarrh, 454 ; con- siderations as to its causes, 455 ; details of the process, 455. Chronic catarrh or coryza, 456. Tumors, especially mucous polypi, 456. CONTENTS. xvii Laktnx and Trachea. — Malformations, 457. Croup and Diphthbria, 458. Catarrh, 460. (Edema glottidis, 460. Chronic catarrh, 461. Subglottic inflam- mation, 461. Perichondritis, 461. Syphilis, 462. Laryngeal phthisis, 463. Tumors, 464. The Bronchial Ttjbes. — Bronchiectasis, 465. Catarrh or bronchitis, 467. Fibrin- ous or plastic bronchitis, 469. B. — The XiXTNgs. General Considerations, 469. Maleormations, 471. Atelectasis, 471 ; and collapse, 472. Hypertrophy of the lung, 473. Pulmonary Emphysema.— (1) Interlobular, 474. (2) V^icular ; its causes, 475 ; •expiratory, 475; inspiratory or compensatory, 476; anatomical changes, 477; effects, 480. Senile emphysema, 480. Disorders or the Circulation. — Active hyperasmia, 481 ; sometimes collateral, 481. Passive hypersemia and oedema, 482 ; hypostatic engorgement, 482 ; mode of occurrence of oedema, 483 ; appearances, 483. Passive hyperemia from heart disease ; brown induration, 484. The hemorrhagic infarction, 485. Embolism without infarction, 487 ; oil embolism, 487. Pulmonary hemorrhage, 488. Inflammations. — Acute Pneumonia, 489 ; stages of splenization, 490 ; red hepatization, 490 ; gray hepatization, 492 ; and purulent infiltration with resolu- tion, 493 ; occasional result in abscess, 493; gangrene, etc., 494; condition of pleura, 494. Chronic Pneumonia, 494; producing chiefly induration, 494. Acute Catarrhal Pneumonia, 496 ; related to capillary bronchitis, 496 ; its lobular arrangement, etc., 496 ; occasional interstitial pneumonia, 497. Gangrene or the Lungs, 498. Phthisis Pulmonalis, 499. Causes, 500 ; views as to its pathology, 500. Modern view of a local tuberculosis, 502. Conditions which predispose, 502 ; path of entrance of virus, 502 ; localization at apex, 502. Anatomical Changes, their complicated characters, 503. (1) Condition of bronchi, 503; catarrh, 504; peribronchitis, 504 ; acute with abscess, 505 ; or chronic with induration, 505. (2) Fibroid phthisis, 505 ; pigmentation of connective tissue ; formation of connective tissue, peribronchitio, interlobular, and subpleural, 505 ; bronohiectatic cavities, 506 ; mode of occurrence of emphysema and cavities, 506. (3) Catarrhal or Caseous Phthisis, 507 ; the anatomical changes, 507 ; nature of the caseous necrosis, 509 ; formation of cavities, 509 ; general appearances of the lung, 510. Modes in which cavities form, 512. Sputa, 512. Hemorrhage in earlier and later periods, 512. Condition of pleura, 513 ; mode of occurrence of pneumothorax, 514. Condition of bronchial glands, 514; intestines, etc., 514. Acute Miliary Tuberculosis, 515. Bovine tuberculosis, 515. Syphilitic Disease, 516^ Tumors. — Barely primary, 516. Lympho-sarcomas, 516. Cancers, 517. Inhalation of Foreign Substances, 518 ; the ordinary pigmentation, 518 ; an- thracosis, 519 ; and other kinds of pigmentation, 520. C— The Pleura. Pleurisy, 521 ; its causes, 521 ; anatomical changes, 522. Empyema, 222. Pleural adhesions, 523. Hydrothorax and pneumothorax, 523. Tumors, 524. XVm CONTENTS. DISEASES OE THE ALIMENTARY CANAL. A. — The Mooth. Inflammations.— Catarrh, 525 ; follicular stomatitis, 526 ; thrush, 526 ; gangrenous stomatitis, 527. Inflammation of the tongue, 52$. Inpectivb TtTMOKS. — Syphilis, lupus, 528. Tumors, chiefly cancers, 529. Macboglossia, 530. Eanitla, 530. Thb Teeth. — Caries, 531. Inflammations of pulp, cement, and structures around, 532. Hypertrophy of cement, exostosis, 533. B.— Soft Palate, Phabtnx, and Tonsils. Inflammations. — Acute catarrhal angina, 533 ; chronic catarrh, 534 ; acute phleg- monous inflammation of fauces (quinsy), 535 ; diphtheria, 536 ; tonsillitis, 536 ; and hypertrophy of the tonsils, 586. Syphilitic and tubercular diseases of the fauces, 537. C. — The (Esophagus. Dilatation, general and partial, 537 ; the diverticulum, 538. Gbsteitction, 538. Inflammations, 539. Perforating ulcer, 539. Tumors, especially epithelioma, 540. D. — The Stomach. Introductokt, as to structure and function, 541. Post-mortem changes, 542 ; in- cluding softening of the stomach, 543. Dilatation and Hypertrophy, 543. Inflammations, 545. Catarrh, acute, 545 ; and chronic, 546. Simple Perforating Ulcer, 546 ; its peculiarities, 547 ; effects, 547 ; and mode of origin, 448. Hemorrhage from the stomach, 549. Tumors.— Cancer in its epithelial, 550 ; medullary, 551 ; scirrhous, 552 ; and colloid forms, 552. Other tumors, 553. E. — The Intestines. Introductory as to structure and function, 554. The movements of the contents, 5S4. Post-mortem changes, 555. Malformations, 555. Meckel's diverticulum, 556. Hernia, external and internal, 556. Mode of occurrence, 556. Eorms of external, 557; and internal hernia, 557. Contents of hernias, 558. Strangulation, 559. Twisting of the intestine, 560 , occurrence in sigmoid flexure and elsewhere, 561. Intussusception, 561. Prolapse of intestine, 568 ; two forms, 563. Simple Inflammations. — Catarrh, 563 ; ulcers : follicular catarrh and ulcers, 564. Localized inflammations ; typhlitis and perityphlitis, 564 ; connection of these with vermiform appendage, 565 ; proctitis and periproctitis, 566. Specific Inflammations.— Dysentery, 567 ; acute and chronic, 567. Cholera, 568. Typhoid fever, 569 ; conditions of intestine, 570; and mesenteric glands, 571. Tuberculosis of intestine. — Eormation of the tubercular ulcer, 572. Tumors. — Chronic epithelioma, 575 ; colloid cancer, 575. Obstruction of the intestine, 576 ; the various lesions producing it, 576. Effects of accumulation of contents, 576. CONTENTS. XIX DISEASES OP THE LIVEE, PANCREAS, AND PERITONEUM. A. — The Livkk. Introditctokt. — -As to structure and function, 578. Malformations and Misplacements, congenital and acquired— the female liver, 579 ; folds in the liver, 580 ; changes in position, 580. Passive Hyperemia, 580. Thrombosis and Embolism of portal vein and hepatic artery, 582. Hypertrophy of the liver, 583. Retrograde Changes, chiefly fatty infiltration, 583 ; and amyloid degeneration, 585. Acute Yellow Atrophy, its probable nature, 586 ; characters of yellow and red tissue, 587. Inflammations of the liver, 587. The tropical abscess, 587 ; pysemio abscesses, 588. Chronic Interstitial Hepatitis or Cirrhosis, 589 ; nature of the process, 589 ; the new-formed connective tissue, 589 ; hypertrophic cirrhosis, 591 ; atrophy of hepatic tissue, 591 ; effects on circulation in the liver, 591. Perihepatitis, 650. Syphilitic Diseases of the liver : gummata and hepatitis, 594 ; congenital syphilis, 595. TtTBERCTJLOSis of liver,, 595. Ttjmors, chiefly adenoma, 596 ;. and cancer, primary and secondary, 598. Parasites, 600. B. — The Bile-Ducts and Oall-bladder. Gall-stones, 601 ; single and multiple, 601 ; effects of their shifting, 602. O'Bstrttction of ducts, causes, 602 ; results under diflTerent circumstances, 602. Tumors, 608. C. — The Pancreas. Hemorrhages, inflammations, 604 ; atrophy, fatty infiltration, tuberculosis, cancer, 604 ; concretions and dilatation of pancreatic duct, 605. D. — The Peritoneum. Its relations and function, especially the power of absorption, 606. Disorders of the Circulation. — Active hyperaemia, 607 ; hsematoma of the peri- toneum, 607. Ascites, 607. Inflammations. — Peritonitis, chiefly septic, 608. Chronic peritonitis, 610. Tuberculosis of the peritoneum — tubercular peritonitis, 610. Secondary tubercu- losis, rare, 611. Tumors, 612. The Secondary Extension or Cancers of the Abdominal Organs. — The secondary cancers of liver, 612 f probable path of invasion, 612. Cancerous in- fection of the peritoneum, 614; relation to great omentum, diaphragm, etc., 615. DISEASES OF THE URINARY ORGANS. A. — The Kidneys and Ureters. Normal Structure and Eunction, 617. Arrangement of tubules, and blood- vessels, 617. Locality and conditions of secretion of urine, 618. Malformations and Misplacements, 620. Congenital malformations, including defect of one kidney, and horse-shoe kidney, 620. Movable kidney, 621. Compensatory Hypertrophy, 622. XX CONTENTS. Disorders of the Circulation. — Active hypersemia, 623 ; and passive, 623. Thrombosis, 623. Embolism, 624. Bright's Disease, or Nephritis, 624. Caused by irritants brought by the blood, 625; may attack specially one tissue, hence parenchymatous and interstitial nephritis, 626 ; acute nephritis from scarlet fever, cold, 626 ; chronic nephritis from gout, lead-poisoning, pregnancy, 626. Anatomical details. Glomerulo- nephritis, in acute nephritis, especially of scarlet fever, 626. Parenchymatous nephritis also chiefly acute, 627. Large white kidney, partly parenchymatous, partly interstitial, 631. Interstitial nephritis, usually chronic, 633 ; changes in glomeruli, 634 ; tubules, 634 ; formation of cysts, 635 ; bloodvessels, 636 ; the contracted kidney, 637. Albuminuria, 638 ; conditions of its occurrence, 639. Tube-casts, 639. Changes in heart and arteries and increased arterial tension, 640; arterio-capillary fibrosis, 641 ; hypertrophy of middle coat, 641. Origin of increased tension from the kidney lesions, 641; its possible explanation from these, 643. Septic Inflammations, 645. Pysemic lesions, 645. Pyelonephritis, 647 ; path of entrance of septic organisms, 647 ; formation of abscesses, 648. Pyonephrosis, 648. Pyelitis, 649. Retrograde Changes. Simple atrophy, parenchymatous infiltration, 649 ; fatty degeneration , 650. Amyloid degeneration, structures involved, 650 ; combination of amyloid and contracted kidney, 651. Concretions and calculi : biliary, 653 ; uric acid, etc., 653. Syphilis and TtrBERCULOSls, 654. Penal phthisis a local tuberculosis, 654. Hydronephrosis, causes and mode of occurrence, 655. Occurrence of pyonephrosis, 657 ; and independent cysts, 657. TtTMORS. — Simple cysts, 657. Cystoid degeneration, 658. Primary cancer, 659. Secondary cancers, 659. Sarcoma, etc., 659. Parasites. — Echinococcus, 660 ; filaria sanguinis, 660. B. — The Urinary Bladder and Urethra. Congenital Malformations. — Extroversion, etc., 660. Eupture and perforation, 661. Results of extravasation of urine, 661. Dilatation and hypertrophy, 661 ; hypertrophy of muscular coat, 662 ; diverticula, 662. Disorders of the Circulation. — Passive hypersemia, hemorrhage, 662. Inflam- mations, chiefly from decomposition of urine, 663 ; character of urine, 664. Tuberculosis of the bladder, 664. Tumors, chiefly papilloma, cancer, cysts, 665. Parasites, 666. Concretions and Calculi. — Their chief constituents and causation, 666. Calculi composed of uric acid ; urates ; oxalate, 667 ; phosphates ; carbonate ; cystine ; xanthine, 668. Diseases of the Urethra. — Gonorrhoea, stricture, 668. DISEASES OP THE FEMALE GENERATIVE ORGANS. Malformations, including the various forms of Hermaphroditism, 670 ; and Pseudo- hermaphroditism, 671. Defect of uterus, etc., 672. Double uterus, 672; horned uterus, 673. A. — The Uterus and Vagina. Misplacements of the Uterus. — Arrangements for retention of the uterus in place, 674. Prolapse or descent, 674; procidentia, 675. Prolapse of vagina, 675. Inversion of uterus, 675. Elexions and versions, 675. CONTENTS. XXI Atrophy, Hypertrophy, and Dilatation. — Atrophy and hypertrophy, 676 ; hypertrophy of cervix, 677. Dilatation from accumulation of contents, 677. Inflammations of Utertts anb Appendages. — Endometritis, 678. Metritis, 678. Pelvi-peritonitis or perimetritis, 678. Pelvic cellulitis or parametritis, 679. Puerperal Peter, a septic disease, 679. The local lesions and their extension, 680. Phlegmasia dolens, 681. Periuterine H^aiMATOCELE, 681. Extrauterine Pregnancy, 682. Syphilis and Tuberculosis oe Uterus, 683. Tumors. — Hasmatoma, 684. Myoma, 685 ; subserous ; intraparietal ; submucous forms, 685 ; structure and secondary changes, 680. Cancer, soft or medullary, 688; epithelial; the cauliflower excrescence, 689 ; colloid, 690. Mucous polypi, sarcomas, etc., 690. Parasites, 691. B. — Ovaries, Fallopian Tubes, Ligaments. Ovarian Hernia, usually congenital, 691. Inflammations, of Fallopian tubes, 692 ; of ovaries, 692 ; chronic oophoritis, 692 ; formation of cysts, 693. Tuberculosis of the ovary and tubes, 693. Tumors. — Simple cysts, 694. Colloid ovarian cyst, or Cystoma, 695 ; origin and structure, 695: appeararces, 697; secondary changes, 697; chiefly fatty degen» eration, hemorrhage, inflammation, 698; perfoi'ation, 698. Dermoid cysts, 698. Cancer, 699. Sarcoma, 700. Cysts of the broad ligaments. Parovarian, 700 ; their origin, 701 ; and connections, 701. Comparison of ovarian and parovarian cysts, 702. C. — The Mammary Gland. Malformations, 703. Inflammations, acute and chronic, 703. Tumors. — Adenoma, 704; adenoid sarcoma and sarcoma, 704; cysto-sarcoma, 706. Cancer, parenchymatous and duct cancers, 707 ; connection with Paget's disease of the nipple, 708. Creighton's views of cancers of breast, 708. Porms of cancer : scirrhus, 708; medullary, 710; acute scirrhus, 711; colloid, 711. Other tumors, 711. DISEASES OP THE MALE GENEEATIVE ORGANS. A. — The Testicles. Malformations and Misplacements. — Imperfect descent ; congenital hernia, 712. Inflammations, 712; acute and chronic orchitis, 713. Syphilitic disease, 713. Tuberculosis, 714. Tumors — Sarcoma and cysto-sarcoma, 714; cancer, 715; other tumors, 715. Hydrocele and hsematocele, 715. Congenital hydrocele, 716. Spermatocele or encysted hydrocele, 716. B. — The Penis and Scrotum. Ulcers or chancres. Condyloma, Cancer, 717. Lymph-scrotum, 717. Hypertrophy of prostate, 718. Concretions in prostate, 718. XXU CONTENTS. DISEASES or THE BONES AND JOINTS. A. — The Bones. Introduction. — Structure and growth ofbone. Metaplasia, 719. KiCKETS. — Its causes in malnutrition, 721; artificial production, 722. Normal ossification from cartilage and periosteum, 724. The ossifying cartilage in rickets, 724. The periosteal ossification, 726. Deformities of the bones in rickets, 726 ; of the long bones, chest, vertebras, pelvis, head (craniotabes), 728. Eecovery from rickets, 729. Osteomalacia, 729. Causes, 730. Forms of softening of the bones, 730. De- formities resulting, 731. Inflammations of Bone.— Changes chiefly in the soft structures, 731. Condensing and rarefying osteitis, 732 ; part taken by osteoblasts and osteoclasts, 732. Caries, 733. Absorption of bone, 733 ; (Transplantation of bone, 734 ;) process of absorp- tion of dead, 734 ; and living bone, 734. Healing of fractures, 736 ; callus, 736. Periostitis ; chronic periostitis frequently secondary, 737 ; suppurative or malig- nant, and simple acute periostitis, 737. Osteomyelitis, 738. Necrosis of Bone.— Separation of dead from living, 738 ; formation of new bone, 739. Phosphorus-necrosis, 739. Syphilitic Disease of Bones. — Gumma, with periostitis, 740. Hereditary syphilis, changes chiefly in long bones, 740. Ttjbercitlar Disease of Bones, 742. Spinal Cttrvatures. — The normal structure and curves of the spine, 743. Forms of curvature, 744. Pott's disease, 744. Kyphosis, 745. Lordosis, 745. Lateral rotatory curvature, 746. Tumors of Bone. — Osseous tumors, related to inflammation, osteophytes, hyper- ostosis, exostosis, 748. Osteoid chondroma, 748. Sarcoma, 750 ; myelogenous, 750; interstitial, 750; and periosteal, 751. Cancers, 751. Cysts, especially of the jaws, 752. B. — The Joints. Dislocations and Misplacements. — Congenital dislocations, 753. Talipes, con- genital and acquired, 753 ; its forms, 753. Traumatic dislocations, 754 ; mode of occurrence, 755; secondary changes, 755. Spontaneous dislocations, 755. Anchylosis, 755. Inflammations of Joints, 756. Simple acute arthritis, 756. Pysemic arthritis, 757. Acute rheumatic arthritis, 757. Gouty arthritis, 758. Chronic rheumatic arthritis and arthritis deformans (morbus coxEe senilis), 759. Scrofulous or tubercular arthritis, 760 ; changes in synovial membrane, ends of bones, carti- lage, etc., 760 ; caries, 761. DISEASES OF THE SKIN. Introduction. — Normal structure, 762. HTPERiEMiA, Hemorrhage, and (Edema, 764. Eetkogradk Changes. — Simple atrophy of skin, 765; hairs (alopecia, canities), 765 ; and nails, 766. Inflammations. — General subject illustrated by case of flea-bite, 766. Causation of cutaneous inflammations and connection with nervous system, 767. Forms of cutaneous inflammations. I. Symptomatic, in acute fevers, 768 — smallpox CONTENTS. XXUl eruption a typical example, 768. II. Inflammatory skin eruptions, 770. (1) Brytliema and roseola, 770. (2) Eczema in its various forms, 770. (8) Psoriasis, 772. (4) -Pityriasis rubra, 772. (5) Lichen ruber, 772. (6) Prurigo, 773. (7) Pemphigus, 773. (8) Acne, 773; its connection with comedo, 774; and milium, 774; acne rosacea, 774. III. Traumatic and non-infective inflammations. (1) Bums and scalds, 774 ; in their three degrees, 775 ; collapse after burns, 775. (2) Frost-bite and chilblain, in three degrees, 776. (3) Boil and carbuncle, 776. (4) "Wounds and excoriations, 777. (5) Ulcers, 777. IV. Infective inflamma- tions. (1) Lesions from cadaveric poisons, 778. (2) Erysipelas, 779. (3) Phleg- monous inflammations, 780 ; malignant oedema, 780. (4) Splenic fever or malig- nant pustule, 780. (5) Infective tumors, especially framboesia, 781. Syphilitic Skin At'FKCTIONS. — Chancre, 782; skin eruptions, 782; and gumma, 783. Teopho-neukoses. — (1) Herpes, its anatomical characters, 784 ; caused by lesions of nerves, spinal cord, brain (general herpes), 784. (2) Glossy skin, 785. (3) Morphoea and scleroderma, 785 (sclerema neonatorum, 786). (4) Acute bed- sore, 787. Hypertrophies and Tumors. — Callosity, 787 ; corn, 787 ; ichthyosis, 787. "Wart and horn, 788. Keloid, true and false, 788. Soft warts and moles, 789. Mol- luscum contagiosum, 789. Fibroma moUuscum, 789. Xanthoma, 790. Ele- phantiasis, 790. Sarcoma, 790. Epithelioma in its infiltrating, 791 ; and flat forms, 798 (rodent ulcer, 793). Ordinary cancer, 794. Parasitic Affections. — Eavus, 794 ; ringworm, 796 ; pityriasis versicolor, 796. Scabies, 797. Larvffi of insects, 797. Addendum. — Actinomycosis, 798. LIST OF ILLUSTRATIONS. FIG. 1. Blood in pernicious anaemia 2. Medulla of bone in pernicious aniemia 3. Endothelium in normal capillaries 4. Capillaries in passive hyper^emla 5. Crystals of liEematoidin from thrombus in vein 6. Organization of blood-clot 7. Diagram of embolism of end-artery 8. Embolic infarction of kidney . 9. Infarction of kidney undergoing absorption . 10. Oil embolism of lung .... 11. Crystals of hsematoidin from hemorrhage in brain 12. Crystals of hsemin, prepared artificially 13. Cells containing red-blood corpuscles 14. Serous spaces and lymphatic capillaries 15. Injection of capillary bloodvessels, serous spaces, and 16. Charcot's crystals in leukaemia 17. Bone-marrow in leukaemia 18. Leukasmic formations in liver 19. Leucocytes of frog containing granules of vermilion 20. Liver in melanaemia 21. Leucocyte showing amoeboid movement 22. Inflamed human omentum 23. Fibrinous exudation in pneumonia 24. Bloodvessels of granulating wound 25. Granulation cells in their various forms 26. New formation of bloodvessels in a granulating wound 27. Semidiagrammatic section of a granulating wound, 28. Coagulation necrosis in muscle 29. Coagulation necrosis in muscle 30. Necrosis in pysemic lesion in kidney . 31. Cloudy swelling in renal epithelium, 32. Eatty degeneration in vessels of brain 38. Eatty degeneration in atheromatous aorta 34. Eatty degeneration in cancer cells 35. Crystals of cholestearine 36. Eatty infiltration of voluntary muscle 37. Eatty infiltration of hepatic cells 38. Colloid degeneration in ovarian cyst . 39. Calcareous infiltration in a tumor, 40. Calcareous infiltration of cysts of trichina 41. Calcareous infiltration of middle coat of artery 42. Amyloid disease of liver lymphatic capillaries XXVI LIST OF ILLUSTEATIONS. ria. 43. Amyloid capillaries of liver 44. Corpora amylaoea, .... 45. Division of cells . . . • 46. Elongation and curvature of tibia from hyperemia 47. Regeneration of epithelium in cornea of rabbit 48. Section of hard chancre (syphilitic) 49. Gumma of kidney .... 50. Gumma of liver .... 51. Portions of same more highly magnified 52. Miliary tubercles in lung 53. Tubercle from a bronchial gland 54. Tubercle in artery of pia mater 55. Tubercular ulcer of intestine . 56. Tubercular bacillus .... 57. Lung in bovine tuberculosis 58. Appearance of face in leprosy . 59. Elephantiasis of labia majora . 60. Hyperostosis of bones of leg in elephantiasis . 61. Lipoma in wall of stomach 62. Pendulous lipoma of appendices epiploicte 63. Portion of hydatid mole 64. Microscopic section of subcutaneous myxoma 65. Myxoma of nerve stem 66. Multiple internal enchondromata of fingers . 67. Spongy exostosis of femur 68. Ivory exostosis of frontal bone (internal surface) 69. Multiple exostoses of frontal bone 70. Microscopic section of myoma, stained 71. Isolated muscle cells from a myoma . 72. Calcareous infiltration in a' myoma 73. Amputation neuroma .... 74. Microscopic section of a neuroma 75. Section of painful subcutaneous tumor 76. Structure of same after maceration in nitric acid 77. Section of skin in venous nsevus 78. Cavernous angioma of liver 79. Adenoma of mamma .... 80. Psammoma ..... 81. Formation of mucous cysts 82. Hydronephrosis with granular atrophy of kidney 83. Congenital cystic kidney 84. Dropsy of Graafian vesicles 85. Papilloma of larynx .... 86. Hair-follicle, etc., from dermoid cyst of ovary 87. Round-celled sarcoma .... 88. Spindle-celled sarcoma .... 89. Large fungating spindle-celled sarcoma of foot 90. Adenoid sarcoma of mamma . 91. Giant-celled sarcoma .... 92. Stroma of soft cancer .... 93. Section of growing margin of an epithelioma LIST OF ILLUSTRATIONS. XXVll FIG. 94. Tubule from margin of cancer of kidney .... 95. From epithelioma of skin, penetrating cylinders witli signs of irritation 96. Cancer cells showing fatty degeneration 97. Structure of flat-celled epithelioma . 98. Structure of cylinder-celled epithelioma 99. Trom scirrhus of mamma showing cells and stroma 100. Cells from cancer of mamma . 101. Colloid cancer ..... 102. Colloid cancer, changes in cells 103. Colloid cancer, infiltrating muscle 104. Swarms of bacteria .... 105. Bacteria in pus-corpuscles 106. Two forms of bacilli .... 107. Tubercular bacillus .... 108. Blood in septicsemia of mice and in splenic fever 109. Vein in septicsemia of mice . 110. Pyemic abscess in kidney 111. Micrococci in capillary of kidney in pysemia, 112. Bacillus anthracis and that of septicsemia of mice 113. Yillus of intestine in splenic fever 114. From same, more highly magnified . 115. Spirillum Obermeieri .... 116. Typhoid bacillus .... 117. Micrococci in skin in erysipelas 118. Bacteria in capillary of kidney in scarlet fever 119. Sarcinse ventriculi in vomited matter 120. Aerial growth of penicilium . 121. Formation of conidia in submerged portion of same 122. Fungous growth in kidney . 123. Hair containing spores of fungus from ringworm 124. Leptothrix buocalis .... 125. Oidium albicans in thrush 126. Distoma hepaticum .... 127. Distoma sinense .... 128. Taenia solium, head .... 129. Taenia solium, unripe proglottis 130. The globular body, or Mellis's body . 131. Taenia solium, branching of uterus . 132. Taenia solium, fully developed uterus 133. Taenia solium, ova .... 134. Tffinia solium, cysticerci in muscle 185. Taenia solium, head of cysticercus cellulosae . 136. Taenia solium, development of cysticercus . 137. Taenia solium, hooks of cysticercus . 138. Hooks of echinocoocus 189. Taenia solium, movements of head in intestine 140. Taenia mediocanellata, head, extended aiid contracted 141. Taenia mediocanellata, unripe proglottis 142. Taenia mediocanellata, ripe proglottis 148. Taenia echinocoocus, adult or strobila 144. Taenia echinocoocus, diagram of development of brood-capsules XXVlll LIST OF ILLUSTRATIONS. riG. 145. Tfenia eohinococcus, brood-capsules .... 146. Tffinia echinococous, chitinous membrane of old hj-datid cyst 147. Bothriocepiialus latus, natural size . 148. Bothriocephalus latus, head and part of the body 149. Bothriocephalus latus, proglottis showing female organs 150. Trichina spiralis in muscle .... 151. Klaria sanguinis, embryo with sac . 152. Klaria sanguinis as seen in drop of blood 153. Defect of inter-ventricular septum 154. Congenital adhesion of curtains of pulmonary valve 155. Congenital malformation of aortic valve, two curtains 156. Exaggerated fenestration of aortic valve, approach to condition of cuspid valve ..... 157. Hypertrophy of left ventricle 158. Hypertrophy of right ventricle 159. Patty degeneration of the heart, low power . 160. Patty degeneration of the part, higher power 161. Calcareous infiltration of muscular tissue of heart 162. Calcareous infiltration of muscular tissue of heart, other form 163. Aortic valve in acute endocarditis, warty vegetations 164. Mitral valve in chronic endocarditis . 165. Ulcerative endocarditis, section of edge of valve 166. Ulcerative endocarditis, lesion in kidney 167. Soldier's spot on pericardium 168. Aneurism of valve, diagram of formation 169. Diagram of funnel-shaped deformity of mitral valve 170. Diagram of aortic insufficiency 171. Globular thrombi in left ventricle 172. Longitudinal section of artery at seat of ligature 173. Atheroma of aorta ..... 174. Atheroma of femoral artery .... 175. Patty degeneration of middle and internal coats in atheroma 176. Atheroma of cerebral artery .... .177. Normal cerebral artery .... 178. Endarteritis obliterans .... 179. Calcareous infiltration of middle coat of artery 180. Calcareous infiltration of middle coat of artery 181. Syphilitic arteritis, ..... 182. Aneurism with tunnelled clots at openings of branches 183. Section of dissecting aneurism 184. Hemorrhoids of rectum 185. Section of normal lymphatic gland 186. Section of normal spleen 187. Section of sago spleen . 188. Diffuse amyloid disease of spleen 189. Transverse section of a nerve . 190. MeduUated nerve fibres 191. Transverse section of a neuroma 192. Sections of spinal cord from cervical and lumbar swellings, showing groups of ganglion cells 193. Similar section from dorsal region LIST OF ILLUSTRATIONS. XXIX FIG. 194. Cervical enlargement showing arrangement of fibres 195. Medulla oblongata at various levels . 196. Gray degeneration or sclerosis of cord 197. Descending gray degeneration in medulla and cord 198. Ascending and descending degeneration in cord 199. Amyloid bodies from cord 200. Posterior sclerosis in early stage, limited extension 201. Anterior poliomyelitis on one side 202. Cord in progressive muscular atrophy 203. Medulla oblongata at level of fourth ventricle 204. Muscle in pseudo-hypertrophic paralysis 205. Cervical enlargement in pseudo-hypertrophic paralys 206. Lumbar enlargement from the same . 207. Section of pons varolii 208. Horizontal section of brain of child . 209. Lateral aspect of cerebral hemisphere 210. Internal aspect of cerebral hemisphere 211. Arteries of brain showing cortical distribution 212. Pons in descending gray degeneration 213. Atheroma of small cerebral artery 214. Sacculated miliary aneurism of nutritive artery 215. Fusiform miliary aneurism 216. Crystals of hsmatoidin from cerebral hemorrhage 217. Patty degeneration ef vessels in cerebral softening 218. Bloodvessel surrounded by leucocytes from medulla oblongata phobia ..... 219. Prom parotid gland in hydrophobia . 220. Prom a glioma of the brain . 221. Arteries of the pia mater in tubercular meningitis 222. Section of spina bifida 223. Papilloma of larynx .... 224. Section of lung in early, stage of emphysema 225. Perforation of alveolus in emphysema 226. Lung alveolus from a hemorrhagic infarction 227. Pat embolism of lung .... 228. Cast of infundibulum and air-vesicles in pneumonia 229. Alveolus filled with fibrine and a few leucocytes in pneumonia 230. Lung in gray hepatization .... 231. Chronic pneumonia ..... 232. Tubercular ulcer of bronchus. 233. Lung in caseous form of phthisis 234. Lung tissue from sputum in phthisis 235. Embolic cancer of lung .... 236. The same showing epithelial masses . 237. Sputum with carbonaceous particles from anthracosis 238. Oidium albicans or thrush-fungus 239. Section of syphilitic chancre of lip . 240. Section of tooth, showing caries and secondary dentine 241. Perforating ulcer of the oesophagus . 242. Large polypoid myoma of the oesophagus 243. Dilatation of the stomach .... hydro- PAGB 883 884 385 386 389 894 394 398 401 402 408 404 405 407 408 410 412 413 415 417 422 423 425 426 432 433 440 447 451 464 478 479 486, 488 490 491 492 495 604 508 510 517 518 520 527 529 582 539 540 544 XXX LIST OF ILLUSTRATIONS. PIG. 244. Twisting of the intestine 245. Large cyst of vermiform appendage 246. Typhoid bacillus 247. Peyer's patch in typhoid fever 248. Typhoid Peyer's patch, diagrammatic representation 249. Tubercular ulcer of the intestine 250. Tubercular ulcer, microscopic section 251. Cylinder-celled epithelioma of rectum 252. Passive hyperemia of the liver 253. Patty infiltration of liver, general view 254. Fatty infiltration in isolated hepatic cells 255. Acute yellow atrophy of liver 256.. Cirrhosis of livor, early stage . 257. Advanced cirrhosis of liver . 258. Gumma of liver 259. Miliary tubercle in liver 260. Cavernous angioma of liver . 261. Secondary cancer of liver 262. Disseminated cancer of the peritoneum 263. Section of normal kidney 264. Diagram of course of uriniferous tubules 265. Horse-shoe kidney 266. Embolic infarction of kidney 267. Glomerulo-nephritis, exudation of leucocytes 268. Glomerulo-nephritis, hemorrhage 269. Glomerulo-nephritis, increase of epithelium . 270. Glomerulo-nephritis, great increase of epithelium . 271. Large white kidney, microscopic appearances 272. Normal kidney for comparison .... 273. Interstitial nephritis, sclerosis of glomerulus 274. Section of contracted kidney, showing contortion of structures 275. Normal kidney, for comparison .... 276. Endarteritis obliterans in contracted kidney . 277. Arteries of pia mater in chronic Bright's disease and normal case 278. Septic embolism, of kidney ..... 279. Micrococci in capillary of kidney in pyasmia 280. Bacteria in capillary of kidney in scarlet fever 281. Cloudy swelling of renal epithelium .... 282. Amyloid degeneration affecting basement membrane of uriniferous tubules . 283. Amyloid and contracted kidney .... 284. Kidney in hydronephrosis ..... 285. Cystoid degeneration of the kidney .... 286. Uriniferous tubule at border of advancing cancer . 287. Stratified chitinous membrane from hydatid cyst of kidney 288. Large diverticulum of the urinary bladder 289. Tuberculosis of the bladder . 290. Rudimentary uterus . 291. Uterus bicornis 292. Uterus unicornis 293. Polypoid hsematoma of the uterus 294. Section of myoma of uterus showing nuclei LIST OF ILLUSTRATIONS. XXXI ^'''- PAGE 295. Myoma with calcareous infiltration ...... 687 296. Cancer of uterus, infiltrating muscular wall ..... 688 297. Cancer of uterus and vagina, naked-eye appearance . . . 689 298. Cauliflower cancer of uterus ....... 690 299. Cystic formation in ovary from dilatation of Graafian vesicles . . 693 300. Tuberculosis of Tallopian tubes ...... 694 301. Glandular tissue in wall of ovarian cyst ..... 695 302. The same showing goblet cells ...... 695 303. Prom wall of ovarian cyst, showing smaller cysts . . . 696 304. Trom wall of dermoid cyst, showing sebaceous glands . . . 699 305. Hair and appendages from wall of dermoid cyst .... 699 306. Diagrammatic view of uterus and appendages .... 701 307. Section of adenoma of mamma ...... 704 308. Adenoid sarcoma of mamma ....... 705 309. Dilated glandular spaceSj and intra-cystic growth in cysto-sarcoma of mamma ......... 'J06 310. Cartilage from sarcoma of mamma ...... 707 311. Section of scirrhus of mamma ...... 709 312. Cells from scirrhus of mamma ...... 710 313. Section of fractured rib, showing new-formed connective tissue, cartilage, and bone . . . . . . ... . 720 314. Prom same, showing continuity of cartilage and bone . . . 721 315. Normal ossification from cartilage ...... 722 316. Longitudinal section of ossifying margin in rickets .... 723 317. Bone in osteomalacia ........ 730 318. New formation of bone in connection with inflammation . . . 733 319. Bone in process of absorption showing Howship's lacunae . . . 734 320. IProm same, showing giant-cells (osteoclasts) and Howship's lacunse . 735 321. Hyperostosis of bones of leg in elephantiasis .... 737 322. Rotation of vertebrae in lateral curvature . . > . . 746 323. Section of chest in lateral curvature, compared with normal . . 747 324. Multiple exostoses in bones of leg ...... 749 325. Osteoid chondroma ........ 749 326. Cyst of head of fibula .... . . 752 327. Urate of sodium in the articular cartilage in gout .... 758 328. Section of normal skin, epidermic layer and hair .... 763 329. Section of smallpox pustule of skin ...... 769 330. Section of smallpox eruption with necrosis . . . . . 770 331. Micrococci in pus corpuscles from cadaveric pustule . . . 779 332. Skin in erysipelas, micrococci in lymph-spaces .... 780 333. Section of skin in framboesia ....... 781 334. Epithelioma with penetration of epidermis ..... 791 335. Epithelioma showing laminated capsules, etc. .... 792 336. Epithelioma, showing ingrowing precedes and irritation of skin . . 793 337. Achorion Schoenlenii from favus ...... 794 338. Tricophyton tonsurans in a hair from ringworm .... 795 339. Microsporon furfur from Pityriasis versicolor .... 796 A MANUAL OF PATHOLOGY. INTRODUCTIOxH. Pathology may be defined as the study of diseases not in their manifestations merety, but in their essential nature. There are various conditions met with from, day to day which we name diseases. " They produce certain alterations in the feelings of the person affected which induce him to say he is not well, and they in many cases lead to changes in the condition of the bodily frame which can be actually observed by the physician, and may enable him to come to a conclusion as to the actual disease which is present. These subjective phenomena and those objective signs are mere indications of the presence of something which we call the disease or morbid process ; and it is surely incumbent on every one who undertakes to treat disease, not to content himself with a knowledge of its manifestations merely, but to satisfy himself as to its real nature. And here, at the very outset of our study of Pathology, it is to be remarked that we have to do with diseases, not disease in the abstract. There are certain definite conditions which the body presents, and which are recognized as morbid states, or conditions different from those of health, and our object is to find out what is the nature of those morbid states. Endless discussions might be raised as to the nature and causes of disease in the abstract; but we shall arrive at much more reliable conclusions if we study the individual states of disease and leave those more general dis- cussions aside. Without going into any general discussion as to the nature of disease as a whole, there is one subject which here calls for some consideration, namely, the relation oe diseased to healthy con- ditions. Physiology is the study of the body and its actions in health, and it is not to be supposed that in disease these physio- logical processes suddenly cease. So far as the diseased condition is concerned, these processes are modified, and they must be studied under the altered circumstances; but in the study of each * pathological condition the physiological must be taken as the basis. A knowledge of physiology is the necessary preliminary to the study of Pathology. It may be said, indeed, that the pathological processes are naerely the physiological ones altered. In disease 2 18 A jiajs'ual of pathology. there is something disturbing the natural processes, and there is an endeavor, as it were, on the part of the body to get over the disturbance, and the phenomena of the disease are not infrequently the expression of the resistance which the natural processes present to the disturbing element. These normal inrocesses must be taken into account, therefore, and, as we shall see further on, the physio- logical laws are really in essence identical with the pathological. We have to study the nature of diseases, and this will bring us into close connection with their causes. Much has been written concerning the causes of disease in general, and much that is valuable, but this study of itself would be almost sufficient to fill a volume. It will be enough here if we consider, as each disease comes under review, whether it is traceable to any definitely dis- tinguishable cause or causes. In some acute febrile diseases, we are able to predicate the existence of viruses, and even the nature of some of these viruses is to some extent known. Wliatever is known as to the cause of diseases will assist in elucidating their nature. In the study of diseases in their nature, there are three main sources from which assistance is to be obtained ; one may be desig- nated Experimental Pathology, another Pathological Anatomy, and the third Clinical Observation. John Hunter may be said to have laid the foundation of experimental pathology. So far as it can be prosecuted, this mode of study is calculated to afford us the most directly trustworthy information as to the nature of dis- eases, and much of the advance in modern pathology is due to this line of study. If we can actually induce a given disease in an animal, we have found out much as to its causation, and are in the way of finding out much as to its nature. In some cases we are able actually to observe the morbid processes in the living animal. Or, we can kill the animal at various periods after the onset of the disease, and observe the results at various stages. "We can vary the experiment in different ways, so as to eliminate on one side and another the various elements, and so reduce the problem to its simple and necessary parts. Experimental pathology has carried us far towards understanding many of the conditions in disease. Reference need only be made to the reformations which this line of study has effected in our knowledge of Inflammation, Em- bolism, Tuberculosis. _ The study of morbid anatomy is not likely to effect such revolu- tions in Pathology as experimental pathology, but in the training of the individual medical student it is calculated to play an even more important part in giving him an understanding of the nature of the diseases he has to deal with. Morbid anatomy gives us the physical changes which disease produces in the body. These changes are, as it were, the expression of the pathological pro- cesses, and are only to be regarded as indications of the existence of these processes. It is probable that all morbid processes pro- duce changes in structure, although the changes may elude our INTRODUCTION. 19 observation. For the most part, however, we are able to associate the change of structure with the morbid process, and the observed change leads us up to the actual nature of the disease. In fact, the nature of disease might be studied on the basis of the morbid structure, advantage being taken also of all information from the side of experimental pathology and clinical observation. Morbid Anatomy is the study of the structural changes in all periods and stages of the disease. It is sometimes objected to this mode of study that in observing the state of the tissues after death we see only the last stages of disease, and in some cases only the results. This, however, is not the case. Every clinical observer will admit that in the same disease the fatal issue occurs in different cases under the most diverse circumstances. Death ensues, as a rule, when by reason of defective nutrition, or a deficiency in the supply of oxygenated blood mainly by interference with the respi- ration, the functions of the body can no longer be carried on. ]!^ow there is in different individuals an infinite variety in the vigor of the vital processes, so that a condition which in one will very slightly affect the essential phenomena of life, will, in another, seriously compromise them. This is an experience of our every- day life. And so it happens that patients die in all stages of dis- ease. Even in the same case we are often able to study the various changes in their different stages. As an illustration of what is meant, take the case of pneumonia or acute inflammation of the lungs. Patients die in this disease, as a rule, from failure of the heart and consequent cessation of the circulation ; but the paralysis of the heart is not related solely to the condition of the lungs. It is often much more closely related to the elevation of temperature which is to be traced to changes in the nervous system, while the powers of resistance of the heart in each person are an important element in the matter. And so it happens that one man will die with a limited and advancing pneumonia, while another will survive through a very extensive condensation. The lung at death in the one case is in the same stage of disease as in the other at a certain date during life. We can study the nature of the disease in the former and we are surely warranted in assuming that in the patient who survived, the state of the lung is virtually identical with that of the patient who died. Again, in a carcinoma growing up to death, we have, at the growing margins of the tumor, changes which are the same as those by which the tumor has all along been extending, and we can study the methods of its growth as well as its relations to the structures in which it has been growing. Thus it is that, although morbid anatomy by itself may in some cases throw little light on the nature of the disease, yet, taken as an expression of the morbid process, it is of the highest value. It may be added that as similar processes must have similar changes as their correlatives, we may take these changes as a kind of test of the existence of the processes. In referring to processes and changes, it must be understood that 20 A MANUAL OF PATHOLOGY. the finer structure of the body is taken into account. In Patho- logical Anatomy, we include Pathological Histology, and it may indeed be said that, as the coarser, naked-eye appearances are merely the expression of the finer structural details, so we shall not understand the former unless we are able to refer them to the latter. We can have no accurate idea of the proper structure of the normal liver by simply looking at it with the naked eye, and we can have little insight into its morbid conditions by the same method of observation. The morbid conditions, however, do gen- erally cause changes in the naked-eye appearances, and this is of great consequence as enabling us, when roughly examining an organ, to infer that its structure is changed. But these macro- scopic appearances are only useful when they are used to throw light on the microscopic changes or to direct attention to them. The really important processes are those which concern the finer elements of the tissues, and so it is to these that we shall chiefly attend in studying the various forms of disease. Clinical observation is of great importance in the study of pathology, and that in various ways. If what has been stated above be correct, then it is the processes occurring during life that are the real subject of study in pathology, and it is only by careful clinical observation that we are able to get, as it were, into close relations with these processes during their actual currency. Clinical Observation and Pathological Anatomy should thus be taken as mutually elucidating each other, and as working together towards just conceptions as to the nature of the conditions con- cerned. There is another aspect in which clinical observation is of im- portance in relation to pathology. The pathologist, if conversant only with morbid anatomy and experimental pathology, is apt to form a too mechanical and simple conception of the processes in- volved, and is likely to theorize on the basis of a too-limited view of the subject. Clinical Observation is a needed corrective to this, bringing the pathologist back to the practical aspects of the matter, and checking the tendency to theorize by the discipline of facts. In the systematic treatment of the various forms of disease, the plan adopted has been to take up first the diseases in their general aspects, and afterwards the diseases of the special organs and systems. The work, therefore, divides itself naturally into a G-eneral Part and a Special Part. In the General Part will be taken up those diseases which are not confined to any organ or tissue; most of them, indeed, may affect any organ of the body. In this part are included the follow- ing subjects : The Affections of the Circulation and of the Blood, Inflammation, Eetrograde Changes, Hypertrophy, Repair, and Eegeneration, Infective Tumors, Tumors proper, and Parasites. In order to make this general part complete, the subject of Mal- formations should be included. With the general subject of Malformations, however, the author has little practical acquaint- INTRODUCTION. 21 ance, and he has thought it better to leave it to special works on that subject. In the Special Part, the diseases as they manifest themselves in the individual organs and tissues will be considered. It is clear that the diseases described in the General Part will again come under review in each division of the Special Part, and they will be taken up very much in the same order as in the G-eneral Part. But each disease presents various specialties according to its locality, and, from a practical point of view, it is important to understand the modifications thus occurring. The Special Part will be, in a certain sense, an expansion and amplified illustration of the general principles educed in the General Part. PART I. GENERAL DISEASES. AFFECTION'S OF THE CIRCULATIOISr AND OF THE BLOOD. We have here two somewhat diverse conditions to consider, namely, the abnormal variations in distribution of the blood, and the changes in its actual condition. In regard to distribution, we may have too much or too little blood in the vessels, or the blood or its constituents may get outside the vessels. On the other hand, the blood may undergo changes in its constitution, or it may change its condition by coagulating inside the vessels. In order to understand what is to follow it will be necessary, in the first place, to refer briefly to certain points in the PHYSiOLoaY OP THE CIRCULATION. If wc are to study alterations in the dis- tribution of the blood, then we must have in our minds clear ideas as to the arrangements by which the normal distribution is regulated. In the distribution of the blood the capillaries and veins may be regarded as virtually passive channels. They are able to accommodate more or less blood accoi'ding to circum- stances, but of themselves they have probably little to do with the variations in the supply. It is obvious that the supply of blood to the tissues varies, chiefly according to their needs ; the working brain or muscle requires and gets a fuller and more rapid supply of blood than when at rest. Although there may be some assist- ance to the circulation by the attraction to the tissues of needed material, yet essentially the supply is regulated by the arteries ; when they dilate more blood passes into the capillaries and on to the veins, and when they contract less blood reaches the capillaries and veins. We may regard the arteries as regulating the supply of blood, the capillaries as distributing the blood, bringing it within reach of the elements of the tissues, and the veins and lymphatics as carrying it off. The amount of blood admitted by the arteries depends on the state of contraction or relaxation of the muscular fibres in the middle coat, and this, like all other muscular actions, is under the command of the nervous system. When the vaso-motor nerves are stimulated the muscular coat contracts, when these nerves are pai'alyzed it relaxes, and when a 24 AFFECTIONS OF CIRCULATION AND BLOOD. moderate amount of stimulus is supplied, then we have that state of slight contraction to which the name of tonicity is applied. Much attention has been bestowed on the exact nervous rela- tions of the middle coat of arteries. There is no doubt that it is under the influence of centres situated in the cerebro-spinal axis, but there is reason to believe that there are, as well, in or near the walls of the arteries, peripheral ganglia, which are the immediate regulators of their calibre. The heart is often compared with arteries in its structure, and we know that it possesses intrinsic ganglia. By means of these ganglia it is able to persist in its contractions after separation from all higher centres or even when cut out of the body. "We know, also, that the higher centres influence these ganglia in two ways, either by stimulating them (through the sympathetic) or by inhibiting them (through the vagus). In the arteries we see somewhat similar phenomena. When arteries are cut ofl:" from all central connections they are still capable of varying their calibre. If the sciatic nerve in a frog is divided the arteries indeed dilate, but after a time they resume, at least partially, their state of tonicity, and are capa- ble of still further variations. Again, an excess of carbonic acid in the blood will cause arteries to contract after all their central connections have been severed, and they may be made to dilate by means of chloral or atropine. It is well known that irritation of the vaso-motor nerves causes contraction of the arteries, and this is readily enough understood without supposing the existence of peripheral ganglia, but it has now been shown that the arteries may be caused to dilate by the stimulation of nerves passing to them, and this can only be by means of local ganglia. It is known, for instance, that dilatation of the arteries of the salivary gland may be produced by irritation of certain nerves passing to them, and so is it with the vessels of the penis. Lately, it has been shown that the arteries of the skin may be thus caused to dilate. In these cases the nervous influence paralyzes the local ganglia. In studying inflammation we shall see still further proof of the existence of these peripheral nerve-centres, the exist- ence of which Lister long ago inferred. Besides these local centres, there are higher and more general centres situated chiefly in the spinal cord and medulla oblongata. From these centres there seems to pass a continuous slight stimu- lation inducing that moderate contraction which we name tonicity. If the connection be severed, the tonicity ceases, the arteries dilate. There is a general centre for the whole vaso-motor system in the medulla oblongata. When this is stimulated all the arteries appear to contract. When it is destroyed all the arteries in the body dilate. But without being destroyed the centre may be paralyzed or inhibited. It is inhibited by the inhalation of nitrite of amyl, and the arteries dilate. It may also be inhibited by the stimula- tion of a nervous branch which passes upwards from the heart, the depressor nerve. This general centre, therefore, has nervous connections of a similar kind to the local ganglia. GENERAL HYPERiBMIA. 25 It may be added that each organ seems to have nervous arrange- ments of its own, by means of which, either reflexly through the spinal cord and sympathetic system, or more locally, it is in a position to regulate the contraction of its arteries and the supply of blood. HYPEK^EMIA AND ANAEMIA. These physiological considerations would lead us directly to the consideration of the local variations in the distribution of the blood in the body. But prior to that, we have to consider alterations in the quantity of the blood as a whole. It is clear that with regard to both local and general variations the blood may be either excessive or deficient in quantity, and to express these the terms HYPEREMIA and ANiEMiA are used. It will, therefore, be possible to consider this subject under the four divisions of General Hy- persemia. General Anaemia, Local Hypersemia, and Local Ansemia. 1. General Hyperemia. — This term designates the condition in which the total quantity of blood is in excess. The term Plethora is used in a similar sense. The first question that arises here is, whether the vascular system is capable of accom- modating more blood than it contains normally. There is no difficulty in answering this question in the affirmative. If the vessels as a whole could contain no more blood than they normally hold, then there could be no local variations, no blushing, no in- crease in the quantity of blood during activity of organs. The capillaries present great varieties in the amount of blood they contain at different times, and if we take the whole capillaries of the body into account, it will appear that in them there is a great reserve space, which may possibly on occasion be used for the accommodation of an excess of blood. This matter has been brought to the test of experiment, and as there are several points of interest in this regard, we shall refer more specially to the observations made. Transfusion op blood is the artificial introduction into the vas- cular system of blood from another animal. In the experiments of AVorm Muller, which are chiefly of im- portance here, the defibrinated blood of dogs was injected, with precautions, into the vessels of animals of the same kind. It is not remai'kable that the vascular system can accommodate a large additional quantity of blood, but it is remarkable that it should do so with little disturbance to the health of the animal. A quantity equal to one-half or three-fourths of the blood normally present in the animal may be injected without endangering the life of the animal, and the quantity needs to be double the normal, or over it, before the animal's health is seriously impaired. It might be expected that when the vascular system is thus overfilled the blood-pressure would be greatly raised, but actual registration 26 AFFECTIONS OF CIRCULATION AND BLOOD. of the pressure, by a canula introduced into the carotid and con- necting with a kymographion, shows that though during the actual operation there is a rise of pressure, yet it soon falls to within normal limits. If a quantity is injected beyond double the normal bulk of the blood, then the pressure begins to show remarkable elevations and depressions, and the animal usually dies in the course of the same day, or the next. Life is immediately endangered when one and a half times the normal bulk is injected. When blood is transfused, then, in large quantity it finds accom- modation chiefly in the capillaries and veins, the arteries being relaxed in order to admit of its passing into these, and the blood- pressure is not raised. It appears that the capillaries and veins of the abdominal organs form a great reservoir for the accommoda- tion of excessive blood, and that the blood lodges here chiefly after transfusion. The excess of blood thus supplied to an animal does not, how- ever, remain permanently as a part of its organism. There seem to be arrangements in the body for disposing of it. "Worm Miiller endeavored to determine what time it took to dispose op a large EXCESS OP BLOOD. After the transfusion the animals were starved, and the blood and urine examined at intervals. It was concluded that the fluid of the blood is rapidly disposed of, being excreted by the urine. A few hours after transfusion much of the excess of liquor sanguinis had already gone, and even when sixty to eighty per cent, of the entire blood was injected, the whole excess had dis- appeared in the course of two or three days. The rapid disposal of the liquor sanguinis leaves the blood-corpuscles greatly in ex- cess, and the rate of disappearance was determined by counting them by means of Malassez' method. If the quantity transfused is small, the corpuscles may be disposed of in a few days; but in the case of large transfusions it may take two or even three weeks. In this comparatively short period of time, however, the whole excess of blood, both plasma and corpuscles, is removed, and we may infer that there are arrangements in the body for the regula- tion of the amount of blood. These experiments all refer to the transfusion of defibrinated blood. If blood is injected when just about to coagulate, or if when it has just begun to coagulate some of the serum is pressed out and injected, then in some cases the animal dies rapidly with symptoms referrible to pulmonary embolism. The blood in the right side of the heart and pulmonary artery is found after death to be coagulated. The explanation of this is, that at the time of coagulation of the blood, the tibrinoplastic substance and the fer- ment, which Schmidt's observations have shown to be so directly concerned in coagulation, are both set free. It appears that even a small quantity of these substances introduced in the free state into the blood of a living animal induces coagulation of it. The importance of these facts in regard to transfusion in human beings Avill not be overlooked. Hitherto the transfusion of blood from an animal of the same GENERAL qyPER^MIA. 27 kind has been referred to, dog's blood injected into a dog. But when blood from a different species of animal is used, there are frequently symptoms of poisoning developed. The urine is blood-colored, and it contains albumen and tube-casts; there is vomiting of bloody material, diarrhoea, etc. It is as if the foreign blood had acted as a poison, and we may inquire what is the nature of the poison. The observations of Ponfick (Virchow's Archiv, vol. Ixii.), and others, have thrown considerable light on this matter. It has been already mentioned that the urine is blood- colored, but microscopic examination shows that this is due, not to the presence of red blood-corpuscles, but to that of the coloring matter of the blood in solution. It is not a bloody, but a blood- colored urine, not a hsematuria but a hemoglobinuria. The fact seems to be that there is no poison in the foreign blood-plasma, but that the corpuscles are unable to survive in the alien blood; they dissolve, and their haemoglobin being dissolved in the plasma acts as a poison, and is eliminated by the kidneys. It seems to exercise its deleterious influence chiefly on the kidneys themselves, the tube-casts and albumen in the urine being evidences of the irritation of these organs. The general symptoms, in fact, are largely referrible to the irritation of the kidneys. If haemoglobin be introduced into the blood in other ways, it acts equally as a poison. The red corpuscles of animals may be destroyed by repeatedly freezing and thawing the blood, and when that has been done, the blood of the same kind of animal will produce symptoms such as those referred to. It is to be observed that all animals are not exactly in the same relation to each other in this respect. It is found, for instance, that a much smaller quantity of lamb's blood than of hen's blood produces hsemoglobinuria in a dog. The importance of these facts in regard to transfusion in the human species will be apparent. In this place it may be mentioned that the blood transfused does not, according to Panum, act as food or take its place. If an animal is undergoing starvation, transfusion does not avert or delay the process of inanition ; it rather hastens it by increasing the waste. In using transfusion as a means of treatment the object is to make up a deficiency of red corpuscles or blood-plasma. Having now seen that, by transfusion, an artificial plethora may be induced in animals, we may be prepared to admit the possibility of its existence in the human subject. It will presumably occur when the blood-forming organs are unduly active, and will mani- fest itself in an over-fulness of the capillaries and veins through- out the body, but especially in those of the abdominal viscera. Persons of vigorous digestion and active habits have often a florid appearance, as if the vessels, of the skin at least, were overfilled. The excess of blood is used, to a considerable extent, in the for- mation of fat, and we know that the subcutaneous adipose tissue and that of the abdomen are often much increased. But the ob- servations mentioned above show that any excess of blood is dis- 28 AFFECTIONS OF CIRCULATION" AND BLOOD. posed of with considerable ra]:>idity, and we may infer that in the human subject a moderate tendency to plethora will be overcome. It will develop when the formation of blood keeps in advance of its destruction by the arrangements provided for that purpose. 2. General Anemia. — By this name is meant strictly a defect in the blood as a whole, a real want of blood, but the term is habitually used to designate conditions in which the blood is defective in any of its important constituents. A true ansemia or want of blood, such as occurs in consequence of a severe hemorrhage, is designated Oligemia, and this term may be regarded as virtually equivalent to Acute Traumatic Anaemia. When such a condition develops from a single large hemorrhage, the condition of simple reduction of the bulk of the blood does not long remain, but various processes occur which modify the state of the blood. We have now to consider what these processes are, and how they modify the condition of the blood. To begin with, the bulk of the blood does not long remain under the normal; it is rapidly made up, but not by a plasma of normal concentration. The blood is unduly watery, and so the oligeemia gives place to a Hydremia. The process by which this is brought about is not very obscure. As the hemorrhage pro- ceeds the arterial blood-pressure diminishes ; in slight hemorrhages it soon recovers, but in severe cases the reduction continues for some time. The consequence of this must be a diminution in the transudation of the normal parenchymatous fluid from the capil- laries. If the reduction of pressiire is considerable, there may even be a reverse current, the fluid from the tissues being absorbed into the blood. Again, the secretion of urine depends on the blood-pressure in the vessels of the Malpighian tufts in the kidneys, and the pressure here depends largely on the general arterial ten- sion. Any diminution of the general blood-pressure will therefore lessen the amount of urine secreted, and will diminish the loss of water by the blood. In this way, and by the absorption of water from the alimentary canal, the bulk of the blood is soon made up, but, as already mentioned, it is a watery blood. After such a hemorrhage also, there is an excess of leucocytes in the blood, especially as compared with the red corpuscles, which are much diminished. This condition of Leucocytosis is brought about in various ways. During the actual hemorrhage the white corpuscles being more adhesive pass less freely out of the ruptured vessels, and so fewer are lost than of the red corpuscles. But the principal cause of the leucocytosis is, that the white corpuscles are much sooner replenished than the red. The thoracic duct pours into the jugular vein lymph containing leucocytes both during and after the hemorrhage. Moreover, the organism seems to have a very great power of forming leucocytes. If we consider the excessive quantities of them which are formed during an active suppuration, we may have some idea of the rapidity with which they may be produced. GENERAL ANEMIA. 29 The red corpuscles are much more slowly regenerated. If the hemorrhage has been at all severe, it takes many weeks to make up their number. The number of corpuscles to a given bulk of blood can readily be estimated by the instruments devised for the enumeration of the corpuscles, of which one of the most conven- ient is that of Thoma, manufactured by Zeiss, of Jena. By this method it can be observed how the corpuscles are gradually re- plenished. The exact mode of formation of the red corpuscles, even the site of their formation, is very obscure. It has been generally believed that the spleen, lymphatic glands, and bone-marrow, have to do with the formation of these corpuscles. The observations of ]Sreumann and others have caused great importance to be attached to the bone-marrow in this regard, and the fact that nucleated red corpuscles are to be found here, especially in young persons, has been regarded as an indication that this tissue is specially con- cerned in the formation of these bodies. It has generally been supposed that the red corpuscles develop out of the white, but considerable doubt has always existed as to this. Recently, it has been asserted that they arise by a process of budding from existing red corpuscles. It is not necessary to assume that the red corpuscles are replen- ished only by an excessive activity in the blood-forming organs. It may be, rather, that with an ordinary, or even reduced, activity, the corpuscles are made up by fewer of them being consumed than under ordinary circumstances. The coloring matters of the bile and of the urine are derived from the blood, and their existence implies that red corpuscles are destroyed in order to yield their coloring matter. In the case of the bile, this destruction probably takes place in the liver, but in the case of the urine, the coloring matter exists pre-formed in the blood, and the destruction of cor- puscles takes place elsewhere, perhaps in the spleen. After a severe hemorrhage, there is much less activity of all the functions of the body, and, presumably, less consumption of red corpuscles. In accordance with this the bile and urine are paler than normal; often very much so. It may be, then, that in the generally re- duced activity of the body, there is no increased formation of red corpuscles, but that their slow replenishment is really due to an economy of them. In the above, the case of a single considerable hemorrhage has been taken. Where there are frequent small hemorrhages, as from piles, bleeding from the uterus, etc., there will be a recurrent loss of blood, and a continuous hydrsemia. Spontaneous anjemia is a term used to designate conditions in which, without any loss of blood, there is a deficiency chiefly in the red corpuscles. There is generally an actual deficiency in the number of the corpuscles as determined by counting, but there are cases where, without any great reduction in number, there is a great deficiency of haemoglobin. The normal proportion of red 30 AFFECTIONS OF CIRCULATION" AND BLOOD. corpuscles to the plasma is thirteen per cent., and in spontaneous ansemia it has been found as low as six, five, and even four per cent. Various forms of spontaneous ansemia are met with, of which two call for special note, namely. Chlorosis and Pernicious Ansemia. Chlorosis occurs most frequently in young women about the age of puberty, and it is remarkably amenable to treatment by means of iron. There is reason to suppose that this condition may be due to a congenital defect in the organs for preparing the blood — they are unable to meet any extra strain on them, such as occurs at puberty. It is interesting, in this regard, that chlorosis has been found in a certain number of cases to be associated with a visible defect in the circulatory system, which gives some corroboration to the supposition of a defect in the blood-preparing organs (Virchow). The most constant defect is narrowness and thinness of the aorta. There is also frequently an irregularity in the origin of the branches from the aorta, especially the intercostal ones. The narrowness of the aorta may lead to hypertrophy of the heart. It is sometimes stated that chlorosis is related to congenital defect of the organs of generation, but there is no sufficient evidence in support of this. There are certain anaemias of a very serious kind which come on without any apparent connection with other abnormal condi- FlG. I. Fig. 2. Blood in pernicious ansemia. The larger bodies are the normal red corpuscles. The smaller are the round, more deeply colored ones usually found — so-called microcyte?. (BiCHHORST.) From red medulla of bone |in per- nicious anaemia.* u. Nucleated red corpuscles, c. A red corpuscle with granular nucleus, b. Large nucleated cells, forming the bulk of the altered marrow. X 350. tions. These are sometimes designated Essential Anemias, of which the most important is Peenicious Anemia. This name is used to designate a disease in which, without apparent cause, the blood deteriorates, becoming deficient in red corpuscles. The de- terioration goes on progressively to a fatal issue, and nothing has been found to arrest it. In this disease there is a marked defici- ency in red corpuscles, but besides that there are corpuscles pres- ent which are not represented at all in normal blood. These are red corpuscles of a much smaller size than the normal ones, as shown in Fig. 1. They are usually about half the size of the red ones; instead of being biconcave they are globular, and GENERAL AN.EMIA. 31 they have a much deeper color than the ordinary red corpuscles. They are generally present in considerable abundance, and may even exceed in number the normal ones. It is asserted that these small corpuscles (microcytes) are present in all cases of this dis- ease. This is denied by some, but they are certainly present in a large proportion of cases. In addition, red corpuscles of larger size than normal and nucleated red corpuscles, have been met with in the blood in some cases of pernicious anaemia, and nucle- ated corpuscles may be found in the blood after death when exami- nation has failed to detect them during life. In some cases also of this disease, the medulla of bone is altered. Instead of the yellow adipose tissue, which is the normal structure in some parts of the medulla, a red semi-fluid marrow has been found, in the shaft of the femur for instance. Under the microscope, in these cases, the normal adipose tissue is found to be replaced by aggre- gations of cells, in the midbt of which are found nucleated red corpuscles, while the non-nucleated corpuscles present great variety in size (Fig. 2). This change in the medulla, however, can hardly be regarded as distinctive of this form of anaemia. It has been found in ordinary forms of ansemia, and it is sometimes absent in pernicious ansemia. Probably it indicates an alteration in the organs having to do with the preparation of the blood, but nothing further can be definitely asserted. Besides these forms of ansemia already described in which there is an actual loss of blood or else a grave defect in the formation of the blood, there are some conditions in which the blood is impoverished in consequence of some other disease which either causes a waste of the constituents of the blood, or, by lowering the nutrition as a whole, leads to defect in the formation of the blood. This is called secondary anemia, and it may occur in all debilitating diseases such as malignant tumors, febrile conditions, albuminuria, etc. Anemia, in its various forms, not unfrequently produces sec- ondary CHANGES in various organs, and it will be proper briefly to refer to these. The foundation of all these chaiages is the deterio- ration of the blood, and we must be prepared to find functional activity reduced, and, above all, the nutrition of the tissues inter- fered with. A prominent result of this interference with the nutrition is the frequent occurrence of degenerative changes. Fatty degeneration of the muscular tissue of the heart is one of the commonest of these. Experiment on dogs shows that succes- sive large hemorrhages leading to inanition rapidly produce fatty degeneration of the muscle of the heart. The author has met with a case in which, after a single very severe hemorrhage from the stomach, with a fatal issue three weeks later, there was extreme fatty degeneration of the heart. Fatty degeneration also occurs in the epithelium of the uriniferous tubules of the kidney and in the hepatic cells of the liver. A fatty degeneration of the intima 32 AFFECTIONS OF CIRCULATION AND BLOOD. of the aorta, producing a figured appearance in the wall of the vessel, has been seen in chlorosis and in other forms of anaemia (Virchow). This may be part of the defect of the vascular system in chlorosis already mentioned, but more probably it is a secondary degeneration. The state of the medulla of bone in pernicious anasmia has been referred to, and it has been remarked that a similar red marrow has been seen in other forms. "We meet with it in secondary antemias, and, perhaps, especially in old persons. 3. Local HypBRiEMiA. — We have next to consider the local variations in the distribution of the blood. The term local hyper£emia is applied to conditions in which there is an excess of blood in the vessels of a particular part. It may be due to an ab- normal amount of blood being admitted by the arteries, and in that case the blood will generally be at a higher pressure and flow more quickly than normal ; or to some interference with the passage of the blood away from the part by the veins, in which case the current will probablj' be unduly slow. In this way we distinguish two forms of local hyperemia — an active or arterial and a passive or venous. Active Hyperemia or Active Congestion. — This occurs when an excess of blood is admitted by the arteries into a part. The terms Atonic and Arterial Hyperaemia may be regarded as synony- mous with active hypersemia, and also the expressions Fluxion and Determination of Blood. This condition will come about either when there is some increase of the blood-pressure forcing more blood in, or when the arteries are dilated so as to allow the blood freer access. Increase of blood-pressure is not often local, and even when it is, a rapid accommodation is usually effected by which the press- ure is brought to an equilibrium. This accommodation is effected, as we have seen, by means of the arteries, their state of contrac- tion being subject to variation. There is one situation, however, in which arteries possess little tonicity, and hardly at all regulate the supply of blood except passively, and that is in the lungs. It is to be noted, therefore, that any increase of blood-pressure affect- ing the pulmonary circulation is apt to be followed by an active hyperajmia. In studying active hyperemia of the lungs, we shall see that increased activity of the heart may lead to active congestion in the lungs. There is a condition designated collateral hyperemia, and it might be supposed that this is due essentially to increase of blood- pressure. It occurs when, on account of deficiency of blood in one part (local anemia), there is excess of blood in another. If the blood is deficient in one part, it must be excessive in another or in the system in general. The local angemia is due to some im- pediment to the circulation, chiefly obstruction of the arteries, and it may be supposed that the direct result of such obstruction will be to raise the blood-pressure in the neighboring vessels and so lead to an active hypersemia. As we shall see afterwards, this is ACTIVE HYPEREMIA. 33 probably the explanation of the congestion of the lungs which follows the drinking of large quantities of cold water. The cool- ing of the stomach causes contraction of the arteries in the ab- domen, and this increases the blood-pressure. But for the most part the bloodvessels are so fully under the control of the nervous system, and the mechanism for the regulation of the circulation is so well arranged, that when a local aneemia occurs the accommo- dation of the excess of blood is not left to mere accident, but is provided for according to the needs of the organism. Thus, if the carotid artery is obstructed, the dilatation and hypersemia do not occur in the arteries of the arm, which are the nearest to the ob- structed artery, but in the other arteries passing to the brain. If one renal artery is obstructed, there is a collateral hypersemia of the kidney opposite, and the secretion of urine is restored to the normal. Most collateral hypersemias, therefore, are due rather to dilatation of the arteries, tlian to increase of blood-pressure. Turning to cases in which the hyperemia is more directly due to DILATATION OF THE AETERiES, a simple example is atforded by the congestion which follows the application of warmth to the skin in the form of poultices, etc. It is believed that this hyper- semia causes a collateral ansemia in certain subjacent parts, and this, like collateral hypersemia, has not a merely accidental dis- tribution. On this principle, as some suppose, poultices and fomentations are useful, although probably this is not the entire explanation of their action. But, again, the arteries dilate when an unusual pressure to which they have long been subject is suddenly removed. The arrangements for the regulation of the circulation are such that when arteries are subjected to pressure, as the arteries of the abdomen in ascites, the circular muscular fibres become less active, the external pressure causing narrowing of the arteries without their contraction. Should the pressure be suddenly removed, however, these vessels, taken as it were at a disadvantage, dilate, and an active hypersemia results. Hence, after removal of a large accumulation of ascitic fluid, it is usual to apply a supporting- bandage which will partly take the place of the pressure removed, till the arteries accommodate themselves afresh to their new cir- cumstances. After removal of an ovai'ian tumor there may be a hyperemia of the kidneys, which may even lead to a transitory albuminuria. Further, paralysis of the vaso-niotor nerves may lead to relax- ation of the arteries. The author met with a case in which an accident caused a traumatic lesion of the medulla oblongata. The injury had apparently destroyed the vaso-motor centres of the kidneys. There was a most remarkable active hypersemia of these organs, evidenced after death by an enormous overfilling of all the vessels with blood. During the few hours of life after the acci- dent, a very excessive quantity of watery urine was twice drawn oft' by the catheter, and after death the bladder was found highly distended. Division or injury to the spinal cord is likely to pro- 3 34 AFFECTION'S OF CIRCULATION AND BLOOD. duce hyperfemia in the parte supplied with nerves by the cord beneath the point of injury. JSTerve-stems may be interrupted in their continuity and dilatation of arteries so produced. Lastly, in neuralgias, we sometimes have dilatation of the arteries. "Whether this is produced by the vaso-motor fibres being directly involved in the morbid process, or reflexly by stimulation of sensory fibres, it is impossible to say. As a RESULT of the dilatation of the arteries, there is not simply an increased access of blood to the part, but the blood flows more quickly. The first eftect of a sudden dilatation of a considerable number of arteries Avill be a reduction of the arterial blood- pressure. But, by contraction of arteries elsewhere, this will soon be restored unless the number of arteries dilated be vei'y great. If the blood-pressure remain the same then, the blood will pass with less resistance through the dilated arteries, and will reach the capillaries and veins at a higher pressure than normal. As a matter of tact, the blood-current is accelerated and the pulse may be propagated through the capillaries into the veins. The most obvious signs of active hypersemia are redness, slight swelling, and elevation of temperature. The swelling is due partly to the overfilling of the vessels, but also to an increased ti'ansudation from the vessels into the lymph-spaces. It has been found that if a canula is introduced into a lymphatic vessel in the leg of a dog, and the sciatic nerve cut, there is an increased flow of lymphatic fluid from the canula. If the hypersemia continues long, and no other element occurs, there will probably be a hyper- trophy of the aft'ected part. The vessels especially are liable to enlarge, and very insignificant ones may become of considerable size. It has been said that active hypersemia may lead to hemorrhage, but experiment seems to prove that even a very great rise in the blood-pressure in the capillaries does not lead to hemorrhage unless the vessels are badly supported, or else defective in some way. By obstructing the respiration in a dog, you may raise the arterial pressure enormously, but there is no rupture of the capil- laries, or only in such delicate structures as the retina, brain, or conjunctiva. The increase in pressure in a pure active hypersemia is, of course, greatly less than this. Passive HypERiEMiA or Passive Congestion is a condition in which the blood stagnates in the vessels ; they are overfilled with blood, which, as it remains too long in the vessels, has a venous character, hence passive hyperaemia is also called Venous Ilyper- aemia. This condition frequently occurs as a consequence of weakness OF the HEART. In the normal state the forces of the circulation have to overcome gravitation, in order to remove the blood from depending parts. The force of the heart propagated through arteries and capillaries to the veins is genei'ally sufficient to do PASSIVE HTPER^MIA. 35 this. But, if the heart is weak, the blood is apt to linger in depending parts, or in parts far removed from the centre. Weak- ening of the heart occurs in many forms of disease. It is often very marked in fevers, such as typhus and tj'phoid, or in long- continued debilitating diseases, vphich produce ansemia. In these cases the blood often stagnates in the dependent parts of the lung, where it produces the so-called hypostatic engorgement. It also stagnates frequently in depending parts of the skin, over the sacrum and shoulder-blades in persons lying on their backs, over the trochanters in persons lying on their sides. In these situations the weakness of the circulation, along with the mechanical effects of the weight of the body and irritation of decomposing material, leads frequently to sloughing of the skin and the formation of bed-sores. In fevers there may be hypersemia of the extremities of the fingers or toes, resulting even in necrosis or gangrene. Again, there may be difficulty in overcoming gravitation on account of the force of the heart being partly lost by reason of ABNORMAL CONDITIONS IN THE ARTERIES. If there be partial obstruc- tion in the arteries, as in atheroma, where there is thickening of the internal coat sometimes with a deposition of thrombi on the surface, the force of the heart may be lost in friction, and conse- quently the blood may stagnate in the pai'ts supplied. Obstruction of veins, however, is the most direct cause of passive hypersemia. This may be produced by pressure of tumors, exudations, bandages, the pregnant uterus, even hard masses of feces, by coagulation of blood within the veins, or by the bursting of tumors into veins, or their growth through their walls. Lastly, DISEASE of the valves of the heart produces in a large proportion of cases a general venous hypersemia. We have now to consider the results of this engorgement of the vessels. Taking the simplest case, that of obstruction of a venous stem, the first result is an increase of blood-pressure in the veins behind the point of obstruction, and an accumulation of blood in the part. Considering the rapid manner in which increase of pressure in the arteries is compensated, it might be expected that the increase of pressure would soon be relieved, and the engorge- ment recovered from. If the vein have abundant anastomoses, then to a considerable extent the blood will find its way by other channels, and the normal conditions be restored. But, from the list of causes of passive hypersemia, it will be seen that most pf these involve sets of veins," or whole regions of the body; even in the case of thrombosis, the coagulation usually extends to a nuniber of veins. Apart from relief by anastomosis, however, it might be supposed that, when obstruction in a vein occurs, the increase of pressure would, as in the case of obstruction of an artery ,_ be compensated by changes in the state of contraction of the arteries. But a local relaxation of the arteries would only intensify the result by superinducing an active hypersemia ; consequently the desired compensation could only be effected by a reduction of the 36 AFFECTIONS OF CIRCULATION AND BLOOD. blood-pressure throughout the system, which will scarcely happen. The increase of pressure remains, and it atiects not only the veins, but, more particularly, the capillaries, the blood in which is, as it were, jammed between two pressures, the normal pressure from arteries and the abnormal from the veins. The further effects are to be traced to the excessive pressure in the capillaries. The blood accumulates in excessive quantity in these vessels and at an excessive pressure. In consequence of this, an increase in the natural transudation of fluid through the capil- laries occurs, and the blood-corpuscles, especially the red ones, escape from the vessels. Each of these phenomena merits more special consideration. The term Diapbdesis, or hemorrhage by diapedesis, is applied to the escape of the red corpuscles from the bloodvessels when it occurs, as in the present case, without rupture of their wall. This process occurs mainly, if not entirely, in the capillaries, and it can be shown by experiment that it does not involve rupture of these vessels. If the tongue of a frog is ligatured at its base so as to include all the veins, but excluding the artery, there will be the phenomena of hypersemia greatly intensified, and among these phenomena diapedesis. But, if the ligature be loosened within a moderate period, the circulation is restored, and the phenomena disappear. If the escape of blood-corpuscles had been by rupt- ure, it would have continued after resumption of the circulation. As to the manner in which the corpuscles escape, it is believed by some that they are pushed through the endothelial plates, but by others it is asserted, with more probability, that they pass between the endothelial cells. Fig. 3 shows the appearance of the endo- thelium of a capillary mapped out by treatment with nitrate of silver, and Fig. 4 shows capillaries similarly treated after passive hyperffimia had existed. The latter illustration is taken from Arnold, who asserts that while in the normal condition there are minute apertures between the endothelial cells, chiefly at the angles where two or three meet, these are found much enlarged in passive hypersemia. The small apertures may be called stigmata, and the larger ones stomata. The excessive pressure in the capil- laries seems to be the chief agent in causing the escape of the corpuscles, as well as the increased transudation of fluid. That there is an increased transudation of fluid can be directly proved by experiment. The flow in the lymphatic vessels has been proved to be excessive. If the lymphatics are not capable of disposing of the entire excess, then the fluid accumulates in the serous spaces and cavities of the body, giving rise to (Edema AND Dropsy, which are to be more fully considered afterwards. This accumulation will occur if, on the one hand, the transudation be too excessive for the lymphatics to dispose of it, or if, on the other, for some reason, the lymphatics do not take it up sufficiently. The current in the lymphatics depends on the blood-pressure, and we have just seen that the cause of the increased transudation is excess of blood-pressure, and so the same condition which deter- PASSIVE HYPEE^MIA. 37 mines the increase will, to a certain extent, cause it to be moi-e rapidly disposed of. Hence it is that a simple passive hyperemia from obstruction of a vein, let us say, is not usually associated with much oedema. "When the hypersemia depends on weakness of the heart, then the attraction of gravity which prevents the return of blood will also interfere with the flow in the lymphatics, Jig. 3. Fig. 4. Normal capillary, with endo- thelium mapped out by treatment "with nitrate of silver. Capillaries after passive hyperajmia. Apertures between the cells greatly enlarged ; the so-oalled stomata. (Arnold.) and there will be no excessive blood-pressure to accelerate the flow. Hence, in these cases, oedema is more common and more serious. The exuded fluid, as may be inferred, contains red corpuscles, but it does so much less in actual pathological processes than might be supposed from experiments in animals. In the latter there is a sudden obstruction, with exaggerated results ; in actual disease in man the processes usually develop slowly, and there is some accommodation of the vessels. It should be added that the white corpuscles pass out of the vessels as well as the red, but not to such an extent, and that the corpuscles, both red and white, escape from the small veins as well as from the capillaries. When oedema does not occur, there is frequently developed some swelling of the connective tissue of the parts concerned. This is a true hypertrophy, and is not to be confounded with inflammatory increase of connective tissue which will afterwards come frequently before us. The increased transudation, by providing an increase of nutritious material, causes hypertrophy of the connective tissue. 38 AFFECTIONS OF CIRCULATION AND BLOOD. wliicli is swelled, and also denser. This increased density is often seen in the heart, when, from disease in its own valves, there is a general venous engorgement in which the veins of the heart take part. We see it also very often in the kidney and in the lungs in cases of valvular disease. The tissue, as a whole, is rendered hard and resistant. The part which is the seat of passive hypertemia will be unduly red, and the color will be dark or livid. It will be swollen, both from the overfilling of the vessels and from the oedema, and it will usually be lowered in temperature. 4. Local Anaemia. — In this condition the vessels of a part are more or less deficient in blood. It may be due to various causes. The capillaries may be emptied by pressure on the part. For instance, an abscess approaching the surface may, by its pressure, prevent the blood reaching the capillaries of the skin, and a slough is the result. A cavity in the lung may, by undermining the pleura, cause sloughing of it. Tumors or clots of blood, etc., by their pressure, may cause ansemia of surrounding parts, and if the part thus rendered ansemic be a structure whose function is important to life, such as the brain, serious results may follow. Interference with the arteries will produce ansemia if the flow of blood through them be obstructed. There is such a thing as spasm of arteries — this, probably, produces the shivering which is so common at the outset of fevers, the arteries/of the skin being spasmodically contracted. So also in some neuralgias a spasm of the arteries has been seen. The application of cold causes con- traction of the arteries — the ether spray causes complete aniemia by this means. Besides this, the arteries may be narrowed by disease of their coats. There is a rather common disease in small arteries which consists in a thickening of the internal coat and has somewhat the character of atheroma. This condition is often called endarteritis obliterans, and is in some cases a syphilitic manifestation. It is clear that, by reducing the calibre of arteries, it will produce angemia. In arteries of the brain, atheroma pro- duces narrowing of the calibre which may be so considerable as to produce ansemia. More frequently, however, anfemia is pro- duced to a serious extent only when blood coagulates on the atheromatous patch and completely occludes the artery. Again, tumors, blood-clots, exudations may cause narrowing of arteries by pressure. Arteries also may be completely obstructed by ligature or by plugging. In considering the results of local ansemia, the case of complete closure of arteries will be here omitted, because it will come up for consideration under the head of embolism. In cases where there is incomplete obstruction, some blood will pass by the arteries, but the capillaries will be imperfectly filled. The part will be pale, reduced in temperature, flaccid. Its nutrition will be diminished, and its elements prone to undergo atrophy and degeneration, and even, as we have already seen, necrosis. The function will be interfered THROMBOSIS. 39 with if the nutrition is depreciated. If the anasmia affect an important organ, the results may be serious. Thus, obstruction of the coronary arteries may cause paralysis of the heart from this cause. Again, anaemia of the bloodvessels interferes so much with the nutrition of their own walls that, if after its suspension the circulation be renewed, the vessels may rupture and serious hem- orrhage result. Lastly, a local ansemia produces a hypersemia elseAvhere, but this has already been considered under collateral hypersemia. THROMBOSIS AND EMBOLISM. These two conditions are often associated, but must be carefully distinguished. Thrombosis is the coagulation of blood within the vessels or heart. Embolism is the obstruction of a vessel by a plug brought from a distance. The coagulum which forms in throm- bosis is a thrombus, the plug which obstructs in embolism is an embolus. A thrombus detached from its place becomes an embolus, and an embolus, whether consisting of coagulum or not, may grow by successive deposition of clot or thrombosis. 1. Thrombosis. — In considering the mode of occurrence of throm- bosis, it is necessary to refer to the conditions under which the blood coagulates. According to the views which are identified with the name of Alexander Schmidt, three agents are necessary for coagulation, the fibrinogen, the fibrino-plastic substance or paraglobulin, and the fibrin-ferment. The two former unite to form fibrine in the presence of the latter. The fibrinogen is dis- solved in the blood-plasma, the paraglobulin and ferment reside in the white corpuscles. It is only by destruction of the white cor- puscles that the paraglobulin and fei'ment are set free; so long as the white corpuscles circulate in the blood and remain alive, fibrine cannot form. Fibrine will form when the conditions are such that the white corpuscles are no longer preserved alive. Fibrine, it will thus be seen, is the result of a chemical combination, and the resulting albuminous substance, the fibrine, is not a vita] structure but a dead chemical compound. In order to the preservation of the white corpuscles, they must not be exposed to the contact of dead matter. You may keep blood fluid for a long time if you simply ensure that it is in contact with living tissue. Lister long ago showed that if an artery be ligatured in two places, and cut out while full of blood, it may be hung up and the blood will remain fluid for some days. Within the body if a vessel is liga- tured carefully in two places, the middle portion remaining in con- nection with the living tissues, then the blood may be kept fluid from twelve to fifteen days. The main cause of coagulation, then, is the contact of the white corpuscles with dead matter or altered living tissue. In the living body anything which interferes with the integrity of the vessel-wall or the endocardium is likely to predispose to coagulation. Stagna- tion of the blood is often set down as a cause of coagulation, but 40 AFFECTIONS OF CIECULATION AND BLOOD. this will act chiefly by altering the vessel-wall , and by keeping the white corpuscles removed from contact with the living tissue. As it is the endothelium of the vessels and endocardium which is in most immediate contact with the blood, it will be interferences with it that will conduce to coagulation. If a portion of blood inside a vessel be cut oft" from the circula- tion, then it will by and by coagulate just as it does outside the body, the main agent in the coagulation being the disintegrating white corpuscles. In this way a red thrombus is produced. But vessels are rarely so situated as to allow of a complete coagulation such as this ; much more frequently the thrombus is formed from the blood which is still moving, although, it may be, slowly, and it is of gradual growth. The formation of thrombi in the living vessels has be'en carefully studied by Zahn (Virchow's Archiv, vol. Ixii.), whose experiments throw much light on the process. The mesentery of a frog is exposed and subjected to microscopic examination. A vessel of some size, an artery or vein, is chosen, and its wall in some way injured, as by twitching it slightly with the forceps, or placing a small crystal of common salt near it. Yery soon white blood-corpuscles begin to adhere at the injured part. As the blood passes over it, successive layers of white cor- puscles adhere, and a growing clump of them is formed. Along Avith the white corpuscles a stray red one may be insinuated, or there may be several red ones. The clump so formed, be it wholly Avhite or partly mixed with red corpuscles, may be carried off, in Avhich case a new one begins to form; but the clump may remain hxed and be continuously enlarged by successive depositions of cor- puscles from the circulating blood. In course of time a change occui's in the appearance of the clump, the white corpuscles lose their individual outline to a great extent, and the clump gathers itself together into a gray granular mass in which neither by acetic acid nor by staining are the majority of the white corpuscles to be discovered. It has, indeed, very much the characters of fibrine which has been obtained by whipping the blood outside the body. The clump of white corpuscles, in fact, by the disintegration of the corpuscles and the attraction of the fibrinogen from the blood- plasma has converted itself into a fibrinous coagulum. All the white corpuscles, however, are not disintegrated, some are still recognizable in the mass. A similar mode of formation is observed when a vessel is injured by pricking with a needle, or by cutting it. The presence of foreign bodies if they are rough on the sur- face, produces adhesion of white corpuscles and their conversion into thrombi in similar fashion, but when smooth pieces of glass are introduced, there does not seem to be the same tendency' to adhesion of the white corpuscles. It will be understood that thrombi formed in this way often contain a few red corpuscles. If by any alteration in position, or tearing of the clump, a channel is formed, then the red corpuscles will be wedged in and retained. The WHITE THROMBI and the mixed thrombi are therefore to be I regarded as forming a single class. The red thrombi composed of the entire blood form another class. THROMBOSIS. 41 Having learned so much as to the formation of thrombi, we may be prepared to consider the special circumstances under -which they occur in actual cases. It may be said that in most cases of thrombosis there is either such a stagnation of the blood as to cause a serious deterioration of the endothelium, or else some pal- pable INJURY to the vessel Compromising its endothelium, and the various thrombi may be studied according as the}' are formed in one of these ways or the other, while in some cases the action of both may be traced. As we have already seen, the stagnation is rarely complete, and accordingly the thrombi are mostly white or mixed, being formed in the way just described. Thrombi form in the heart from the blood stagnating in its chambers. This will occur when, from any cause, the cavities of the heart are imperfectly emptied, as from dilatation or weakness of the muscular substance. The coagulation will occur most readily in the parts of the cavities from which the blood is least likely to be emptied during the imperfect contractions. Hence ■ we find them near the apices of the ventricles and in the auricular appendages more frequently than elsewhere. So also they form most commonly behind the columnae carnese, and are frequently found peeping out between these muscular columns. These thrombi are frequently of a pearly-white color, and are never composed of the whole blood, although they may be brown from admixture of red corpuscles. As dilatation occurs more frequently in the right heart than in the left, these thrombi (which were called by Lfennec, globular vegetations), are more frequent in the right cavities than in the left, although by no means rare in the left ventricle. "Weakness of the heart not infrequently produces thrombosis in THE VEINS. In debilitating diseases, such as typhoid fever, phthisis, etc., the heart is weak, and the blood-current sluggish, especially in the veins. These thrombi are, at their commencement, usually related closely to the valves. In the sluggish state of the circula- tion the valves lie half closed, the force of the blood being insufh- cient to press them back against the vessel-wall. Hence the blood will stagnate in the pouches of the valves and coagulation will begin there. Coagula so formed grow up the veins, but even when they have become continuous, they often present a knotted condition, from the parts corresponding with the valves being bulkier. In such cases the knotted character can often be detected through the skin. The coagulation occurs primarily in the larger veins, the femoral, jugular, sinuses of the dura mater, but accord- ing to Virchow, this is only due to certain local relations. In the cases hitherto mentioned, stagnation of blood has been the primary factor, but in the thrombosis sometimes occurring IN THE UTERINE VEINS after childbirth, we have this combined with a palpable injury to the vessel-wall. In some cases, after parturition, the uterus contracts imperfectly, and the blood, stag- nating in the uterine sinuses, is apt to coagulate. In this case the starting-point of the coagulation is often the open mouths of the 42 AFFECTIONS OF CIECULATIOlSr AND BLOOD. veins on the raw uterine surface, which in many respects resembles the surface of a wound. A more definite wound of a vessel may induce coagulation. The coagulation may occur at the ruptured edges, or a clot may form in the effused blood outside the vessel, and by successive deposition from the escaping blood grow through the gap into the vessel. In case of ligature of a vessel the internal and middle coats are ruptured, and coagulation occurs as in the case of a wounded vessel. If stagnation already exists in a vein, a very trivial wound may induce coagulation. Thus in cardiac disease where passive hypersemia has led to oedema, the punctui'es made to relieve the oedema or the ulcers which form spontaneously, not in- frequently lead to thrombosis in the veins. It is important to bear this in mind in connection with the general venous hypersemia of valvular disease of the heart. .Diseases of the vessels and heart which interfere with the endo- thelium induce coagulation on the surface. Thus acute endo- carditis produces thrombosis on the valvular structures of the • heart, and chronic endocarditis does so sometimes b}'- the forma- tion of calcareous plates, which may, b}' and by, tear through and expose themselves in the current. Atheroma of arteries, by causing roughness and ulceration, or by producing calcareous plates, may lead to coagulation, which is more serious in such small arteries as those of the brain, where thrombi may completely obstruct, than in such a vessel as the aorta. The well-known coagulation of blood in Aneurism is susceptible of similar explana- tion. Here the internal wall is much altered, and usually deprived entirely of its endothelium. Another occasional cause of throm- bosis is the protrusion oe tumors through the walls of vessels. It is very seldom that arteries are thus involved, and, as we shall afterwards see, thrombosis does not occur in the capillaries, but veins are occasionally attacked by malignant tumors and their walls so altered as to induce coagulation. Thrombi which have once formed are liable to grow. The thrombus is composed of dead tibrine, and the surface is rough, so white corpuscles adhere and disintegrate, and coagulation occurs readily in successive layers. In the case of the veins the blood will be for the most part stagnant above and very often below the thrombus, and it is in these vessels particularly that they are apt to grow very extensively. Thus a coagulation starting in the uterus may travel along to the internal and , common iliac veins, and thence pass into the veins of the legs. In a case observed by the author, coagulation had its origin m a cancer of the kidney, which involved the wall of the renal vein, and it extended thence to the inferior vena cava, and to the veins of both legs which were distended with old thrombi. In regard to the character of the thrombi formed under these various circumstances, it maybe said that almost all are of the white or mixed character, as most of them form where the circu- lation, although it may be stagnant, is not absolutely at a stand- THROMBOSIS. 43 still. The more the blood is at rest, however, the more it is likely to contain red corpuscles. It is clear that thrombi forming at the edges of a wounded vessel as the escaping blood passes over them will be white thrombi, and, indeed, Zahn determined this in his experiments. Thrombi forming on the inflamed valves, on the diseased endocardium or intima of vessels, or in consequence of the projection of foreign bodies or tumors, will be white. The globular vegetations of the heart are also white or mixed — they are, indeed, often of a pearly whiteness, and even those occurring in veins from weakness of the heart are largely composed of white corpuscles. Growing thrombi will be mainly white or mixed, but as the blood above and beneath a growing thrombus is usually at a stand-still, or nearly so, we are apt in this case to have more nearly the entire blood entering into the constitution of the thrombus, and these are often reclder than most. The stratified clots in an aneurism are white or mixed, and it may almost be said that, except in the case of coagulation in an aneurism after ligature of the artery, it is seldom that the whole blood is concerned in the formation of a thrombus. It is important to distinguish thrombi which have formed during life from mere post-mortem coarula. It will be clear from what has gone before that the thrombi are mostly either white or gray, but being formed largely of white corpuscles, they are of a dead or opaque white or gray appearance. Post-mortem clots are some- times pale from the sinking of the red corpuscles or otherwise, but they are gelatinous and smooth on the surface and mostly trans- parent, whereas the thrombi are firmer, drier, more opaque, and granular on the surface. The thrombi also adhere to the wall to some extent, whereas the clots do not, although in the heart, from getting entangled among the columnse carnese, they may have an appearance of adhesion. Lastly, the thrombi are often stratified, indicating their deposition in successive layers. We have now to consider the changes which thrombi undergo after their formation. It is to be remembered that the coagulum is virtually a piece of dead matter, fibrine being merely a chemical compound, not a living structure. There are two indications, chiefly, in which thrombi are liable to change — the one is softening, and the other an apparent organization. Softening is a frequent result, especially in the coagula in the heart and veins. It should be said that the softening which occurs in connection with pysemia is here left out of account, as the whole processes in connection with this disease will be studied afterwards. The globular vegetations in the heart frequently present very good examples of softening. It begins in the central parts of the thrombus, and the coagulum breaks down into a turbid brownish juice, the softening extending gradually outwards. The juice is often like a mixture of pus and blood, or in very white thrombi it may be like pure pus. It consists of the debris 44 AFFECTIOXS OF CIRCULATION AXD BLOOD. of the thrombus, and no well-preserved corpuscles are to he found in it. The softening may extend outwards till a mere rind of clot is left, and this may give way and cause the juice to be launched into the circulation. In veins, also, softening may take place, and here the coloring matter of the blood Fig. 5. may be deposited in the form of A hfematoidin crystals (see Fig. 5). Of ca course, where softening has occurred, ^ E! ^ there is much more probability of g^ bits of the thrombi being torn away ^ ^ or carried forward so as to produce ^ ^.■^ embolism. Thrombi, instead of softening, may ^ '^ IB dry in and shrivel. In such case we 5^ may have lime salts deposited, and even through time the formation of <> little stony masses — vein-stones or ^ Phleboliths. „ , , , , , .,. , , The Organization of a thrombus Crvstala of h^matoiam found . - , , a .1 closely aggregated in the midst of an IS a prOCCSS of SOme mtcrest. As the old thrombus in a vein. The crystals COagulum IS dead, it IS clcar that it have a deep red color. X 350. canuot take part in the process of organization. In studying inflamma- tion this subject will come up for fuller discussion, but it may here be stated that when a piece of dead animal substance is present among the living tissues, the first step towards its absorption is usually its replacement by an elementary tissue, the dead structure forming, as it were, a mould on which the new tissue forms itself. The constituents of the thrombus are, therefore, pushed aside or disintegrated by masses of round cells (as shown in Fig. 6, 6); and at the same time bloodvessels springing from the vasa vasorum extend into the substance of the new-formed tissue. The thrombus is thus converted into, or replaced b}', a vascular tissue, which subsequently develops into connective tissue. Like other new- formed connective tissue of this kind, this tissue tends to contract. The result of this sometimes is the drawing together of the walls of the vessel, and the permanent obliteration of its calibre. The vessel is thus converted into a solid cord. In other cases the con- traction acts on the walls of the proper vessels of the new-formed tissue, dragging them outwards. By this means the vessels are widened, and in time may come to assume a cavernous character. This may result in the reestablishment of the circulation, the wide spaces of the sponge-like tissue coming to communicate with the regular calibre of the vessel. A favorite place for the forma- tion of this cavernous tissue, is the place of union of the iliac veins to form the vena cava. Here, the vessels are sometimes found filled with a spongy tissue through which the circulation is carried on. By a still further contraction of the new-formed tissue, the calibre of the vessel may be completely reestablished, the sinus-like blood-channels expanding into the calibre of the vessel. THROMBOSIS. 45 Before leaving this subject of thrombosis, it may be well to con- sider WHETHER COAGULATION OCCURS IN THE LIVING CAPILLARIES. It is to be remembered that the deterioration of the endothelium is the proximate cause of the coagulation of the blood in the vessels. The capillary wall consists entirely of endothelium, and the dete- rioration of it means the deterioration of the entire capillary wall. Such an interference with the capillaries as to induce coagulation Fig. 6. Organization of blood-olot. a represents the clot little altered ; red corpuscles are chiefly seen, with a few solid round cells, which are like white corpuscles, but more numerous than in normal blood. In b the red corpuscles are entirely replaced by round cells. In c the round cells have given place to large spindles. X 350. will only occur when actual necrosis takes place. Moreover, as the tissues depend on the capillaries for their nutrition, obstruction by thrombosis will involve the death of the tissues themselves. Hence thrombosis of the capillaries, or even complete stagnation in them, may be put out of the question except in connection with necrosis. The non-occurrence of thrombosis in the capillaries is of great practical consequence. If it were not so, the thrombi in veins, growing against the current as they so readily do, would grow into the capillaries, and through them into the arteries. The capillaries, not admitting of this, form a barrier to the extension of the coagulation. It thus happens that, after extensive coagula- tion in the veins, the circulation is largely maintained by arteries, capillaries, and lymphatics, and necrosis rarely occurs. It is worthy of note in connection with this matter that the blood found in the capillaries after death is nearly always fluid. In studying thrombosis, we have left out of account all cases of 46 AFFECTIONS OF CIECUL ATIO jST AND BLOOD. what is called septic thrombosis, where the coagulation arises in connection with the introduction of decomposing material into the veins. Such processes will receiA^e consideration in another part. We have still to consider the effects of thrombosis. Apart from the occurrence of emholism, which may result from throm- bosis anywhere, it will be mostly thrombosis of the veins that is followed by serious results. The most direct eflect of obstruction of veins by thrombi is, of course, passive hypkr^mia with its consequent (edema. The occurrence of serious oedema depends large!}' on the extent of the anastomosis of the obstructed vein, and also somewhat on the rapidity with which the thrombosis has occurred. If the thrombus forms slowly, the functions of the plugged veins may be largely taken up by the lymphatics and by other veins which remain unaffected. In the case already referred to, Avhere a cancerous tumor in the kidney had burst into the renal veins, and thrombosis had extended to the vena cava and down the veins of both legs, there was comparatively little cedema at any time, although all the main venous trunks of both legs were plugged. One circumstance renders this compensation, especially by the lymphatics, the easier, namely, the fact that the thrombosis does not extend into the capillaries, and consequently not into the arteries. The cause of this has been already explained, biit it is clear that if the circulation is still maintained in the arteries and capillaries, the lymphatic circulation will not sulfer. It is important to know that these secondary effects of throm- bosis, and especially cedema, will not usually show themselves for some time after the onset of the process. A coagulation begin- ning in a vein will take some time before it completely obstructs it, and even when it has done so, it may be necessary for it to grow into other veins before any pronounced oedema will develop. Hence it is that a thrombosis may lead to embolism by detachment of portions of the thrombi before it has manifested its presence by hyperemia and oedema. Thrombosis in veins seldom leads to Gangrene, and in the few cases in which gangrene actually occurs some additional interfer- ence with the circulation will usually be discoverable. Weakening of the heart, in conjunction with thrombosis, may cause it, and so may disease of the arteries diminishing the force of the blood. 2. Embolism. — This, as we have seen, is a process frequently associated with thrombosis. Embolism will affect arteries or capillaries, and, aa the portal vein is distributed in the liver like an artery, it is also liable to embolism. The plug or embolus is most frequently a thrombus or a part of one. It may be a bit of tumor which has found its way into a vessel, or a foreign body which has obtained entrance. It may be a piece of cretaceous material from a degenerated valve or vessel. It may be a parasitic animal, as the echinococcus, which has found its way into the cir- culation. EMBOLISM. 47 In the ease of many arteries the effects of embolism are very trivial. The anastomoses are so fkee that they readily compen- sate completely, and the circulation is restored almost at once. For the purposes of the tissues it is the capillary circulation which is of importance; and if the blood, by any route however circui- tous, reaches the capillaries, there is no serious result. "When an artery with free anastomosis is obstructed by an em- bolus, there will be at once an increase of blood-pressure on the proximal side of the plug. The anastomosing branches by dilata- tion will reduce this excessive blood-pressure, but the excessive blood-pressure may itself assist in opening up the anastomosing channels. In this way the circulation is restored. At the seat of obstruction thrombosis occurs on each side of the embolus, and goes on upwards and downwards to the nearest branches. By the organization of the thrombus the calibre of the artery is destroyed and the vessel reduced to a solid cord. In this way a piece of artery is lost, and that is all the permanent result. It is similar with capillary embolism. The ultimate result is the loss of a piece of capillary between the two nearest communi- cations. At the time of its occurrence the embolus in a capillary will produce very little disturbance, as the communications are so free in the capillary system, It sometimes happens, however, that multiple embolisms cause more serious derangements of the circu- lation. It is very different in the case of arteries which have no anas- tomoses. There are parts of the body in which the arteries are distributed to a perfectly definite piece of tissue, and have no anas- tomotic connections. In the case of such arteries, to which Cohn- heim gives the name of End Arteries, the results of obstruction . are very serious. The part is entirely deprived of its blood-supply through the arteries, and if any blood reaches it, it must be by the connection with neighboring capillaries or by the veins. The most direct result of obstruction of an end arter}^, therefore, is ansemia, and consequent death or necrosis of the tissue. But there are some cases in which an apparent exception to this occurs ; there is the necrosis, but instead of anaemia, there is an excessive engorgement with blood. This is very well seen in the case of the lung, where embolism often produces the hemorrhagic infarc- tion. We have to consider how this is to be explained. Cohnheim's experiments in elucidation of the pathology of em- bolism are of such importance in this regard that more particular reference to them may be here permitted. The subject of experi- ment was the tongue of the frog. The two main lateral arteries of the tongue are not end arteries, but their lateral branches are. Cohnheim introduced little blackened pellets of wax into the division of the aorta which communicates with the arteries of the tongue, and these were sometimes carried to the tongue, obstruct- ing the arteries there. Sometimes one pellet obstructed the anas- tomosing branch between the main arteries, while another stuck 48 AFFECTIONS OF CIRCULATION AND BLOOD. in one of the main arteries, so that the latter was converted into an end artery. Whether a main artery thus conditioned or a plugged lateral branch was observed, the process was virtuallj' the same. The blood was, immediately after the plugging, at a stand- still, in artery, vein, and capillaries. These vessels might be mod- erately full of blood or might contain on\j blood-plasma. Soon, however, a backward flow of the blood from the veins was observed (diagrammatically shown in Fig. 7), and by and by this produced Pig. 7. Diagram of coniJitions following embolism of an end artery. In the figure to the left the state of ansemia after the embolism is shown. In the other figure the regurgitant current from the vein is indicated (after Cobnheim). an engorgement of the entire vessels, veins, capillaries, and arteries. After a time a remarkable diapedesis began to manifest itself through the capillaries into the surrounding tissue, which became engorged with blood. The portion of tissue concerned would, in accordance with the area of distribution of the artery, be wedge- shaped, and the result was a wedge-shaped, red, pulpy piece of tissue, not unlike a blood-clot — the Hemorrhagic infarction. If the frog survived, the piece of tissue by and by sloughed off. The explanation of these phenomena is not very difiicult. The obstruction of the artery reduces the pressure in the vessels sup- plied by it to nothing. The veins are still in open communication with the veins of the part, in which, although the blood-pressure is low, it is still something. Accordingly, the backward flow occurs from the veins to the capillaries, and so to the obstructed artery. Thus the engorgement of the vessels is not difficult to explain. The diapedesis is to be referred to the fact that the capillai-ies, being deprived of blood, have the integrity of their walls impaired. "We have already seen that passive hypersemia produces diapedesis, owing to interference with the capillary wall. Much more serious is the nutritive deterioration in this case, and so the diapedesis is very great, leading to a marked infiltration of blood into the tissues around. The deprivation of fresh blood causes death of the tissue, which here, as it is an external part, sloughs. EMBOLISM. 49 In applying these facts to human pathology, we have to consider, in the iirst place, what arteries of the body are end-arteries. These are the renal and splenic arteries and their branches, the nutritive arteries of the brain, the central retinal artery, the pul- monary artery and its branches, to which we may add the portal vein, as in its relations an end-artery. We have not, in all of these, the typical hemorrhagic infarction, and it is necessary to consider each individual case separately, and endeavor to explain the divergencies which they present. Embolism in the lungs frequently presents the most typical hemorrhagic infarction, but it has been known since Virchow's important researches that embolism of the pulmonary artery does not always lead to its formation. In the same lung you may have a number of obstructed arteries, in connection with some of which there is the hemorrhagic infarction, while in the case of others it is entirely absent. This apparent puzzle is explained when we come to consider more closely the relations of the circulation in the lungs. It has already been said that it is the circi;lation in the capillaries that is of consequence in considering the results of em- bolism, and we know that the capillaries everywhere anastomose freely with each other. It is conceivable, therefore, that the anas- tomosis of the capillaries might come to act like an arterial anas- tomosis, and that the circulation might be maintained through the capillaries. In the lung the capillaries of the pulmonary artery .are wider than those of most other parts, and so the loss of force .by friction will be less than elsewhere. There is, besides, less ten- dency to necrosis of the tissue here, as the connective tissue of the lung, the bronchi and the larger vessels, are supplied with blood by the bronchial arteries. In some eases, then, the circulation in the capillaries behind the plug is sufficient to maintain the capillary wall and prevent the formation of the hemorrhagic infarction, and,^ indeed, experiment seems to show that in normal animals embolism seldom results in the infarction. If we consider the usual situations of the hemorrhagic infarc- tions of the lung, we shall obtain still clearer views on the subject. If an artery is obstructed near the root of the lung, then the capillaries of the piece of tissue concerned will be in communica- tion on all sides with capillaries in which the circulation is still active. The piece of tissue is, as it were, buried in the spongy lung substance whose capillaries are filled with actively moving blood. It is not surprising that, in this case, the capillary circula- tion in the affected piece of tissue, although rendered sluggish, is still maintained; the movements of respiration also assisting in maintaining the circulation. In accordance with these considera- tions the hemorrhagic infarction seldom occurs in the central parts of the lung. But if the obstructed artery has a peripheral distri- bution, if the piece of tissue is covered on one side by the pleura, or if, being situated at the edge of the lung, it has two sides covered by pleura, or even, being at the edge of a lobe as well as of the lung, it has three sides covered with pleura, then it will be 4 50 AFFECTIONS OF CIRCULATION AND BLOOD. in a much less favorable position. On one, two, or three of its sides the capillaries are not in communication with other capillaries in which the circulation persists. It is not surprising, therefore, that the hemorrhagic infarction is nearly always peripheral, and that it frequently has its seat at the edge of the lung, or at the edge of a lobe. The infarction is wedge-shaped, and it is interest- ing, in relation to the points we are considering, to observe that the plug is usually not exactly at the apex of the wedge but a certain distance nearer the heart, so that sound tissue intervenes between the beginning of the plug and the infarction. The ex- planation of this is, that in the neighborhood of the plug, that is to say, at the apex of the conical piece of tissue supplied at the artery, the, tissue is still surrounded on all sides by capillai'ies in which the circulation is active, and for a certain distance this is sufficient to carry on the circulation. It may even be said that all around the periphery of the infarction, so far as it is in connection with lung tissue, there will be a zone in which the surrounding capillaries keep up the circulation in the affected capillaries, and that the actual infarction is less in all these directions than the area of dis- tribution of the obstructed artery. It appears that if the heart is of normal strength, it, with the movements of respiration, is capable of maintaining the circula- tion in the capillaries, even when a peripheral branch is the seat of embolism, and it is mostly in cases of weakness of the heart, or Avhen the pulmonary circulation is already in a state of engorge- ment, or where multiple embolisms obstruct numerous neighbor- ing trunks, that the infarction occurs. When embolism occurs in the pulmonary artery, there will always be stagnation of the blood, and even if the hemorrhagic infarction does not form, there will be great interference with the circulation. In the case of the spleen there are no such compensating con- ditions as in the lung, and here the hemorrhagic infarction seems to occur with great uniformity. In the KIDNEY, embolism always produces necrosis of a wedge- shaped piece of tissue, but even in recent embolism this is not always engorged with blood. The very wideness and freeness of communication of the capillaries in the lung which so frequently prevents the formation of the hemorrhagic infarction, will ensure that when it does occur there will be a very great engorgement of the vessels and abundant diapedesis. In the case of the kidney, the capillaries are smaller, and their communications with the veins more circuitous, and so it often happens that necrosis occurs before the backward flow has been established. In that case the whole wedge-shaped piece of tissue coagulates into a solid mass (see Fig. 8). This is an instance of the so-called coagulation-necrosis, which we shall have a better opportunity of studying afterwards. We may have, therefore, a hard, solid, whitish Avedge"^, instead of a hemorrhagic infarction. A true hemorrhagic infarction is some- times met with, especially when a small artery is obstructed. In the case of the brain, necrosis of the tissue occurs, and some- EMBOLISM. 51 times so rapidly that the capillaries are rendered incapable of receiving the blood before the backward flow from the veins is sufficient to cause engorgement. The necrosis here does not result in coagulation of the tissue, but iu its softening, so that as a result of embolism of the brain we have softening which may, or may not, be accompanied by hemorrhage, but is never associated with very considerable bleeding. Embolism of the retina is similar to that of the brain. We have still to consider the case of the poetal vein, Avhich, in its distribution, is comparable to an end-artery. The conditions Tig. 8. Embolic infarction of kidney, showing the wedge-i (after Rayer) ed piece of tissue affected here, however, are peculiar, inasmuch as the liver is supplied with blood from the hepatic artery as well as from the portal vein. It has already been more than once noted that it is the condition of the capillaries which is of importance in relation to the hemor- rhagic infarction. A study of the circulation in the liver shows that when the portal vein is closed, blood still passes from the hepatic artery into the hepatic capillaries. The hepatic artery supplies blood to the connective tissue, the walls of the ducts and larger bloodvessels of the liver. The capillaries from these are collected into veins which open into the interlobular veins, which, of course, are the terminals of the portal vein. So that when the portal vein is obstructed, the blood from the hepatic artery passes into the interlobular veins, thence into the hepatic capillaries, and so on into tEe intralobular and hepatic veins. The capillaries of the portal system are thus kept supplied with blood, and their nutrition does not suffer. Experiment has even shown that when the entire portal vein is obstructed the secretion of bile is not entirely at a standstill ; the blood of the hepatic artery affording material for a limited production. It has been said that the hemorrhagic infarction forms in the case of end-arteries, but there is an apparent exception to this in 52 AFFECTIONS OF CIRCULATION AND BLOOD. the cabe of the superior mesenteric artery. If the superior mesenteric artery or one of its larger branches be obstructed, hemorrhage occurs in the intestine and mesentery, and the portion of gut suffers necrosis, but it is well known that the anastomosis of the mesenteric arteries is tolerably free. The explanation of this apparent anomaly has been worked out by Cohnheim and his pupils in a very interesting manner. As a rule, it may be said that main stems have, in proportion to their size, much less con- siderable anastomotic communications than the smaller branches. -Thus the anastomotic communications of the iliac or femoral artery are proportionally much less considerable than those of the tibial or of smaller arteries still, and the anastomoses of the superior mesenteric are much less voluminous in proportion than those of its branches nearer to the gut. If the main stem be obstructed, therefore, the restoration of the circulation occurs much more slowly than when a small stem is the seat of obstruction. Another illustration of this is afforded by embolism of the femoral artery. The temperature falls rapidly, the limb is numb and half-paralyzed, and this is doubtless due to insufficient supply of blood by the artery. It takes some days before the collateral vessels dilate suf- ficiently to I'estore the temperature and functions of the limb. The contrast is very great when a small stem is obstructed; in that case comparatively little inconvenience is suffered, and recovery is rapid, unless, indeed, several small stems are simultaneously affected, in which case, as we shall afterwards see, the results may be very serious. It is similar in the case of the superior mesen- teric and its larger branches. Obstruction here is slowly recovered from, and for a time the circulation is virtually at a standstill. But here a very important element comes into consideration. The vessels of all parts of the body are not equally resistant. Those of the skin and muscles (and here it is of course the capil- laries and small veins that are concerned), are peculiarly resistant, and are able to stand a considerably prolonged deprivation of blood. It is different with those of the intestines. In order to test the vulnei-ability of the vessels of the intestine, the following experiment was' made. A ligature was tied on the superior mesen- teric artery, and the precaution was taken of tying it over leather, so that it might not destroy the vessel, and thus admit of its being subsequently unloosed. It was found that if after two to two anii a half hours the ligature was untied, hemorrhage occurred from the capillaries. The meaning of this is that within this period the deprivation of blood so seriously disorganizes the capillaries that they are no longer able to prevent the escape of^blood at the normal pressure. A much longer time is required in order to the occurrence of hemorrhage at the pressure of the venous blood; a period of ten_ or twelve hours is needed. But it was found that for the establishment of the collateral circulation a period exceed- ing even this was required, namely, fourteen hours. Accordingly, before the anastomosis can be established, the backward flow from the veins has already begun, and even the diapedesis. The rees- EMBOLISM 53 tablishment of the circulation even increases the tendency to hem- orrhage, as it subjects the blood to a higher pressure than that of the venous blood. The experiments referred to showed that when the superior mesenteric artery is obstructed, the hemorrhagic infarction forms with a backward flow from the veins just as in other cases. It will be obvious that arteries possessing free anastomoses MAY BE REDUCED TO THE CONDITION OF END-ARTERIES if their auas- tomoses are no longer available. If, as sometimes happens, an embolus passing to the leg breaks up, sa}', by being propelled against a bifurcation, and is scattered to a number of stems simul- taneously, then the circulation will be reestablished verj' slowly or not at all, and necrosis is liable to occur, especially if the circula- tion is already feeble. Thus, we may have gangrene of the toes occurring in this way. It is to be added that in old people ob- struction of a number of arteries sometimes occurs from throm- bosis as a result of atheroma, and this may likewise lead to necrosis. Hitherto we have considered only the more immediate results of embolism in end-arteries, we have still to pass under review the FURTHER CONSEQUENCES. We havc secu that the regular result is necrosis of the piece of tissue concerned with or without the occur- FiG. 9. Infarction of kidney undergoing absorption. The infarction is white and depressed below the level while the tissue is puckered around it (after Rayer). rence of hemorrhage. In the case of the lungs there is a doubtfu,l exception to the uniform necrosis of the piece of tissue. 'The lung tissue is nourished to a great extent by the bronchial artery, and obstruction of a branch of the pulmonary artery will not interfere 54 AFFECTIONS OF CIRCULATION AND BLOOD. with the nutrition of the connective-tissue stroma and the bronchi, and it is probable that only a partial necrosis occurs. The air- vesicles, however, are nourished by the capillaries of the pulmonary artery, and it is to be expected that, for the most part, these at least will either necrose or atrophy. As a matter of fact, the whole infarction often undergoes necrosis, and in cases of hemor- hagic infarction of the lung which recover, symptoms like those of phthisis sometimes develop, and lung tissue has been known to be spit up. As the necrosed lung tissue is disposed of, a cicatrix will take its place. In the case of the spleen and kidney, the solid infarctions are gradually absorbed (see Fig. 9) like foreign animal matter in the living body generally, a preliminarj- decolorization first occurring. Their place is taken by cicatrices in the midst of which, even at a late date, little pieces of solid, cheesy -looking material may often be seen. The softened brain tissue is also ab- sorbed, and a cicatrix or a cyst takes its place. So is it with the retina; the piece of tissue is lost and absorbed. In the case of the superior mesenteric artery, the slough of the bowel and hemorrhage lead on mostly to a fatal result, but cases do occur in which, after the separation of a slough, an ulcer is left which may ultimately cicatrize. We have still to consider two rarer forms of embolism, namely, by OIL and by air. Oil or fluid fat not unfrequently gets into the bloodvessels. It does so where, by fracture of a bone or injury to the subcutaneous adipose tissue, the fat cells in the bone mar- row, or adipose tissue are broken up so as to set free the oil, and, at the same time, the vessels, and especially the veins, are laid open so as to absorb the oil. Oil also occurs in the blood in cases of diabetes, and, as in Fig. 10, may produce embolism. The oil is carried, of course, to the right heart, and on into the lungs, where it sticks in the capillaries and the smallest arteries. If the capillaries are obstructed at considerable intervals, then no evil results, the anastomosis being so free that no serious disturbance occurs, and the oil itself does not irritate. But, if a considerable number of small arteries near each other be obstructed, or even a large number of capillaries, we may have a condition resembling the hemorrhagic infarction. It has been found on experimen't that abundant fat embolisms in the ear of a rabbit, by obstructing numerous capillaries, may lead to necrosis. In some cases the oil may, to some extent, pass through the lung capillaries, and it is found mostly in the Malpighian tufts of the kidney, one or two loops being here and there filled. There are a few rare cases on record in which extensive embolism has occurred in the smallest vessels of the brain, conjunctiva, skin, muscles, heart, intestines, liver, and kidneys, and has apparently been the cause of death. It is well known that the admission of a considerable quantity of air in^o veins near the heart often leads to a fatal result, and some have supposed that the embolism in the lungs is the cause. It need hardly be said that, as the pressure in the veins near the HEMOBRHAGE. 55 heart is very low, and there is even a degree of suction during inspiration, there is great danger in opening sucli a vein as the jugular. In regard to the cause of death in these cases, it is im- portant to notice tliat a repeated admission of small quantities of air does not produce serious results, whereas a single large admis- sion is rapidly fatal. This hardly looks as if embolism were the cause, and, as a matter of fact, the air is found after death mainly in the right auricle and ventricle, which are usiially enormously Fig. 10. Oil embolism of lung. The fat is seen in larger nnd smaller drops in branches of the pul- monary artery (a a) as well as in the capillaries. From an osmic acid preparation (Sanders and Hamilton). dilated. The fact seems to be that the right ventricle, in contract- ing, merely squeezes together the elastic air, which again expands during the diastole. The force of the heart is thus fruitlessly expended and the blood is not sent into the pulmonarj' artery. Moreover, the over-distention of the right auricle with air prevents the admission of blood from the venic cavas. Thus the circulation is at a standstill, and death results. HEMOREHAGE. This is the escape of blood from the living vessels or the heart. It may take place in minute drops, perhaps frequently repeated, 56 AFFECTIONS OF CIRCULATION AND BLOOD. or in larger quantities. The blood may pass outside the body or make a place for itself and form an extravasation inside the body, or it may infiltrate the tissues over a considerable area, forming an ecchynlosis. From what has gone before, it will be understood that there are two forms of hemoi'rhage, which should be kept apart, namely, that by kupture of vessels, and that by diapedesis. The former may affect any size or kind 'of vessel, and when it occurs, there will be an escape of the whole blood. The latter occurs only in the finest vessels, mainly the capillaries, and it is chiefly th« red corpuscles which escape, and with them, of course, some fluid, but the fluid has not the constitution of the entire blood-plasma. These two forms of hemorrhage are difterent, not only in kind, but in the CAUSES which lead to them, and j'et in some cases it may be difficult to determine which is the form present. Taking first the case of hemorrhage hy rupture, it is most obviously produced by some agent acting on the vessel from with- out, as in the case of a wound by a weapon or a jjiece of broken bone, etc. Then also ulceration may cause penetration of a vessel. Disease of the walls of vessels, or of the heart, may lead to rupture, as aneurism, atheroma, varix. It may here be said that new-formed vessels, whether in inflammations, or in tumors, are peculiarly prone to rupture, presumably from the thinness of their walls. There are further some cases of hemorrhage in which we have to assume some change in the vessels arising from an altered condi- tion of the blood, as the cause of hemoi-rhage, and in most of these cases it is doubtful whether the hemorrhage takes place by rupture or by diapedesis. In scurvy there is a deterioration of the blood which presumably has a direct effect on the structures comprising the vessel-wall. The hemorrhage here is probably by rupture, judging from the rapidity with which sometimes large extravasa- tions occur, but it is not impossible that it may be by diapedesis. In purpura hemorrhagica (or morbus maculosus Werlhofii), there is also hemorrhage traceable to weakening of the walls of the vessels from a change in the constitution of the blood. In anaemias and leukaemia, hemorrhages are very frequent, and doubtless the altered constitution of the blood has to do with it. In these the hemorrhage is probably by diapedesis. Alteration of the constitu- tion of the blood is also frequently a cause of hemorrhage in the acute specific fevers. The petechias of typhus, and the frequent hemorrhages in smallpox are examples, the latter being often so marked as to warrant some cases being called hemorrhagic small- pox. In the hemoi-rhagic diathesis there is a peculiar fragility of the walls of the vessels, and this is doubtless congenital and often inherited. In such persons a slight injury produces rupture, and there is difficulty in getting the hemorrhage stopped. Even a temporary excess of pressure in the vessels may lead to hemor- rhage in these cases. In poisoning by phosphorus the vessels become fatty, and there HEMOERHAGE. 57 is a tendency to hemorrhage, but whether by rupture or by diape- desis is unknown. Of hemorrhages undoubtedly by diapedesis we have already con- sidered two good examples, in passive hypereemia and the hemor- rhagic infarction. In inflammation also there is escape of the blood-corpuscles by the same method. We have next to consider the stoppage of hemorrhage, and in regard to diapedesis it is clear that it will cease when its cause ceases to act. There is in this case no rupture of the vessel, and so soon as circumstances restore the vessel to its normal state of impermeability to the blood-corpuscles the hemorrhage will cease. In the case of hemorrhage by rupture, the problem is more com- plicated, and various elements enter into it. It is well known that such hemorrhages tend to cease spontaneously, and we have now to see how that result comes about. The direct means of stoppage is coagulation oe blood, so that a thrombus obstructs the oriiice. The thrombus may form at the ruptured edges, or the blood may coagulate outside the vessel, and the coagulum by successive deposition, grow in. The actual thrombus, as it is formed by flowing blood, will be a white or mixed one. The stilling of the hemorrhage being directly the result of thrombosis, it is to be added that various circumstances favor the formation of the thrombus, and aid in preventing its displacement. These circumstances are for the most part the direct results of the hemorrhage itself. In the first place, as a hemorrhage proceeds the white corpuscles become proportionately excessive, and this is itself favorable to the formation of thrombi. In the case of an artery again, the narrowing of the ruptured orifice by contraction of the muscular coat favors the stilling of the hemorrhage, and so does its retraction within its sheath, thus leaving a space in which the clot has room to form. This contrac- tion of the muscular coat is brought about in the first instance hj the stimulus of the agent which caused the rupture, and it will be kept up by the irritation of the blood on the exposed and torn structures. Then the bleeding as it progresses leads to ansemia, and this in two different ways assists in stilling the hemorrhage. It causes weakness of the heart, and so the arterial pressure is reduced and the thrombus is not so liable to be washed awaj. It also produces irritation of the vaso-motor centre in the medulla oblongata, and this leads to contraction of the finer arteries throughout the body. It is clear that in the case of an artery a longitudinal wound will be more diflicult to close than a transverse one, as the contraction of the muscular fibre will only make it gape further. On this account it is customary Avhen bleeding is serious from an artery thus wounded, to cut it right across in order to still the hemorrhage. "We have now to study the further history of the blood which HAS ESCAPED. Blood wWch has escaped by diapedesis is mostly carried off by the lymphatics, but there is no doubt that to some 58 AFFECTIONS OF CIRCULATION AND BLOOD. extent it may also undergo partial transformations such as will be described immediately, and which result in pigmentation. In the case of hemorrhage by rupture the blood is sometimes entirely absorbed, and that with considerable rapidity, especially when it is infiltrated into the tissues, where it occupies the serous and lymphatic spaces, as in ecchymoses. In the case of larger hemorrhages the blood either accumulates in an existing cavity, or by tearing makes a cavity for itself. It may remain for some time as an independent mass, forming a kind of permanent tumor, the hsematoma, which is specially considered below. The blood may remain for some time fluid, but usually it coagulates by and by. After a longer or shorter period of time the blood is disposed of, and we have now to consider the manner of its disposal. It is easy to understand how the fibrine is dealt with, it disintegrates, and is through time absorbed. The red corpuscles undergo moi'e considerable changes, and their history we have to trace. The coloring matter is frequently dissolved out of the red corpuscles, and in solution it is largely absorbed. The solution may stain the intercellular substance of the tissues, and possibly may lead to a more or less permanent pigmentation of them. In true pigmen- tations, however, the coloring matter is in cells, and it is doubtful whether living cells are capable of being simply stained hj a solu- tion of coloring matter. The peculiar bright red color which one sees in the neighborhood of a hemorrhage in the brain, or the various colors seen in the skin after an effusion of blood into it, are due to staining of the tissues with the dissolved coloring matter of the blood, but neither of these is permanent. The coloring matter after being dissolved out of the corpuscles is often, after a time, deposited in the solid form, appearing as crystals of hsematoidin (see Fig. 11), or as granules. Pig. 11. I, ^ Crystals of hEematoidin from an old hemorrhage in the brain. Their color is reddish-brown. X 350. Again, the red blood-corpuscles may be taken into the substance of other cells, and so disposed o£ The effused blood acts as an irritant in the tissues, producing inflammation around, and numbers of leucocytes collect in the neighborhood. These take into their substance red corpuscles, thus becoming blood-corpus- cle-holding cells (see Fig. 13), concerning which much has been HEMOEEHAGE. 69 written. The leucocytes, as shown in the figure, may take up several red corpuscles, and of course they become greatly enlarged. Besides that, the giant-cells which we shall afterwards refer to in connection with inflammation, may take up red corpuscles. These cells pass in part into the lymphatics, and the red corpuscles are thus absorbed. But it appears that to some extent they remain Fm. 12. Pig. 13. Crystals of hsemin prepared artificially by adding glacial acetic acid to a drop of blood, heating and evaporating to dryness. X 350. Cells containing blood-corpuscles from the neighborhood of a hemor- rhage : a, with fresh corpuscles j 6, ■with dark granules from disintegra- tion of red corpuscles. permanently, or else that the red corpuscles are taken up also by the fixed connective-tissue cells, and so a true pigmentation is brought about. In either case the red corpuscles within the cells shrink into reddish-brown irregularly shaped bodies (see Fig. 13, b), which lie in the substance of the cell. Subsequently the pigment may break up and be dissolved out of the cell, 'and so the colora- tion will disappear. In the case of diapedesis, a similar process of pigmentation may occur by the red corpuscles being taken up by cells. It has already been stated that the blood acts as a foreign body, and leads to inflammation around it. This inflammation some- times leads to what is called the organization of the blood-clot. In this case the process is very similar to that already referred to in the organization of the thrombus, and the result is usually the formation of a cicatrix. Sometimes a process in some respects similar to the formation of the cavernous tissue in place of a thrombus occurs, but instead of the meshes being filled with blood they are filled with serous fluid. Thus in the case of a hemor- rhage in the substance of the brain the new-formed connective tissue which replaces the eft'used blood, is unable, from the brittle nature of the brain tissue, to form a cicatrix by its contraction. 60 AFFECTIONS OF CIECULATION AND BLOOD. Instead of that, by its contraction it leaves spaces which are filled with serous fluid, and so we have the apoplectic cyst. An old clot which is not in a position to be readily disposed of in any of the ways described may dry in and finally become im- pregnated with lime salts. It need hardly be said that, when ex- posed to septic influences, a clot is liable — perhaps very liable — to undergo decomposition. Blood which has been eff'used occasionally takes up a somewhat permanent position in the body, and when masses of blood thus remain for a time they may assume the appearance of tumors. Sometimes a clasS' of blood-tumors is distinguished under the name Hematoma, although thej' do not come under the strict definition of tumors. It will be proper here to enumerate the various conditions to which this name is given. The CEPHALHEMATOMA is a condition sometimes met with in the child immediately after birth, and produced during delivery. In the act of delivery the pericranium is separated from the surface of the skull and vessels are ruptured. Blood .collects between the pericranium and the skull, and is apt to remain long there, retain- ing its fluidity for an unusual time. The raised pericranium pro- duces new bone, and at first chiefly at its margins. There is thus a shell of new bone in the shape of a ring covering in the edges of the collection of blood. This produces the peculiar character that when the prominence is handled the impression is as if there were a gap in the skull. The shell of new bone is continuous with the cranium, and as the fingers pass inwards they suddenly dip into the gap, and it feels as if they dipped into the soft brain- substance. In some cates there is also hemorrhage inside the skull. The Othpematoma, or hematoma auriculare or insane ear, is a condition in some respects comparable to the last mentioned. In it the perichondrium is raised from the cartilage of the ear, some- times bringing li|,tle bits of cartilage with it; and blood collects between cartilage and perichondrium. This occurs on the anterior surface of the concha, and the result is that the hollows are filled up and become prominences. It appear to be sometimes produced by violence, such as blows, but only in persons predisposed to it. It is met with almost alone in insane persons, and chiefly those suftering from general paralysis. As the blood is absorbed the ear does not recover, but shrivels up with great consequent deformity. The hematoma of the dura mater is also of most frequent occurrence in insane persons, though by no means confined to them. In persons dying with apoplectic symptoms there is some- times found a flat layer of blood on the internal surface of the dura mater, in some cases an inch or an inch and a half thick. On careful examination there is a thin false membrane on the surface of the clot, and the disease is usually the result of a chronic inflammation of the dura mater, pachymeningitis chronica htemor- rhagica. aSDEMA AND DROPSY. 61 The HEMATOMA OF THE HEART is an interesting form. It some- times happens that large masses of fibrine are deposited on the valves or elsewhere, and these may come to form permanent pro- jections. In one case met with by the author there were immense festoons hanging from the mitral valve and filling the greatly enlarged left ventricle. In some parts there was calcareous infiltration of the hard dry clot, but no proper organization had occurred. The UTERINE HEMATOMA is a polypoid mass of blood, coagula- tion having occurred on a placental surface or retained placenta. It is sometimes called the fibrinous polj'pus. It projects into the cavity of the uterus and may simulate a polypoid myoma. Blood may collect in the peritoneal pouch behind the uterus, forming a kind of retro-l'tekine hematoma. OEDEMA AND DEOPSY. In order to understand these conditions it is necessary to refer to certain points in the normal relations of the lymphatic circu- lation. The connective tissue throughout the body is, as it were, permeated with spaces of various shapes in which the connective- tissue corpuscles lie. These lacunse or serous spaces are lined with endothelium like the blood and lymphatic vessels themselves. The serous spaces are provided (as shown in Fig. 14) with numer- ous anastomosing processes, and they communicate on the one hand with the interior of the bloodvessels, and on the other with the lymphatics. Arnold and others (see Fig. 15) have succeeded in injecting the serous spaces from the bloodvessels, especially when, as in passive hypertemia, the channels of communication between the bloodvessels and spaces have been widened. We are to suppose that a circulation is continually proceeding from the capillary bloodvessels into these spaces, and so into the capillary lymphatics. The serous cavities of the bodj' are to be regarded as large serous spaces. They are also lined with endothelium, and are continiious with the lymphatic capillaries. The serous spaces, therefore, and the serous cavities, are virtually the same in nature, and their pathology is similar. (Edema is overfilling of the serous spaces with fluid, dropsy is overfilling of the serous cavities, and so the two conditions are virtually identical. Anything which causes an excess of fluid in these spaces or cavities will produce oedema or dropsy, and the first condition which suggests itself is obstruction of the lymphatics. The force which carries on the lymphatic circulation is largely the blood- pressure propagated from the capillaries, and it may be expected that OBSTRUCTION TO A LYMPHATIC STEM would produce accumula- tion of fluid in the spaces. But it is to be remembered that the serous spaces are in as close relation to the blood capillaries as they are to the lymph capillaries, and any obstruction to the lymphatics will probably have the effect of causing the transuded 62 AFFECTIONS OF CIECULATION AND BLOOD. fluid to return to the blood capillaries. The fluid flows from the bloodvessels because the pressure is higher in them than in the lymphatics, but an obstruction in the lymphatics will tend to equalize the pressure, and so prevent further transudation. At any rate, experiment has shown that the whole lymphatics of a riQ. 14. Serous spaces (co) and lymphatic capillaries (dd) in pleural surface of diaphragm in prep- aration treated with nitrate of silver. The connection of the branched spaces with the commencing lymphatic vessels is shown. (Recklinghausen.) limb may be ligatured, or, what is equal to that, the entire lymphatic glands excised without producing oedema. The blood- vessels take up the functions till new lymphatic channels are formed. Even when the thoracic duct is obstructed there is not necessarily any oedema or dropsy. It is true that obstruction of the thoracic duct sometimes leads to distention, especially of the chyle vessels, and even the bursting of them so as to lead to a chylous ascites. It may even lead to an ordinary ascites. So far as human pathology is concerned, however, it must be exceedingly rare to And obstruction of the thoracic duct apart from other con- ditions which more directly lead to dropsy. We may say at least (EDEMA AND DROPSY. 63 that, with this possible exception, obstruction of lymphatics does not of itself lead to oedema, or dropsy, although it is clear that it Fig. 15. Capillary bloodvessels, serous spaces, and capillary lymphatics of the frog's swimming web, filled with (blue) injection material thrown into the bloodvessels. (The black branched bodies are the normal pigment cells.) u, a, Capillary bloodvessels filled with injection material, d, b, Lymphatic capillaries also injected, but less full than the blood capillaries. c, c, Serous spaces injected from the bloodvessels. The injection was made after passive hypersemia had been produced by ligaturing the vein. (Arnold.) X 250. may aajgravate an oedema whose cause is to be found in some other condition. Looking to these facts, it may be said that the conditions which lead to oedema and dropsy do so by causing increased traksuda- TiON FROM THE CAPILLARIES iuto the serous spaces. A considerable increase may be compensated by the lymphatics and the blood- vessels carrying off an additional quantity of iiuid, but when the limits of this are passed, the fluid will accumulate in the spaces and distend them, thus giving rise to oedema or dropsy. The most obvious cause of increased transudation is venous HYPEREMIA. Here there is increased pressure in the capillaries and veins, and a greatly increased transudation. From what has gone before, it will appear probable that here the increase of pressure is not the only element in the case. The circumstances of the capillary wall are altered in such a way that we may pre- sume that it is rendered abnormally permeable. This view appears more probable when we And that active hypersemia does not, if uncomplicated, produce oedema. In arterial hypersemia, it is true, the blood-pressure is not so much raised in the capillaries as it is in the venous form; still it is raised, but the transudation is never so much increased as to produce oedema, unless there is an inflam- matory element in the case. In passive hypersemia the fluid exuded will be a watery serum, and as there is diapedesis it will 64 AFFECTIONS OF CIRCULATION AND BLOOD. contain red corpuscles in considerable numbers. The red corpus- cles will be taken up by the leucocytes as already described, and carried to the lymphatic ' glands, where they will disintegrate. It should be added that it requires considerable increase of pressure in the capillaries to produce an cedema hj passive hypersemia when acting alone. It has even been stated that a simple passive hyper- emia, apart from vaso-motor paralysis (producing also active hypersemia), does not lead to oedema. It has been shown that if the iliac vein of a dog be ligatured, there is no oedema till the sciatic nerve is cut. The explanation of this, however, may be that this vein has such free anastomoses that its ligature does not raise the blood-pressure sufUciently to induce oedema, whereas a coincident vaso-motor paralysis producing dilatation of the arteries raises the blood-pressure sufficiently. Experiment proves that if a sufficient number of veins be obstructed oedema will result with- out vaso-motor paralysis. Sotnitchewsky, by introducing plaster of Paris into a peripheral vein of the leg of a dog while the thigh was constricted by an elastic band, succeeded in obstructing a number of veins by the gypsum hardening in them. Iti this case oedema followed without the induction of vaso-motor paralysis. In passive hypersemia from thrombosis of veins there are usually many veins obstructed before oedema occurs. In the case of passive hyperemia from heart-disease, it may well be supposed that the prolonged venous engorgement will produce a more than usual deterioration of the capillary wall, besides a depreciation of the blood itself We now come to a question which is not so easy of answer as that we have just been discussing. It has been customary to say that a watery state of the blood, a uydr^mia, may induce cedema, and the case of the so-called cachectic oedemas is cited. This, however, has been rendered doubtful by a series of experiments by Cohnheim and his assistants. A simple hydrsemia, induced in a dog or other animal by repeated blood-lettings and the replace- ment of the blood withdrawn by a solution of common salt, does not lead to oedema. On the other hand, it may well happen that a prolonged hydrseraia as opposed to this more acute form, such as we meet with in cases of chronic emaciating disease, may so depre- ciate the capillary wall as to give rise to oedema under compara- tively trivial circumstances. In such persons the heart is weak, and the blood has a tendency to stagnate in depending parts, as has already been described, and this comparatively slight increase in pressure may induce the occurrence of oedema. Next we have the frequent (edema of the skin in Bright's DISEASE to account for. There is undoubtedly here in many cases a hydr^emia, induced in two different ways. There is the loss of albumen, which renders the blood directly more watery. But in many cases there is also an abnormal retention of the water in the blood. In acute Bright's disease, especially, there is great reduc- tion in the amount of urine secreted, and this implies an increase in the water of the blood. It is in these cases, it will be observed, OEDEMA AND DROPSY. 65 that the occurrence of oedema is most frequent. These facts naturally suggest that if the oedema in Bright's disease is not due simply to the hydrsemia, it may be due to this in conjunction with the increased bulk of the blood, to a hydk^mic plethora. This view has obtained much support. It has been supposed that, the entire bulk of the blood being increased, there will be increased pressure in the capillaries and increased transudation from the watery blood. But thei-e are some objections to this view. We have already seen that plethora, even when suddenly induced, does not raise the blood-pressure. There is a form of Bright's disease in which the arterial tension is raised, and the increased tension is related to hypertrophy of the left ventricle of the heart. But it is just in this form of Bright's disease (the cirrhotic form) that oedema is least usual, and a case may proceed to a fatal issue with- out the occurrence of any oedema. Then there are cases of abso- lute suppression of urine, as in hysterical females, etc., in which we must presume an exaggerated hydrsemic plethora, but without a trace of oedema. In some experiments by Cohnheim and Lichtheim, a hydrsemic plethora was induced by injecting a solution of common salt into the vessels of animals. Enormous quantities could be injected without seriously compromising the animal. We have seen that when blood is transfused in the dog, the limit consistent with the survival of the animal is one and a half times the bulk of the blood, but more salt solution than three times the bulk of the blood could be injected without killing the animal. From the pre- vious reference to transfusion, it will be understood that these injections did. not produce any permanent rise in the blood- pressure. The most direct result was a great acceleration in the speed of the blood-current, presumably from the diminished fric- tion of the watery blood. There was also a greatly increased transudation and consequent increased flow of lymph. But this was remarkably localized. There was a greatly increased flow of lymph in the thoracic duct, showing that in the viscera the transu- dation was increased; while the lymphatics of the limbs showed no increase, indicating that in the skin and muscles the transuda- tion was not increased. There was also greatly increased secre- tion from the salivary glands, stomach and intestine, liver, lachrymal glands, and kidneys. In these organs an csdema was developed, that is to say, in the mucous membrane and submucous tissue of the stomach and intestines, in the lymphatic glands of the mesentery, in the pancreas, kidneys, gall-bladder, salivary glands ; there was also ascites, but no oedema of the skin. The explanation suggested for this localization of the increased transu- dation and the oedema is, that these organs are all normally con- cerned in the removal of water from the blood, and that probably their bloodvessels are umisually permeable to water. The experi- ments produce a great increase in the water of the blood, and the vessels give ready passage to it. It will be observed that in these experiments the oedema was 66 AFFECTIONS OF CIRCULATION AND BLOOD. present in parts where it is absent in Bright's disease, and was not present at all in the skin. So that the oedema of Bright's disease cannot be ascribed altogether to the hydrfemic plethora, however much that may predispose to it. To explain the csdema of Bright's disease, it seems necessary to suppose some alteration in the vessels of the skin rendei'ing them unduly permeable. There are many facts indicating a relation between the skin and the kidneys in Bright's disease, and it is very possible that the morbid agent which affects the kidney may also affect the skin. In scarlatina we have during the fever an inflammatory hyperaemia of the skin, and it is natural to suppose that when subsequently a kidney affec- tion induces a hydrsemic plethora, the oedema will manifest itself in the previously damaged skin. In the experiments above re- ferred to, it was found that although the normal skin did not become cedematous, yet when it had been previously inflamed, as by pencilling with iodine solution, or by exposing to a strong sun, then oedema shows itself It may hence be inferred that, although hydrasmic plethora is not by itself a cause of oedema of the skin, it is a strong predisposing element. We shall find in studying inflammation that the alteration in the vessels produced by this condition induces oedema, so that inflam- matory oedemas are of frequent occurrence. LEUKEMIA. By this name is meant a condition in which the white blood- corpuscles are greatly increased, the name meaning literally white blood. This was the name applied by Virchow. Another name — Leucocythsemia — applied by Bennett, although literally more cor- rect, is cumbersome, and is now generally disused. The condition of the blood gives its name to the disease, and this will first engage our attention. The normal proportion of white corpuscles to red in the blood is stated as about one in three hundred to one in four hundred and fifty, but it may vary within normal limits. There is after hemorrhage, as we have seen, a slight increase in the proportion of white corpuscles, a leucocytosis, but it is of no special signifi- cance. In leukffimia the relative proportion of white to red cor- puscles is greatly altered. A case is not a very severe one in which the corpuscles are as one to ten, and they may be as one to two or even equal. This alteration in the proportion of white and red is not the only alteration in the blood. The white corpuscles are more varied in size than normal, some larger and some smaller, and they are sometimes more distinctly nucleated. Then the red corpuscles are not only proportionately few in number, but they are absolutely reduced, and that to a very high degree. Occasion- ally nucleated red corpuscles have been found in the blood, these corpuscles being of larger size than the normal red corpuscles. The specific gravity of the blood is considerably reduced ; it may fall from 1065, which is the average normal, to 1040 or 1035. The LEUK^JIIA. 67 Tig. 16. ^ ■^ ^^^ blood has thus the character of anemia along with a great increase of the white blood-corpuscles. In leukfemic blood, after death, there are found small, colorless, glancing crystals of an octahedral shape, which are usually called from their discoverer Charcot's crystals (see Fig. 16). There are also certain other abnormal chemical constituents, chiefly glutine and hypoxanthine. With regard to the probable explanation of this peculiar condi- tion of the blood, it must always be remembered that there is a very great diminution in the red corpuscles as well as a great increase in the white. There must be either a greatly increased new formation of white corpuscles and destruction of red ones, or a serious interference Avith the conversion of the white into the red cor- puscles. This latter is the view originally taken by Virchow, and is the more probable. There maj' be an increased formation of white corpuscles, but the diminution in the number of the red is probably due to a re- duced conversion of white into red. The nucleated red corpuscles have been regarded by some as transition-forms, their presence indicating a delay in the conversion. The blood in persons affected with this dis- ease is unduly pale, but it has not a watery appearance. It is even a thicker fluid than usual and distinctly naore opaque, resembling a mixture of pus and blood. The alteration in the constitution of the blood is associated with changes in certain organs which have generally been regarded as concerned in the preparation of the blood, namely, the spleen, the lymphatic glands, and the medulla of bone. In different cases of leuksemia these structures are vari- ously affected. The medulla of bone seems to be affected in all or nearly all cases, the spleen with the medulla in a considerable number, the lymphatic glands with the medulla in a smaller num- ber, and all three in many cases. The condition of the spleen in leukaemia will first concern us. In all stages of the disease it is enlarged. The enlargement in the earliest period appears to be due to an active congestion, and is accordingly of rapid development. Eindfleisch mentions a case which he saw at Virchow's demonstrations in 'which the enlarge- ment had been so rapid as to cause a rupture of the capsule of the spleen. This enlargement is merely from overfilling of the vessels, but it is succeeded by, or develops into, a solid enlargement. The Malpighian bodies of the spleen have the structure of lymphatic follicles, and it is raaiidy by the enlargement of these that the permanent solid enlargement occurs, a great increase, therefore, of lymphoid tissue. But the new formation often occurs in the pulp as well as in the Malpighian follicles. The spleen thus be- Charcot's crystals from the blood in leukaemia after death. In h, the crystals are partly inside the white corpuscles, (Zenker.) X 500. 68 AFFECTIONS OF CIRCULATION AND BLOOD. Pig. 17. comes converted into a hard, dense, bulky organ, sometimes like a piece of wood. It is also paler than normal, and we can often see the enlarged Malpighian bodies as whiter areas on the cut surface. In addition, there are frequently hemorrhages in the spleen, and these may take the form of the regular wedge-shaped infarction. In the MEDULLA OF BONE the changes are very similar. There is a great neAV formation of round-cell tissue which occurs at the ex- pense of the adipose tissue and also of the bone. This new tissue consists mainly of cells as large as white blood-corpuscles, and has the structure of lymphatic tissue, showing the reticulum and round cells as in Fig. 17. Sometimes there are larger cells than these, and there may be also nucleated red corpuscles. There is thus a great new formation in the medulla and that mainly of lymphatic tissue. As the medulla of bone, especially the red medulla of spongy bone, normally contains lym- phatic tissue, the change in leukaemia may be regarded as a hypertrophy of this, and the amount of hypertrophy is sometimes very great. Thus, the whole yellow mar- row of the hollow shaft of the femur may be replaced by lymphatic tissue. The cavity of the shaft may also be widened at the expense of the bone, and many smaller trabeculse here and in the spongy bone may be destroyed. In this respect, as well as in intimate structure, the leuksemic bone-marrow difi'ers from the red marrow of pernicious ansemia, as the latter does not cause a proper atrophy of the bony tissue. The occurrence of hemorrhages or even infarctions has been observed in the' bone-marrow just as in the spleen. The appearance of the medulla is, of course, greatly altered. It has generally a grayish-red color without any of the normal greasy appearance, but it may be pale so as to look Jike solidified pus, or dark i^ed, these differences depending on the de- gree of the new formation and the state of fulness of the vessels. It has, however, the character of a tolerably solid tissue, not a semi-fluid material as in antemias. These changes may occur in all the bones in the body, and in both spongy and hollow bones, the affection being, however, variously distributed. The lesion in the lymphatic glands consists in an enlargement of them. This begins mostly in a particular set of glands usually situated externally, as in the axilla, groin, neck, etc., and spreads to other sets, generally first to those nearest. The enlarged glands may be three, five, or even ten times their normal size, but^'there is no tendency to any degeneration of their tissue. The KELATiON OF THESE ORGANIC CHANGES in the Spleen, bone- marrow, and lymphatic glands to the disease in its essence is ex- Medulla of bone in leukaemia, from the cavity of the shaft of the femur. Adenoid reticulum and lymphoid cells are shown X 350. LEUKEMIA. 69 eeedingly obscure. An attempt has been made to associate the disease in its origin with the bone-marrow, but even this is by no means certain. There seems little reason to doubt, however, that the bone-marrow along with the lymphatic glands and spleen, and perhaps in a more important manner than they, is concerned in the formation of the blood-corpuscles. The discovery of nucleated colored cells in the normal red marrow of spongy bone seems to show that the red corpuscles are either formed or undergo impor- tant changes here. Besides these organs others are frequently attacked, but the lesions in them are of later manifestation, by no means uniformly present, and undoubtedly secondary. The liver is nearly always enlarged, and this enlargement may be due simply to parenchy- matous changes in the hepatic cells, but is often associated with a Fig. 18. Leukffimic formations in the liver. X '»• distinct new formation in the liver. This is in the form of minute collections of round cells occurring in myriads throughout the organ, as shown in Fig. 18. These are, at first sight, not unlike miliary tubercles, but they have no giant-cells and do not present 70 AFFECTIONS OF CIECULATION AND BLOOD. any tendency to degeneration, while they are much less definite in size and shape. Sometimes, instead of definite aggregations, there is an extensive infiltration of the connective-tissue stroma of the liver with round cells. The exact nature of these lesions is doubtful. They may be simple aggregations of white blood-corpuscles, but they have usually too regular a form for this, and they have been regarded as small lymphatic formations. The kidney is affected not infrequently, and here the appearance to the naked eye very often is as if the organ were greatly enlarged by the presence of large pale tumors in the cortical substance. On microscopic examination, the lesion is seen to consist in an enormous infiltration of the stroma of the kidney with round cells, the proper secreting tissue remaining, but, of course, greatly pressed on. This infiltration occurs in definite areas, as if some agent had addressed itself to certain defined portions of the organ. The CLOSKD FOLLICLES OF THE INTESTINES, both the Solitary ones aud those aggregated in Peyer's patches, may be enlarged, and as they are of lymphatic structure, their enlargement is a simple hyperplasia. This is not of frequent occurrence, and still less frequent is the formation of leuksemic tuinors in the skin, these tumors consisting of infiltrations of round cells. The connective tissue in other regions may also be infiltrated. The author met with a case in which the connective tissue of the mediastinum was enormously infiltrated, so that the tissue formed a bulky tumor. The infiltration extended to the pericardium much in the fashion of a lympho-sareoma. It is proper here to mention that there is a disease called variously Hodgkin's disease and PSEUDO-LBUKiEMiA, in which the organic lesions appear to bo identical with those of leukaemia, but without the increase of white blood-corpuscles, the blood being simply auEemic. There may be great enlargement of the spleen and of the lymphatic glands, and the characters of the enlarge- ment may be essentially like those mentioned above. MELAK^MIA. By this name is meant, literall}', black blood. It is used to designate a condition in which pigment occurs abnormally in the blood and is deposited in the tissues. The pigment is in the form of solid granules, and, although black in color, it is derived from the blood pigment, and contains iron. It is met with in cases of malarial fever, but not in every case, as a rule only in the more severe forms. The view usually entertained is that during the acute paroxysm of an ague, blood-corpuscles are destroyed in the spleen, and their pigment is set free in the granular form. Lately, Arnstein (Virchow's Archiv, vol. Ixi. p. 494) has brought forward the view that the destruction of blood-corpuscles occurs not in the spleen, but in the blood generally. "Whether the spleen be the seat of its formation or not, it is certainly stored up there for MELAX^MIA. 71 years, and may pass into the blood by degrees, although it is more abundant immediately after the acute paroxysm. When the pigment gets into the blood it is rapidly taken up by the white blood-corpuscles, so that these appear in the blood as pigmented cells. These pigmented cells are often larger than the white corpuscles, being enlarged by their abnormal contents. It will thus be seen that very little free pigment will be present in the blood except immediately after the acute paroxysm, the white corpuscles picking up the solid granules just as they do when a solid pigment, such as vermilion, is artificially introduced into the blood of an animal (see Fig. 19). The white corpuscles containing Fia. 19. tV%-A > .' "White blood-corpuscles of the frog, containing granules of vermilion, and showing amoeboid movement. (After Klein.) the pigment accumulate in certain organs, especially the spleen, liver, and bone-marrow! In the spleen and bone-marrow the pigmented cells appear' to leave the capillaries readily, and pass Pig. 20. A lobule of the liver in melanajmia. The black pigment-granules are seen between the hepatic cells, being really in the capillaries. X ^5. into the tissues, producing an actual pigmentation of them, but in the liver they linger longer in the capillaries, which may be seen with many such corpuscles in them (see Fig. 18), although here also the latter may pass out into the surrounding tissue. In very 72 AFFECTIONS OF CIRCULATION AJSD BLOOD. severe cases, other organs and tissues may be pigmented in this way. The brain is very often pigmented, especially in cases where there has been much cerebral excitement. This will be in very acute cases, but it is doubtful whether the pigment has much to do with the cerebral symptoms, which may be merely a consequence of the acute attack. The kidneys are sometimes the seat of it as well as other tissues, such as pancreas, intestine, etc. This abnormal pigmentation of course produces changes in the color of the organs affected. The spleen is slaty-gray or almost black, the liver is steel-gray or blackish, the gray substance of the brain is of a dark chocolate or graphite color, and the kidneys present grayish spots. This is a condition characterized by nervous symptoms, vomiting, sleepiness, headache, convulsions, coma, and it occurs in cases of kidney disease in which the secretion of urine is diminished. The result of the defect in the secretion of urine is accumulation in the blood of the constituents of the ueinb, and it was natural to infer that these constituents, acting as poisons, produced the symptoms; hence the name uraemia. In animals, symptoms essentially similar may be produced by tying both ureters, and here also doubtless there is retention of urinary constituents. The urea is readily detected in the fluids and tissues in such animals, and it has been frequently detected clinically in cases of ui'Eemia. And yet it is very difficult to be sure that the symptoms are due to poisoning by the urinary constituents. For one thing, the injection of urea, and even of filtered urine, into living animals does not produce ursemia, the only effect being an excessive secre- tion of urine. These facts have led to theories to account for the ureemic symptoms apart from the presence of urea in the blood. Frerichs' theory at one time received great acceptance. He said that the symptoms were due, not to the urea or other urinary constituents, but to the products of their decomposition, anS mainly carbonate of ammonia. It was asserted that carbonate of ammonia was to be found in the blood of ursemic patients, and that it was often to be detected in their breath. But there is a mistake here. More correct chemical investigation shows that there is no excess of carbonate of ammonia in the blood. Car- bonate of ammonia is to be found abundantly in the intestines, where it is the result of putrid decomposition. Moreover, the injection of carbonate of ammonia into animals does not produce ursemic symptoms, but symptoms of a diflferent kind. Again Traube started a very ingenious theory, according to which the urasmic symptoms are due to osdema of the brain and its membranes, and consequent anemia of that organ. It is known that oedemas occur sometimes very suddenly in Brio-ht's disease, and it Avas supposed that a sudden cedema of the brain DIABETES MELLITUS. 73 would produce such sj'mptoms, tlie varying locality of the cedema determining the variations in the symptoms. But this theory is also scarcely tenable, because cedema of the brain is by no means constant in uraemia. It is rather probable that the original view is fundamentally the correct one. So long as there is a free outlet, the blood may contain a large quantity of urinary constituents, and so when urine is injected into the blood of animals it passes rapidly through the system and does little harm. But if the ureters be first liga- tured and then the urine injected, the ursemic symptoms will rapidly manifest themselves. It will be understood that the urea is not the only constituent concerned, but that the other nitro- genous substances and salts probably take part in the production of the entire set of symptoms. It has already been said that in urfemia urea is present in excess in the blood and fluids of the body, and has frequently been detected during life, and it is in cases where the secretion of urine is diminished or suppressed that these symptoms occur. The secretion may be diminished in various ways — by obstruction in the outflow, by disease of the secreting tissue, by defect in the water of the blood so that the urinary constituents are not duly carried off", or even, as has been supposed in the case of eclampsia, by spasm of the renal arteries preventing the due passage of blood through the kidneys. In all these cases the one common element is a defective separation of the urinary constituents, and their coii- sequent accumulation in the blood, and the presumption is that these constituents have a poisonous effect, although it may be impossible to say whether one or more of them is specially dele- terious. DIABETES MELLITUS. The pathology of diabetes is a subject of considerable difficulty, and it may be well at the outset to set forth the problem which requires solution. The BLOOD AND URINE CONTAIN NORMALLY A SMALL QUANTITY OF GRAPE SUGAR, but in diabetes this undergoes an enormous increase. In the normal condition the sugar is at a constant minimum, un- affected by the amount or kind of food taken. In diabetes there is commonly a very obvious relation between the food taken and the sugar. There are some diabetics who cease to excrete any excess of sugar so long as they abstain from starch or sugar, but whenever they take any such food it is mostly converted into grape sugar and so excreted in the urine. On the other hand, there are diabetics who excrete an excess of sugar whatever the kind of food they take, and though the sugar may be diminished by the use of a mainly nitrogenous diet, yet it cannot be thus made to disappear. In that case it is obvious that sugar is formed not only from carbo-hydrates, but also from the albuminous principles of the food. According to Traube, diabetes is divided into a 74 AFFECTIONS OF CIECULATION" AND BLOOD. slighter and a more severe form according as the sugar is formed from the carbo-hydrates alone, or from nitrogenous principles as well, and it is probable that these forms represent an earlier and a later stage in the disease. Donldn, in view of the relation of the sugar production to the food, distinguishes three stages; first, that in which only the starch or sugar of the food furnishes the grape sugar; second, that in which fats as well as these are converted; and third, that in which albuminous foods, as well as starchy and oily, undergo conversion into grape sugar. It is obvious that in this latter stage there is a great consumption OF ALBUMEN, and in the process of formation of the sugar urea is formed as a waste product in the chemical transformation. We find, therefore, that the urea is also greatly increased in the urine, amounting sometimes to two or three times the normal quantity in the twenty-four hours. In this stage of the disease there is no doubt that the fatty and albuminous constituents of the tissues are also used for the formation of sugar, and that the albuminous principles of the tissues, like the albumen of the food, furnish sugar and urea Avhich appear in the urine. The problem which we have to face then is, that in diabetes there is, for some reason or other, an excessive demand for sugar in the organism. The greed for sugar seems to acquire intensity as the disease advances, so that while at first it is only the carbo-hydrates -which fall a victim to it, there is ultimately a consumption of the nitrogenous foods and even of the nitrogenous tissues. We have to inquire what may be the meaning of this immense demand for sugar. Looking to the manner in which the processes of the body are arranged, we may take it for granted that there is some need to be supplied or else such an excess of material would not be furnishecl. Sugar is a erystallizable substance, and wherever it is formed it will readily be dissolved by the juices and find its way into the blood. Its occurrence in the blood and its excretion by the urine are therefore simply a result of the ready solubility and difliusibility of the substance. Its presence in these fluids throws no direct light on its place of origin. It is natural to look to the liver as the source of the sugar. It is well known that the liver is the place of formation of a substance nearly allied to sugar, namely glycogen. This substance, as its name implies, has a great tendency to become converted into sugar. It is true that in the living body the liver, apparently, contains glycogen and not sugar. If the liver of an animal be cut out immediately after death and without delay placed in boiling water after being cut into small pieces, then it will be chiefly glycogen that will be found, and any sugar that exists has probably formed after death by the transformation of the glycogen. It is diflicult indeed to avoid the occurrence of traces of sugar in this experi- ment, and if the removal of the liver be delayed a large amount of sugar will be found. These facts show that glycogen is always just ready to be converted into sugar; its conversion is, as it were. DIABETES MELLITUS. 75 every moment imminent. During life this conversion does not take place to any considerable extent, and it is even doubtful whether the small amount of sugar existing normally in the body is due to a conversion of the glycogen in the liver, a comparison of the blood in the hepatic vein with that in the portal giving doubtful results. We have to consider, however, whether a pathological cojjver- SION OF THE GLYCOGEN INTO SUGAR may not occur in the liver, and in this regard the observations of Bock and Hoffmann are of great interest. These observers succeeded in the production of an akti- FiciAL DIABETES melUtus by injecting into the blood of rabbits large quantities of a watery solution of common salt. The animals, soon after the injection was made, began to secrete a large quantity of urine, and this urine soon became saccharine. If the injection of salt solution was persisted in, the sugar by and by diminished in the urine and ultimately disappeared. The question now was as to the source of the sugar, and the condition of the liver was examined with this in view. It became abundantly clear that the sugar in the urine came from the liver and was caused by the conversion of the glycogen into sugar. In all cases where the animal was killed after the diabetes had passed off, the liver was found free both of the glycogen which exists normally and of sugar. If, on the other hand, the animal was killed while the mellituria existed, then glycogen and sugar were both present in the liver. The inference from these observations is perfectly obvious. The abnormal condition of the blood causes the transformation of the liver glycogen into sugar, and the latter being a crystalloid and readily diffusible, it is at once washed out of the hepatic cells and passes into the circulation and on into the urine. The diabetes ceases because all the glycogen in the liver has undergone conversion into sugar and the source of supply is exhausted, the liver in these cases being found free of both gly- cogen and sugar. We may say, therefore, that a glycosuria may be produced by the conversion of the glycogen within the liver into sugar. It may be said that the diabetes thus produced is temporary and not comparable with the permanent disease in the human subject. Let us suppose, however, that diabetes is due to the conversion of the liver glycogen into sugar, then the problem with which we started will undergo a considerable modification. We sa'w that there is an excessive production of sugar, but in the view now brought forward this will resolve itself into an excessive produc- tion of glycogen which undergoes conversion into sugar. The problem therefore presents itself — Is there anything to account FOR the excessive FORMATION OP GLYCOGEN? It is to be presumed that glycogen has an important function in the animal body. Whether it be used in the production of muscular force, as many suppose, or otherwise, it seems clear that such an organ as the liver Avould not be engaged in its formation unless it had an important part to play. It is to be presumed then 76 AFFECTIONS OF CIRCULATION AND BLOOD. that glycogen supplies some need in the organism, and that it is formed in the liver for that purpose. But if, as soon as it is formed in the liver, it is transformed into sugar, then the need in the organism will not be supplied. The sugar being a crystalloid will be washed out, and very little glycogen will get into the blood. In such circumstances the or- ganism will have, as it were, a hunger for glycogen, the liver will be stimulated to supply it, and will produce more glycogen. As soon as it is formed, however, the glycogen will be transformed into sugar, and the excessive demand for glycogen will only result in an excessive supply of sugar. In this case the liver will be stimulated to an ever-increasing formation of glycogen which will immediately pass into sugar. We can understand how in the earlier stages all foods which are near to glycogen in their chemical composition will be at once utilized, and how as the disease goes on and the demand becomes more urgent, the other kinds of foods and even the tissues of the body will be used. So long, therefore, as the hepatic cells retain their activity we may presume that they will react to the hunger for glycogen, and the production of sugar will be the result. If the hepatic cells be destroyed or weakened, the probability is that the diabetes will diminish, the disease requiring that the hepatic cells retain their energy. It would appear from the above that diabetes is explainable on the supposition that the glycogen undergoes abnormally a trans- formation into sugar, and that this occurs in the liver itself. We have now to inquire whether any indication exists as to the cause OF THIS TRANSFORMATION OF THE GLYCOGEN. In the experiments of Bock and Hoffmann already alluded to it appears that a particular abnormal condition of the blood is capable of producing this transformation. An enormous dilution of the blood with salt solution seems capable of inducing the liver gly- cogen to pass into sugar. A temporary diabetes has been produced in a variety of other ways, and all of them are explicable on the ground of an abnormal condition of the circulation of the liver. The inhalation of nitrite of amyl induces a temporary glycosuria. "We know that this agent produces a general vaso-motor paralysis, and a general dilatation of the systemic arteries. With the other arteries those of the abdomen will dilate, and the blood passing through the capillaries at an increased rate will reach the portal vein at a higher pressure than normal. The circulation in the liver will thei-efore be accelerated and the blood will be less venous in character, having passed rapidly through the capillaries of the intestines and other organs. The celebrated diabetic puncture of Bernard is made in the medulla oblongata, and we know that in this part of the nervous system are situated the principal vaso-motor centres of the body. There is, therefore, here also a paralysis of the arteries just as after the inhalation of nitrite of amyl. Injuries to the brain, spinal DIABETES MELLITUS. 77 cord, and sympatlietic sometimes produce a temporary glycosuria, and they also may cause vaso-motor paralysis. The observations of Pavy are important in this regard. He pro- duced glycosuria by the injection of defihrinated arterial blood into the portal vein, and here again there is an excessive supply of blood to the liver. But then Pavy also produced glycosuria bj^ ligaturing the portal vein, and so cutting off the blood-supply ex- cept through the hepatic artery, and at first this result seems a very contradictory one. The effect of that experiment would be to cause the liver to be supplied with arterial blood alone, and we may presume that the hepatic artery would dilate and so allow of an additional flow of blood. According to the researches of Cohnheim and Litten (Virchow's Archiv, vol. Ixvii.) the blood of the hepatic artery, after supplying the connective tissue, gall-ducts, and walls of the large bloodvessels, passes into the inter-lobular veins and on into the proper hepatic capillaries, so that the blood of the hepatic artery is finally distributed with that of the portal vein. When the portal vein is closed, the circulation in the liver will be kept up, but only by the blood of the hepatic artery. From these observations Pavy concluded that the cause of the glycosuria when the portal vein was ligatured was the circulation of arterial blood in the liver, and he proceeded to determine whether it was possible in animals to produce diabetes by super- saturating the whole blood with oxj^gen, so that the blood in the portal vein would be virtually arterial. He effected this in various ways : by causing the animals to inhale oxygen ; by using artificial respiration till the fact that the animals ceased to make any spon- taneous respiratory movements showed a deficiency of carbonic acid; by causing the animals to inhale cai'bonic oxide. In all these ways glycosuria was produced. It would appear, therefore, that when diabetes is artificially produced in animals, the one essential condition is that the liver should be supplied with unduly oxygenated blood, such blood causing the glycogen to be trans- formed into sugar in the liver itself. We have now to consider the question whether this view will explain the occurrence of diabetes in the human subject. Is there any evidence of such an alteration of the circulation in tue liver IN CASES OF DIABETES? It is to be noted here that in order to an active hypersemia of the portal circulation there must be an active hypersemia in the parts to which the coeliac and mesenteric arteries are distributed. The circulation in the portal vein depends en- tirely on that in these vessels, and unless the blood passes in greater abundance and more rapidly than it does normally through the vessels of the abdominal viscera from which the portal blood comes, then it cannot pass more quickly through the portal vein. It is not, therefore, as is sometimes stated, a question directly of vaso-motor paralysis of the liver. Moreover, if diabetes depends on the blood in the portal vein being unduly oxygenated, then the only possible explanation of this will be that the ,blood passes so 78 AFFECTIONS OF CIRCULATION" AND BLOOD. quickly through the capillaries of the alimentary canal and other organs that it is imperfectly deoxygenated. The question to he answered then is, whether thei-e is any evidence of diabetes being due to a vaso-motor paralysis inducing an active hypersemia of all these organs. Such a vaso-motor paralysis might arise by disease of the central nervous system, or of the local centres in the abdomen, mainly the coeliac plexus. In regard to the latter, some cases have been recorded (by Frerichs,"Klebs, and Recklinghausen) in which dia- betes has coexisted with atrophy, formation of calculi, or cancer of the pancreas. In cases observed by Klebs there was, along with the atrophy of the pancreas, a very marked change in the coeliac plexus, consisting of a great destruction of ganglion cells. It seems very probable, considering the nearness of the pancreas to the coeliac plexus, that a cancer or the changes resulting from the formation of calculi in the ducts of the gland, might extend to the coeliac plexus, and Klebs accounts for the diabetes in his cases on the view that there was vaso-motor paralysis produced by the destruction of the ganglion cells of this plexus. In one of his cases, indeed, there was observed after death an extraordinary dilatation of the hepatic and splenic arteries and the gastric branches of the coeliac axis, the last-named branch attaining the size of a goose-quill and presenting a highly convoluted course. These facts seem to confirm the view that in man diabetes may be produced by paralysis of the arteries in the domain of the coeliac plexus. There have been also cases in which diabetes seemed to follow injury to the spinal cord or medulla oblongata, but these have been cases of teniporary glycosuria comparable to that following Bernard's diabetic puncture. On the other hand, there have been a few instances of softening of the brain and intra-cranial tumors in cases of diabetes, but these have been too rare to be regarded as of miich importance in the pathology of diabetes. For the most part there is little or no alteration visible to the naked eye in the central nervous system. Eecently Dickinson has described minute changes in the central nervous system, consisting mainlj in excavations around the arteries, produced apparently by exudation from these vessels with disintegration of the brain substance around. In very recent cases there was even accumulation of leucocytes or hemorrhage arouud the arteries, but in the older cases a cribriform appearance, the arteries being surrounded by widened canals. These lesions are scattered through the brain, the largest and most striking being present in the corpora striata, optic thalami, pons, medulla oblongata, and cerebellum. They are less marked in the cord, where in addition there is usually great dilatation of the central canal. The white matter of the cerebral convolutions also fre- quently p)resents similar changes. These lesions are held by Dickinson to be primary and directly related to the cause of the disease. If this view be correct, then DIABETES MELLITUS. 79 we should have lesions of the central nervous system leading to diabetes, and doing so probably by vaso-motor paralysis of the arteries of the abdominal viscera. This view is open to the objection, however, that these lesions in the nervous system may possibly be secondary, due to a dilatation of the arteries, not to exudation from them, especially as we know that exudation occui'S rather from capillaries and veins than artei'ies. Turning to the abdominal organs themselves, there have been in many cases indications of congestion observed. We have already referred to the enlargement of the arteries in one of the cases described by Klebs. The liver itself is generally described as congested, and in a few cases there has been thrombosis of the portal vein. The characteristic red tongue of advanced diabetes has been cited by Pavy as evidence of a progressive congestion of the alimentary canal. The congestion at first is confined to the ab- dominal organs, but in the later periods extends to the mouth, the vaso-motor paralysis being progressive. All the facts may be held as indicating that diabetes depends on the liver being supplied with blood of an abnormal character and at an accelerated rate of speed. The congestion of the liver de- pends on abnormal nervous arrangements, and these may be local, affecting the coeliac plexus, or possibly situated in the central nervous s^ystem. The observations of Dickinson would seem to point in the latter direction, but they stand in need of confirmation, and besides, the lesions may possibly be the efl:ect rather than the cause of the affection. In regard to the other changes in diabetes mellitus, little has to be said. The tissues appear to be peculiarly vulnerable, wounds heal badly, inflammations are generally very severe, often going on to suppuration and gangrene, phthisis pulmonalis often closes the scene, and is frequently very acute. General emaciation is a striking feature in advanced cases. The kidneys may be found enlarged and their epithelium fatty, but this has no direct connec- tion with the essential pathology of the affection. INPLAMMATIOK This is a subject whose importance in pathology can hardly be over-estimated. From the time of John Hunter its phenomena have been taken as the basis of various speculations on the nature of pathological phenomena in general. Following the course we have hitherto adopted, we have first to consider the conditions under which inflammation occurs. Etiology of Inflammation. — In many cases the causes of inflam- mation are obscure, and this applies mainly to internal organs whose actions are greatly hidden from our view. Inflammation is PEODUCIBLB artificially, and if we study the modes of pi'oduction we shall find that agents are used to which the general name of irritants is applied. The inflammation is produced, it is said, by irritating the part in some Avay. This name irritant is apt to be misleading, as it very readily gives rise to the conception of a stimulating action; whereas if we consider the nature of the so- called irritants we shall find that they are rather of a deadening than of a stimulating kind. They are agents which, when acting strongly, are calculated to kill the tissues, and acting less strongly they may be supposed to damage it ; it is in this case that they produce inflammation. A certain degree of heat or cold will kill, . a less degree will lead, if sufficiently prolonged, to inflammation. Such agents as croton oil, nitrate of silver, chloride of zinc, have a damaging action on the tissues, and they are some of the com- monest in use when inflammation is to be produced. Again, trau- matic causes produce inflammation; a direct injury inflicted may kill, but acting less vigorously it may produce inflammation. It may be said, perhaps, that in inflammation of internal organs there is no such definite cause to be discovered. In pneumonia it might be supposed that there is no direct irritant or deleterious agent attacking the lung tissue. But even here there is reason to believe that there is some such agent at work. In one of the hospitals in Glasgow a medical man prescribed a tablespoonful of cough-mixture; the nurse gave a tablespoonful of carbolic acid instead. The result was an acute pneumonia presenting the usual physical signs and symptoms. In this case there was a deleterious agent introduced into the stomach and so into the circulation, and it acted on the tissue of the lungs (perhaps mainly on the blood- vessels), possibly during the process of excretion by these organs; the result was an acute inflammation. Again, when large blisters are applied, it sometimes happens ETIOLOGY OF INFLAMMATION. 81 that the active chemical principle is absorbed, and, passing into the blood, produces inflammation of the kidneys probably during the process of excretion. We have seen also that after transfusion of blood, the hsemoglobin is sometimes dissolved out from the blood-corpuscle and produces inflammation of the kidneys. And so in all inflammations we are to infer the existence of some dele- terious agent, although it is very often difficult to tell whence it has come and what is its nature. At this point it may properly be inquired, whether the nervous SYSTEM has anything to do with the causation of inflammation. There are not a few' facts which suggest, at least, some connection. In some of the instances the connection is clearly an indirect one. For instance, when inflammation of the eye results from division of the flfth nerve, the inflammation is really traumatic in its origin. By the severance of the nerve, the reflex action of winking is abolished as well as the secretion of tears, and so the organ is ex- posed to injuries, and unable to get rid of foreign bodies. The inflammation is the result of irritation from without, and, if the eye be carefully preserved against such injuries, the inflammation does not occur. But there are cases where nervous action has a very important and apparently direct relation to the cause of the inflammation. A man with a stone impacted in his urethra will have an inflam- mation of the testicle. Or after the passage of a bougie through an urethra with a partially healed wound, there will be a rigor with immediate suppression of urine and an acute inflammation of the kidney. These results can only be effected by reflex action, and there are various ways in which we may suppose them to occur. Reflex irritation may produce, through the vaso-motor nerves, a contraction of the arteries of an organ, and in the case of the kidney this contraction may conceivably be sufficient virtually to bring the circulation to a standstill. The immediate suppression of urine resulting on the passage of a bougie can scarcely be accounted for, except on the supposition of such a spasmodic con- traction amounting almost to occlusion of the renal arteries. If such a stagnation of the blood continues long enough, the vessels will be so damaged that when the circulation is restored inflam- mation must result. But there are cases of internal inflammations which cannot be explained merely on the supposition of a reflex stimulation of the vaso-motor nerves. The manifest relief which many inflammations undergo in consequence of counter-irritation has been pointed out by Lister as indicating the influence of the nervous system in pro- ducing inflammation. The application of the actual cautery to the skin over an inflamed and painful joint will often relieve the pain and inflammation instantaneously. It is as if there was in the nerves of the part a state of over-action which affected in- juriously the tissues. This over-action being relieved by a still greater stimulation of nerves connected reflexly, the inflammation subsides. 82 INFLAMMATION. It is probable that even in such cases nervous action alone is not sufficient to produce inflammation. It is more likely that under certain conditions of the local nei'vous arrangements the tissues are especially ■weak, and are liable to be damaged by agents vphich, under normal conditions, they would resist. It has been shown that a mild inflammation of the bone-marrow produced by caustics may be converted into an intense inflammation by causing the animal to eat putrid food. Here an existing damaged state makes the tissues unable to resist the attack of a further damaging agent, which normally they are able to withstand. It may be similar in the case of many internal inflammations produced apparently by exposure of the surface of the body to cold. Such exposure may produce, by reflex action, a state of the nervous system rendering the organ peculiarly liable to damage from conditions of the blood, which otherwise would not produce any such effect. In all these cases, also, it is to be borne in mind that the reflex action may affect specially the vascular sj'stem. It may be added that besides conditions brought about through the nervous system there may be individual peculiarities, hereditary or acquired, rendering different persons variously liable to the action of irritants, and even in the same person the various organs of the body may show difterent degrees of resistance. The char- acter of the inflammation also will, to some extent, be influenced not merely by the nature of the agent causing it, but also by the state of the individual. In studying individual cases of inflammation it will be impor- tant to consider by what path the irritant has reached the part which has become inflamed. In many cases it reaches it by the blood, and as the blood is distributed in every part of the organ, the inflammation will not probably show any special localization. And so, when we find two symmetrical organs, both of which are attacked in every region, we generally infer that the agent causing the inflammation has come by the blood or, at least, by a path common to both. Of course, there may be local diflerences in the organ itself of such a character that every part will not be equally susceptible to the action of an agent calculated to produce inflam- mation, and so the disease may develop more in one part of the organ than in another, although the general character of its distri- bution will generally still suggest the path by which the agent has come. THE PEINCIPAL PHENOMENA OP INFLAMMATION. The classical signs of inflammation are redness, swelling, heat, and pain, but in studying the nature of the process it will not be proper to follow this division. AVe have to investigate the exact nature of the processes occurring in the inflamed part, and in order to obtain a comprehensive view of the subject we shall, in the first instance, give au illustration which exhibits the main phenomena, THE PEINCIPAL PHENOMENA OF INFLAMMATION. 83 and afterwards consider tlie subject under headings suggested by that illustration. A simple experiment may be performed to illustrate the prin- cipal phenomena at the outset of an acute inflammation. If a frog be paralyzed with curare, the web of the foot may be spread out and observed under the microscope. With a pair of scissors a superficial longitudinal wound may be made, taking care to remove little more than the epithelium. ]3y this operation the connective tissue of the web, with its vessels, is exposed ; the action of the scissors in cutting, and the unusual exposure to the air, affect these structures, and the various phenomena of inflammation soon begin to manifest themselves, care being taken to keep a moist atmos- phere around the web so as to prevent the wound, deprived of its epidermis, from drying. At first the circulation goes on in the bottom of the wound as before, the area is merely more trans- parent from the absence of the epithelium. But very soon, if an artery is near or in the wound, it dilates, and there is an acceleration of the stream in the capillaries and veins. But this soon disappears, and the circulation, especially in the capillaries, becomes slower and slower, till here and there the blood-corpuscles now and then stand still for a moment or two. By and by a pecu- liar condition becomes visible in the veins. ITormally, the blood- corpuscles flow down the middle of the vein, and the peripheral zone contains plasma with a few white corpuscles rolling along. As the inflammation proceeds, the white corpuscles come to occupy this zone, and to adhere to the inner surface of the vessel. The individual corpuscles may not be all absolutely stagnant, they adhere for a time and then depart, but the result of the process is that there is a nearly complete filling up of the zone with white blood-corpuscles, so that the vein seems pavemented internally with these cells. This is seen not only in anj'' vein which may happen to be in the bottom of the wound, but also in those for a short distance outside it. If the attention be now directed to the surface of the wound, it soon becomes manifest that certain peculiar bodies are appearing there. These are at first seen mostly towards the edge of the wound, and are especially numerous in the neighborhood of veins where the white corpuscles are adherent. They are of various shapes, and present a transparent gelatinous appearance. If ob- serve^ carefully they are seen to be altering their shapes, presenting the well-known amoeboid movement, such as shown in Fig. 21. These cells gradually increase in numbers, and by their contractile power they move from the periphery towards the centre of the wound till they may come to cover it entirely. These bodies may be removed from the wound by placing the end of a capillary glass tube on the surface. A fluid I'uns up into the tube, and in this fluid are these free cells. The fluid may now be blown on to a glass slide and examined under a higher power of the microscope, when the slow amoeboid movement will be still more manifest. If, in the drop of fluid, these bodies are allowed to die or are 84 INFLAMMATION. killed by the addition of a reagent, they become globular and granular, in fact, have the characters we recognize as those of white blood-corpuscles, lymph-corpuscles, pus-corpuscles — of leu- cocytes in general. The addition of acetic acid to the living cells will first cause them to assume the globular form, and then will bring out the nucleus or nuclei as in an ordinary white corpuscle. The fluid in which these corpuscles are found is coaguable, and if Fig. 21. ^«5■■•^ /=^ SP" #'"^ ''''^'' ^ ■< ^ M^ A leucocyte from human blood showing amoeboid movement. (Klein.) it be kept till the corpuscles have died, strings of fibrine will be found in it. If this experiment be made in summfer, the whole of these phenomena will manifest themselves in a few hours, and in five or six hours the entire wound may be plastered over with amoeboid cells. In the course of a few more hours the wound begins to be covered in with new-formed flat epithelium. This begins at the margins, and if the wound is small it may be wholly covered within twenty-four hours. The amoeboid cells are covered in, but they very soon disappear, and the connective tissue of the web remains with a thin transparent epithelium covering it. Without following out this experiment further, we may now proceed to consider the principal phenomena of inflammation, which have been partly illustrated. "We shall consider, first, the state of the vessels; secondly, the condition which is illustrated in this experiment by the fluid on the surface of the wound con- taining amoeboid cells; and lastly, the condition of the tissues in inflamed parts. I. — THE STATE OF THE VESSELS IN INFLAMMATION. When an irritant is applied to a transparent vascular tissue, such as the tongue or web of the frog, it produces effects which vary slightly, according to its nature. If croton oil be applied, there is first a slight contraction of the arteries, soon followed by a dilata- tion of them. If ammonia be used, there is dilatation without previous contraction. The dilatation of the aetemes leads to an ACTIVE hyperemia, the current is accelerated in the arteries, capil- laries, and veins, and these vessels are overfilled; there is a great excess in the quantity of blood passing through the vessels. The acceleration of the current does not persist, however, in the most affected parts; on the contrary the blood-corpuscles begin to lag, THE PEIISrCIPAL PHENOMENA OF INFLAMMATION. 85 especially in the capillaries and veins, although there is still accel- eration in the arteries, and. in the capillaries and veins in the less inflamed parts. This stagnation in the capillaries and veins may assume a high degree, especially in the part most acted on by the irritant. Although the current is slow in these vessels they remain overfilled, a passive hypergemia supervenes on the active hypersemia ; at the same time the white corpuscles accumulate on the internal wall of the veins in the manner already described, and they also adhere at intervals in the capillaries. The circulation may come almost to a standstill in the capillaries of the parts most affected, while at various distances out from this there will be manifest a less and less amount of retardation till a zone is reached where the retardation disappears, and by and by gives place to acceleration. We have now to consider what may be the explanation of these various phenomena which the vessels manifest. The observations of Lister {Phil. Trans, for 1858, vol. 148) present us with a view of this subject which has been largely confirmed by other observers, and has only been corrected in one or two particulars. Saviotti has also published some very excellent researches (Virchow's Archiv, vol. 1.) which are for the most part confirmatory of Lister's views. • CoNTEACTioisr OF THE VESSELS, which is in some cases the primary phenomenon, is probably reflex. It is frequently absent, and when it occurs is always very transitory. Irritation of sensory nerves is known to produce contraction of arteries by reflex action. If the web of the frog be observed under the microscope, and, at the same time, the skin irritated by tapping or by twitching with the forceps, the arteries will be seen to contract, and this contraction does not occur if the sciatic is first divided. In the case of inflammation, therefore, we may conclude that the primary contraction when it occurs is reflex, produced by the irritation of the sensory nerves. The dilatation of the arteries leading to acceleration of the stream, or active HYPEHiEMiA (also called dbteemination op blood), is not, like the contraction, of reflex origin. In order to enforce what follows, it is important here to recall the fact that irritants act injuriously on the tissues, and, in a certain sense, paralyze them. That the effect of irritants is to paralyze the tissues was long ago shown by Lister in his. important researches on inflammation. The skin of the frog is supplied with pigment-cells. These cells are branching bodies (they are shown in Fig. 15, p. 63), and they possess the power of scattering the pigment into many branches, or of concentrating it more or less into the central parts of the cell. They are under the command of the nervous system, and by their means the animal is capable of changing its color, presenting a dark hue when the pigment is dispersed, and a lighter color aecordina; to the deo-ree of concentration. Some irritants have the immediate eflect of dispersing the pigment, and this itself is so far an evidence of paralysis as the dispersed condition seems to be the 86 INFLAMMATION. state of rest of the cells; but whether the pigment is dispersed or not, the animal loses control of its pigment in the affected area, which does not change its color Avith the rest of the skin, and may be found dai-k while the animal is pale, etc. We have already had occasion to remark that, as Lister long ago inferred, that there are probably, in connection with the arteries, peripheral ganglia which are the immediate regulators of the state of contraction of these vessels. If these ganglia be paralyzed the arteries will dilate, and this is apparently the cause of the dilata- tion under consideration. That the dilatation is not eeflex seems sufficiently proved by the fact that it occurs after all connec- tion with the central nervous organs has been severed. For instance, the sciatic nerve has been divided in a frog's leg with resulting dilatation, but the application of an irritant to the web produces an increase of the dilatation. Again, the brain and spinal cord in the frog have been destroyed (Cohnheim), but the application of an irritant to the tongue still produces dilatation of its arteries. The acceleration of the blood-current in the arteries, capillaries, and veins, will be understood from what has gone before to be a direct result of the dilatation of the arteries; we have, in fact, an active hyperemia. It will not be understood, however, that, apart from inflammation, active hypersemia is never produced by reflex action; it is frequently so, but inflammatory active hypersemia is a local phenomenon. It is not impossible that an inflammatory may be associated with a reflex hyperaemia, and the problem may in this way be complicated. The cause of the eetardation may not at first be apparent, but the researches of Lister atford an explanation of it. The cause of the retardation is an increased adhesiveness of the blood-corpus- cles. This is a matter of direct obseiwation. The corpuscles in the inflamed area can be seen to move sluggishly along the wall as if attracted hj it, and the pavementing of the veins with white corpuscles is clearly due to increased adhesiveness. It has been pointed out by Lister that, when the blood is removed from the vessels and comes in contact with dead matter, the blood-corpus- cles acquire an adhesiveness which they do not possess inside the normal vessels. The red corpuscles stick together by their flat surfaces and form the well-known rouleaux. The adhesiveness of the white corpuscles is not so obvious when a drop of blood is ex- amined outside the body, but we have-reason to believe that it is even greater than that of the red. Now inflammation damages the walls of the vessels, with the result that the corpuscles behave as if in the presence of dead matter — they become adhesive. This is excellently shown in an experiment of Lister's. He ligatured the leg of a frog, producing thereby stagnation of the blood in the vessels, but on examining the web it could be seen that the corpuscles were able to move freely among one another — there was obviously no adhesiveness. But now, if a piece of mustard was applied to the web, this free movement ceased in the area affected; the corpuscles became adherent among themselves. THE STATE OP THE VESSELS IN INFLAMMATION. 87 and to the wall of the vessels. The result of this was an accumu- lation of the corpuscles m the irritated area; any corpuscles which happened to glide into the area remained adherent there, and so, by degrees, the vessels became overfilled — a state of hyperaemia superinduced on stagnation. If any corpuscles happened to escape from the affected area, it ceased to be adhesive, and moved freely about. "We may therefore infer that the retardation of the current and the pavementing of the veins with white corpuscles are the result of the injury to the vessel-wall, and it may be added that, in con- nection with inflammations, all degrees of stagnation up to abso- lute stoppage or stasis may be produced, and are often manifested together in the same case. "We may now sum up the conditions presented by the blood- vessels in the early periods of inflammation as follows : the arteries dilate by a relaxation of their muscular coats, due to a paralysis of the peripheral ganglia. In some cases this dilatation is pre- ceded by an evanescent contraction. The immediate result of the dilatation of the arteries is active hypersemia, or determination of blood, involving overfllling of the artei'ies, capillaries, and veins, with acceleration of the current. This is followed by retardation of the current, the vessels remaining dilated and hypersemic, and this retardation may go on to almost complete stasis in the capilla- ries. The retardation is due to adhesiveness of the corpuscles, and to the same cause is to be traced the pavementing of the veins with white corpuscles. It is sometimes possible in acute inflammation of the skin, as in the case of a boil, to observe conditions directly traceable to the state of the vessels here indicated. Thus at the peripheral parts of such a focus of inflammation the skin presents a fiery-red ap- pearance due to determination of blood; the red color may be pressed away with the finger, but it immediately returns. Inside this zone there is an area in which the redness is not so vivid, and when the red color is pressed away it returns sluggishly; the corpuscles are here alreadj' adherent, and the current retarded. Then in the more central parts.a dusky-red appearance is presented, and on pressure it may be impossible or very difficult to remove the redness; here a condition of extreme stagnation exists. In connection with the state of the vessels, we have to consider the TEMPERATURE OF INFLAMED PARTS. It is Well kuowu that hcat is one of the so-called cardinal symptoms of inflammation, and in external parts a feeling of heat is almost universally complained of. The nerves of internal parts seem incapable of communicating the sense of differences in heat and cold. A hot potato swallowed gives an impression of pain, and it maj be argued that the pain in internal parts during inflammation is partly due to increase of temperature. "We have to inquire whether there is an actual pro- duction of heat in inflamed external and internal parts. There is no doubt that the temperature of inflamed external 88 INFLAMMATION. parts is increased in inflammation. John Hunter long ago deter- mined this by actual observation. He had a case of hydrocele to deal with, and undertook its treatment by the old operation of laying open the sac and inserting lint dipped in an irritating salve, with a view to producing inflammation. At the time of the opera- tion he found that the temperature in the tunica vaginalis was 92°, but next day, inflammation having been induced, the temperature had risen to 98f °. The question here arises whether this increase of temperature is due to an actual production of heat in the in- flamed part, or to an increased supply of hot blood, due to dilata- tion of the arteries. That there is a greatly increased supply of blood to inflamed external parts has been proved by experiment (Cohnheim). If the foreleg of a dog be inflamed by scalding or by painting with croton oil, or any other method, the quantity of blood coming from the limb may be compared with that on the sound side by introducing canulas into the corresponding veins on the posterior aspects of both legs. In a recent inflammation the amount of blood on the inflamed side may reach nearly the double of that on the sound side, and it may even be as great as when the arteries have been relaxed in a limb by dividing the axillary plexus of nerves. This extreme degree of difference may not continue long, but even for some days it is frequently very considerable. The relaxation of the arteries, it is clear, produces a determination of blood which extends beyond the immediate focus of the inflamma- tion, and is not counterbalanced by the retardation. John Hunter, having determined the great increase in tempera- ture above referred to, yet came to the conclusion that it was due to the determination of blood, for he found that the temperature of an inflamed external part never exceeded or even quite reached that of a normal internal part, or, in other words, of the blood in internal organs. Since Hunter's time, Simon has thought to prove that there is some development of heat in inflamed parts. His experiments seemed to show that the arterial blood passing to an inflamed external part is not so warm as the focus of inflammation, and that the venous blood returning from the part is warmer than the arterial blood, although not so warm as the focus of inflamma- tion. But the experiments of Jacobsen, made with more exact instruments, entirely confirm the views of Hunter. It appears that the most acute inflammation of the skin or muscle never causes an elevation of temperature sufficient to reach that of the rectum, vagina, or abdomen, the difference being generally 1° or 2° C. Again, in artificial infiammations of internal parts, as in peritonitis or pleurisy, the temperature was never raised to that of the left ventricle, being always from .2° to .5° C. under it. This means that in these parts, the temperature being already near that of the blood in the left ventricle of the heart, inflammation, lead- ing to an increased supply of blood of a similar temperature, causes virtually no elevation above the normal heat. Again Cohn- heim has found that, when in one forepaw of a dog, a state of THE INFLAMMATORY EXUDATIOK. 89 acute inflammation is induced, while in the other active hypersemia is produced by dividing the axillary plexus of nerves, the tempera- ture in the inflamed foot is always slightly less than that in the other. "We may safely infer, then, that in inflammation there is no local production of heat. II. — THE INFLAMMATORY EXUDATION. In the experiment sketched at the outset the inflammatory exudation was the fluid which collected on the surface of the wound. We saw that this fluid contained amoeboid cells, and that it was coagulable. We may thus consider the inflammatory exuda- tion as consisting of cells, serous fluid, and fibrine, and we shall in the first place pass each of these under review. The Exudation-cells. — The resemblance of the cells met with in acute inflammations to the leucocytes in the blood long ago sug- gested the idea that they are white blood-corpuscles. In the year 1846, Waller observed the pavementing of the internal coat of the veins with white blood-corpuscles in the inflamed tongue of the frog, and as he saw similar cells outside the vessel he inferred that the white corpuscles had got through the wall. It was, however, difficult to believe that the solid globular white corpuscles could pass through the intact wall of a bloodvessel, and Waller's views, although supported by Wm. Addison, were lost sight of By and by, however, liecklinghausen demonstrated that pus-corpuscles and white blood-corpuscles possess contractile power by virtue of which they are able to move from place to place, and to alter their shapes in the most diverse fashion. This paved the way for the actual observation of their passage through the walls of the vessels made by Cohnheim. He made his observations on the mesentery of the frog. When this exceedingly delicate and transparent structure is drawn out of the body through a wound in the lateral aspect of the abdomen, the mere exposure to the air is sufficient to set up an acute inflammation, the phenomena of which can be readily observed under the microscope. Let us suppose that the pavementing of the veins has occurred, and that there is an occa- sional white corpuscle adherent in the capillaries, and the following surprising phenomena show themselves, as described by Cohnheim himself. " One sees, as a rule, first, in a vein which presents the pavementing with white corpuscles, but sometimes in a capillary, a pointed projection in the external contour of the vessel; it pushes itself farther and farther outwards, it increases in thickness, and the pointed projection develops into a colorless rounded knob; this increases in length and thickness, sends out fresh points, and draws itself gradually outwards from the vessel-w^all, with which it comes to be connected only by a long thin stem. Finally, this also lets go the vessel, and there lies outside a colorless, dull, glancing, contractile corpuscle, with several short processes and a 90 INFLAMMATION. long one, of the size of a white Hood-cell, with one or several nuclei; in a word, a white blood-corpuscle." In the investigation of inflamed tissues in the usual way after death, there are often indications to be met with of this process of emigration of the white blood-corpuscles. The leucocytes in the tissues, for instance, are frequently aggregated especially around the bloodvessels. In the accompanying Fig. 22, the appearances in the human omentum are shown in a somewhat diagrammatic form, and the appearances there are sufficiently suggestive. Thei'e is no longer any doubt then that the white corpuscles of the blood wander out of the vessels, and they become the so-called exudation cells of recent inflammations. But, besides the leu- cocytes, the KED CORPUSCLES also pass out of the vessels, and this Pig. 22. Inflamed human omentum. The phenomena of inflammation are seen in the veins and capillaries, the condition being normal at the artery (o), where b represents endothelium covering the trabecula (a). In the vein (i) there are many white corpuscles along the wall. Some of these are emigrating (e); /, desquamated endothelium; g, extravasated red cor- puscles. (ZlEGLER.) they do by the process of diapedesis, of which we have already seen examples. The white corpuscles are active contractile cells, and they generally pass through the vessels to a larger extent than the red ones, but there are some inflammations in which these red corpuscles also pass through in large numbers. So far then as the cells which appear at the outset of an inflammation are concerned, they are doubtless, mainly, if not entirely, blood-corpuscles. THE INFLAMMATOEY EXUDATION". 91 The Serous Exudation. — This has obviously its source in the blood. In inflammation there is a greatly increased transudation of the fluid of the blood from the vessels, and this passes primarily into the serous spaces. If these are, naturally or by reason of a wound, in communication with a surface, the fluid will appear on the surface. The inflammatory cedema indicates a greatly increased circulation in the serous spaces and lymphatics, and this can be proved by actual observation. If the leg of a dog be irri- tated with croton oil, the foot swells greatly, and if the lymphatics on the external aspect of the leg be then exposed they will be found greatly dilated; a canula being introduced, the lymphatic fluid will flow from it, drop rapidly following drop, whereas in the sound leg the circulation is very slow. If before setting up the inflammation a canula be introduced, and an inflammation set up by placing the foot in hot water, then it will be seen that almost immediately an increase in the flow of lymph occurs, while the oedema comes on later and is not followed by further increase in the flow. The meaning of this is that the oedema only develops when the increase of transudation is too great for the lymphatics to dispose of. But not only is the transudation increased, it is altered in quality. We have seen that in passive hypersemia the transudation is a watery fluid, more watery than the normal lymphatic fluid. In inflammation it is a concentrated fluid, containing a great deal more albumen and corpuscles, and on being shed, or even in the canula, it coagulates. The Fibrinous Exudation. — It is a familiar fact that after the infliction of a wound there occurs a glazing of the surface within a few hours, and this glazing is due to the coating of the surface with a layer of fibrine. In addition to this there is discharged from the surface a greater or smaller quantity of serous fluid. This deposition of flbrine on the surface of a wound may be taken as typical of the fibrinous exudation, but a similar deposition of flbrine occurs in many other inflammations, in acute inflam- mations of serous membranes as in pleurisy, in acute inflammation of the lungs, etc. The fibrinous exudation has all the characters of fibrine seen in a blood-clot. Figure 23, for instance, is taken from the lung in acute pneumonia, and it is seen that a lung alveolus is filled with a network of fine fibres. The fibrinous exudation, especially the yellow layer seen on serous membranes, is often called lymph, but this term is a some- what confusing one. It has its origin in the coagulable lymph of John Hunter, and has very interesting historical relations. As the term is used, however, to designate other structures besides the fibrinous exudation, and as it involves a theory as to the rela- tions of the exudation, its use had better be avoided. The fibrinous exudation, for reasons which will appear after- wards, is mostly met with on surfaces. It seldom forms in the serous spaces of the tissues unless the inflammation has been 92 INFLAMMATION. severe enough to kill the tissue, as in the case of a boil or car- buncle- where the slough which forms is composed, partly of dead tissue and partly of fibrine deposited in the meshes. Fig. 23. Lung alveolus in acute pneumonia. A plug of fibrine, with a few leucocytes in it, fills the alveolus. X 350. Mode of Production of the Inflammatory Exudation. — As the constituents of the exudation come from the bloodvessels, it is natural to look to the state of their walls in order to account for the extraordinary passage of the constituents of the blood through them. We have seen reason to believe that the acquired adhesiveness of the WHITE CORPUSCLES in the veins and capillaries is due to a change in the walls of these vessels in the direction of dead matter. In the normal vessels the white corpuscles roll along in the plas- matic zone or in the capillaries, without presenting any independent movement, whereas outside the body they at once present amogboid movement. It is very possible that the living tissues have a cer- tain power of restraining this amcEboid movement, or at least of preventing the amoeboid cells penetrating them. If a piece of dead tissue containing canals and cavities, such as the cornea, be placed in the peritoneal cavity, then the leucocytes in the cavity THE INFLAMMATORY EXUDATIOS-. 93 penetrate into these cavities. In the state of inflammation the capillaries are altered, their walls have undergone a change which renders them more permeable, and, being more like ordinary matter, they may allow a freer contractility of the corpuscles. It is, therefore, the alteration of the wall of the vessel which is the principal agent. It has been supposed that an increase in pressure of the blood in the vessels may have something to do with the emigration of the white corpuscles. But we must be certain, to begin Avith, that there is an increase of pressure. As Cohnheim has pointed out, the conditions here are not such as to cause an increase of pressure. There is no obstruction in the veins; in fact, the circulation through them is unduly abundant, as has already been seen, and any stagnation which exists in the capil- laries has its origin in the adhesiveness of the blood-corpuscles. If this stagnation in the capillaries produces any increase of press- ure, it will do so not in the veins, where it will rather diminish pressure, but in the arteries. I^Tow there is no emigration from the arteries, but from the capillaries and veins alone, and so it can hardly depend on the increase of pressure. The same applies to the diapedesis of the red corpuscles. They pass through the ves- sels not because the pressure is increased, but because the capillary wall is so deteriorated that even at the existing pressure they are pressed through. We have already seen that in the ease of the embolic infarction a diapedesis occurs under conditions in which the pressure is presumably less than the normal. It is to be re- marked that here as there the diapedesis of red corpuscles occurs in the capillaries alone, and not in the arteries and veins. The INCREASED TRANSUDATION OF THE BLOOD-PLASMA is tO be accounted for on similar principles. Alteration in the vessel-wall is again the main condition; and seems in inflammation to be much more serious than in passive hypersemia, as a much greater amount of albumen and salts pass through. The FORMATION OF FiBRiNE, as wc have seen, is a prominent occurrence in many inflammations, and as the constituents of the fibrine come from the blood, it also is to be regarded as part of the inflammatory exudation. The fibrinogen is contained in the exuded blood-plasma. The white blood-corpuscles contain the paraglobulin and ferment, but in order to yield these, it is necessary, as we have already seen in studying thrombosis, that they should disintegrate. In the case of thrombosis, an alteration of the wall of the heart or bloodvessel is necessary in order to the disintegration of the white corpuscles. In the present case it is the tissues outside the vessels that are concerned, and these, as w^e have seen, are damaged as a necessary condition of the inflamma- tion. It has already been noted that firine forms usually on inflamed surfaces, and rarely in the substance of the inflamed tissues unless necrosis has occurred. This may be set alongside the fact that thrombosis does not occur in the capillaries unless they have undergone necrosis. The serous spaces in the tissues, like the 94 INFLAMMATION. capillaries, are lined with endothelium; and these spaces, being small, the white corpuscles will hardly be sufficiently removed from the endothelium to allow of coagulation, so that this will not occur unless the endothelium be dead or shed. In some very acute inflammations of connective tissues (acute phlegmon) there is, however, not uncommonly a fibrinous exudation in the meshes of the tissue, forming a kind of fibrinous oedema. This may be seen not uncommonly in the skin in erysipelas. But where the exudation occurs on a surface and the white corpuscles are removed from immediate contact with the endothelium, then many of them perish and coagulation occurs. In this connection it may be remarked that the epithelium, like the endothelium, seems to have the power, and perhaps to a greater extent, of preventing the disintegration of the white corpuscles and the formation of librine. As a rule, a fibrinous exudation does not form on a mucous membrane, and when it does form it may be taken for granted that the epithelium has died or been shed. It will be understood that the inflammatory exudation presents VARIOUS characters, uudcr different circumstances, even apart from the question of coagulation. In some cases it is exceedingly watery, partaking chiefly of the characters of an ordinary transu- dation. This will be the case mainl}^ in slight inflammations, and in those occurring in persons whose blood is watery. For instance, the inflammations which so frequently occur in Bright's disease have usually a watery exudation. In such cases the exudation-cells will be also small in number. On the other hand, there are inflammations in which the exuda- tion-cells are exceedingly abundant, so abundant that the inflam- mation rapidly assumes a suppurative character. This is peculiarly the case with septic inflammations. For instance, in septic in- flammation of joints such as occurs in pyaemia, we have the exu- dation rapidly becoming purulent, the pus-corpuscles having all the characters of the ordinary exudation-cells, and being doubtless white blood-corpuscles. It will be observed that these suppurative inflammations are severe in chai-acter, and presumably imply serious alteration of the vessel-walls, such as to allow of the enor- mous emigration of the white corpuscles which is here presupposed. It may further be said regarding inflammatory exudations that they VARY considerably according to their site and other rela- tions. We have already said that a serous exudation may flow from a surface, may accumulate in a cavity, or may lie in the serous spaces, causing oedema. We shall afterwards see that the serous fluid may be taken up by cells. Again, the exudation may be mixed with the secretion of a mucous membrane or gland. In the former case, the exudation will have more or less of the characters of the mucous secretion, variously modified according to the amount of the constituents; thus, we may have a mucous, sero- mucous, muco-purulent exudation, and in these exudations epi- thelium cells, cihated and otherwise, will often be found. In the NEW FORMATIONS. 95 case of the kidney, the exudation is to be found mixed Avith the urine, so that we have albuminuria. It may here be remarked that the exudation passes in the di- rection OP LEAST RESISTANCE, and wiU be found to accumulate or escape where it best can; thus, in the kidneys it passes largely into the uriniferous tubules, in the lungs it occupies the air-vesicles, in the connective tissue it tills the serous spaces, producing oedema. In some cases the oedema manifests itself mainly where the tissue is loosest; for instance, in inflammations of the larynx, oedema occurs mainly at the base of the epiglottis and the aryteno-epiglot- tidean folds, giving rise to so-called oedema glottidis. "We have still to consider how inflammatory exudations are DISPOSED OF. In slight cases the exudation is carried off by the lymphatics, passing by that route back into the circulation, the exudation-cells being perhaps partly retained by the lymphatic glands. In more severe cases, and especially when the exudation is retained in cavities, its disposal is more difiicult. The serous fluid will rapidly be absorbed, but the fibrine and the exudation- cells, where these are so abundant as to constitute a purulent in- flammation, or are entangled in the fibrine, are not got quit of so easily. Pus-corpuscles readily undergo fatty degeneration, and we shall afterwards see that structures which have undergone this change, by and by disintegrate, and the fat is absorbed. Some- times, however, the fat is too abundant, or the conditions are not suitable to absorption, in Avhich case the pus may dry into a cheesy mass, which may afterwards be impregnated with lime-salts. Similarly the fibrine may disintegrate and be absorbed, or dry in and become calcareous. III. — CHANGES IN THE TISSUES AND THE INFLAMMATORY NEW FORMATION. We enter here on a somewhat debatable department, especially as under this heading will be included the subject of new formation in inflammation. It is undoubted that the tissues in inflammations sometimes UNDERGO RETROGRADE CHANGES. The inflammation, if very severe, may kill the tissue, but short of that there are certain inflamma- tions which are characterized by the occurrence of fatty degenera- tion in the cells constituting the tissues. It may be said that in severe inflammations, and probably at the outset of all acute in- flammations, the tissues take no active part in the processes, and if affected in their structure at all, are aftected for the worse. "We have already seen that inflammations paralyze the tissues. But it may be presumed that when an inflammation has lasted for some time and has diminished in intensity, the tissues may recover, and it will not be surprising to find that they undergo changes of a kind different from the retrograde processes already mentioned. 96 INFLAMMATION. This leads us up to the question of the new formation of tissue which is so characteristic of many inflammations. It may here be stated that two views are held as to the origin of such new forma- tions, the one being that the formative cells are the white blood- corpuscles, and the other that the existing tissues, and especially the connective tissues, supply the formative cells. We shall tirst mention certain facts connected with new formation and afterwards recur to this disputed point. It need hardly be said that by new formation is meant the production of a properly organized tissue, the form of tissue produced being for the most part connective tissue containing bloodvessels. A GRANULATING WOUND, with the resulting cicatrix, may be taken as typical of the inflammatorj'^ new formation, and by considering the occurrences which present themselves there, we shall become acquainted with certain facts connected with the subject. Granu- lation-tissue is already an imperfectly organized but highly vascular tissue. In the accompanying Avoodcut (Fig. 24), the injected blood- vessels of a granulating wound are shown, and the degree of vascu- larity may be inferred. Pig. 24. Vessels of a granulating wound injected. (Billboth,} It is to be observed in the first place that in order to the produc- tion of granulations, the inflammation must be of some duration. If a wound close within the first few days, no granulations are formed. The damage done by the knife in infiicting the wound produces an inflammatory exudation in the form of a glaze of fibrine and a serous discharge. But if the wound be protected from further irritation it will not produce granulations even should it not heal by the first intention. Under antiseptic treatment, if the wound be protected from carbolic acid vapor and other sources of irritation, granulations do not form. Even in the case of a septic wound, after the preliminary glazing of the surface, there is what surgeons call "a pause" of two or three days before the granulation appear. There is in this case a prolongation of the inflammation for several days before the occurrence of new forma- tion. But, on the other hand, the inflammation must not be too severe, else the new formation will not occur. Inflammations which rapidly pass on to suppuration are not accompanied by new NEW FORMATION. 97 formation. Again, in order to ne\v formation an abundant supply of blood is necessary, and in this connection it may be mentioned that the new formation of bloodvessels is one of the most marked, as it is frequently the earliest visible manifestation of this process. A granulating wound appears, at first sight, to be composed simply of round cells of nearly uniform size. But on more careful examination it is seen that, putting out of view the bloodvessels in the mean time, it consists of two kinds of cells (see Fig. 25). The G-ranulation-cells, a and a, leucocytes j 6, 5, various formative cells ; e, formative cell with two nuclei ; ci, with many nuclei ; d, d, d, formative cells developing connective tissue; e, complete connective tissue. X 500, Picrocarmine preparation. (Ziegler.) one kind has the size and general appearance of the white blood- corpuscle, and gives with acetic acid a similar reaction {a and a^. The others [b, h) are about twice as large as these, and as they present a distinct outline and possess an oval nucleus, they have a considerable resemblance to epithelial cells, and are hence some- times called epithelioid cells. These cells may possess tM'o nuclei (c). Sometimes there are still larger cells with multiple nuclei (cj^ the so-called giant cells, but these are not uniformly present, and may be left out of sight in the further consideration of the subject. In the new formation of the tissue these epithelioid cells are mainly concerned, in so much that Zeigler, whose observations are here of very great value, has designated them formative cells. This author studied the new formation of tissue by introducing under the skin or periosteum, or into the peritoneum of animals, two pieces of glass cemented together in such a way that there was free access between them, while the distance apart was no more than a fraction of a line. One of the pieces of glass was a micro- scopic cover-glass, so that anything between the glasses could be 7 98 INFLAMMATION. studied under the microscope afterwards. These foreign bodies set up inflammation, and through time vascular connective tissue formed around tliem, and penetrated between the plates of glass. In these ingenious experiments the formative cells did not appear till about the fifth day after the occurrence of the inflammation. These cells are, like pus-corpuscles, contractile, but they are much less active, and we shall see immediately that they subsequently assume the characters of fixed cells. By and by these formative epithelioid cells elongate, and send out processes {b, b), becoming stellate or spindle-shaped. After a time the processes grow out and become, with a certain part of the substance of the cell, converted into fine fibres {d). In this way it appears the fibres of the ncAv-formed connective tissue are formed, the rest of the protoplasm of the cell remaining as the spindle- shaped, fixed, connective-tisue cell (e). The fibrillas, developed out of neighboring cells, communicate, and thus is formed the com- plete fibrillated connective tissue. This new formation of connective tissue is necessarily connected with NEW FORMATION OF BLOODVESSELS (see Fig. 26). If epithelioid New formation of bloodvessels in a granulating wound. (After Arnold.) cells are formed in advance of the bloodvessels, they do not pro- ceed to the formation of tissue, but undergo fatty degeneration. The formation of the bloodvessels always occurs in connection with the preexisting vessels, usually the capillaries, and by a process of budding apparently. An elongated process extends out from the wall of the capillary. It meets another process, and so is converted into an arch. The arch and buds increase in thickness, and, by and by, a tunnelling of them begins, and they are by degrees converted into vessels, the blood passing into them. It has been stated by some that in the formation of the bloodvessels from the buds and arches, the tunnelling takes place partly by a conversion of the substance of the solid arch or bud into red blood- corpuscles, in a manner similar to what occurs in the original for- mation of bloodvessels in the embryo. But this seems to be doubtful, and the probability is that no such new formation of NEW FORMATION. 99 blood-corpuscles takes place. The vessels formed are at first mere tubes, and the demarcation of endothelial plates seems to be of subsequent occurrence. The new-formed vessels are then regular capillaries, and by subsequent changes they may increase in size and thickness, and take on the characters of arteries and veins. It is marvellous how rapidly such new formation of vessels occurs not merely in inflammations, but also in the formation of tumors, and we may regard this as consistent with the woiaderful adapta- bility which wo have already seen the vascular system to show to the needs of the system. In the formation of the permanent tissue, we have referred to the important part played by the epithelioid cells, but we have not made any reference to the origin op these formative cells. Their origin is a matter of dispute. Ziegler asserts that they arise by the conjunction or coalescence of the exudation-cells, or leu- cocj'tes from the blood, while others assert that these cells which have to do with the actual building up of tissue have their origin in the fixed cells of the tissues. Many facts may be adduced in favor of this latter view. We have already seen reason to believe that in the early stages of inflammation the constituents of the tissues are mostly passive, and, if they undergo any change, it is in the direction of degener- ation. But when the tissues have had time to recover, it is not inconceivable that, being by the exuded fluid supplied with additional pabulum, they should undergo nutritive changes. Even in some forms of acute inflammation the exuded fluid finds its way into the cells. In parenchymatous inflammation of the kid- neys the renal epithelium enlarges and becomes cloudy, often undergoing degeneration subsequently. But if the inflammation subside to some extent, the epithelium cells may be found with double nuclei and showing other signs of germination. From the researches of Klein and others it is rendered evident that in certain inflammations of the peritoneum the endothelium shows active germination, and as a result of such active processes these cells may produce amoeboid leucocytes which are not to be distin- guished from white blood-corpuscles. It is even doubtful whether in the normal condition the endothelium does not take part in the formation of the white corpuscles. Looking to the fact that the connective tissue throughout the body is so intimately related to the lymphatic system we may possibly find here a means of reconciling divergent views. The endothelium cell and the connective-tissue corpuscle may be regarded as essentially similar structures. We have reason to re- gard the serous cavities as virtually the same as the serous spaces in the connective tissue. The endothelium of the peritoneum is normally beset with frequent aggregates of round cells which may be regarded as lymphatic follicles, and similar aggregates are fre- quent in the connective tissues, for instance, in that of the lung, as has been pointed out by Burdon Sanderson and recently confirmed by Arnold (Yirchow's Archiv, vol. 80). In view of all these facts 100 INFLAMMATION. FiQ. 27. ^1 we may, perhaps, regard the connective tissue and the lymphatic system as a single system, and the lymphatic glands as. simply larger developments corresponding with the smaller cellular aggregates Avhich we meet with throughout the connective tissue. In this view the white blood-corpuscles themselves would be con- nective-tissue structures, and have their seat of origin not only in the lymphatic glands, spleen, and bone marrow, but in all parts of the connective tissue. At last we may say that in inflammations, when they have become chronic or subacute, the connective tissue or endothelium produces amoeboid cells which are not distinguishable from white blood-corpuscles. The epithelioid cells which are the immediate formative agents may take origin from the fixed connec- tive-tissue cells or from the amoeboid ones, and there is nothing inconsistent in the view that they may also take origin in white blood-corpuscles. To return now to the case of the gran- ulating wound, we may find in a section of it appearances confirmatory of what has been said above (see Fig. 27). In its superficial layers it is composed of round cells many of which have the size and appearance of leucocytes, while others have the characters of epithelioid cells. The leucocytes are probably in great part white corpuscles in process of migra- tion, but they mary also be to some extent derived from the lixed connective tissue of the part. Some of them pass to the surface and appear in the discharge as pus-corpuscles. Others, however, will pass into the lymph-spaces or even into the capillary vessels, and in either case resume their position as white blood-corpuscles. As we pass deeper in the granulating wound there are evidences of the changes in the epithelioid cells described above. We find parts where large spindle-cells are abundant, forming sometimes an actual spindle-cell tissue. Still deeper, and at the base of the wound, we find new-formed connective tissue. Towards its base the granulating wound shows a striking ten- dency to contract, and we may account for this in two ways chiefly. The leucocytes, to a large extent, disappear when we pass a short distance beneath the surface; and at the same time the epithelioid cells, by becoming spindle-shaped and arranging themselves in parallel bundles, occupy less space than before. The new-formed connective tissue also shows a remarkable tendency to draw together, becoming more compact and drier. This shrinking of the connective tissue continues long after the wound has healed, the cicatrix tending to become smaller and harder. By the con- ^< Semidiagrammatic section of a granulating wound. X 85. NEW FOEMATIOJSr. 101 traction at the base of the ■wound its area is diminished as a whole. The bloodvessels also which form loops passing to the surface are partially constricted, and so the superficial granulations are less supplied with blood. "We may suppose that another consequence of this will be a less ' considerable emigration of the white cor- puscles from the vessels. We have still to consider how the granulating wound becomes COVERED WITH EPITHELIUM. This proccss is One which it is rather difficult to observe, apparently because the new-formed epithelium is very delicate and transparent. The new epithelium always arises from that already existing. The epithelial cells at the margin of the wound enlarge and divide, and so provide fresh cells which gradually cover the surface aud assume the place and char- acter of the usual flat epithelium. It is said that the young epithe- lium sometimes shows even a slight amoeboid movement. The formation of epithelium sometimes begins in the midst of the wound, but this only happens when some epithelial structures, such as hair-follicles or sebaceous glands, have escaped destruction when the wound was made. It is known also that living epithelium may be transplanted from one part of the body to another or even from a different person. When grafting is performed in this way the epithelium germinates like that at the margin and covers the neighboring granulations. The processes which we have sketched as occurring in the granulating wound are repeated with slight modifications in all OTHER INFLAMMATORY NEW FORMATIONS. For new formation to occur the inflammation must be prolonged for some time, and it must not be too severe. These are the chai-acters of chronic inflamma- tions, and it is in connection with them especially that we have new formation occurring. In these chronic inflammations we have a tissue compai-able to granulating tissue, consisting essentially of round cells, but in which when the process is active epithelioid cells may be distinguished. The round cells have the characters of leucocytes, and in some cases they pass outwards from the tissues and form pus. In most cases, however, they pass into the lym- phatics and disappear. If two surfaces in the condition of granulation come in contact they coalesce, and their vessels communicate so that they form a common layer. In that ease when the inflammatory tissue de- velops into connective tissue the surfaces will be united by a permanent vascular connective tissue. In this way the flaps of a stump unite after granulating, and thus also permanent adhesion of the pleura and of the pericardium is often brought about. It should be noticed that the inflammatory new formation does not always develop into connective tissue, but that it may produce OTHER FORMS OF THE CONNECTIVE-TISSUE SERIES, AS BONE AND CAR- TILAGE. A chronic inflammation of the periosteum results in considerable new formation of bone, in which the formative cells 102 INFLAMMATION. take part. The forrnation of callus round a broken bone is an instance of this. Then cartilage is sometimes formed in connec- tion with inflammations, though much less frequently. The callus formed after fractures in the lower animals has often cartilage in it, and it may be so also in man. Of considerable importance is the new formation of tissue ABOUND foreign BODIES. If a foreign body be introduced among the living tissues, if not very virulent in its own nature, it sets up a mild chronic inflammation, with the result of producing a vascular, rudimentary, tissue-like granulation. If the foreign body be permeable by this tissue, then the granulations will grow into it and, as it were, devour it, replacing it first by their own rudi- mentary tissue, which afterwards gives place to connective tissue. As this connective tissue is comparatively small in bulk, and tends to contract more and more, the result of the whole process is an absorption of the foreign substance and the gradual disappearance of all trace both of it and of the tissue which has replaced it. J3ut if the foreign body is not permeable, then the inflammation results in the production of a layer of connective tissue around it, and so the body becomes encapsuled. Many instances of this might be given. If a piece of dead animal tissue be introduced into the body, as, for instance, a piece of liver previously hardened in chromic acid solution, or a piece of prepared catgut used to ligature a vessel, then the dead tissue is first replaced by rudimentary tissue which gradually shrinks away. If a piece of the tissue of the body dies, and if severe inflammation is kept oft", then its replacement by rudimentary tissue and absorption occur. In fractures of bones it often happens that a piece is en- tirely separated and dies. Such a piece of bone may lie exposed in the wound in a compound fracture, and it has frequently been seen how it has been eaten into by the granulations and absorbed by them. This tendency has been recently taken advantage of in a very ingenious manner by Hamilton, of Aberdeen, in the treatment of wounds. He finds that a a piece of sponge decalcified and placed on a granulating wound, becomes filled with granulations and replaced by them. By this means it is possible to encourage the growth of granulations and get them to fill spaces, etc. This pro- cess has been named sponge-grafting. The encapsuling of foreign bodies is frequently seen. A parasite such as the trichina or echinococcus obtains a connective-tissue capsule. Dead material in the body which is not permeable by the granulations is similarly treated, such as dried-in inflammatory products, which have formed first a caseous and then a calcareous mass. We frequently find such calcareous material surrounded by a fibrous capsule in the lungs and elsewhere. INDIVIDUAL FORMS OF INFLAMMATION". 103 IV. — INDIVIDUAL FORMS OF INFLAMMATION. "We have already seen that all the phenomena of inflammation which we have been studying are not always present in the same case, and that they exist in varying proportions in difterent cases. The variations in this regard have been already to some extent indicated, but it may be well briefly to refer to some of them here. In almost all cases of inflammation hyperasmia occurs, even in the more chronic. Some slight inflammations of an acute char- acter show little beyond hyperemia. The redness of the skin produced by exposure to the sun in a single day in summer is an instance of this. Doubtless there is along with the hypersemia increased transudation through the vessels, and the subsequent desquamation of the epidermis shows that it has been damaged, and, in fact, partly killed. It is similar with the cutaneous .rashes in scarlet fever and measles. There is probably more or less exudation in all inflammations. The fluid constituents of the blood permeate the tissues and we frequently find them cedematous, and leucocytes are to be found in the tissues frequently in great abundance. In the examination of the tissues after death the presence of round cells is the most unequivocal sign of inflammation. These cells are found perme- ating the tissues generally in acute inflammations, but they are usually more localized in the chronic forms, and in that case they are associated with the new formation of tissue. In very acute inflammations they may be produced in such abundance as to break up the tissue and come together to form an abscess. In the formation of an abscess there is nearly always some destruction of tissue, not necessarily the death of considerable pieces of tissue so as to form sloughs, but the molecular disintegration of the tissue which breaks down before the crowding leucocytes. These two circumstances, namely, the great exudation of leucocytes and the necrosis of the tissue, imply that the irritant is a very severe one. In a large proportion of cases the irritant is of a septic nature, and we know that abscesses most frequently form in connection with septic wounds, etc. It may be said then, that where we find leucocytes in abnormal numbers in a part we conclude that in- flammation has been present, and if they be in very extraordinary numbers, we infer that the inflammation has been very acute. There are some cases which warrant the application of the term infective inflammation. This term infective is to be carefully distinguished from infectious, which involves the idea of a disease communicable from one person to another. By infective is meant a morbid condition which has a tendency to spread from its original seat to parts around or at a distance. An inflammation is infective when it is what is called " spreading," and it is to be inferred that in these cases the products of inflammation contain some irritating or phlogogenic material. The products of ordinary inflammations are not infective, and inflammations are not naturally " spreading." 104 INFLAMMATION. When an inflammation has the infective characters there are always bacteria present in its products, and we may presume that these are related to this peculiarity. The term phlegmonous inflammation is used to designate an acute inflammation of the connective tissue of the body, usually that beneath the skin. The inflammation is nearly always due to some specific infective material, as in erysipelas. There is rapid development of redness and osdematous swelling of the tissue, generally going on to suppuration, and frequently with some necrosis, evidenced by the formation of sloughs. Sometimes an inflammation of a surface is associated with pro- gressive destruction of tissue called ulceration. This means that the vitality of the tissue is being gradually destroyed and the structure breaking down, the process being well expressed by the designation molecular necrosis. Now, in order to this the presence of some very virulent irritant is necessary. Probably it does not occur except under the action of very specific forms of irritation, such as we shall have an opportunity of studying afterwards. Sometimes the ulceration progresses very rapidly, so that consider- able sloughing may combine with the molecular necrosis. Ulcers of this kind are sometimes called PHAGEDiENic. The irritation may be so intense and the necrosis so rapid that there is no time for much exudation of leucocytes. As a rule, however, profuse sup- puration exists along with ulceration, the intense irritation inducing a very abundant emigration of leucocytes. Again, an acute inflammation sometimes produces degeneration of tissues in a more pronounced manner than usual. This applies especially to cases in which the parenchyma of organs is engaged, as in inflammations of the kidney where the renal epithelium is specially involved. We have already seen that the inflammation produces cloudy swelling in this" case, and this readily goes on to fatty degeneration. Fatty degeneration is also manifested in inflammations of the brain, where it is sometimes almost the only evidence post mortem of the existence of inflammation. We have already adduced a sufficient number of instances of NEW FORMATION in inflammation. It is to be remembered that all such new formations have a striking tendency to contract and form a very dense connective tissue. When chronic inflammation exists in a organ such as the liver or kidney, this contraction frequently gives rise to considerable contortion of the normal tissue, which is often the seat of degeneration. This tissue, by the presence of the new-formed connective tissue, is pressed on, and, after degenera- tion, is absorbed. In this connection, we may speak of indura- tive INFLAMMATION, the strictures being rendered hard by tho dense contracting connective tissue. RETROGRADE METAMORPHOSIS. Under this designation are included a number of conditions, all of wMch imply a degradation of the nutritive processes in the tissues. As the cells are concerned in the nutrition of the tissues, it is for the most part these which are at fault, although it may be that in some cases the most manifest ■s'lsible changes are not in them. The most extreme case is, of course, where the nutrition ceases altogether, and the structure dies. Short of that, we have various forms of change manifesting themselves. Thus there is a simple diminution of the vitality, and the structures dwindle. Again, the chemical constituents of the structures change, split- ting up, it may be, into more elementary principles. Or the tissues are unable to prevent the deposition in them of extraneous ma- terial, which is thus infiltrated into them. These last are called infiltrations, whereas the conditions in which there is a degrada- tion of the normal constituents into lower chemical substances are designated degenerations. NECEOSIS: GANGRENE. Under the designation necrosis are included conditions in which the vitality of portions of the tissues entirely ceases; there is a local death. We have here to consider the conditions under which necrosis occurs, the appearances of and changes in the dead por- tions of tissue, and the effects on neighboring parts and on the organism as a whole. Causes of E"ecrosis. — The vitality of a part will be lost (1) if it be deprived of its supply of nutriment by interference with the circulation, or (2) if by some deleterious agent, or otherwise, the constituent elements, the cells, are so interfered with that they cannot carry on the vital processes. It is obvious that under vary- ing circumstances the tissues will have different powers of resist- ance, and that the tissues differ among themselves in this respect. The tissues of an old person will be less able to survive the attacks of certain agents than those of a young person, and any preceding degradation of a tissue, from whatever cause, will render it more susceptible to necrosis. Interference with the circulation caus'es necrosis, and here it is the CAPILLARY CIRCULATION we have to do with. If a tissue be of normal vigor, there must be complete stasis in the capillaries before necrosis occurs; any survival of the circulation in these 106 RETROGRADE METAMORPHOSIS. vessels, however small, is sufficient to enable the capillaries and surrouiidiniij tissues to live on. We have already seen that ob- struction of AN END-ARTERY, by embolism or otherwise, leads to this stasis in the capillaries and resulting necrosis of the tissues. A complete obstruction of the veins will have the same effect, but they anastomose so completely that this can occur but rarely. It does occur approximately when a piece of intestine is incarcerated in a sac with a narrow neck, and we know that under these cir- cumstances gangrene is very liable to occur. Even extensive thrombosis, especially when other conditions, such as weakness of the heart, conspire-, may lead to gangrene, as in fevers. The obstruction of the capillaries may be directly produced. If a cavity approaches the surface of a lung, it may undermine the pleura, and, by obstructing the capillaries, cause a slough to form. Very often adhesion of the two layers of t^ie pleura occurs, and vessels pass from the parietal to the pulmonary layer and nourish it; but where such adhesion does not take place, there is frequently sloughing, and pneumothorax may result from the partial separation of the slough. Similarly, an ulcer of the in- testine may undermine the peritoneal coat, and so cause sloughing and perforation. Less directly, weakness op the heart may so far interfere with the circulation in the capillaries, especially of distant and dejien- dent parts, as to contribute to necrosis. It is obvious that this cause alone can never produce necrosis, but we shall see after- wards that this is a powerful predisposing cause. Turning next to cases where the necrosis is due to a direct action on the tissues, it may be said that the vitality of the cells of a tissue may be compromised by chemical agents acting on them, by direct traumatic agents, or by excessively high or low temperature. The chemical products of putrid decomposition are often peculiarly virulent. We have already seen that they frequently cause the most intense inflammation, and the inflamma- tion is commonly accompanied by necrosis. In fact, the infective inflammations, such as those of pyaemia, are, for the most part, necrotic. When, in pyaemia, ulcerative endocarditis, etc., bacteria exist alive in the body, and form colonies in places to which they are carried, they produce necrosis of the immediately surrounding tissues, not probably by their direct action, but by that of their products. We know also that decomposing urine in the tissues produces the most intense inflammation, generally along with ex- tensive sloughing. It is obvious that direct traumatic injuries may destroy the vitality of the tissues, either directly or else by in- terfering with the supply of blood. In cases of traumatic necrosis it is probable that, besides killing the tissues, the agent will so far interfere with surrounding parts as to induce inflammation. In fact, it can hardly fail to be seen that there is commonly a close con- nection between the causes of necrosis and those of inflammation. Excessive heat or cold is a cause of necrosis, the vitality of the cells being destroyed by excessively low or high temperatures. A necrosis: gangrene. 107 very short immersion of a living part in water heated to 130° to 136° F., or in a freezing mixture reduced to 4° to 0° F., suffices to kill it. If the temperature be slightly less extreme, a short immersion produces a violent inflammation, and a long immersion may still result in necrosis. There are certain forms of necrosis still to be considered that depend on causes which cannot be absolutely brought under one or other of the categories already mentioned. One of the most interesting of these is senile gangrene. It is known that in certain cases a slight injury to the toe, such as cutting the nail too deeply or tearing off of a rag-nail, may lead to a necrosis which spreads from the seat of origin to the foot, or even to the lower part of the leg. Such a trivial injury in a healthy person would lead at most to a trifling inflanimation, but in these old persons gangrene is the result. The explanation is that, to begin with, the circulation is so seriously interfered with that the tissues are already, as it were, half dead, and a very slight cause suffices to suspend their vitality altogether. In addition to weakness of the heart, there is in these cases always atheroma of the arteries, and sometimes even thrombosis on the atheromatous patches. To this must be added the weakness of the tissues which may be presumed to exist in old age. Of someAvhat similar significance is the softening of the brain which often occurs in old people from simple atheroma of the arteries, even without thrombosis. In a healthy person complete obstruction of an artery is necessary in order to softening of the brain-substance, but in old persons the mere lessening of the cali- bre of an artery by an atheromatous patch is often sufficient to cause softening. These softenings are very often on the surface of the brain, and lead as much to weakness of mind, etc., as to motor paralysis, whereas the softenings from embolism are much more frequently central, and lead to more definite loss of motion. In former days there used to be epidemics of what is now recognized as ergotism from eating bread made of grain mixed with ergot of rye. In these epidemics the symptoms frequently culminated in gangrene, usually beginning in the toes, but extend- ing thence, and sometimes attacking the ears, nose, etc. The gangrene is usually accounted for by the anaemia due to the spas- modic contraction of the arteries from the action of the ergot. This explanation has been doubted, and the anaesthesia which is a concurrent symptom has been adduced as the cause. Possibly the intei'ference with the circulation, the directly poisonous action of the agent, and the exposure to injury to which a part devoid of sensation is liable, may all have to do with the occurrence of gan- grene. In HOSPITAL GANGRENE there is a pirogressive necrosis of the tissue, beginning usually in a granulating wound, and resulting either in considerable sloughing or molecular necrosis. The gan- grene travels mostly along the connective tissue, and so may undermine the skin, or isolate muscles or bloodvessels. The dis- 108 RETROGRADE METAMORPHOSIS. ease is due to a specific virus, which spreads in the spaces of the loose connective tissue. Changes in the dead tissue. — When a tissue dies in the living body there is, at first, no obvious change in its anatomical charac- ters by which it could be distinguished after death from that which has survived. But the dead tissue is liable to undergo changes, chiefly chemical, by which its structure is altered, and it becomes obviously different from the remaining tissue. The different forms of necrosis, indeed, have been divided according to the character of the changes assumed by the dead tissue. It will be understood that, in the case of external parts, ordinary putre- factive decomposition will often occur and dominate all other changes, so that it is chiefly in internal parts that we find those which occur independently of decomposition. 1. Coagulation-necrosis is a term which has recently come into use to designate a condition described very fully by "Weigert (Vir- chow's Archiv, vol. 79). The process is to be compared with the coagulation of the blood, the coagulated tissue being equivalent to the fibrine. In fact, the formation of a thrombus is a kind of co- agulation-neci'osis implying the death of leucocytes, and the forma- tion of a dead structure, the fibrine. We have already seen that the coagulation of the blood is related to the death of white blood-corpuscles. In dying, these cells set free the paraglobulin, which is one of the principles that go to form fibrine. Now the active cells of the tissues generally con- tain paraglobulin, and if the fibrinogenetic substance be present, as it is present in the lymphatic fluid which bathes the tissues, then coagulation may take place if the cells die and yield their paraglobulin and ferment. In order to this coagulation the tissue must be a very cellular one, and an abundant supply of fluid con- taining the fibrinogenetic substance must be present. We meet with this change, chiefly in cases where death has occurred suddenly, in a limited piece of tissue, while the parts around remain vigorous. It is seen very typically in many cases as a result of embolism ; the embolic infarction owes its dense character largely to the coagulation of the tissue. Sometimes this occurs without much hemorrhage, and, in the kidney for instance, we often find a pale, wedge-shaped infarction of almost cheesy consistence. But even when there is hemorrhage the tissue is commonly coagulated as well. Another example is sometimes afforded by muscle which under-, goes a change to which the name colloid degeneration is some- times given, but which is perhaps better called waxy or hyaline degeneration. In typhoid fever, and, to a less extent, in. acute tuberculosis, scarlet fever, smallpox, etc., this peculiar change is frequently observed in the muscles, chiefly the adductors of the arms, the rectus abdominis, diaphragm, etc. To the naked eye a portion of the muscle is seen to be pale and glassy-like, resembling the flesh of uncooked fish. This occurs in patches, and where COAGULATION-NECEOSIS. 109 thus affected, the muscle appears to be more brittle, hemorrhages sometimes occurring in the patches. Under the microscope, the primary change is seen to be a disappearance of the transverse strife, and a greatly increased transparency of the muscular fibre. Fibres affected in this way may be seen close beside unaffected ones. The affected fibre is obviously unduly brittle, having a tendency to break transversely, and to crumble (see Fig. 28). By Pig. 28. Coagulation-necrosis or hyaline degeneration of muscle. X 75. this process it often happens that an oval piece of degenerated fibre gets isolated, the two tapering ends being irregularly crumbled (see Fig. 29) while the sarcolemma collapses on the ends of the oval piece. A similar glassj' transformation occurs in the un- striated muscle in the acute diseases mentioned. Fig. 29. A coagulated clump of muscle more highly magnified. Tfie sarcolemma surrounds it, drawing together at the ends. X 350. A somewhat similar condition is occasionally seen in paralyzed muscles, where it may exist side by side with ordinary atrophy and fatty infiltration. It has also been produced artificially in living animals by freezing the ipuscles. 110 RETROGEADE METAMORPHOSIS. The process here is a coagulation of the contractile substance. This coagulation may even be brought about in the muscles after death if they be injured before the occurrence of the cadaveric rigidity, which may be regarded as the expression of the normal post-mortem coagulation of the sarcocele. In the case of typhoid fever it may be supposed that there is a premature death of in- dividual muscular fibres, induced by the phenomena of the disease, and, perhaps, assisted by traumatic causes. Another example of coagulation-necrosis is afforded by diph- theria. In this disease the exudation which appears on the fauces is, indeed, in part a true fibrinous exudation, but it is also in part composed of the coagulated superficial portions of the mucous membrane. The TUBE-CASTS of the kidney are also, to some extent, the result of coagulation of the epithelium of the uriniferous tubules, the Fig. 30. ■0] ),o (B' % Q^ Formation of a pyaemic abscess in the kidney. Section stained with aniline brown. The necrosed portion, a, shows no structure and is not stained. The surrounding inflamed area {i, b, b) is deeply stained. death of the epithelium occurring in connection with inflamma- tion of the organ. In all cases of coagulation-necrosis the tissue becomes more firm and sohd. Sometimes the coagulum assumes a fibrillated character, DESICCATION AND MUMMIFICATION. Ill but perhaps more frequently it is homogeneous, the structure of which the tissue is composed being obscured. It is characteristic of the process that the nuclei of the cells become obscured and are no longer brought into view by staining the tissue. Referring back to the formation of the white thrombus (p. 40) it will be remembered that the disappearance of the nucleus is there a characteristic occurrence, and in coagulation-necrosis it may be regarded as of similar significance, implying the death of the cell. This peculiarity may be used to distinguish the exist- ence of this process. If we stain a section of a tissue, as in the accompanying figure (Fig. 30), and find that a piece shows no nuclei, we may infer that necrosis has occurred. 2. Caseous necrosis is a condition in many respects analogous to coagulation-necrosis. "We have seen that the latter is an acute process, but caseous necrosis mostly occurs when the loss of vitality is brought about more gradually. It is met with mostly in tuber- culosis and syphilis, and in both of these we have a specific virus acting on the tissues. It may be a question how far the death of the tissue is due to the action of the virus or to the obstruction of the circulation. This form of necrosis also occurs occasionally in tumors and inflammatory products. The structures involved are cells, and so we have material for the resulting coagulum. But before the actual necrosis fatty de- generation occurs in the cells, so that the coagulum is furnished with fine fat-granules which give a very opaque appearance to it. To the naked eye the density of the tissue with its opaque appear- ance is suggestive of cheese, and hence the name. Under the microscope, the necrosed tissue presents the same obscuration of the nucleus as Ave find in coagulation-necrosis, but in addition all details of structure are completely obscured by the general opaque granular appearance presented by the caseous material. In fact, this general granular opacity frequently renders the orig- inal constitution of a structure exceedingly obscure. 3. Desiccation and mummification is a simpler process than those we have been considering. The part dies,. and instead of coagulating, it simply dries in and shrivels. An example of this on the large scale is afibrded by some cases of extra-uterine preg- nancy, where the mother survives the death of the foetus. The latter may remain for years in the abdomen, simply drjdng up. Virchow found muscle, connective tissue, and vessels still quite recognizable after twenty years. In twin pregnancy, also, one of the foetuses may die at an early period, and be born as a flattened, shrivelled object Avith that which reached the full time. It will be obvious that cases of caseous metamorphosis and coagulation- necrosis may be brought under this heading, the resulting material having often a tendency to dry and contract. Calcareous infiltra- tion frequently overtakes such structures finally if they are not absorbed by the processes to be presently considered. 112 RETROGRADE METAMORPHOSIS. But under certain circumstances an external part also undergoes desiccation, and the condition is called dry gangrene or mummi- fication. In some cases the drying-in will be facilitated by the part being at the time of death deficient in moisture, as where the gangrene has resulted from embolism or in senile gangrene. It will not probably occur if there has been much coincident inflam- mation. The part undergoes a gradual deepening of color; at first merely livid, it passes on into purple, deep blue, and even black. This is due to the blood-coloring matter being dissolved out and staining the tissues, which deepen in color as the pigment becomes concentrated by drying. The cuticle by and by gets raised by red fluid accumulating beneath it, and when it has separated evaporation goes on more rapidly, and the piece of tissue withers, shrinks, and is converted into a hard black mass, often with a mouldy smell. In the case of dry gangrene, the deficiency of fluid prevents the agents of decomposition obtaining a proper nidus. 4. Softening or colliquefaction is seen typically in those ne- croses of the brain-substance which are so frequent in connection with embolism. The breaking down of the brain-substance is accompanied by fatty degeneration, so that a kind of fatty emul- sion is formed. When external parts die they very often undergo softening with decomposition. This occurs chiefly in cases where there has been considerable inflammation, so that the parts are saturated with fluid. An ordinary slough in an external wound is an in- stance of this. When a considerable portion of a limb is killed and separated by sloughing, then we speak of it as moist gan- grene. The appearances are well seen where a portion of a leg has died in consequence of a traumatic cause. The parts which were at first hot, red, and painful, become mottled with brown, blue, and black, and may even present blisters. They become cold and darker, except at the margin where a dusky-red line of demarcating inflammation appears. The tissues get universally stained with blood-coloring matter, the cuticle gives way, and decomposition advances and causes breaking down of the tissues, which are separated as sloughs in all stages of softening, and exhaling a strong odor. The fluid which permeates the tissues contains fat, phosphates, and other salts, as well as extractives from the tissues. We have now to trace the further course of events in necrosis. In many cases the necrosis limits itself almost at once; the agent has been at work once for all, and has killed a certain por- tion of tissue, and it only remains, by processes which we shall now describe, to get rid of the dead piece. In other cases the agent acts also on surrounding parts, though, being less severe, it only produces inflammation, while necrosis may occur at a subse- quent period. This will happen the more readily if decomposition SIMPLE ATROPHY. 113 occurs in the gangrenous part. The juices of decomposition ex- tending to the inflamed parts may cause a further serious extension of the necrosis. Thus in traumatic gangrene it may be long before a proper line of demarcation forms, and the necrosis becomes definite. The importance in such cases of preventing decomposi- tion in the dead part will be obvious. But, again, in predisposed tissues, which are less able to resist than normal ones, as in old persons, or in persons the subject of diabetes, the gangrene may extend without there being any considerable inflammation or de- composition. The final disposal of the dead tissue. — In this, inflammation plays a most important part. "We have seen that violent inflam- mation is often produced by the same cause as the necrosis, or may supervene on it. This will mostly be the case in external parts where decomposition often comes in to increase the inflam- mation. The inflammation is accompanied by exudation and hypersemia, like other inflammations, and commonly goes on to suppuration. A layer of pus comes thus to divide the dead tissue from the living, and the dead is cast ofl' as a slough. There re- mains a suppurating wound or ulcer. This loss of tissue, whether molecular or as a massive slough, is the essential feature of an ulcer of whatever kind, and a suppurating surface will usually be left. In internal parts, if the necrosis be accompanied or followed by the production of irritating chemical substances, then a violent inflammation will be produced around. It is so in the case of pysemia, where there is septic embolism. In this case the inflam- mation will usually be violent enough to produce suppuration, and the result will be the formation of an abscess. (See Fig. 30.) In the case of internal parts where there is no disturbing de- composition, or even in external parts which are protected from septic contamination, the inflammation is of a much milder char- acter. The necrosed portion now comes to act as a foreign body or dead piece of tissue, and is subject to the changes already- described at p. 102. The dead tissue is often eaten into and replaced by vascular granulations, which finally contract and leave a small residue of connective tissue; or the dead piece is encapsuled and may lie quiescent. ISTot infrequently the encap- sulecl tissue undergoes infiltration with lime-salts, as we shall see afterwards. In the case of necrosis in bone the external capsule is frequently composed of new-formed bone. SIMPLE ATEOPHY. There comes up here for consideration, to begin with, what may be called physiological atrophy. At certain periods, for instance, the milk teeth drop off", and this is effected by an atrophy of the fang so that the crown is shed. At a still earlier period the thymus 114 EETEOGRADE METAMOEPHOSIS. gland atrophies. Then again throughout life there is a continual shedding of the hair, and if a cast-oif hair from the eyelash, for instance, he examined under the microscope, it will be seen that its bulb is atrophied, and this is the cause of its being shed. In some persons the hair of the scalp is largely shed at a compara- tively early age, without being properly reproduced, there being here an atrophy of the hair-sheath and };iapilla. Then there is the normal atrophy of the tissues generally, which occurs in old age. The atrophy of old people may in many cases be due to some organic disease whose symptoms are not manifest; but we are all familiar with the healthy old person with shrivelled hands and face and plicated skin. In all these cases there is a kind of intention in the tissues, so to speak, according to which they live a certain period and then decay. As Paget has pointed out, such atrophies may almost be regarded as active processes. The fall of the leaf is due to an active absorption or atrophy of the fibres uniting it to the stem ; if the leaf dies before its time, or is killed, it remains hanging, but in the natural course it drops when its time is come. So with our tissues and the whole organism, there is a period to their activity. The period varies in different persons, and in this regard hereditary influences have an important bearing. Just as these largely deter- mine the period of growth of the body and its rapidity, so do they influence the duration of activity of the tissues. This is plainly seen in the case of the hair; l)aldness runs in families, just as lon- gevity does. Turning to more strictly pathological atrophies, we may distin- guish three forms : 1, those dependent on the supply of nutrition being defective; 2, those in which disuse of a structure causes its atrophy; and, 3, those in which the atrophy is related to some .change in the nervous system. General emaciation is the most obvious example of the first class, occurring, as it does, either directly from interference with the supply of food, or from impoverishment of the blood by exces- sive waste. The food may be procured in insuflicient quantity, or a stricture of the oesophagus may interfere with its passage to the stomach, or the stomach may reject it after it has been swal- lowed. On the other hand, there is frequently, in advanced phthisis or ulcerating cancers, a large consumption of the nutri- tious material available to the body, and the tissues suffer accord- ingly. In these and other cases of general atrophy, the tissues dwindle in different proportions, the fat most; next to it the spleen, testicles, liver, muscles, bones, and least of all the central nervous system. As belonging to this class also may be mentioned the atrophies OP fevers, although perhaps the atrophy here is to some extent more of an active process. In fevers there is, with the high tem- perature, an increased combustion of the nitrogenous constituents of the tissues. If the supply of nutritious material were abundant, SIMPLE ATEOPHY. 115 then this would not necessarily lead to atrophy, but the febrile patient eats little or nothing, and, besides, the constitution of the blood is altered, and so the structures atrophy, sometimes with great rapidity. To the same class belong local atrophies from local interference with the blood-supply. The overgrowth of connective tissue in interstitial inflammations of parenchymatous organs causes atrophy of the secreting structure of these organs, as in the case of the liver, kidney, testicles, etc. Growing tumors or aneurisms cause atrophy of the tissues around, etc. Of the second class, the most obvious are the atrophies of muscles FROM DISUSE. Paralysis or anchylosis of a limb results in its emaci- ation. In conjunction with the atrophy of the muscle, there is often an overgrowth of the adipose tissue between the muscular fibres. The retrograde changes which occur in the uterus after delivei'y may possibly be regarded as another example. As to the ATROPHIES DEPENDING ON NERVOUS LESIONS, these are somewhat obscure in their essential pathology. It is true that after motor paralyses of all sorts, atrophy of the muscle occurs, after hemiplegia, for example; but the atrophy in this case may be from disuse of the muscle, just like atrophy after anchylosis of a joint. There are, however, some atrophies following nervous lesions which are rapid in their development, and appear to be due not directly to the paralysis, but rather to an interference with the nerve-centres concerned in the nutritive processes. It has been abundantly shown by experiments in animals that when a nerve- stem containing motor fibres is divided, there is a coagulation, dis- integration, and subsequent absorption of the medullary sheaths of the nerve-fibres in the stem. Erb states that the axis-cylinder per- sists, while others assert that it too atrophies. In any case, the muscles supplied by the nerves also atrophy. Even in the first week there is considerable wasting, and after a month the muscle has scarcely half its former thickness. This is a simple atrophy, the muscular fibres getting thinner, and presenting the nuclear change to be referred to afterwards. The atrophy which occiirs in a common hemiplegia is not nearly so rapid as this, and is often scarcely perceptible after a month. In comparing the lesions in the nervous system in these two cases, the diflference will at once appear; in the one the interruption to the motor fibres is high up above the spinal cord, while in the other it is low down, after the fibres have left the cord. But there are some forms of paralysis in which atrophy is a peculiarly pronounced feature. Infantile paralysis is one example; progressive muscular atrophy is another ; and glosso-pharyngeal or bulbar paralysis a third. In these the atrophy is even more strik- ing than the paralysis, and in other forms of paralysis there is often a greater loss of function with much less atrophy. These forms of atrophy have been classed as tropho-neuroses, as it is evident that besides the mere paralysis there is some lesion of the structures which command the nutrition of the muscles. These structures 116 RETEOGEADE MET AMOEPHOSIS. are, presumably, trophic nervous centres situated in the spinal cord, and, as we shall see afterwards in connection with diseases of the nervous system, it is to be inferred that these trophic centres are near the motor centres, or are identical with them. ITow the motor centres of the cord are in the anterior gray cornua, and the trophic centres are presumably there also, taking part in the de- struction which affects the cornua in this class of diseases. In infantile paralysis, for instance, there is an acute inflammation, with destruction of centres in the anterior cornua. Another case of a supposed tropho-neurosis is the atrophy with paralysis which occurs in lead-poisoning. Here the paralysis and atrophy affect the extensors of the arm, and the localization of these to a group of muscles has led to the view that here also the ganglion-cells of the anterior cornua are involved. This localiza^ tion has not been made out, and there is no apparent reason why the lead should specifically attack this particular group of ganglion- cells. Still we know that poisons have frequently special affinities, and the possibility is not to be excluded. In all these forms of muscular atrophy certain changes occur in the muscles. There is an increase in the nuclei of the muscular fibres, and sometimes an increase of the connective tissue, a con- dition which some have regarded as an interstitial inflammation. Sometimes also a great development of fat occurs in the connective tissue of the muscles. These changes are secondary; they are found in the muscles after division of nerves, and are therefore not to be regarded as the cause of the atrophy and paralysis. The muscular fibre itself becomes smaller, 'and is occasionally the seat of fatty degeneration. As the disease proceeds, the muscular fibre may altogether disappear. Among the tropho-neuroses is also commonly included that peculiar axkophy of half the face, of which a few cases have been published. This atrophy affects all the structures, bones, muscle, skin, etc., but is not accompanied by paralysis. It does not follow strictly the distribution of any nerve, although closely approxi- mating to that of the fifth. The pathology is obscure, but it is usually regarded as due to an affection of the trophic centres wherever they are. ALBUMINOUS INPILTEATION. This is a term having a meaning equivalent to Cloudy Swelling as used by Virchow, and to Parenchymatous Degeneration. The condition has been incidentally referred to in considering inflam- mation. Its essential nature may be expressed by stating that in it cells increase in bulk, while the added material is not properly assimilated and so deposits in the cells in visible albuminous granules. The enlarged cells are therefore clouded (see Fig. 31), and the nuclei obscured. The condition implies a qualitative defect in the nutrition of the cells, while quantitatively there is ALBUMINOUS IXFILTEATION. 117 increase. The qualitative defect is very often still further mani- fested by the occurrence of fatty degeneration (an in the figure) along with the cloudy swelling, and these two conditions, in fact, frequently run into each other. Fig. 31. '■-<»- ( „ '// Cloudy swelling of renal epithelium with slight fatty degeneration. A portion of a tubule is shown, and some isolated cells. From a case of acute phthisis pulmonalis. X 350. The condition is brought about by causes which irritate cells and at the same time increase their supply of nutritious fluid. One of these is inflammation, and cloudj- swelling is the most pro- nounced change in the earlier stages of the parenchymatous inflammations of organs, especially of the kidneys. Besides by inflammation, it is produced by nearly all febrile diseases, and seems to bear some relation to the elevation of temperature. It is met with in the acute specific fevers, in pneumonia, erysipelas, pyaemia, acute phthisis pulmonalis with high temperatures, etc. It is as if the blood, altered by the elevation of temperature and otherwise, acts as an irritant, producing a kind of sub-inflamma- tory condition. As the blood is carried throughout the body the parenchymatous change is not limited to any single organ, but is found in the liver, kidneys, muscular fibre of the heart, voluntary' muscle, and elsewhere. The name cloudy swelling implies that the affected cells are enlarged. It is to be observed also that the cells concerned here are the proper cells of organs, that is to say, the structures which are concerned in their functions and make up the greater part of their bulk. Hence it arises that considerable enlargement of the organs as a whole may occur from this cause, and this is especially seen in the liver, which sometimes shows great increase in size and weight in acute fevers. The kidneys are also sometimes con- siderably enlarged from this cause. 118 RETROGRADE METAMORPHOSIS. FATTY DEGENERATION. In this condition, which aifects the cells of tissues, we have a change in the chemical composition of the cell-contents; the albu- minous constituents split up and yield fat. Before going fui'ther it may be well to remember that fat exists in the tissues in two conditions; in the first place as free fat, and in the second place in such close chemical union with the albuminous constituents that it no longer responds to the ordinary reactions of fat. For instance, besides free fat in muscular fibre there is much combined fat, and in order to detect the latter, by extraction with ether for example, it is necessary in the first place to decompose the albuminous com- binations. When these combinations are decomposed the fat can be seen in the muscle as minute drops, and it can be extracted with ether. It may be well, in the first place, to take one or two typical examples of fatty degeneration, and endeavor to gather from them some conception of its pathology. The well-known experiments of Bauer on the effects of poisoning dogs 'WITH PHOSPHORUS aftord an excellent example to begin with. This author deprived a dog of food for a period of twelve days, till it had consumed all its available store of fat, and the excretion of nitrogen in the urine had reached a constant minimum of eight grammes in the twenty-four hours. He then gave the animal small doses of phosphorus and found that the excretion of nitrogen markedly increased on to death, reaching treble its former amount, namely, 23.9 grammes. The phosphorus in the blood had in- duced a marked consumption of the albuminous tissues, manifested in a great increase in the urea excreted. But now when the animal was killed, an enormous increase in the free fat in the organs was found; the liver and muscles contained about three times their normal amount of fat, and other structures such as the renal epithelium, and the walls of the bloodvessels, presented marked fatty degeneration. Here was an agent circulating in the blood, whose effect was the decomposition of the albuminates and the formation of fats. Again, it has been mentioned above that in anemias there is often a marked fattj' degeneration of the muscle of the heart, of the hepatic cells, and of the renal epithelium. In this case a de- terioration of the blood, and especially a defect in the hemoglobin, determines the occurrence of fatt}' degeneration. "When an artery in the brain is occluded we have already seen that necrosis frequently occurs, accompanied Ijy softening; but, along with this or preceding it, there is a pronounced fatty degeneration affecting the brain-substance and resulting in the formation of large cells filled with finely divided fat (the so-called compound granular corpuscles). A similar aggregation of fat occurs at intervals in the walls of the capillaries (see Fig. 32). It is true that the fat here may be partly derived from the myelin of the disintegrated medullary sheath, but it is not probable that the FATTY DEGEXERATIOX. 119 fat of the capillary nuclei can have this source. Here is a case in which a local deprivation of blood has the eifect of inducing a fatty degeneration. We have also instances of fatty degeneration in inflammations, where the vitality of the cells is compromised, and in quickly Pm. 32. Fatty degeneration in the cerebral vessels in softening of the brain. (Paget.) growing tumors, where, perhaps, the nutritive processes are sub- ordinated to the unduly active formative ones. "We have now to endeavor to explain the occurrence of fatty degeneration in these various circumstances. There are some of them which we can account for on the same principles as we account for the fatty degeneration in phosphorus-poisoning. In acute yellow atrophy of the liver the hepatic cells break up, and present the characters of pronounced fatty degeneration ; this is, presumably, due to the action of some poisonous agent, and it has even been supposed that phosphorus is the agent. Then, again, we have fatty degeneration frequently associated, as we have seen, with cloudy swelling in fevers, etc. In this case the fatty degen- eration may be due to the splitting up of the loosely combined fatty-albuminous principles. The same applies to some of the more local fattj' degenerations. The mere degradation of the tissue may allow of these decompositions occurring, as when fatty de- generation occurs in yellow softening of the brain. But there are some cases in which more fat appears in the tissues than the mere breaking up of the normal combinations- would account for. In these cases we must suppose a different mode of origin. It seems to be a function of most of the active cells in the body to form fat, which is oxidized or burnt either in the same place or elsewhere. The cells may form fat even from albuminous material. The mammary glands secrete milk just as abundantly when the 120 RETEOGRADB METAMORPHOSIS. animal feeds on meat free from fat as on a ricUy fatty diet. Mus- cular tissue contains fat loosely combined with the albumen, and probably it is continually forming fat, which is continually bemg oxidized. But something may interfere with its oxidation. The supply of blood may be insufficient, the quality of the blood may be altered, or the vitality of the cells may be so reduced as to ren- der the process of oxidation imperfect. It is possible, then, that there may be in these cases, not so much an increased decomposi- tion of the albumen as a decreased oxidation of the fat, and the latter will appear in the tissue as free fat, with all the appearances of fatty degeneration. We have now to consider the actual anatomical _ changes presented in fatty degeneration and visible under the microscope. The degeneration occurs mainly in the cells of the tissues. The fat, arising as it does by the chemical decomposition of the proto- plasm of the cell, appears in the form of fine drops or granules, which are strongly refracting. These granules are still separated from each other by the remains of the cell contents and are there- fore isolated. It may happen in this way that, as in Fig. 33, a Fig. 33. Pig. 34. Fatty degeneration in an atheromatous aorta. The shapes of the cells brought out by the fat; a, from internal coat; 6, muscle-cells from middle coat. X 350. Fatty degeneration of cells in a cancer of the mamma ; a, slightly affected ; 6, more so ; c, completely fatty — the compound granular corpuscle. X 350. fatty degfeneration occurring in a structure may render its con- stituent cells unusually distinct, their form being brought prominently out by the fat in them. As time goes on, the fa1> granules increase till the whole cell is filled with fine refracting oil drops, which still remain isolated (see Fig. 34), being each surrounded by an albuminoxis envelope. The process is, in fact, \Qvj much like what occurs in the cells of the mammary gland in the secretion of milk, the colostrum cells being like the fully degenerated cells, which are often described as compound granular corpuscles. When finely divided fat suspended in fluid is present in the living FATTY DEGENEEATIOX. 121 tissues, it is very readily absorbed. We know how readily the emulsionized fat in the alimentary canal is taken up by the epi- thelium, and passed on into the lacteals. When milk is injected into the abdominal cavity of a living animal, or even laid on the surface of the diaphragm after death, it very quickly passes into the lymphatics. In the case of fatty degeneration of cells, if fluid be present, the cells disintegrate, an emulsion is formed, and absorption occurs just as in the case of milk. But sometimes the fatty degeneration occurs in connection with structures not adapted to absorption, as in a hydrocele, where the tendency is rather to transudation, or in an ovarian tumor. In that case, the fat undergoes further changes, resulting usually in the production of crystals of cholestearine (Fig. 35). This sub- FiG. 35. Crystals of cholestearine; o, large ones from an old hydrocele; h, from stagnant bile in gall-bladder. X 350. stance occurs as a normal constituent of the central nervous tissue and bile, in which latter it is dissolved. Its crystals are rhombic tables whose angles measure 79° 30' and 100° 70'. On adding strong sulphuric acid to a crystal of cholestearine, letting it gradu- ally run in and act on it, the crystal appears to melt from the edge inwards, and take on a fatty appearance, and by and by it gathers into a brown drop. On adding iodine and sulphuric acid to a crystal, there is at first a beautiful display of colors. The changes mentioned above occur when there is abundant fluid in connection with the fatty debris, converting it into an emulsion, which either is absorbed or deposits crystals of cho- lestearine. But when the fluid is deficient, as when the vessels are few and the cells are heaped together closely, in that case the fatty 122 RETROGRADE MET A JIOEPHOSIS . degeneration is often associated with necrosis, and there is a shrink- ing and drying-in of the structure, resulting in the formation of a cheesy-looking material. This process we have already considered under the designation caseous necrosis. The cheesy material used to be regarded as crude tubercle, and the metamorphosis was called TUBERCULIZATION. We have already seen that although caseous necrosis is far more frequent in connection with tubercu- losis than any other condition, yet the name must not be monopo- lized by this process. FATTY INFILTKATION". By this term is meant the deposition of fat in the tissues. The normal fate of fat is, for the most part, to be burnt, thereby assist- ing in the maintenance of the animal temperature. But there may be too much fat formed or absorbed for the uses of the organism or for the purposes of particular parts, and it is then laid down, as it were, in store. In some persons digestion is active, and they assimilate more carbo-hydrates than their organism can oxidize. Such persons are often rather sluggish in their movements, and respiration is not very vigorous, and so the oxidation is less than normal. In that case the spare fat is deposited in the subcutaneous tissue and great omentum mainly. It is infiltrated into the connective-tissue cor- puscles, and it is well known that adipose tissue and connective tissue are to a certain extent mutually convertible. This general deposition is called obesity. Then there are local depositions that are more difficult to explain, which occur mainly in connection with structures that are in some way put out of use. A most typical example of this is afforded by muscles which have become fixed at their two ends by stiffen- ing of joints. The muscle can no longer produce any movement, and its fibres gradually atrophy as we have already seen. At the same time, in the connective tissue around the muscle and in that which supports it, there is a great infiltration of fat, so that adipose tissue appears between and around the fibres (see Fig. 36). Then, again, in pseudo-hypertrophic paralysis — a disease chiefly of chil- dren — there is a similar process. The muscular tissue atrophies, but there is at the same time an excessive transfoniration of the connective tissue into adipose tissue, so that the wasting of the muscle is more than counterbalanced by the excess of adipose tissue, and there is thus a pseudo-hypertrophy. A similar fatty infiltration occurs in the heart. jSTormally, there is a certain amount of adipose tissue beneath the pericardium. But sometimes this becomes excessive in quantity and extends into the muscular substance, between the muscular fibres, so that the wall of the ventricle may be largely composed of adipose tissue. If this fatty infiltration were primary, then we could understand how, in these cases, there should be great wasting of the proper FATTY IXFILTEATIOX. 123 muscular fibre, and there are cases in which the over-loading of the heart seems to be part of a general obesity. But, more "fre- quently, there is reason to believe that the weakening of the heart and the atrophy of the muscle are the primary occurrences, and the fatty infiltration secondary. Fig. 36. Fatty infiltration of muscle from a case of stiffening of the nnkle by an epithelioma of the skin over it. The mus.cular fibres are narrowed, and adipose tissue appears between them. X80. It is difiicult to account for this local deposition of fat in con- nection with muscle. It may be that as normally fat is largely oxidized in mviscle, or largely produced there in connection with the active process of contraction, when the demand is gone it is laid down by the vessels in the neighboring connective tissue. Eat is often deposited in excessive quantity around diseased and USELESS glands, especially the kidney. In hydronephrosis there is often an enormous increase of the fat which normally surrounds the kidney. This is also difiicult to account for. The INFILTRATION OF FAT INTO THE LIVER, which wc meet with very frequently, is also difficult to explain. It is met with, in the first place, in persons addicted to the excessive use of alcohol, and in that case often goes along with an excess of fat in all the organs, probably due to the oxidation of the fat being interfered with by the alcohol. The fat, in these cases, is often very fluid, and the organs have a greasy appearance and feeling. But, in the second place, fat is often found in large quantities in the liver in cases where, in the subcutaneous tissue or elsewhere, there is an actual deficiency of it. The fat in the liver is in the peripheral parts of the lobules, and from this it is to be inferred that it has been brought by the portal blood. This fatty infiltration occurs fre- quently in phthisis pulmonalis, and in other cachectic diseases. Its accumulation under these circumstances may, in part, be ac- counted for by supposing that the fat which is normally used for the formation of the fatty acids and the cholestearine of the bile is not so used and is therefore stored in the hepatic cells. It is known that the secretion of bile is greatly diminished in such 124 RETROGRADE METAMORPHOSIS. cases, and that the bile is watery. In that case the fatty infiltra- tion here would be like that in muscle, due to diminished activity of the organ. Another view, and one having some appearance of probability, is based on the theory that one of the functions of the liver is to prepare fat for oxidation. Naumann (Reichert and Du Bois Reymond's Archiv, 1871, p. 41) has shown that the liver fat is much more oxidizable than ordinary fat, and that in the verte- brata the size of the liver is in inverse proportion to the activity of the respiration, being largest in fishes and smallest in birds. It is, therefore, suggested that in phthisis and cachectic diseases the liver may produce an excess of easily oxidizable fat and store it up ready for use. Hence, perhaps, the utility of liver oils in cases of phthisis, etc. "We have seen that in fatty degeneration the fat appears in the form of fine granules or drops, and that as these increase they re- main isolated. In fatty infiltration there are, of course, first fine fat-drops, but as more fat is added the drops grow in size. In the case of the conversion of connective tissue into adipose tissue, there is a single fat-drop in each cell, as in Fig. 36. In the case of fatty liver the fat-drops are of various sizes (see Fig. 37), but, as a FiQ. 37. Fatty infiltration of the liver. Isolated hepatic cells with drops of fat of various sizes. X 350. rule, much larger than in fatty degeneration. The size is by no means an absolute criterion, but it is an important practical indica- tion. It is only in the liver that there can be much difliculty in distinguishing between fatty degeneration and fatty infiltration, and here the fact that in the latter the fat is deposited at first in the cells at the peripheral parts of the lobules, and always con- tinues more abundant there, is sufficiently distinctive. PIGMENTARY INPILTRATION. In studying hemorrhage we have already seen that a common result of the extravasation of blood is the pigmentation of the tissues around. This pigmentation may be brought about in various ways, and is of various degrees of permanence. In the first place, the blood-coloring matter may be dissolved out of PIGMENTARY IXFILTEATIOX . 125 the corpuscles and stain the tissues, this being an evanescent pig- mentation. Then the dissolved coloring matter may be deposited in the solid form after a time. We may thus have crystals of hsematin in the form of oblique rhombic pillars, or simply amor- phous granules ; the crystals occur mostly in large extravasations. Lastly, there is the pigmentation which results froKi the cells in the neighborhood of the hemorrhage taking up the red corpuscles and becoming pigmented by these. Probably much of the pigmen- tation which occurs as a consequence of chronic inflammation or passive hypersemia is due to this last process, the hemorrhage here being by diapedesis. Chronic catarrhs of the stomach and intes- tinal canal are often distinguishable after death by the slaty color of the mucous membrane. In chronic passive hypersemia of the lungs from heart disease there is a brown pigmentation, frequently called brown induration. The pigmentation occurring in tumors, especially cancers and sarcomas, is often regarded as due to minute hemorrhages, and there are many facts Avhich appear at least to connect it with the bloodvessels. Gussenbauer (Virchow's Archiv, vol. Ixiii. p. 322) asserts that in melanotic tumors there is a thrombosis in the smaller vessels, and that the blood-coloring matter is dissolved out, and is taken up by the cells of the tumors. It is to be remarked that in pigmented tumors there is not a homogeneous distribution of the pigment, but the majority of the cells are unpigmented, and there is often an arrangement suggestive of local foci of origin. It is to be presumed that in these tumors there is some peculiarity of the bloodvessels which allows either of ready extravasation or thrombosis. It is to be added, however, that it is denied by some that the pigment in tumors is derived from the blood pigment, chiefly on the ground that it does not contain iron. Pigment is to be found in thrombi, and in the case of veins espe- cially it may be deposited in crystals as well as in granules (see p. 44). Pigmentation of the lungs may be regarded as a normal con- dition, although it is acquired after birth. It is due to inhalation of particles of dust which are carried into the lung-substance by amoeboid cells, and partly remain in the connective tissue of the lung, and partly are carried to the bronchial glands. "Where this pigmentation is excessive, as in the case of miners, we have a rec- ognized morbid state designated Anthracosis. Other forms of pigmentation occur in the lungs from the inhalation of variously colored stuflr's by workers exposed to them. Icterus is a yellow staining of the tissues with a coloring matter dissolved in the blood serum. This is usually the biliary coloring matter absorbed from the bile-ducts after its secretion. It implies an obstruction to the ducts in some part of their course. A similar staining may be a consequence of the destruction of red corpuscles, their coloring matter becoming dissolved in the blood — the so- called hsematogenous icterus. The BRONZE COLORATION OF THE SKIN in Addison's disease is related to disease of the supra-renal capsules, in which there is a 126 EETROGRADE METAMORPHOSIS. caseous condition, a local tuberculosis. The solar plexus of nerves is probably affected along with the capsules, but the exact path- ology of the condition is not understood. Lastly, a tissue may be unduly deep in color simply from ATROPHY of the other constituents, and a ooncentration of the nor- mal pigment. ^Thus when emaciation occurs, and the fat is absorbed from the subcutaneous tissue, this often assumes an unusually dark yellow or brown hue. An emaciated heart presents in its muscular substance a very dark color from the diminution of the contractile substance and concentration of the pigment. MUCOUS AND COLLOID DEGENEBATION. These two conditions present considerable similarity, and in individual cases it is often difficult to say which of them is actually present. They are characterized by the abnormal occurrence in the tissues of two chemical principles, which are albuminates, and doubtless arise by transformation of the normal tissue-albumen. One of these substances is known as a definite chemical principle, and is named mucin ; the other is not well known in its chemical relations, and is somewhat indefinitely named colloid material. Both have the peculiarity that in the presence of water they swell up and acquire a gelatinous consistence. "With very similar physical characters, and arising under somewhat similar circum- stances, they are distinguished by their difference in chemical ' reaction. Mucin forms a somewhat membranous precipitate with acetic acid, and its solutions are also rendered turbid by alcohol and chromic acid. Colloid material is not obviously altered by these reagents. A PHYSIOLOGICAL TYPE of mucous and colloid degeneration is afforded by the normal secretion of mucus. Here it is known that the epithelial cells, whether of the surface of the mucous membrane or in the proper glands, become converted into goblet-cells, by the formation of mucus within them. The mucus is secreted by the rupture or disintegration of these cells, and the discharge of the material which has swelled them up. In certain pathological conditions this secretion of mucus is exaggerated, notably in the catarrhs of mucous membranes. But this can hardly be regarded as a proper mucous degeneration. In OVARIAN TUMORS a proccss is often visible which closely resembles the secretion of mucus. "We shall see afterwards that the larger number of ovarian tumors originate in a glandular for- mation, and in this gland-tissue most characteristic goblet-cells are often to be seen (see Fig. 38), the gelatinous contents of the cysts formed being obviously secreted in this way. But then, the gelat- inous material does not usually give the reaction of mucin with acetic acid, and is clearly an albumen of a different kind, whose chemistry is not well known. Hence this would be included under MUCOUS AXD COLLOID DEGEXEE ATIOX . 127 colloid degenei'ation, although in histological details resembling the mucous form. Again, in the thyroid gland there are often, even normally, little gelatinous particles visible on dividing the gland, and in the commonest form of goitre (colloid goitre) there is a great increase of this clear gelatinous material. On microscopic examination it is clear that the gelatinous material arises by transformation of the epithelium lining the saccules which form the parenchyma of the Pig. 38. Erom internal surface of a colloid ovarian cyst. The lining epithelium is mostly in the form of goblet-cells, the superficial parts having clear, transparent contents. X 350. gland. The cells swell up and become filled with clear gelatinous material ; by the discharge of this or the disintegration of the cells the colloid contents of the saccules are formed. But this material has not the reactions of mucus. In COLLOID CANCERS there is a similar transformation of the epithelium, so that the cellular masses are transformed into colloid masses, which till the spaces in the stroma. This form of cancer is most frequent in the stomach and large intestine, and it may be thought that this colloid transformation, so closely resembling the normal secretion of mucus, is related to it, as the cancer takes origin in the mucous membrane. But colloid cancer occurs also in the mamma and even occasionally, to a partial extent, in epithe- lioma of the skin. In all the instances given hitherto, the mucous or colloid degen- eration has affected epithelial cells. But a mucous transformation sometimes occurs in the intercellular substance of connective tissue, including bone, cartilage, adipose tissue. The intercellular substance is converted into a gelatinous material, while the cells remain unaffected or undergo fatty degeneration. When this change occurs the tissue is softened, and this will produce a very striking result in the case of bone and cartilage. In these tissues it mostly takes place in old people. 128 RETROGKADE MET A JIOEPHOSIS . We shall see afterwards that there is a form of tumor which is characterized by the fact that its tissue contains mucin in its inter- cellular substance. This is not a case of mucous degeneration, but sometimes a portion of a tumor of a different kind will acquire these characters, and then we may use this designation. It is mostly in fatty tumors and sarcomas that this occurs. CALCAREOUS INFILTRATION. This is a condition of very frequent occurrence, and therefore deserving of very careful attention. By the designation is meant the deposition of lime-salts in abnormal fashion in the tissues. The lime-salts are for the most part the same as those which nor- mally take part in the structure of bone, namely phosphate and carbonate of calcium. There is a certain proportion of the salts of lime existing nor- mally in all the tissues and juices; these all leave an ash on burning, and lime-salts form part of this ash. But the lime-salts here are dissolved in the juices, or form combinations with the albumen, so that they do not appear on mici'oscopic examination. In calcareous infiltration there is a deposition of the lime in the form of insoluble carbonate and phosphate, and there is also an accumulation of these insoluble salts, so that the ash on burning the tissues is greatly increased. There is a precipitation of the lime, and as lime-salts in solution are continually being brought in along with the fluids of the tissue, they are continually pre- cipitated and thereby fixed. In considering the circumstances which induce this precipitation, we encounter what Virchow has called metastatic calcification. In some cases where there is rapid destruction of bone, as by multiple caries, or by cancer or sarcoma advancing on bone, there has been found after death calcification of portions of the lung or digestive canal, the lime being deposited in the connective tissue in such a way as sometimes to make the tissue almost like pumice stone. In several of the cases disease of the kidney has coexisted, and there may have been therefore some interference with the due excretion of the absorbed lime-salts. In any case we may presume that the deposit is related to excess of lime-salts in the blood and fluids. There must, however, have been some cause determining the locality of the deposition, in the lung in some cases, in the in- testinal walls in others, but this is quite obscure. Turning to other cases of calcareous inflltration, we find that wherever there is a structure which has lost its vitality and yet is left as a kind of dead and foreign body in the midst of the tissues, there is apt to be deposition of lime in and around such structure. It may be said that obsolete or obsolescent structures are liable to be impregnated with lime. It has already been stated that lime is present in all the fluids and tissues of the body, and in the fluids it is probably kept in solution by the presence of an excess of car- CALCAREOUS INFILTB ATION . 129 bonic acid. In the case of a structure which is obsolete the fluids will stagnate^ will lie about in it, and it is not remarkable that their lime, which is so readily precipitated from solutions, should deposit. As the fluid is renewed, more and more lime is de- posited, and the structure may finally be converted into a stony mass. The lime-salts are deposited in the first instance in the form of fine globular granules, either in the protoplasm of cells or in the inter-cellular substance. The structure is as if dusted with re- fracting granules, and the appearances in many respects resemble those of fatty degeneration. (Fig. 39, a.) As the salts accumulate, Pig. 39. Calcareous degeneration in a tumor ; u, cells of smooth muscle filled with lime granules : b, a bloodvessel converted into a solid rod. X 3oO. the appearance of granules is somewhat lost, and a more contin- uous petrifaction results. (Fig. 39, b.) The addition of a dilute mineral acid causes the salts to dissolve, and, as carbonates are nearly always present, solution occurs with evolution of gas. Examples of this process are very numerous. A minute parasite, the trichina spiralis, occurs in the embryo form in the muscle of man and animals; it lies there quiescent, coiled up spirally and surrounded by a capsule. It is virtually a foreign body, and the capsule is by degrees impregnated with lime, assuming an opaque appearance at its poles (Fig. 40). If the embryo itself dies, it also may become impregnated with lime (see Fig. 40, lower part). Sometimes an extra-uterine foetus dies and remains inside the ab- domen as a foreign body. It becomes surrounded by adhesions and partially encapsuled. The capsule and superficial parts of 130 RETROGRADE METAMORPHOSIS. the fo3tu8 become through time encrusted with lime. Again, an inflammatory exudation in the pericardium may dry' in and remain as a half-caseous material, which finally becomes impregnated with lime, and something like a shell may form around the heart. In phthisis pulmonalis, if healing occurs, the contents of cavities and Pig. 40. Trichina spiralis in muscle. The capsules infiltrated with lime, and in one case a dead worm shrivelled and impregnated with lime. inflammatory products may dry in and become surrounded by a capsule. Impregnation with lime results, leading to a pultaceous or mortary material, which may ultimately condense into a stony Pig. 41. Calcareous infiltration of the middle coat (6) of an artery. At the tapering borders of the patch the elongated shape of the opaque structures indicates that the muscular fibre-cells are specially affected. The internal coat (c) is thickened. X 60. mass. These stony masses are sometimes coughed up if the lung afterwards breaks down, but it is very common to meet with them in the midst of cicatrices at the apices of the lungs after death. Again, in Valvular disease of the heart, due to chronic endocarditis. AMYLOID DEGENERATION. 131 the new-formed connective tissue, by its contraction, becomes hard and dry, and virtually obsolete, and deposition of lime-salts occurs. In regard to the frequent deposition of lime-salts in the middle COAT OF ARTERIES (Fig. 41) there seems to be little doubt that this is frequently associated with atheroma, which is a chronic inflam- mation of the internal coat, and we may suppose that the indura- tion of the internal coat affects the neighboring middle coat. This calcareous infiltration is peculiarly liable to occur in old persons, and ^^■e may believe that in them there is a defective vitality of the walls of the artery, perhaps specially affecting the more active middle coat. But there are cases, and sorae of them in not very old persons, where there is a remarkably extensive calcareous impregnation of the middle coat, so that the arteries are largely converted into rigid tubes. In these cases we may presume that, from some unknown cause, the middle coat is prematurely de- fective in vitality. In the cartilages of old people, especially those of the larynx and ribs, there is very commonly a deposition of lime-salts. But, in this case, there is not simply a calcareous impregnation, rather a true ossification occurs, and the process may be regarded as virtu- ally a physiological one, a late development of bone from cartilage. AMYLOID DEGENEEATION. This name is applied to a condition in which the constituents of the tissues are converted into a substance whose chemical charac- ters are different to those of any normal principle in the body. The degeneration is also called waxy and lardaceous from the physical characters of the substance produced. This may be called for convenience amyloid substance, and, as the name suggests, it was originally supposed to be allied to starch. It has really no chemical relation to starch, being a nitrogenous substance and a modified form of albumen. It resembles starch, however, in re- spect that it gives a color reaction with iodine. "When a solution of iodine in water^ is poured on the surface of an organ which presents amyloid degeneration, then the amyloid substance takes on a mahogany-red color. If, afterwards, a very dilute sulphuric acid be added, the color will sometimes assume a darker brown or bluish tint. More recently it has been found that amyloid sub- stance presents a peculiar reaction with methyl violet, one of the aniline dyes. "Watery solutions of this, dye color the normal tissues blue, but stain amyloid substance of a rose-pink color. Other aniline dyes show differences of tint with amyloid substance. The substance itself has a peculiar, bright, translucent, glancing appearance (see Fig. 42), and, as the structures in which it occurs are enlarged, they are often remarkably prominent under the ^ A convenient solution is, iodine, ten grains ; iodide of potassium, twenty grains ; water, four ounces. For microscopic sections a solution half this strength is sufficient. 132 RETROGRADE METAMORPHOSIS. microscope. It is a very dense, heavy material, and after death, at least, is somewhat brittle, so that the structures have often a kind of broken-up appearance. Fig. 42. Advanced amyloid disease of the liver. The arrangement of the transparent amyloid material suggests its formation in the capillaries. The round bodies at the peripheral parts of lobules are fat-drops, there being slight fatty infiltration. X 70. (Thierpelder.) Amyloid disease may affect any organ of the bodj^ but it is particularly frequent in the spleen, liver, kidneys, intestine, and lymphatic glands. In all these organs it begins in the connective tissue or the WALLS OF THE BLOODVESSELS, more especially the walls of the capil- laries and smaller arteries. As the disease is a progressive one and the amyloid substance accumulates in large quantity, it is im- portant to observe the condition in the very earliest stages. If a section of the liver be made at a time when the disease is not far advanced, and the section, after staining with iodine and sulphuric acid, or with methyl violet, be examined under the microscope, it will be seen that, besides the smaller arteries, the capillaries are the seat of degeneration (see Fig. 43). Their walls are swollen and translucent, and the calibre encroached upon. At the same time, the hepatic cells are compressed and are undergoing atrophy. In advanced stages, on the other hand, the whole tissue of the liver seems to be replaced by the amyloid substance, and it is diffi- cult to say in what structures the degeneration has originated, but even here there are often, as in Fig. 42, indications of its origin in the capillaries. In the spleen, as we shall see afterwards, there are two forms of amyloid disease, and in one form it seems to begin in the reticulum of the Malpighian bodies, methyl violet or iodine AMYLOID DEGENERATION. 133 revealing a fine network having an amyloid reaction in these bodies in the earliest stage. In the other form it affects the walls of the vascular sinuses of the pulp. In the kidney it is chiefly the vessels that are affected, but the basement membrane of the urin- iferous tubules is also sometimes involved. It would seem, therefore, that the amyloid substance first appears in the walls of the vessels and in the connective tissue in these three oi'gans. It remains to be considered whether it passes beyond these to the other elements of the organs. In the case of Fig. 43. Vt '^'^A 'rt^ ^■^ ox^ ^c^D Amyloid disease of liver in early stage. The walls of tlie capillaries swollen and translucent. V 350. the liver there does not seem to be any undoubted evidence that it does so. In the earlier stages it is found in the vessels alone, and in the later stages there is such enlargement and contortion that the seat of origin is somewliat obscure. In the Icidney, also, it seems to confine itself to the vessels and connective tissue of the organ. In the spleen it does not, according to the observations of the author, confine itself to the vessels and connective tissue proper. Even in very early stages he has generally found that here and there in the sago spleen the round cells of the lymphoid follicles are affected. These cells, from what has been said on a previous occasion, may be regarded, however, as belonging to the connective tissue. In the lymphatic glands, again, it is the blood- vessels and reticulum that are affected. In the intestine it is the capillaries and arteries, and to a less extent the muscular fibre-cells. Prom this it will appear that the view formerly held, according to which the disease might attack the epithelial cells of such organs as the liver, is erroneous, and that the degeneration is confined to the structures constituting the supporting framework of the tissues, including the vessels. We have now to consider the effects of amyloid dbgenbeation. We have referred to the brittleness of the amyloid substance, but it is not to be inferred that this exists to any considerable extent during life, otherwise we should have frequent hemorrhages as a 134 RETKOGRADE METAMORPHOSIS. result of amyloid disease. Hemorrhages rarely occur, and so we infer that the substance is tolerably elastic during life. In exam- ining amyloid organs after death, especially such organs as the intestine, great care should be taken in handling them lest de- struction of the amyloid structure should take place. It is clear from symptoms observed during life that the amyloid substance is very pervious to fluids, the prominent symptom of amyloid disease in the bowels being diarrhoea, and in the kidney excessive discharge of watery urine. It has already been said that the calibre of vessels is reduced when amyloid disease occurs in their walls. This will cause ansemia in the structures supplied ; and atrophy, sometimes with fatty degeneration, is frequently the result. This we see in the kidney and in the liver, the atrophy of the proper secreting sub- stance of the liver being, however, to a great extent, the direct result of pressure by the swollen capillaries. The amyloid structures are greatlj' increased in bulk and weight, and this tells on the organ as a whole. The liver, spleen, and kidneys are often greatly enlarged, and they present a peculiar dense translucent ■ appearance which has given rise to the names waxy and lardaceous disease, often applied to amyloid degeneration. Besides the generally diffused amyloid disease occurring in a number of organs, and present in every part of the individual organs affected, we sometimes meet with a localized amyloid DEGENERATION. This mostly occurs in new-formed inflammatory tissue and cicatrices, especially when of syphilitic origin, and also in tumors. As jet this local amj'loid degeneration has only been observed in pathological structures such as those mentioned. It has been seen in syphilitic cicatrices in the liver, in the tongue, and larynx, in degenerating cartilage, etc., and in some cases the amyloid piece of tissue is of considerable size, and as it differs in its hard translucent character from the tissues around, it maj itself look like a tumor. We may now consider the nature of the process which has been described. Looking to the history of the cases in which it occurs, it is clear that it is to be referred primarily to an alteration in the blood, probably an impoverishment of it in albumen. The disease is not an independent one, but comes on in certain cachectic states due to chronic tuberculosis, syphilis, diseases of bone in- volving prolonged suppuration, chronic dysentery, chronic albu- minuria, etc. It is more difficult to determine the nature of the connection between the vice in the blood and the disease in the tissues. By some it is supposed that the amyloid substance arises in the blood by modification of the albumen, and is then infiltrated into the structures. But this view cannot be accepted, for various reasons. In the first place, the substance is eminently insoluble, and it is difiicult to understand how it can be carried ; besides this, it does AMYLOI]) DEGENERATION. 135 not displace the normal structures simply, but replaces them, these structures being converted into the amyloid substance. It is more consistent to suppose that the tissues are reduced in vitality by the altered condition of the blood, and that the albumen received enters into combination with the protoplasm in such a way as to produce this peculiar substance. The process may perhaps be compared to the coagulation of the tissues, which, as we have seen, sometimes occurs when they undergo necrosis, the tissues entering apparently into a chemical union with the fibrinogen in the fluid exuded from the bloodvessels, so as to form fibrine or some substance allied to it. Amyloid substance has been often regarded as akin to fibrine, and fibrinous casts in the tubules of the kidney are sometimes converted into amyloid substance. The existence of localized amyloid disease is strongly confirmatory of some such view as this. Here abnormal structures enter into, this peculiar chemical combination with the albumen of the blood, while normal structures do not. In this connection also, the fact that amyloid disease affects the connective structures of the body is not to be forgotten. It is as if the chemical basis of these structures had a special relation to the amyloid substance. Amy- loid disease is therefore essentially a degeneration, although, in order to the formation of the amyloid substance, it is necessary to have added to the tissue material from without, and this adds greatly to the bulk and weight of the structures. We have still to refer to bodies occasionally met with, and des- ignated AMYLOID CONCRETIONS Or CORPORA AMYLACEA. In old CX- FlG. 44. Corpora amylacea : a, from the prostate; &, from a hemorrhagic infarction of the lung; c, from the spinal cord. X 400. (Ziegler.) travasations of blood we sometimes meet with round or oval stratified bodies of small size (see Fig. 44, b), M'hich give a typical amyloid reaction. Sometimes they contain in their central parts 136 RETROGRADE METAMORPHOSIS. a foreign body, such as a blood-crystal. Again, in the prostate gland {a) we meet with concretions of considerable size, it may be visible, as brown granules, to the naked eye, with all the characters of stratified amyloid concretions. They are also met with in the tissues of the central nervous system (c), they are present in the normal brain, especially in the ependyma of the ventricles, but in cases of sclerosis they may be present in enormous numbers. The significance of these amyloid bodies is not usually very great in a directly practical point of view, but their presence under these various conditions seems to prove that the various albu- minous substances may undergo conversion into the so-called amyloid substance. HYPERTROPHY, RE 1' AIR, AND REGENERATION. I. HYPEPvTKOPHY. Hypertrophy, in its most literal sense, means overgrowth, or excessive growth, and it is so that we shall use it here. In order to understand overgrowth it will be necessary to make some ob- servations on the characteristics of normal growth. In the NORMAL GROWTH of the body each tissue has the power of reproduction up to a certain point. By some hidden power the tissue grows and moulds itself into particular anatomical forms, and ceases growing when it has attained the proportions necessarj- for its function in the organism. We do not know what this power is, but we can say that it is inherited by the germ from its parents, and that in the variations which are presented in different individuals heredity plaj^s a very important part. In order to this growth the new formation of bloodvessels is necessary, but here, as in pathological conditions, the formation of vessels is secondary, and takes place merely according to the needs of the organism. The amount of blood supplied and its distribution strictly follow the necessities of the growing tissues, and the vascular system shows a wonderful power of adaptation to the requirements of the tissues. It is true, as we shall see afterwards, that an excessive supply of blood may lead to increased growth, but such an excessive supply' of blood never occurs nor- mally, is an accident, and as such may lead to morbid or excessive growth. When tissues cease to grow, it is not that the formative power inherent in them has ceased to exist, but simply that, being sub- ordinate to the general law of the organism they have attained the full size requisite for their intended uses. Should occasion occur for their renewed growth, then it will very often happen that a fresh start will be made. Looking to the details of normal growth, we find that it is the cells which are the essential factors in the process. It is by DIVISION OP THE CELLS, a proccss frequently designated proliferation, that growth is ultimately aiSected. Much careful observation has been bestowed on the process of division of cells. There are frequent indications that first the nucleus and afterwards the cell separate into two. Before the actual division begins the nucleus undergoes a transformation, the details of which may be studied in Fig. 45. In a the condition of an epithelial cell in its normal quiescent state is shown. By particular methods of staining it can 138 HYPEKTKOP]! Y, EEJ'AIK, AND E EG EX E RATION . be shown that the nucleus contains a fine network of fibres, but here the substance of the nucleus as well as the fibres is stained. In h the condition preliminary to division is shown. The nucleus now contains a collection of convoluted tubes, and those alone are stained while the substance Ijetween does not take on the color. These fibres are apparently contractile and vary their position somewhat, but gradually tend to assume a radiating arrangement as in c and d. There now comes a separation in the middle, as at e, and the two sets of fibres retreat from one another towards the Fig. 45. Division of cells. Explanation in te.\t. (After Flemmisg.) poles of the cells as in /. The division of the nucleus is thus effected, and that of the cell follows as in g. Subsequently the irregular bundle of fibres in each new cell assumes the shape of the regular nucleus and gets surrounded by a membi-ane. The fibres also give place to a fine network as in the original cell, and the substance of the nucleus between the fibres again takes on the staining as in *. This process of division has been observed in the fixed cells of many tissues, and it is probably the only one which occurs in the normal process of growth. In white blood-corpuscles, and probably also in the embryonic cells a more direct division of the nuclei appears to occur, but the details of that process are not very clear. Bearing in mind the facts mentioned as to normal growth we have now to consider the processes in overgrov^'th or hypertrophy, and the conditions under which it occurs. The simplest form of hypertrophy is that which arises from the necessity for the excessive performance of a normal function. We saw that growth ceases when the requirements of the organism HYPERTKOPHY. 139 are satisfied, but if increased requirements develop, then the tissues may take on a fresh growth to meet them. This is illus- trated chiefly by the muscular and epidermic tissues. Many instances of hypertrophy of muscle, from this cause, might be cited. If, in consequence of stricture of the urethra or obstruction at the neck of the bladder, the passage of urine is obstructed, and the muscular coat of the bladder must contract with more vigor to expel the urine, the muscle will undergo hypertrophy. In this way there maj' be a very remarkable thick- ening of the muscular coat. In like manner, we may have hypertrophy of the muscular coat of the intestine in connection Avith stricture of the rectum or colon. The muscular tissue of the heart also undergoes an exactly similar hypertrophy when, in order to expel the blood from its cavities, more forcible contractions are requisite. We know also that the voluntary muscles hypertrophy Avhen they are repeatedly exercised in a forcible way. In all these cases of hypertrophy of muscle it is usually said that frequent exercise is the cause, but this is hardly a full descrip- tion of the circumstances. The exercise must not only be frequent, but the work to be done must require an unusually forcible EXERTION In the cases already cited it will be seen that the essential condition is the necessity for additional power, usually to expel the contents of a cavity through a narrowed orifice. The heart does not hypertrophy because its muscle undergoes frequent exercise, but only when additional force is required. It is so also in the case of voluntary muscles. Mere agility and rapidity of movement does not cause hypertrophy of muscle, whereas repeated severe exei'tion calls it forth. The muscles of the hand and arm do not hypertrophy in persons who use them frequently in writing, but they do in artisans who use great force in their occupations. It may be added that a muscular action which is ordinarily per- formed with moderate force may, from abnormal conditions, come to be performed frequently with excessive force, and so lead to hypertrophy. For example, the urinary bladder may be induced to contract frequently and with exaggerated force, although there is no obstruction, and this may induce hypertrophy. A question arises here as to the finer details of the hyper- trophy OF MUSCLE. In the case of involuntary muscle there can be no doubt that the hypertrophy occurs by division of the mus- cular fibre-cells by a process similar to that already described in referring to noi-mal growth. But some question has been raised as to the exact nature of the process in striated muscle, and careful measurements have been made of the diameter of the muscular fibres in hypertrophy of the heart. It is stated by some that the diameter is increased and by others that it is not. It may be said, however, that the increase in thickness, if it occurs, is not so great as to account for the large additional bulk of the muscular sub- stance as a whole, and that there is, as well, a numerical increase in the muscular fibres effected by division. Enlargement of a tissue by such numerical increase has been 140 HYPERTEOPHY, EEPAIK, ANlJ KEGEXE K ATIOIST . designated by Virchow hyperplasia, and this is sometimes distin- guished from true hypertrophy, in which there is merely an enlarge- ment of the elements of the tissue. This distinction, however, cannot be rigidly carried out, and the term hyperplasia will only be used here in order to indicate that the hypertrophy is by pro- liferation. The EPIDERMIS is the other tissue which fretjuently shows hyper- trophy when the necessities of the organism call for it. The func- tion of the epidermis is chiefly to protect the true skin from injury l)y friction against external objects, and, in its primary formation in the foetus, the epidermis is thicker or thinner according as the parts of the skin are liable after birth to be exposed to greater or lesser amounts of friction. But, if afterwards, certain portions of the skin are frequently exposed to friction, then an additional growth will occur in the epidermis, a hypertrophj'. We have abundant instances of this in the horny hands of workmen. The thickening of the epidermis which results in the so-called corns is another instance of hypertrophy, in order to protect a portion of the sensitive skin from undue friction or pressure. In regard to these thickenings it is to be pointed out that they only occur when the friction or pressure is not constant, but recurs at frequent intervals. A constant pressure, as by a splint pressing on a part, causes atrophy, whereas a frequently repeated pressure results in hypertrophy, apparently by allowing the struct- ures to recover and afford time for increased nutrition. The same law applies to tissues in the interior of the body. When exposed to constant pressure they atrophy; when the pressure is intermit- tent they hypertrophy. It is here to be noted, however, that pressure from within (as by tumors, aneurisms, etc.) is usually con- stant, while that from without is mostly intermittent. Hence the original statement of John Hunter is justified, that pressure from without produces thickening, while that from within causes atrophy, although it is not to be taken without reservation. The hypertrophy of the epidermis in these cases is undoubtedly effected by division of the cells; it is a hyperplasia, and the process is similar to that already described. Hypertrophy from increased blood-supply. — In what has been already stated we have not exhausted the subject of hypertrophy, and, in order to appreciate what follows, it is necessary to refer again to normal growth. It was observed above that in ordinary growth of tissue the bloodvessels strictly follow the growing tissue, and are formed according to its needs. But if, from some acci- dental circumstance or by artificial interference, the blood-supply be greatly increased, then excessive growth may resu.lt. If the spur of the cock be removed from the leg and successfully trans- planted into the comb, it will grow with excessive vigor, forming a prominent horn-like structure. Here the excessive supply of blood, the comb having a much more active circulation than the & THE REPAIR OF INJURIES. 141 Fig. 46. leg, induces an excessive growth of the epidermis forming the spur. In human pathology we have numerous instances of hypertrophy analogous to this. Increased activity of the circulation will often lead to hypertrophies. AVe see it in the neighborhood oe inflam- mations. "We have already seen that determination of blood exists outside the immediately inflamed area, and if this is prolonged it may lead to overgrowth of the tissues. In this way we may account for the excessive growth of hair sometimes seen in the neigh- borhood of ulcers, near diseased joints, and at the ends of stumps which have remained long inflamed. A very striking instance of hypertrophy of this kind is sometimes ajfForded in bones. In the neighborhood of inflamed joints the sur- face of the bones is often nodulated, and the bones greatly thickened by new formation from the periosteum. In cases of periostitis, the new formation of bone is perhaps more strictly to be regarded as a part of the inflam- matory }irocess, as we shall see afterwards. There arc some curious instances of limited necrosis of bone occurring during the period of growth in which the bone, as a whole, has grown larger than the other. If a boy has a necrosis of the femur, the whole bone is probably more richly supplied with blood, and the normal growth is accelerated. The ne- crosis may be recovered from, and the person is left with a permanently elongated femur which may be as much as two inches longer than the other, and may lead to considerable lameness. The tibia is differently situated to the femur. Its two extremities, are tied to the ends of the fibula by firm ligaments, and so the bone cannot elongate. If over- growth occurs, the bone must curve so as to accommodate itself. An example of this is shown in the accompanying Fig. 46, from a preparation in St. Bartholomew's museum (quoted by Paget), in which the bone, measured over its curve, was two inches longer than the healthy one. Elongation and cur- vature of tibia, the result of necrosis during period of growth. (Paget.) II. THE RBPAIK OF IN.JURIES AND EESTORATION OP LOST PARTS. The term Regeneration is applied to the restoration of portions of the body which have been lost by injury or disease. The regeneration of a part is to be carefully distinguished from mere growth. A tissue may be able under suitable stimulation to fij 142 lEYPERTROPIIY, RKPAJ.K, AND REGKXEK ATIOX . reproduce its elements, and increase in size; but for the replace- ment of a lost part, if at all considerable, there must be, virtually, a renewal of the process of development. This REPRODUCTION OF LOST PARTS in their entirety occurs readily in some of the lowest forms of animals. In the hydra, if the creature be cut in two, each half will develop into a complete animal, and the process may be repeated indehnitely. This power of reproduction of the whole animal from a part seems confined to those creatures -which can propagate by spontaneous fission or gemmation. "When we come to animals higher in the scale the power of reproduction seems to be limited to the restoration of lost limbs, antennse, etc. Without going into details, which will be found by reference to Paget's "Lectures on Surgical Pathology," it may be said that there are indications which seem to show that there is some kind of LA\v according to which the reparative power in each perfect species is in inverse proportion to the amount of change Avhich the animal has passed through in its development from the embryonic to the perfect state. It is as if, in the process of development, the formative power as distinguished from mere growth were gradually exhausted, and the process of reproduction, which we have seen to be, as it were, a renewal of that of development, only occurs when this -power has been comparatively little expended. It appears, for instance, that in insects the power of reproducing antehnaj or limbs is limited to those species which have attained the perfect state through a comparativelj^ simple and direct course of develop- ment. It is consistent with this view that in the larval state insects show a much greater power of reproduction than when perfect. The larva of one of the higher insects will be able to reproduce its limbs, while the perfect insect is not. In man, and in the vertebrata in general, the long course of development seems largely to exhaust the reproductive power of the hodj, and, in the adult state at least, the power of restoration of lost parts is very small, and the processes concerned are almost as much related to growth of tissue as to development. In the embryonic state it is probable that the power of restoring lost parts is much greater than in the adult. Some children are born with a short arm, at the extremity of which are imperfectly developed fingers; it is probable that in these cases amputation of the arm has occurred in utero, and an attempt at restoration has followed. In the adult it may be said that restoration of lost structures is almost confined to the blood and the epithelial and connective tissues. Along with the connective tissues we have, of course, bloodvessels which are readily reproduced, and we may also, to a limited extent, include nerve-fibres, which, as we shall see afterwards, are some- times restored. ^ While, therefore, the absolute restoration of complete and con- siderable portions of the body is scarcely possible in man, yet the body is by no means unprovided with powers by which injuries ARE RBPAiRKD and loss of structures is made good" It may be said THE EEPAIR OF IXJURIES. 143 that the higher and more complex animals are endowed with greater ability to protect themselves from injury, and that their tissues possess the necessary powers of restoration in the case of those injuries to which they are specially liable. In the various processes' here to be considered, it will be seen that what may be called the definite intention to attain a certain result which is shown in the process of development, is distinctly Adsible, and that the tissues have a remarkable power of meeting adverse conditions. Healing op ■vyounds. — The power of repair is well seen in the various processes concerned in the healing of wounds. There are some wounds which heal by a process fitly designated immediate UNION. That is to say, the surfaces are brought together and coalesce without any new-formed material being produced to serve as a bond of union. This occurs mostly in clean-cut wounds, which, shortly after their infliction, are closed so as to bring the cut surfaces into close contact. It is necessary for this process that all inflammation lie avoided either at the time of infliction of the wound or afterwards. The wound should therefore be clean- cut and made with a sharp instrument. We are to think of the living tissues not as mere mechanical pieces of texture, but as possessed, by virtue of their vitality, of wonderful powers of adapt- ability to circumstances. When two living surfaces are brought into contact and all disturbing conditions are averted, then the bloodvessels will form communications, the nerves will by and by unite and become continuous, and the connective tissue coalesce. In this way it frequentlj- happens that a wound in the skin, or even in muscle, unites, and no trace of a bond of union or even of the line of union can be found after a few days. The epidermis probably does not unite so directly, and the wound is covered by new-formed epidermis. In union by pkimaey adhesion avc have a process of a more complicated kind. In it inflammation plays a part. When a wound is inflicted, the mere mechanical injury, or exposure after- wards, frequently leads to a trivial but acute inflammation, re- sulting, as we have seen, in the coating of the cut surface with a fibrinous exudation, the so-called glaze. If two surfaces thus coated with fibrine be brought in contact they unite, the fibrine acting as a glue or cement. But the fibrine does not form a per- manent bond of union, and if no attempt is made to efiiect union bj' other methods, then the wound will subsequently gape by the breaking down of the fibrine. In order to effect a permanent union we must have formative cells produced, such as we saw, when studying inflammation, to be necessary for the formation of connective tissue out of granulation tissue, and we must have a similar new formation of bloodvessels. The new formation of a uniting tissue here is very trivial in amount ; there is no produc- tion of proper granulation tissue, but merely a limited production of formative cells which replace the thin layer of fibrine, and a budding of the bloodvessels till communications are formed be- tween the two surfaces. This whole process may occupy only a 144 HYPERTKOI'HY, RETAIE, AND RKGEN KK A TION . day or two, and the permanent new-formed tissue forming the cicatrix is usually very small in amount. This form of union is sometimes spoken of as union by the first intention, but that term is also applied sometimes, but not correctly, to immediate union, and so it is, perhaps, better to use the term primary adhe- sion for this form. In studying inflammation we have already considered the method of UNION BY THE SECOND INTENTION which occurs when two granu- lating surfaces come in contact. It is necessary now to refer more particularly to the processes of REGENERATION as manifested in the individual tissues of the body. In the first place we may regard the blood as a tissue, and we have already seen that after a severe hemorrhage its constituents are gradual!}^ regenerated, the fluid part most quickl}', the white corpuscles comparatively soon, and the red corpuscles somewhat slowly. The EPIDERMIS and epithelium of the surface, of the skin and mucous membranes are restored with considerable rapidity. In the case of the skin and mucous membranes there is normally a continuous shedding of the surface epithelium, and a new forma- tion in the deeper layers to replace that which is lost, a kind of physiological regeneration therefore. When, bj- accident or other- wise, a superficial portion of epithelium is shed before its time, it will be replaced by the normal growth of the deeper layers, prob- ably accelerated by the requirements of the body. When the whole thickness of the epithelium is destroyed, the gap is by de- grees filled by the proliferation of the epithelium at the edges of the wound, as we have already seen in the case of the cicatrization of a granulating wound. According to the observations of Klebs, the new-formed epithelium acquires a slight power of amoeboid movement, so that it can proceed to the spot which it is to occupy. The proliferation of the epithelium proceeds by a process similar to that already described in considering the normal division of cells. In the accompanying illustration (Fig. 47) from a paper by Eberth (Virchow's Archiv, 67) the fibrous transformation of the nucleus and the other changes, as seen in the cornea of the rabbit, some days after a portion of the epithelium had been removed, are shown. In the normal cornea there are traces of a similar process by which, we rnay presume, the physiological regeneration occurs. It is here of interest to observe that the epidermic cells may be transported from their original seat and survive and piroliferate on the surface of a wound, even in another individual. It is well known that advantage is taken of this fact in the process of graft- ing which surgeons resort to in order to accomplish the cicatriza- tion of large wounds. The whole thickness of the skin or mucous membrane may be transplanted from one place to another, or even from a different person ; or the skin may be made to occupy the place of the mucous membrane, or vice versa. When the skin or mucous membrane is thus made to occupy a different position with REGENERATION. 145 different relations and duties, it by and by conforms itself to its new position and the epithelium acquires a structure like that in its neighborhood. In the case of the hairs and nails we have normally a process of desquamation and regeneration similar to that of the surface epi- dermis. If a hair be prematurely extracted or a nail torn off, it is restored by a strictly normal process. But if the hair-follicle be Frfi. 47. Regeneration of epithelium in cornea of a rabbit, (a) Fibrous transformation of nucleus. (6) Partial separation of the fibres and hour-glass change of nucleus, (c) Complete division of nucleus, (rf) Complete division of cell. (Eberth.) removed or the matrix of the nail destroyed, there is no restora- tion of the structure, the regeneration of such complex structures being beyond the powers of the ordinary epidermis. In some glands there is in health or disease a desquamation or destruction of the epithelium. Then, in the kidneys there is a form of inflammation in which the epithelium of the tubules is abundantly shed. In this case it is restored by a new formation, and we are sometimes able to observe the old epithelium in the lumen of the tubules, while the small, young epithelium lines them. In the liver there is great destruction of the secreting cells in acute yellow atrophy, and sometimes alongside the remains of the cells there are collections of new-formed cells, as if an attempt were being made at renovation of the tissue. The regeneration of connective tissue has been sufficiently illustrated in what has gone before. It is obvious that in the heal- ing of wounds, except by immediate union, there is a new forma- tion of connective tissue and bloodvessels. As connective tissue seems to be the simplest form of tissue, it is sometimes used to fill up gaps where more complex tissues have been lost. Thus a 10 146 HYPERTROPHY, REPAIR, AND REGENERATION. wound in a muscle is not restored by the formation of muscular but of connective tissue, and so is it with wounds of the liver, spleen, kidneys, etc. The regeneration of bone is frequently exemplified in the repair of fractures. In the various processes observable here we may see conditions analogous to those in healing by primarj^ adhesion and by the second intention. In cases where the broken ends are kept closely together and at rest there may be very little inflammation, and the permanent uniting medium may be produced by the im- mediately neighboring tissue. As we shall see afterwards, although the periosteum usually supplies the new bone, yet it is not neces- sary to its formation, but the bone itself, perhaps rather the tissue occupjnng the Haversian canals, is capable, under certain conditions, of producing new bone. In other cases there is more considerable inflammation, it may be with suppuration, and granulation tissue is produced. This granulation tissue, arising largely from the periosteum, develops according to circumstances bone, cartilage, or connective tissue, forming the callus and ultimately supplying the permanent bond of union between the broken ends. It has recently been shown by the observations of Dr. Macewen, of Grlasgow, that bone may be transplanted. Pieces of bone have been taken fi'om a person, and used to fill up a gap in a bone, and they have both lived and grown larger in their new position. N^brve-fibres show a certain power of new formation when divided or when portions are excised. When a lierve is thus divided, even if the two ends are separated for some distance, there is often, after a time, a full reestablishment of the conduc- tion. It appears that from the central end pale fibres grow out. These pass to the peripheral end, and constitute the axis-cylinders, which afterwards acquire medullary sheaths and so become com- plete nerve-fibres. In this way a considerable length of nerve may apparently be restored. There is another form of regeneration sometimes described, but it is of a more doubtful nature. When a nerve is divided, the fibres in the peripheral portion, from its cut end downwards to its ultimate distribution, show a peculiar change, consisting mainly in degeneration of the medullary sheath. It is doubtful whether the axis-cylinder takes any part in this process. After the cut ends join, the nerve-fibres are restored, and this by a process which may be called regeneration of the medullary sheath. It has alreadj' been mentioned that when a muscle is wounded the gap is filled hj connective tissue ; there is no proper regenera- tion. But there may be loss of the contractile substance by de- generation, as in fatty degeneration of the heart. When such a process is intense, it seems impossible that the muscular fibres can be restored, and as the heart often recovers there must be a regeneration of the contractile substance. But in this case there is not a destruction of the muscular nuclei, and therefore not a regeneration of the muscular cell as a whole. In the case of unstriped muscle there is probably also an occasional degeneration and renewal of the contractile cells. IISrPECTIVE TUMORS (aRANITLATIOX-TISSUE TUMORS). This class of tumors is taken up here chiefly because they show- in their structure and general relations considerable analogies to inflammation on the one hand and tumors proper on the other. As indicated in a previous part, the expression infective means that the disease is "spreading," that it depends on some virus which propagates itself, and tends to reproduce the same kind of lesion outside its original seat. In two forms of disease included here, the exact nature of the virus has been made out, namely, in tuberculosis and leprosy; and in both it is found to be a micro- organism in the form of a short rod-shaped bacillus. It may per- haps be legitimately inferred that in all the rest specific organisms are the infective agents. It may be added that several of these forms of disease are not only infective but infectious, communi- cable, that is to say, from person to person; some are capable of being inoculated into animals. The virus acts as an irritant, and the resulting lesions present strong analogies to inflammation. It is not to be inferred that the micro-organisms, where they are concerned, themselves irritate the tissues; it is more probable that the irritation is due to chemi- cal products resulting from their vital processes. The resulting lesions are in some cases indistinguishable from those of inflam- mation, and we shall see afterwards that we have to speak of syphilitic and tubercular inflammations. But the virus also takes usually a more local habitation, and concentrating its action on particular points, it gives rise to numerous lesions, having more or less the character of tumors. Even the tumors present great analogies to inflammation in their structure. They are formed of granulation tissue, and are often called granulation-tissue tumors or granulomas. But the tissue of the tumors presents certain differences from ordinary granulation tissue chiefly in its tendencies. The granu- lation cells tend to undergo fatty degeneration, and so the tissue may become caseous or break down. At the same time there is the more normal tendency' to undergo development into connec- tive tissue, and this may go on in an imperfect way alongside the other change. Hence the tumors frequently present great varieties in structure, and it is sometimes difficult fully to unravel their relations. 148 INFECTIVE TUMORS. SYPHILIS. In this section we have to consider the general relations of this disease. In what has gone before some of the grounds have been indicated for stating that a virus is concerned in its production. In addition the following may be mentioned; it is well known that the discharges from a syphilitic person are contagious; and it is also generally believed that in the secondary stage the blood, and even'the milk, are infectious. In this connection it is to be remem- bered that an attack of syphilis generally confers immunity against a further attack, the analogy with the specific fevers being sug- gested by this. A virus is the cause of the disease, and as a general rule it is usually applied to some part of the organs of generation. It may be applied, however, to some other part, as to the finger (in the case of a surgeon examining a part), to the lip (as in the case from which Fig. 48 is taken), to the eyelids or other external part. The Fig. 48. '^'-'c Section of a bard chancre at its marginal part. The granulation tissue occupies the skin under the epidermis, gradually replacing the latter. X ^5- result is the indurated or primary chancke. This consists of a raised hard structure generally with an ulcerated surface. Ex- amined microscopically, it is found that the epidermal covering of the skin is not necessarily lost, but that beneath it, and in the central part, it may be to some extent replacing it, there is an enormous formation of granulation tissue (Fig. 48). The true skin is entirely replaced by this granulation tissue, and instead of it there is a bulky mass of rpund cells. This structure may be regarded as inflammatory, but it may also be regarded as a kind of tumor, and may be taken as the type of the syphilitic tumor. In its less common seats it may very closely resemble another form of tumor. Thus a chancre of the lip may be mistaken for an epithelioma, and be excised under that impression. This actually occurred in the case from which Fig. 48 was taken. The tissue, SYPHILIS. 149 although like in structure to granulations, does not, like them, readily form connective tissue, but remains long in the same rudi- mentary condition, and when it disappears leaves comparatively little of a cicatrix. On the other hand it sometimes becomes caseous, but this does not so readily occur here as in some other localities. The virus is carried from the indurated chancre by the lym- phatics, and in the first place lodges and is caught in the neigh- boring JCYMPHATio GLANDS, where it again produces similar results, namely a great production of ill-formed granulation tissue which has little tendency to develop into proper connective tissue, but readily undergoes an irregular caseous metamorphosis, and occa- sionally takes on the phagedsenic character. After an interval the virus passes into the blood. There is a period which may be regarded as a period of incubation, or self- propagation of the virus between its first introduction into the system and the evidences of its presence in the blood — the virus seems to take a certain time to reproduce itself in quantity, and it generally does so chiefly in the lymphatic glands. When an agent exists in the blood in a finely divided state it will be carried to all parts of the body, and if it produces lesions they will probably be symmetrical, as the corresponding parts in each lateral half of the body are for the most part in similar circumstances, and are similarly afifected by any agent acting equally on them. The existence of symmetrical lesions is presumptive evidence that a disease is due to something in the blood. In the secondary stage of syphilis then we have the virus in the blood, and the result is symmetrical lesions of the skin, mucous membranes, bones, etc. These secondary lesions are inflammatory in character, and have generally a resemblance to ordinary inflammations. They are most frequent in the skin, and so we have the syphilitic roseola, eczema, etc., but other parts may be affected, and we have syph- ilitic periostitis, pharyngitis, etc. It is a question to what extent inflammations occur in internal organs in this stage, but according to Hutchinson they are more frequent than is generally supposed, but are rarely seen because persons seldom die in the secondary stage. The secondary stage has been aptly compared with the eruptive stage of specific fevers, it is like a fever long drawn out. There is in both cases a virus in the blood, and ijj syphilis, as well as in the acute fevers, there is generally elevation of temperature. The analogy between the rash of secondary syphilis and those of measles, scarlet fever, smallpox, etc., is also suggestive, the skin affections in both classes of cases being inflammatory. During this stage then the virus is active in the blood, and it is generally held that the blood and secretions are contagious. The person is also in the position of transmitting the disease to his offspring, the virus apparently passing into the germ and sperm cells. Just as in the speciflc fevers, the virus dies out of the blood 150 INFECTIVE TUMORS. spontaneously, and the various secondary lesions disappear. When the virus is no longer in the blood this fluid will cease to be con- tagious and the disease will no longer be transmissible to the oflspring. But it is not to be inferred that the disappearance of the secondary lesions is absolute proof of the virus having died out of the blood, and it would not be safe to advise a patient that he could safely marry till at least two years after the subsidence of all secondary symptoms. In this secondary stage it is not common to meet with tumors like the indurated chancre. They are characteristic rather of the next stage, and when they do occur in this stage they are small and accompanied by more pronounced inflammatory manifesta- tions. The TERTIARY sTAiiE IS chieflj' characterized by the formation of tumors to which the name Gummata is applied. They are com- posed similarly to the indurated chancre, namely, of granulation tissue in the first instance, but in them this tissue has a much greater tendency to undergo caseous necrosis, although the trans- formation into connective tissue also occurs. Hence it happens that the gumma of the tertiary stage is very commonly more or less caseous in certain of its parts. Fig. 49. GuDinia of kidney. The opaque central part (d) is caseous; around this there is fibrous and granulation tissue (c). X 20. (Cornil and Ranviek.) To the naked v\e the tumor is a whitish or grayish body, com- monly AA-ith a yellow caseous appearance in its central parts, or irregularly distributed. It varies in size, sometimes as small as a millet seed, in which case it is usually multiple, but it is usually much larger, and may attain the size of an apple. The tumor is not generally sharply defined from neighboring structures, but its periphery merges in a firm connective tissue which usually extends 8YP11ILIS. 151 outwards into neighboring structures, so that the tumor appears planted in the midst of a cicatricial mass. Under the microscope the tumor will be found, as in Pigs. 49 and 50, to replace a certain portion of the normal tissue. The central caseous part will be opaque, as in c, Fig. 50. Externallly Fig. 50. (lumina of liver. E.xplanation in te.\t. ^.Ki. there is more transparent tissue (6), while around and in neigh- boring parts of the organ there is new-formed connective tissue, as at d in the figure. In Fig. 51 the appeai-ances seen under a higher power are shown, the parts taken being from h and c in Fig. 50. It is seen that the peripheral portions (Fig. 51, a) of the tumor present innumerable round cells mixed with fibrous tissue, which latter is often very pronounced. The caseous parts are opaque and present fine fat granules with shrunken cells and nuclei (Fig. 51, b). The tumors are met with in almost all the tissues of the body, skin, mucous membranes, subcutaneous tissue, in the substance of 152 INFECTIVE TUMOKS. muscles (as in the tongue), periosteum, lirer, dura mater, soft membranes of the brain, cerebral nerves, etc. The name gumma does not express their usual consistence, and is stated to have been first applied to the periosteal form. The caseous metamorphosis leads to various results, according to the situation and circumstances of the gumma. If the tumors have a superficial situation, then ulceration results, and we have KiG. 51. K- „."-."';' N-^f-JSiV rriVfi'^ •• ->• '■' '*»''''' t.j..fik.'--*' From gumma of liver, same section as Fig. 50 j a, taken from recent part {h, in other figure) ; d, from caseous (r). X 350. a deep excavated ulcer with swollen infiltrated walls, consisting of tissue like that of the gumma, and with the same tendency to degeneration, so that the ulceration extends. As the tumor in- volves neighboring structures which undergo necrosis along with the caseous process in the tumor, there may be great destruction of tissue brought about. In internal organs the caseous material may long lie apparently unaltered. The gumma may be virtually healed, its granulation tissue absorbed or converted into connec- tive tissue, while the caseous matter remains, and is finally left in the midst of a cicatrix where it may become calcified. It appears that the absorption of a gumma may be promoted by the administration of remedies. The exact process by which this is brought about is hardlj' known, but there seems to be a simple fatty degeneration with absorption, in the way indicated in the section on fatty degeneration. We have still to inquire what may be the relation of these ter- tiary lesions to the virus. The virus no longer exists in the blood, and in accordance with this the lesions are characteristically unsym- metrical. The most probable supposition is that, after the close of the secondary stage some of the virus has remained lying in a par- ticular part. Perhaps a small gumma has formed, and the virus has lain in it quiescent but still surviving. It may be waked up by some accidental circumstance in the life of the patient, at any period afterwards, perhaps as long as twenty years. The virus TUBERCLE AND TUBERCULOSIS. 153 propagates itself, but its effects are local. It may produce a tumor of large size, but it does not pass into the blood, and does not pro- duce the lesions of the secondary stage. It has been matter of dis- pute whether a tertiary gumma is an infectious lesion, and the fact that the blood of the patient does not become infected might seem to answer the question in the negative. It is to be remembered, however, that the person already possesses an immunity by having passed through the secondary stage. The gumma is probably capable of producing syphilis in another person. The tertiary stage of syphilis is often in its later period associated with AMYLOID DISEASE. TMs is uot from the direct action of the virus, but is due to the condition of the blood induced by the serious organic lesions. Syphilis is often associated \\ith a condition of the arteries which will come up for discussion further on. Wherever there is, as so frequently happens, a considerable formation of granulation tissue passing into connective tissue, the arteries take part in the inflammation, and we have especially thickening of the internal coat, sometimes going on to complete obliteration of the calibre of the vessel. This is sometimes very strikingly seen in the neigh- borhood of gummata, and by diminishing the blood supply, it may contribute to the degeneration of the gumma. It also predisposes to degenerations in parts around, as wberei softening of the brain occurs in connection with gummata. Hereditary Syphilis. — We have already seen that sj'philis, in the seeondar}' stage at least, may be transmitted to the offspring. In the acute period the children often die in utero, or they. sicken soon after birth and die within a few weeks. But it often happens that the children do not show am' evidence of syphilis for months or years. In this way we may distinguish cases of congenital syphilis from cases of simple hereditary syphilis, the former being born with syphilitic lesions, the latter only acquiring them after- wards. In congenital syphilis the most constant and unequivocal lesion is the affection of the bones, which will be considered afterwards. In this condition there is the formation of a kind of gummatous tissue apparently, with inflammatory conditions. In the simple hereditary cases the lesious are, like those of the secondary stage, mainly inflammatory. There are inflammations of the skin, mucous membranes, cornea, etc. The characteristic malformation of the teeth which Hutchinson has pointed out seems related to the inflammation of the mucous membrane of the gums during the development of the teeth. TUBEECLE AND TUJ3KR0ULOSI.S. We enter here on a somewhat debatable department of Pathology, but the investigations of experimental pathology have recently given a firmer basis to our knowledge of the subject. 154 INFECTIVE TUM(^KS. GrENERAL TUBERCULOSIS. — We have already seen in the case of syphilis that in the secondary stage there is a virus in the blood which produces secondary lesions in diverse organs. This secondary stage of syphilis has been sometimes compared to a long drawn- out fever, and we saw that the symmetrical character of the lesions was to be regarded as presumptive evidence that the virus is in the blood. N"ow in ACUTE MILIARY TUBERCULOSIS we have a condition in which lesions appear in diverse organs and occur symmetrically, and it may be well to begin our study of tuberculosis with this disease. We have in it an undoubted tuberculosis, and the prin- ciples which we are able to establish in regard to this disease will afford us a criterion by which we may judge of the nature of other processes more doubtfully or less purely tubercular. The disease much more closely resembles an acute fever than secondary syphilis does, and is often mistaken for typhoid fever. In the course of a few weeks there spring up in the lungs, kidneys, liver, lymphatic glands, and frequently also in the soft membranes of the brain, substance of the heart, spleen, and elsewhere, a multitude of small lesions whose structure will be described presently. In the case of bilateral organs, such as the kidneys, the little lesions are Pig. 52. C6*;MfH Miliary tubercles in lung. The opaque oentrul piut: :iie caseous. ;■ 1(1. scattered through both, and are present in all parts of each organ. Looking at a ease of acute miliary tuberculosis, the conclusion can hardly be avoided that there is here a virus which has been circulating in the blood, and sown wherever the blood has reached, although producing its effects only in organs affording a fitting nidus for it. TUBERCLE AKD TUBERCULOSIS. 155 It may be well here at the outset to inquire what is the structure of these multitudinous lesions, each of which is a miliary tubercle. They present certain differences in their various situations, but there are certain points of agreement in all. If we take a very recent case and examine the lung, we shall find an immense num- ber of minute nearly globular bodies (Fig. 52), occupying the stroma of the lung, and very often either involving a bloodvessel or immediately bordering on one. These bodies are the tubercles, and whether in the lung or elsewhere, they present a structure which is virtually identical in every part. Fig. 53 shows a very Pig. 53. "#' Tubercle in a bronchial gland. X ^^0. small tubercle from a lymphatic gland, considerably magnified. It is seen to be a defined, roundish body, presenting at its peripheral parts numbers of round cells like leucocytes; nearer the centre rather larger cells, like the formative cells of granulation tissue, and often called epithelioid cells ; and in its more central parts one or more gigantic cells having numerous nuclei, the so-called giant- cells. These various structures are not to be distinguished in every one of the tubercles, as it depends on the section whether their central parts are shown, and, besides, they are liable to de- generation, which obscures their structure. We can hardly avoid calling these little bodies tumors, and to bodies of this kind we shall confine the name tubercles ; these are miliary tubercles. Their relation to the bloodvessels is often very well seen if the soft membranes of the brain are involved. In the adventitia of the fine arteries of the pia mater, there will lie found aggregations 156 INFECTIVE TUMOBS. of cells, forming sometimes, as in Fig. 54, a prominence on the wall, or, if the vessel be small, a spindle-shaped sheath around it. The cells constituting the tubercles are prone to undergo caseous NECROSIS so that, as in Fig. 52, the central parts are often markedly opaque, and the structure completely obscured. The giant-cells are often dotted vs^ith fine fat granules, and fatty degeneration fre- quently overtakes the greater part of the tubercle. It should be Fig. 54. ■ J Tuberole on artery of pia mater. X 300. added that verj^ frequently what appears to the naked eye to be a single tubercle often turns out, under the luicroscope, to be a group of two or more, and even when completely coalesced this may still be indicated by the caseous metamorphosis having two or more distinct centres joined at the periphery. The tubercles contain no bloodvessels, and this may partly explain their proneness to caseous metamorphosis. We have hitherto referred only to the caseous change which tubercles undergo, but it has to be added that they are liable also to a change which may be called eibrous transformation. We have already seen that tubercles contain the elements of inflamma- tory new formation, in their details having all the ultimate constituents of granu.lation tissue, except the bloodvessels. They may, like the tissue, present a tendency to organization, and be converted into masses of hard, solid, connective tissue. It is note- worthy that when this occurs the inflammatory products around commonly undergo similar changes, making, as a rule, common cause with the tubercles whether the change be caseous or fibrous. This form is less common than the caseous, and its occurrence is probably determined by peculiarities of the constitution or cir- cumstances of the individual. TUBERCLE AND TUBERCULOSIS. 157 Connection of Tuberculosis and Inflammation. — In the above remarks the structure of the typical tubercle has been described, but it is not common to meet with tubercles entirely free from in- flammatory complication, although cases of acute miliary tubercu- losis do occur in children in which the tubercles are virtually pure. In the great majority of cases, however, there are evidences of in- flammation around them. In the case of the lung, for instance, the alveoli immediately bordering on the tubercle are filled with large cells, the products of catarrhal inflammation, and the walls of the alveoli are infiltrated with round cells. These inflammatory products frequently make the tubercles appear to the naked eye much larger than they really are — the tubercle and inflamed lung tissue making a common mass. Throughout the lung also, and away from the immediate vicinity of the tubercles, there are often evidences of inflammation in the form of serous exudation and catarrhal cells in the alveoli. In the pia mater the inflamma- tory products are so abundant that they give their character to the disease called tubercular meningitis, and by their pi-esence obscure the actual tubercles, which are often difficult to see. The inflammations which are of nearly constant occurrence in connection with tubercles may be accounted for in various ways. They may be due directly to the action of the virus, or to an irri- tation springing from the mere presence of the tubercles acting as foreign bodies. Looking to the case of syphilis where we have the virus producing both inflammations and gummata, the pre- sumption is that both tubercles and inflammation are to be traced to the virus. The tubercles themselves, in their structure, present, as we have seen, close analogies to inflammatory product^ and to syphilitic gummata. We have the same round and e;^helioid cells. And even the giant-cells are met with in luxuriant granu- lations. The new-formed cells in tubercles again are prone to de- generation just as those in gummata. The tubercles differ from gummarta in their small size, a single tubercle being, as a rule, just visible to the naked eye; and in the regularity of their structure, which, with great uniformity, agrees with the description given above. It is interesting that in both these diseases there is such a tendency to inflammatory formations, and to the production of tumors, which in their structure show such analogies to inflam- mation. Local Tuberculosis* — -We have seen that in acute miliary tuberculosis there is something analogous to the secondary stage of syphilis in which a virus exists in the blood, and we have now to inquire whether there is anything analogous to the tertiary stage in which the virus is localized, and the lesions are unsym- 'metrical. Doubtless tubercles, like gummata, may become obsolete, and possibly the virus may wear itself out, but it is not known that any patient has ever survived a general miliary tuberculosis, so that we have here nothing strictly analogous to the tertiary stage. But we have such a thing as a Local Tuberculosis, an unsym- metrical tuberctilar lesion. Many instances of this may be adduced. 158 INFECTIVE TUMOES. and in all of them there are evidences to be found of similar char- acters to those seen in acute general tuberculosis. The existence of a virus is indicated by the infective character of the lesions, that is to say, the tendency, when the disease has manifested itself in a part, to propagate itself in the neighborhood ; as if there were a virus, which, reproducing itself in the original centre, was carried outwards and gave rise to similar lesions around. Again, in these local manifestations the tuberculosis is accompanied by inflammation, and here, also, the tubercles as well as the inflam- matory products tend to undergo changes the chief of M'hich is caseous necrosis. . As an example of this we may take tuberculosis of serous CAVITIES, such as the peritoneum or pericardium. If the tubercular virus gets into the peritoneum it is carried up and down in it, and the result is the production of tu^bercles in every region of the cavity. The tuberculosis is accompanied by inflammation, so that tuberculosis of the peritoneum is known under the name of tuber- cular peritonitis. The peritoneum, being a lymphatic sac, is di- rectly related, as we shall see in connection with the spread of cancerous tumors, to the lymphatics in the diaphragm, and through the diaphragm with the pleural cavity, which is another lymphatic sac. The virus appears to be carried through the diaphragm in many cases of tuberculosis of the peritoneum, and produces an eruption of tubercles in the lower part of the pleural cavity. Take, again, local tuberculosis of the kidney, forming the dis- ease sometimes called renal phthisis. When this disease is fully developed there are, usually in one kidney, irregular cavities lined with ragged ulcers, and these cavities often replace the greater part of the kidney tissue. In this disease the course of events seems to be this : tubercles are formed at the apices of the pyramids of the kidney where they project into the calices, or else in the mucous membrane of the pelvis itself These tubercles in the usual way undergo caseous necrosis, and being on a surface, they break down and form tubercular ulcers. Meanwhile the virus has extended deeper into the kidney tissue, and a fresh crop of tubercles has arisen beyond the ulcer. These tubercles in succes- sion undergo caseous necrosis and break down, and at the same time fresh crops are formed, so that a progressive destruction of the kidney tissue results. (A similar process of ulceration is in- dicated in the accompanying illustration (Fig. 55) of a tubercular ulcer of the intestine.) But the virus is not only carried inwards into the kidney tissue, but also downwards into the pelvis of the kidney, and down the ureters. As it is borne along it seems to lodge on these surfaces, and produce similar changes — tubercular ulceration of the pelvis, of the kidney, of the ureter, of the bladder, and sometimes also of the vesiculje seminales or vasa" deferentia. From the bladder the ulceration may extend to the ureter of the opposite side, but usually it confines itself to the portion close to the vesical opening, hardly ascending against the current of the urine. TUBERCLE AND TUBERCULOSIS. 159 In the case of renal phthisis we see how the. caseous necrosis leads to tubercular ulceration, the caseous material be removed, and leaving an ulcerated surface, and this case may be taken as typical of that process. But sometimes in the ureter the caseous material is not carried away, but remains as a dense consistent layer, lining the tube, it may be, in its entire length. There are cases again in which a local tuberculosis occiirring in the midst of an organ leads to a considerable accumulation of caseous material. Fit .- -,\' Tubercular ulcer of intestine. The rounded form of the tubercles around the ulcer (a) is seen, some of them breaking up the muscular coat {h) : one {d) outside this coat, and be- neath the peritoneum. X ^^^ A typical instance of this is presented by the scrofulous TUBERCLE OP THE BRAIN. In the brain substance of children we sometimes meet with a considerable tumor composed of dense caseous material, surrounded by a zone of gray transparent tissue. The course of events has been, that a group of tubercles has first formed, let us say from the virus having lodged here. These have undergone caseous metamorphosis while a fresh crop has been pro- duced at their periphery. And so as time elapses there is ever fresh new formation of tubercles and their death and degeneration. In this way a caseous mass is formed of the remains of myriads of dead tubercles. The gray transparent zone at the periphery is composed of tubercles not yet degenerated, mixed with inflam- matory products. The existence of a virus is here shoM'n by the tendency to extend by the successive formation of crops of fresh tubercles. Artificial Production op Tuberculosis. — In what has gone before it has been shown that in acute general tuberculosis there is IGO INFECTIVE TUMORS. a virus in the blood producing multitudinous tubei'cles in various organs. It has also appeared that in cases of local tuberculosis there is a virus producing tubercles by a process which may be called infective, inasmuch as the influence passes out from a centre and infects the neighboring tissues. We have now to inquire whether the virus can l)e convej^ed from one animal to another by inoculation. ]!Tumerous experimenters since the time of Villemin have shown that in certain animals, especially guinea-pigs, it is possible to pro- duce a GENERAL TUBERCULOSIS BY INOCULATION with Certain products from the body of man. "When pieces of a caseous tubercle or scrofulous lymphatic gland are inoculated under the skin or into the abdominal cavity of a guinea-pig, then the animal in six to ten weeks dies of general tuberculosis. Tubercles are found in the peritoneum, pleura, kidneys, liver, spleen, bone-marrow, etc. By the introduction of the material a virus has been introduced which gives rise to the regular tubercular manifestations. A LOCAL TUBERCULOSIS may also be produced by inoculation. In Cohnheira's experiments, for instance, a piece Of caseous material is introduced by an incision through the cornea into the anterior chamber of the eye of a rabbit or guinea-pig. If the substance has been so fresh as to contain none of the products of decomposition, the irritation produced by its introduction soon passes away, and the inoculated substance gets smaller and smaller and may even, after a time, disappear. For a time the eye appears quite clear and intact. Then suddenly there appears in the iris a larger or smaller number of fine gray nodules, which, just as in man, attain a certain size and then become caseous. In rabbits this eruption of tubercles generally occurs twenty-one days after inoculation, in guinea-pigs it is usually a week earlier, although even in rabbits it may take place in fourteen days. The tuberculosis may confine itself to the eye or it may extend to other organs. It is specially interesting that in this case the virus has appar- ently a period of incubation of fourteen or twenty-one days, in this respect conforming to the viruses of other forms of disease. Experiments have also been made in whicli animals have in- spired AIR containing the sputa of tubercular patients, with the result of inducing tuberculosis of the lungs and bronchial glands. Again, animals have been fed with tubercular matter, and have contracted tuberculosis of the intestines and mesenteric glands, and so on. These experiments prove undoubtedly that tubercular material contains a virus which is capable of transmission to other living animals just as the syphilitic virus is. Nature of the Tubercular Virus. — But now the question arises, Is this a specific virus only produced by itself, or may it arise in the body from other products? Opinions diverge on this point. Villemin, whose experiments are the earliest bearing on this subject, and Klebs have strongly expressed the view that the tubercular virus is specific, and can only be produced by self-prop- TUBERCLE AND TUBERCULOSIS. 161 agation. On the other hand, it is held by many that caseous material, whether the result of the degeneration of tubercular pro- ducts or of those of simple inflammations, is capable of producing tuberculosis. In fact, in the experiments in which tubercular material is inoculated, these observers assert that it first produces a local inflammation, and that the finely divided material which results from the drying in of the inflammatory products is the cause of the tubercular eruption. In this connection it may be mentioned that acute miliary tuberculosis in man is often sup- posed to take its origin in some local mass of caseous material, and that local tuberculosis, say of the lung, is frequently, by such authors, referred to the products of caseous necrosis in the inflam- matory exudation of a simple catarrhal pneumonia. This matter we may now regard as finally set at rest by the recent discoveries of Koch, already confirmed by several others, that the virus of tuberculosis is essentially connected with a par- ticular form of micro-organism, a bacillus. These observations, establishing as they do the parasitic nature of tuberculosis, com- pletely corroborate and carry to their due conclusion the views expressed in the preceding pages. By a particular method of observation, Koch has succeeded in demonstrating the existence of a special bacterium (bacillus) in tubercles, whether occurring spontaneously in man and animals or induced by inoculation. Fig. 56. /^ ■tJ Tubercular bacillus prepared from sputum in phthisis pulmonalis. X 1500. The bacilli are short rods, a quarter or half the length of a red blood-corpuscle (see Fig. 56), but occasionally a little longer. They are often in considerable aggregates, especially where the tubercular process is advancing, and they frequently exist inside the giant-cells. In many cases the rods contain spores, generallv two to four in each bacillus. These organisms have been found in the following diseases — general miliary tuberculosis, phthisis pulmonalis, scrofulous tu- bercle of the brain, tuberculosis of the intestine, scrofulous disease 11 162 INFECTIVE TUMORS. of lymphatic glands, scrofulous synovitis. They have been found also, uniformly, in bovine tuberculosis, in the spontaneous tuber- culosis of guinea-pigs, rabbits, and monkeys. They are also present in the tubercles produced by inoculation in animals. But the bacillus has not only been discovered, it has been culti- vated outside the body. It grows in blood-serum, but very slowly, and only when the temperature is between 30° and 41° C. The organism has been cultivated through many generations, and fi'om various forms of tuberculosis, and at the enct it has been found to retain all its virulence. When introduced it takes about a week or ten days to produce any manifest change, but it ultimately gives rise to a regular tuberculosis in the internal organs. These observations, then, distinctly prove that tuberculosis is a specific infective disease. Considering that the bacillus is present abundantly in the sputum of phthisis, and gets dispersed every- where from that, there is no difficulty in understanding how the organism gets into the body. It is clear, however, that in order to its development there must be some existing condition of the body predisposing. It has alreadj^ been mentioned that the bacillus is of slow growth, and when it is carried into the health}^ tissues it probably gets eliminated before it undergoes considerable increase. In the case of weakly persons, however, the tissues may be less able to resist its inroads, and as different persons are variously con- stituted the locality of the development will vary. The lungs, however, are obviously the favorite seat of attack, and the organism is doubtless inhaled. According to the views already advanced, the relations of the tubercular process and the area covered by it are somewhat more extended than many have hitherto acknowledged. JSTot only such definite tubercular conditions as the scrofulous tubercle of the brain, but also pulmonary phthisis, scrofulous disease of the glands, etc., are essentially tubercular in their nature. The virus is present in all such products, and they are capable of producing tuberculosis by inoculation. The domain of tuberculosis therefore covers that of scrofula. It is here proper to state that histological investigation seems to confirm this latter view. Scrofulous disease of the lymphatic glands is not a simple inflammatory swelling of them, but tubercles of typical structure are to be found in them from the earliest period, and the process is as much a tubercular one as the local tuberculosis of the brain. It is the same with phthisis pulmonalis. There are undoubted inflammatory phenomena here, but tubercles are found as well, and although it may be said that the tubercular formation is secondary to the degeneration of the inflammatory products, the constancy with which tubercles are to be found in the earliest periods rather contradicts this view. The so-called scrofulous diseases are characterized by a rich new formation of cells, apparently inflammatory, in the midst of which tubercles are to be found. Both tubercles and inflammatory products are prone to undergo caseous necrosis. Here the former TUBERCLE AND TUBERCULOSIS. 163 question comes up as to the relation of the inflammatory products to the specific tubercles. Looking to the fact that these pro- ducts undergo precisely the same changes as the tubercles it seems reasonable to infer that they are both due to the action of the same virus. This is only consistent with what we have seen in the case of syphilis where the same virus produces both the inflammatory manifestations and the gummata. Source of the Tubercular Virus. — There are still some ques- tions to be answered after all that has been stated above. If in acute miliary tuberculosis we have a virus in the blood, whence does it come ? If in local tuberculosis there is a virus, what is its source, and how does it reach its local habitation ? It has been stated that in acute miliary tuberculosis the virus is present in the blood, but this does not quite explain the whole. The virus is often present in the blood without producing this general tuberculosis. For instance, in phthisis pulmonalis there are often a few tubercles in the liver and kidneys, and the virus must' have reached these organs by the blood. Then in local tuberculosis it is diflicult to understand how the virus can have reached such organs as the kidneys or the joints except by the blood. We have already seen that the tubercular bacillus is slow of growth, and does not multiply with great rapidity, and the probability is that before acute miliary tuberculosis can be produced there must be a large accumulation of it in the blood. It is often stated that in acute general tuberculosis the source of the virus is to be found in some old caseous mass in the body, such as a scrofulous tubercle of the brain or a caseous gland. But the disease not infrequently occurs without any such caseous focus being discovered, and even when a caseous mass exists it is not clear how the virus is produced in such quantity as we are led to infer. In some cases tuberculosis of the thoracic duct, and in others of the branches of the pulmonary artery, has been found in acute miliary tuberculosis, and in these we have a suflicient source of vivxis in immediate connection with the blood. It may be that careful examination will reveal such sources of supply in most cases of this disease, but meanwhile we raust wait. It is even possible that the virus may sometimes be introduced in a peculiarly virulent form. As Virchow long ago pointed out, epidemics of general tuberculosis occur, and the explanation may be found in this. In regard to local tuberculosis it is to be presumed that the virus is introduced in small quantity, and in order to its propagation two things are necessary. In the first place the virus must be allowed to tarry in the part-, and in the second place it must find a fitting nidus. It seems as if the normal tissues had the power of destroy- ing small quantities of the virus. But if the tissues are defective in vitality, and especially if along with that the blood stagnates in them, then we may have the virus, if introduced, propagating itself and producing tuberculosis. 164 INFECTIVE TUMOES. The source of the virus is not far to seek. If phthisis pulmon- alis is a tubercular disease, and if, as Koch and Ehrlich have shown, the sputum of such patients contains myriads of the spe- cific bacillus, then the air of towns must contain it in abundance, and everyone must inhale it. But it is only persons who have natural or acquired weaknesses that become the subjects of local tuberculosis. But the virus may be introduced by the food as well as the air, and in this connection it is important to note that the bacillus of bovine tuberculosis appears to be identical with that of human tuberculosis. There is reason to believe that the milk of tuber- cular cows contains the virus, which may thus find access to man. The virus then having been introduced by the air or in the food may lodge in the lungs or intestine, and, in persons predisposed, may develop tubercular disease at the seat of its entrance. But if the place of entrance does not afford a fitting nidus, the virus may be carried beyond. It will most readily be carried by the lym- phatics to the nearest lymphatic glands, and may thence pass into the blood. In children it seems as if the virus were peculiarly liable to lodge in the mesenteric glands after being taken in by the food. Again, the virus may get into the blood, but it does not develop unless it finds some part of the body fit for its reproduction. In many cases of scrofulous and tubercular disease, there has been, previous to their development, some injury or disease of the par- ticular part in which they have occurred. For instance, in scrofu- lous synovitis, there is very commonly some history of an injury as the starting-point of the disease, which is really a local tubercu- losis of the joint. BOVINE TUBERCULOSIS. This disease, perhaps better known by its German name of Perlsucht, is rather common among cattle. It is a general disease manifesting itself in a variety of organs like our own general tuberculosis, but running a much slower course. It is an infective disease, and has been communicated to the calf, lamb, goat, pig, and rabbit, by feeding these animals with milk from an afl:ected cow, or with the actual pearl nodules. Like tuberculosis, it is due to a virus, which, as we have seen, is the same bacillus as that of ordinary tuberculosis ; it is generally believed to be hereditary. The disease in the cow is characterized, like general tubercu- losis, by the formation of numerous isolated or conglomerated nodules._ They occur chiefly on the serous membranes, in the lymphatic glands, and in the lungs. The nodules on the serous membranes are the most obvious and characteristic, and it is they which have given the disease its commonest name, Perlsucht or pearl disease. In the pleura and peritoneum appear vascular villous outgrowths in which the nodules ultimately develop (Fig. 57). These nodules are of various dimensions, mostly about the BOVINE TUBERCULOSIS. 165 size of lentils, either sessile or stalked, and very often in the form of flat oval bodies crowded together on the surface like duckweed in a pool of water. They are liable to become caseous or ulti- mately cretaceous. The lymphatic glands are simultaneously affected, especially the thoracic and abdominal ones, and they often grow to enormous dimensions, from the formation of nodules in them. They also are liable to caseous necrosis or calcareous depo- sition. The lungs rarely escape infection, and the nodules here frequently coalesce so as to form somewhat large masses, which Pig. 57. A piece of lung in bovine tubereulosis. On surface of lung many rounded tumors are seen, some pendulous. (VincHow.) are most abundant towards the surface. These masses are often surrounded by distinct capsules, and if softening, which is of common occurrence, supervenes, we have cavities lined with a distinct connective-tissue membrane. Such cavities are regarded by verj' high authorities, and especially by Virchow, as due to dilatation of the bronchi bj^ accunmlated secretion. Besides in these organs, nodules may occur in the liver, intestine, joints, bones, genito-urinaiy organs, and udder, and in these situations they present similar characters to those already referred to. In its essential or minute structure the pearl nodule differs little, if at all, from the tubercular nodule of the human subject. It is made up of a congeries of minute bodies which may be called tubercles, consisting of rounded aggregations of cells, the most characteristic of which are the giant-cells, which are here even more abundant than in ordinary tubercles. It is therefore in its general features, and in the peculiar arrangement of its nodules, that this disease differs from tuberculosis in man. It has been indicated above that the virus of bo\dne tuberculosis, being the same as that in human tuberculosis, may produce the 166 INFECTIVE TUMORS. latter when introduced into the hodj of man. According to Creighton, the resulting lesions often resemble those of bovine tuberculosis rather than those of the human form. LUPUS. This is a disease of the skin, usually of the face, and occasionally of neighboring portions of the mucous membrane. It is character- ized by the formation of rounded prominences, generally of a brownish color, on the surface of which there is often desquama- tion of the epidermis. On microscopic examination of the rounded prominences (which are sometimes called tubercles, in the microscopic sense) they are found to consist essentially of granulation tissue. The cutis vera has been replaced by an abundantly cellular tissue, the cells mainly like leucocytes, but also epithelioid, and even giant-cells. The infiltration of the skin also is not homogeneous, but often in dis- tinct nodular aggregations resembling tubercles. As in the other forms of infective tumor, the cells here present a tendency to degeneration. It sometimes happens that the gran- ulation tissue is partially absorbed, and partially developed into connective tissue, so that a cicatrix results, but it is a cicatrix without previous ulceration (lupus non-exedens). In other cases the epidermis over the prominences gives way and an ulcer forms, the granulation tissue breaking down so as to cause a deep loss of substance. The mode of formation of these ulcers is like that of the syphilitic ulcer from the gumma, or the tubercular ulcer, and, like them, they tend to enlarge by successive new formation of lupus tissue at the periphery, and its destruction. In this way there may be extensive loss of substance of the skin (lupus exedens). There may be a partial healing of the ulcers at one part, and advance at another, so that considerable deformities result. As the disease is an infective one we may presume that it depends on a virus, but the nature of the virus is obscure. There are some cases in which the syphilitic virus seems to be the cause (syphilitic lupus), but these are a very small minority. It is believed by some that we have here a local tuberculosis of the skin, and it is possible that this view may turn out to be correct. There is, however, this objection to it, that it does not appear that the lymphatic glands in connection with the lupus become the seat of scrofulous disease. LEPKOSY. This disease is also called Elephantiasis Grsecorum. It was at one time spread all over Europ6, but is now confined to Iceland, some parts of Norway and Eussia, and the coast of the Mediter- ranean. LEPROSY. 167 The disease occurs in two forms which are designated lepra tuberculosa and lepra ansesthetica. In the first the new formation has its seat in the skin or mucous membrane; in the second it is the nerves which are affected. "When it attacks the skin, it is mostly the face and hands which are affected, and the legs if they are exposed to the weather. There appear larger or smaller swellings, at first red or bluish in color, which become firmer and harder. These tubercles may reach the Pig, Leprosy. The ffice shows nodular swellings, especially on nose, eyebrows, lips, chin, and ears. Pntient had also a large ulcer on right leg, and a small one on left. (Virchow.) size of a hazel-nut or a walnut. They consist of granulation tissue in which cells of the size of leucocytes are most abundant. As in other granulation tumors, we often have ulceration, or, as in the case of lupus, there may be cicatrization without ulceration. By the formation of the swellings and cicatrization, great deformities frequently result, so that the patients have often a peculiarly hideous appearance, the face being knobbed and gnarled (Fig. 58). In the aneesthetic form the nerve-stems become the seat of gran- ulation tissue, forming spindle-shaped swellings, sometimes of con- siderable length. The granulation tissue here is in the interstitial connective tissue, so that the nerve-fibres are separated and com- pressed. In the anffisthetic parts it is not uncommon to find gan- grene occurring, so that fingers or toes drop off". In leprosy there are sometimes tumors formed in internal organs, but this is very rare. By the researches of Hansen and ISTeisser, it has been shown that leprosy is related to a micro-organism, which closely resembles the tubercular bacillus. The bacilli are always to be found in the granulation tissue forming the tumors. Their source, however, is not so clear. They are not acquired by contagion, and experi- 168 INFECTIVE TUMORS. ment has hitherto failed to produce the disease by inoculation, although the possibility of inoculability is not to be denied. The fact that leprosy occurs at the present day only among fish-eating people may perhaps indicate that the organism has its origin in the decomposition of fish, and persons in a low state of health eating decomposing fish are liable to be affected by it. ULANDEES AND FARCY. This is a single disease, although the names to some extent are applied separately. It aflects chiefly horses, and is called glanders when it has its chief seat in the nasal mucous membrane, and farcy when the skin is chiefly affected. It is eminently contagious, and communicated from animal to animal by inoculation. Occurring chiefly among horses and similar' animals, it is met with also in some of the domestic animals, and is not infrequently communi- cated to man, especially to persons who work about horses. The disease in horses manifests itself first in the formation of swellings of the mucous membrane or skin, consisting of granu- lation tissue. The nasal mucous membrane is generally first attacked, and there is either a diffuse infiltration of it or else a more localized series of swellings like those of lupus. From this seat the disease spreads to neighboring lymphatic glands, also along the mucous membrane to the lungs and intestinal tract. The granulation tissue here, even more than in the other infec- tive tumors, tends to break down, so that, as a rule, ulcers soon form, which present a great tendency to spread. These ulcers arise by what is virtually a suppurative process, and if the tumors are situated deep in the skin or mucous membrane there may be actual abscesses, which, by bursting, form ulcers. If the ulcers heal, cicatrices are formed in the usual way. The manifestations in internal parts are largely inflammatory in character. The lymphatic glands of the neck are the seat of inflammatory swelling. In the lungs there are nodules either con- sisting of granulation tissue with caseous central parts, or more distinctly pneumonic. There are also in the mucous membrane of the intestinal canal nodules which are sometimes more solid, at other times breaking down into pus. It is to be added that the above description applies to the acute cases, which are the commoner, but that the disease is sometimes chronic in its course. Chronic cases have usually the nodules in the skin, and there are secondary tumors in the muscles, etc. In man, glanders is usually an acute, rapidly fatal disease. There are nodules and ulcers in the mucous membi-anes and the skin, and frequently phlegmonous inflammation of the skin with abscesses among the muscles, etc. In fact, in man the disease takes the inflammatory character more distinctly than in the horse. We may have in man also nodules, ulcers, and abscesses in internal organs. It is clear that we have in this disease a virulent agent, but the nature of it is unknown. TUMORS OR MORBID GROWTHS. Definition. — A tumor means literally a swelling, and formerly any swelling was called a tumor. Tumor, for example, is often named as one of the cardinal signs of inflammation, and it is still customary to speak of the inflammatoi-y tumor. But now-a-days the use of the word has become limited ; it is applied to a class of new formations of which it is difficult to give a strict definition. It may be said that tumors are pieces of tissue which have a life and growth of their own irrespective of the needs of the organism, and of the general local conditions around them. The structure of a tumor does not differ in any essential particular from that of normal tissues ; in its elements it is wholly analogous to what may be found in the physiological tissues. It is nourished by the same blood, its bloodvessels being continuous with those of surrounding parts, its nerves are connected Avith neighboring nerve-stems, and its tissue, if not always similar to that near it, is frequently iden- tical. But it grows independently and without apparent object. Thus a fatty tumor goes on increasing in size irrespective of the adipose tissue in which it has its seat, and the person may be reduced to the greatest emaciation, most of the ordinary fat being absorbed, while little or no impression is made upon the fatty tumor. It may here be said that tumors usually arise in the midst of tissues of their own nature, and when they do so, they may be called HOMOLOGOUS. But they not infrequently arise in the midst of tissue of a different kind, a tumor composed of muscular tissue, for instance, in the kidney, and they are then called heterologous. These words were at one time used to express the distinction, that in the one case the tissue corresponds to the tissue of the body and in the other is different from the tissue of the body. But as the tissues of tumors correspond in their structure to the physiological tissues, there is no such thing as heterology in this sense. Origin and Development of Tumors. — In the definition given of tumors we have seen that they are composed of tissue which follows in its structure the normal tissues, but grows without reference to the needs of the organism. We have here to inquire how this piece of abuormally growing tissue takes origin. For the most part it may be asserted that it arises in tissue of its own nature, and that it grows by a process perfectly analogous to that of its own kind of tissue. Even in the case of heterologous tumors this is, at the outset, true. A muscular tumor, whatever 170 TUMOES OR MORBID GROWTHS. its seat, must have had embryonic muscle as its primordial basis, and it grows by a process analogous to the growth of muscle. But most tumors in their primary position are strictly homologous, and their tissue presumably has its origin along with that of the tissue in which they have their seat. A fatty tumor has its seat among the adipose tissue, and is at the first a piece of fat indistinguishable from that which surrounds it. We have to inquire how it is that this particular piece of adipose tissue has taken upon itself this peculiar and unusual development. An explanation has been recently suggested by Cohnheim, and enforced by cogent arguments and ingenious experiments per- formed by him and his pupils. Let it be supposed that the pri- mordial tumor is a piece of tissue left over as it were from the embryonic state, and retaining unabated much of the embryonic power of growth and development, and much of the special phe- nomena of tumors will be explained. In the normal growth of the body the various tissues go on repro- ducing themselves up to a certain point, but they stop short when they have produced the proper amount of tissue for the needs of the organism. The finer details of this process are largely governed by heredity, but it is clear that there is a law in the organism regulating the growth of the tissues in relation to each other and to the organism as a whole. It may be presumed that the embryonic basis of each tissue starts with a great power of new formation, but this power is strictly under command of the organism as a whole. But if a piece of embryonic tissue be taken out of its normal relations and placed in a position favorable to its further growth, then it may perhaps grow on irrespective of the needs of the organism, and develop something in the nature of a tumor. We have already referred to a case in which a process like this occurs. When the spur of a cock is transplanted to the comb, it grows rapidly, and by and by forms a prominent tumor. Here is a piece of tissue removed from its proper relations into a position more favorable for its growth in respect to blood-supply, and it grows with a very special vigor. Again, Leopold has found that it is possible to transplant cartilage from a living animal into the anterior chamber of the eye, where it acquires vascular connec- tionswith the iris. If fcetal cartilage be used, it grows in its new position and may form a distinct tiimor of some size, but if it be cartilage from an animal after birth it does not show the same vigor. It appears also that the earlier the period of development of the embryo from which the cartilage is taken, the more likely is there to be a vigorous growth in the new position. These facts would indicate that the normal tissues may under unusual circumstances, when they are disconnected from their normal relations, assume an independent growth, and the tissues of the embryo are more capable of this independent growth than those of the fully developed animal. But there are some facts in the pathology of tumors themselves GROWTH AND EXTEXSIOX OF TUMORS. 171 which indicate that in some cases, at least, they take origin in pieces of tissue left over, as it were, from the embryo. There are tumors which arise, as it is said, by inclusion. A very striking instance of this is the so-called sacral teratoma. In these tumors almost all the tissues of the body may be present, and sometimes there are parts as of a foetus. There seems no doubt that in this case, at an early period, a whole embryo has been included inside the foetus, and the person is born with an embrj'o included in his tissues. The various embryonic tissues grow in their abnormal position not altogether indiscriminately. Again, tumors of striped muscle have been found in the kidneys and other parts of the urino-genital system. The explanation of this seems to be that the "Wolffian body from which the Iddneys are developed is, in the embryo, close to the corneous and vertebral layers, and portions of these being included in the Wolffian body, in the embryonic state, they may afterwards develop into tumors. Again, it is not uncommon to find tumors developing in after- life from congenital moles or soft warts. These little outgrowths present throughout life a somewhat rudimentary structure, but they lie quiescent for many years, till suddenly, it may be, they present an extraordinary power of growth and develop tumors. It may then perhaps be presumed that in the case of many tumors they take origin in pieces of tissue left over from the em- bryo, and retaining largely their power of growth. But this does not apply to all tumors, and especially it does not apply to cancers. We shall afterwards see that these tumors do not grow from a single piece of tissue, but that in a considerable and extending area, the existing epithelial structures take on an unusual growth. At the marginal parts of an epithelioma of the tongue, for instance, it can nearly always be seen how the normal epithelium is extending and penetrating inwards; and again, a cancer of the kidney appears to arise and advance by transforma- tion of the existing tissue of the organ. It appears, therefore, that in this case the tumor arises from the existing normal structures, and that we must look for some abnormal impulse inducing it to grow outrageously. In the case of cancers and sarcomas the abnormal impulse is not infrequently related in some way to a traumatic cause. Many tumors are referred by patients to injuries received, although there must be some local peculiarity before a simple injury can produce such effects. Growth and Extension of Tumors. — For the most part, tumors enlarge by a new formation of tissue within themselves, just as the normal tissues increase during the period of growth. The tissue of the tumor is sometimes continuous with that of surround- ing parts, sometimes it is separated by a capsule composed of connective tissue; sometimes it begins by being continuous and afterwards gets separated. In any case the ordinary tumor simplj' grows by new formation of its own tissue. It often produces 172 TUMORS OE MORBID GROWTHS. effects on neighboring parts, by pressure especially, but apart from these merely mechanical effects, it does not prejudice neighboring structures. Tumors possessing these characters are usually called SIMPLE OR INNOCENT grOWths. But then there are tumors of which this is not true. They have a tendency to grow into and infiltrate neighboring tissues, present- ing characters "of what may be designated local malignancy. This is peculiarly the case with sarcomas and cancers. In the case of sarcomas the tumor seems to penetrate into and develop, as it were, on the mould of the existing tissue — apparently very much in the style that a thrombus or a piece of catgut in the tissue is replaced by granulation-tissue which moulds itself on it. For instance, a sarcoma may penetrate through a bloodvessel, replacing and taking the shape of a thrombus in the vessel. In the case of cancers, on the other hand, their tissue, which is epithelial in character, pene- trates among the tissues, largely destroying them and producing inflammatory disturbances. There is another peculiarity which certain tumors show, and particularly the sarcomas and cancers, namely, metastasis or gen- eralization, which is another feature of malignancy. In the case of these tumors, secondary growths spring up in parts removed from the primary tumor. Doubtless something is carried from the original tumor to the remote part, and we have to inquire by what path this is carried, or what may be the nature of the material. In the case of cancers the epithelial processes penetrating into the tissues readily find their way into the lymphatic spaces. Around a cancer there are often indications under the microscope that the lymphatics are filled with epithelial masses. From these growths in the lymphatic spaces material maj^ be carried off to distant parts of the Ij'mphatic system and cause secondary tumors to form there. Thus, a cancerous tumor sometimes penetrates into the peritoneal cavity, which, of course, is a lymph-sac, and secondary tumors are sown up and down the peritoneum. The lymph-sac of the peritoneum communicates with that of the pleura by lymphatic channels which pass through the diaphragm, and it is quite common to find the cancerous growth extending into these chan- nels, and through them into the pleura, producing secondary tumors there. In other cases the secondary tumors spring up in the lymphatic glands, and it is always those to which the lym- phatics around the tumor pass that are first involved, something passing off' from the epithelial processes in the lymph-spaces and being conveyed to the lymphatic glands. While this is the course in cancers, we find that in sarcomas if metastasis occurs it is by the tumor penetrating through the walls of bloodvessels. The material from the tumor is therefore carried by the blood, and as it is mostly the thin-walled veins which are thus opened into, the metastasis is usually in this case to the lungs. As to the nature of the material which passes from the tumor, it must be either something dissolved in the juices, or else solid par- ticles of some kind. Looking to a secondary cancerous infection SECONDARY CHANGES IN TUMORS. 173 of the peritoneum, we can hardly escape the conclusion that it is a finely divided solid. The secondary tumors are not regularly dis- tributed over the pei'itoneal surface, hut occur here and there or in groups, just as if solid particles had been carried and produced their eifects where they got leave to lie. Then also it must be solid particles which are arrested by the lymphatic glands and give rise to the secondary tumors there, as it were, by embolism. The probability is that the actual cells of the tumor are carried off and deposited at a distance. Perhaps it is not the fully developed cells, but small rudimentary ones. In this connection it is important to note that the secondarj- tumor for the most part exactly reproduces the tissue of the original one, even to the smallest details, and it is natural under these circumstances to believe that pieces of the original tumor are actually transported. It has already been stated that sarcomas and cancers are the tumors ■\\'hich regularly present a malignant tendency, but on rare occasions other tumors also do so. Cartilaginous tumors are not infreqxiently malignant. Next to them mucous-tissue tumors most frequently become malignant, but even fibrous tumors have been ob- served to do so, and lately Cohnheim has recorded a case of colloid goitre in which secondary tumors occurred. So that malignancy is not confined to sarcomas and cancers. On the other hand, tumors having the structure of sarcomas may remain local to the end. It has been usual to believe that this malignancy is dependent on peculiarities of the tumor itself. And when a simple tumor, as sometimes happens, assumes malignant characters, it usually assumes the structure of a sarcoma or cancer. Lately Cohnheim has started another theory, according to which the peculiarity is not in the tumor but in the normal tissues. In the case of a simple tumor the normal tissues are able to prevent its tissue from penetrating into them, but in the case of malignant tumors the tissues have become weakened and are unable to form a barrier to their extension. When a simple tumor becomes sarcomatous, it is because the tissues around have assumed a peculiar weakness. "When pieces of a tumor are transported to a distance, a struggle, as it were, occurs between the tendency of the tissue of the tumor to grow, and that of the normal tissues to prevent its growth. In the case of a simple tumor the tissues assume the upper hand, and cause the absorption of the tumor-tissue. In the case of malignant tumors, however, the tissues are too weak to accomplish this, and the secondary tumor develops. This theory is too strained, and all the facts are much better explained by supposing a special power of growth in the tumor. Wlien a secondary infection of the peritoneum is examined, it is difiicult to believe that there is anything but a peculiarly active agent and not any specialty in the peritoneal tissue. We have still to consider certain secondary changes to which tumors are liable. They are exposed to the same pathological pro- J74 TUMOES OR MOEBID GBOWTHS. cesses as normal tissues, and in a higher degree. Thus we meet with fatty degeneration, which is common, especially in quickly growing tumors; calcareous infiltration in structures which are obsolete; hemorrhages, principally in superficial rapidly growing tumors, when the bloodvessels are ill-formed; and necrosis mostly in tumors near the surface and thus exposed to mechanical irrita- tion, the consequences of such necrosis being ulcei'ation with, it may be, suppuration, hemorrhage, decomposition. Conditions like those last named will seriously affect the or- ganism as a whole, and they will occur most frequently in the case of malignant tumors, which grow quickly, and rapidly come to the surface. Malignant tumors also affect the organism as a whole by the readiness with which they extend to or produce secondary tumors in important organs, and secondary cancers frequentl^^ also induce inflammations, as in the case of the peritoneum or pleura. It is clear therefore that malignant tumors, especially by bleed- ing, by ulcerating and sloughing, by invading important parts, by producing inflammations, etc., have a tendency to deteriorate the system, producing antemia and general weakness. If growing quickly, they also tend to emaciate b^' using up the nutritive material of the body. A simple tumor, if it happens to be at the surface and exposed to mechanical violence, may also ulcerate and produce serious constitutional results, but it will be mainly in the case of malignant tumors that these results will follow. To these conditions of the body as a whole the name cachexia is often given. Sometimes also the term dyscrasia or diathesis is used with the meaning that there is some peculiar condition of the system preceding and inducing the formation of malignant tumors, but of this there is no evidence, and the changes in the general condition are always secondary. CLASSIPICATIOX. In considering the individual forms of tumors the simplest pos- sible method of classification will be adopted. In a work pro- fessedly on pathology it will be admitted that the structure of a tumor is the essential basis of classification and nomenclature, and in what follows terms will be used in what may be called their anatomical_ sense. It may be clinically convenient to designate tumors which present malignant properties as cancers, but it will npt do here to group together in one class tumors of totally different structure. The various tumors will be divided into three groups. In the first will be included tumors whose tissue reproduces a single simple physiological tissue, such as adipose tissue, connective tissue, bone. In the second group are tumors into whose structure more than one simple tissue enters, such as tumors consisting of such complex structures as papillge, or even made up of a systematic formation of bone, skin, etc. In the last group we have tumors SECONDARY CHANGES IN TUMOES. 175 which are mainly composed of cells, or iu which cells predominate. The individual cells are not different from those of the normal tissues, but there is an enormous new formation of them, with little tendency in them to develop into a proper physiological tissue. The first group may be called simple-tissue tumors, the second compound-tissue tumors, and the third cellular tumors. This classification, it may be remarked, is only used for conveni- ence, and does not lay claim to logical consistency. A very great advance has been made in our knowledge of tumors by the publication of Virchow's classical work. Die krankhaften Geschwulste. From this work many of the following illustrations are borrowed by the kindness of the author. A.— SIMPLE-TISSUE TUMOES. 1. THE CONNECTIVE-TISSUE TUMOK OE PIBEOMA. "We have already abundantly seen that connective tissue is fre- quently produced in inflammations, and it is not surprising to find that one class of connective-tissue tumor lies on the borderland of inflammations and tumors. EiQ. 69. Elephantiasis verrucosa from the labia majora. A tumor the size of a child's head, with a small base. The surface is lobulated, and each lobule presents warty projections, some fine and delicate, others thick and knobbed. The epidermis is everywhere somewhat thick. The internal parts are composed of thick, interlacing connective tissue, which is oedematous. (ViECHOW.) Elephantiasis arabum (E. grsecorum is leprosy) is a localized thickening of the skin, beginning in attacks resembling erysipelas, at first passing off and then recurring. There is finally a pernaa^ nently progressive and apparently unaccountable new formation of connective tissue, and so the characters of a tumor are assumed, The tissue produced is a loose, succulent connective tissue, like CONNECTIVE-TISSUE TUMOR. 177 that of the skin, but containing more cells, and so more like in- flammatory tissue. The epidermis is also thickened, so that the whole partakes of the character of an exaggerated hypertrophy of the skin (Fig. 59). The new formation may extend inwards to the fasciee, the in- termuscular tissue, and even to the perios- teum, inducing thickening of the bones (Fig. 60). The conditions here present considerable analogies with those in the infective tumors. There is in both a spreading new formation of tissue like that produced in inflamma- tion, although in the present case the tissue does not remain so long in the granulation stage. To one of those forms of tumors, namely leprosy, there is the further resem- blance, that elephantiasis is endemic in certain localities. All these facts may be held as pointing to the inference that this disease is due to a virus of a similar nature to that of leprosy. The resemblance in pathology of the two diseases is further indicated by both having been designated by the same name, the disease under con- sideration being E. arabum, and leprosy E. grsecorum. The disease is frequently re- garded as taking origin in obstruction of the lymphatics. This view is supported by the fact that the new-formed tissue is gen- erally very succulent, as if the spaces were overfilled with lymph, and there are some- times dilated lymphatics visible in the hypertrophied skin. The obstruction pro- duced by filaria sanguinis (see section on Parasites) in the lymphatic glands has been assigned as the cause, as well as mere simple indurations of the glands. The commonest seat of elephantiasis is the leg, and here alone is the name prop- erly applicable ; but it is also very frequent in the external generative organs. It occurs also not infrequently in a localized piece of skin, especially in the scrotum or labia pudendi, where a prominent outgrowth is Hyperostosis and synostosis of the bones of the leg and foot in elephantiasis. The bones present everywhere flat or pointed projections. At +-+ the tibia and fibula are united, as they are also above the ankle-joint. The astragalus and OS calcis are also united. (ViRCHOW.) the result. This may assume very large dimensions, becoming by and by pendulous. To such tumors Paget gives the name Cutaneous outgrowths, and they sometimes grow to enormous size, hanging down from the genital organs as far as the knee. The surface of the skin in these tumors, as well as in the more simple cases of elephantiasis, has a rough tuber- 12 178 SIMPLE-TISSUE TUMORS. culated appearance, and sometimes a highly warty aspect, as in Pig. 59. Smaller tumors of similar structure sometimes occur in large numbers, and to these the name Molluscum fibrosttm, or fibroma molluscum, or even elephantiasis mollusca is given. There are cases of elephantiasis having a certain resemblance to molluscum, inasmuch as there are multiple tumors outside the main one, and the growth seems to be increasing by the coalescence of these. These tumors at the margins are sometimes related to the seba- ceous glands, and appear to be formed around them. In the proper molluscum, however, we have multiple isolated tumors beginning as little growths of connective tissue in diverse regions of the skin, by and by growing out and becoming pendulous. Thus we may have hundreds of more or less pendulous tumors in various parts of the body. This purely fibrous molluscum must be carefully distinguished from molluscum contagiosum, a totally different disease, which will be considered in the section on Dis- eases of the Skin. In all the forms hitherto described the tumors have been con- tinuous with the skin. Tumors are sometimes met with, however, composed of a similar soft connective tissue, but enclosed in a capsule, so that they are separable from the skin. To these Paget gives the name Pibro-cellular tumors, and they are met with chiefly in the same regions (namely the external organs of genera- tion) as the fibro-cellular or cutaneous outgrowths with which they may be combined, the skin over the tumors being greatly thickened. Hard Pibromas or true Pibromas are exceedingly dense tumors composed of firm connective tissue tightly interlaced, and resem- bling tendon in its structure. On section they show a brilliant white surface, and often a concentric arrangement of the connec- tive-tissue bundles. We do not include here the uterine fibromas, which are really muscular tumors, and will be described as such. Pibromas are frequent in connection with periosteum and bone, especially on the jaws. Growing from the periosteum, they are sometimes intimately connected with the bone, which may be as if buried in the tumor. Sometimes the fibroma originates inside a bone. Pibromas also occur on fascias and membranes, as the dura mater, also rarely in the subcutaneous tissue and on nerve-stems. Just as dense connective tissue formed in chronic inflammation may become calcified, so may dense fibromas be partially infil- trated with lime-salts. 2.— THE FATTY TUMOE OR LIPOMA. This form of tumor consists of adipose tissue exactly like that of the body, as for instance the subcutaneous adipose tissue. Adi- pose tissue contains bands of fibrous connective tissue which carry FATTY TUMOR OR LIPOMA. 179 the vessels and nerves, and so do lipomas, but in difi'erent tumors this is variously abundant, the hardness or softness of the tumor depending on this. If there is little connective tissue, the tumor will be soft, and may even feel fluctuant. If there is much, it will be hard, and we may even have an approach to the fibrous tumor, the fibro-lipoma. The fibrous character may be increased by irri- tation, as where a tumor is exposed to friction, producing a kind of productive inflammation in the tumor. Fatty tumors are mostly sui'rounded by a distinct capsule, but sometimes they are continuous with the surrounding fat. Thus the fat around the mamma may undergo such an enlargement as to warrant the name of tumor (Lipoma capsulare). Billroth men- tions a lipoma which had grown in between the muscles of the thigh in such a way as that it could not be removed completely. Lipomas which are not definitely circumscribed may be called DIFFUSE LIPOMAS. Lipomas are of common occurrence. Their most frequent seat is under the skin, especially of the trunk. They are rare under mucous membranes, as that of the stomach (Fig. 61), were there Fie. 61. Lipoma in the wall of the stomach. It was the size of a hazel-nut, situated near the pylorus in the submucous tissue. Natural size. (Virchow.) is normally a small quantity of fat corresponding with the sub- cutaneous fat. They are occasionally met with in connection with serous and synovial membranes, in the appendices epiploicse of the intestines or the synovial fringes. Very rarely they occur where fat is not present normally, as in the kidneys, brain, etc. The author met with a case in which an elongated piece of fat lay on the upper surface of the corpus callosum. Lipomas are for the most part single, rarely multiple. Fatty tumors sometimes become pendulous. Those in the ap- pendices epiploicse (Fig. 62) are so from the first, and the neck of the polypoid tumor may get severed, the tumor becoming a loose 180 SIMPLE-TISSUE TUMOKS. body in the peritoneum; it is similar with the lipomas of the synovial fringes. But subcutaneous lipomas may become pendu- lous and polypoid, and may grow to great dimensions in this form. There is apt to be ulceration of the surface of such tumors, and even hemorrhage. Besides these changes we have the occasional Fig. 62. Pendulous lipoma of appendices epiploiofe of colon, A pedunculated tumor (a) projects from the general mass of subserous adipose tissue {d). It is twisted twice on its axis, and the peduncle is very thin. (ViRCHOW.) induration already mentioned, and sometimes calcareous infiltra- tion follows. Softening with the formation of a cyst inside the tumor is a rare occurrence. 3.— THE irUCOUS-TISSUE TUMOE OE MYXOMA. This form of tumor is composed of mucous tissue, and as this is not one of the physiological tissues of the adult, it will be proper to refer more specially to its characters. The bloodvessels of the umbilical cord are padded and protected from pressure by a gelatinous substance called "Wharton's jelly. Under the micro- scope, this consists of variously shaped cells separated by a clear, transparent, intercellular substance. The intercellular substance is of gelatinous consistence, and owes this character to the fact that it consists of a watery solution of mucin. This substance is nearly allied to albumen, but has the physical characters that, when present in even small quantity in a solution, it gives it a sticky gelatinous character. Its chemical reactions also differ from those of albumen, in respect that though like it precipitated by alcohol, the precipitate is redissolved by water. Also, acetic acid and other organic acids precipitate mucin, but not usually albu- MUCOUS-TISSUE TUMOR OR MYXOMA. 181 men. The precipitate of mucin by alcohol or acetic acid is more membranous than that of albumen. The reaction with acetic acid can be readily brought out in "Whai-ton's jelly, a microscopic section showing, on adding acetic acid, a reticulated precipitate. These reactions can also be studied in the mucus from any mucous membrane, or in the bile, in which mucin is normally one of the dissolved constituents. Besides, in the umbilical cord, mucous tissue is present in the villi of the chorion of the foetus, the villi consisting of a covering layer of epithelium with mucous tissue internally. In the foetus, it is also present in early stages in the subcutaneous tissue where Pig. 63, Portion of a hydatid mole showing the berry-like masses. Natural size, (Viucflow.) it has the place of the subcutaneous adipose tissue, being, in fact, related to fat very much as the temporary cartilage is to bone. Some remains of this tissue may be met with in the adult. Thus, the vitreous humor of the eye is really composed of soft mucous tissue, and traces of it have been found in places where normally adipose tissue exists, as under the pericardium, at the hilus of the kidney, subcutaneously and in the medulla of bone. It appears that in these positions there is sometimes a partial recurrence to 182 SIMPLE-TISSUE TUMORS. the foetal condition. The connective substance of the brain, the neurogha, is allied to mucous tissue, and seems to present a prone- ness to return to that form. Of MUCOUS-TISSUE TUMORS a vcrj interesting form is the hydatid MOLE. Here the mucous tissue of the villi of the chorion under- goes great increase, and the result is the transformation of the villi into congeries of oval, cyst-like bodies which hang like grapes on a stalk, and often hang one on the other (Fig. 63). Thus a bulky mass often results, consisting of an enormous multitude of these berry-like cysts. If the change has begun early in foetal life, then the whole chorion is thus converted; if later, when the villi have become confined to the placental surface, then only one surface is aflfected. The dead and blighted foetus will be found inside the mass, generally in an early stage of development, but sometimes more advanced. Proper mucous-tissue tumors are met with principally in the subcutaneous tissue, where they may be regarded as perhaps due to a' piece of embryonic tissue left over when the mucous tissue was converted into adipose, in this respect resembling the chon- dromas of bone. They form rounded or oval tumors generally soft, sometimes almost fluctuant in consistence and gelatinous in appearance. Examined under the microscope we have a very translucent tissue in the midst of which there are irregularly shaped cells. The tissue is intersected by more or less frequent bands of connective tissue (Fig. 64). The proportion of cells varies Pig. 64. Microscopic section of a myxoma of the subcutaneous tissue. Isolated cells and strands of fibres are shown. Between them a clear gelatinous material was present. X 350. considerably in different cases, and even in different parts of the same tumor. Myxomas are also of somewhat frequent occurrence in the brain as compared with other tumors in this organ. Here they some- times grow to considerable size, and are liable by softening to take MUCOUS-TISSUE TUMOR OE MYXOMA. 183 the form of cysts filled with a mucous fluid. They are also met with on peripheral nerves. They occur in the mamma, where not infrequently they appear to have the character of a diflfuse forma- tion of mucous tissue between the glandular acini, so that the gland as a whole is converted into a tumor. In the salivary glands they occur, but are usually of mixed structure, being partly formed of other kinds of tissues. Considering the relations of adipose tissue and mucous tissue it is not remarkable that mixed forms occur in which apparently a Fig. 65. "^^^''S^s, ^^a£ Malignant myxoma lipomatodes of the long saphenous nerve. A, Section. B, External appearance. The tumor measured 2^ X 1| inches. At A, the nerve-fibres are seen to be for the most part on the outside of the tumor, which, however, was completely covered by the neuri- lemma. Internally the tumor is lobulated, and it presented a gelatinous appearance, but somewhat opaque. A similar tumor was seated on the short saphenous nerve. (Virchow.) partial conversion of the myxoma into a lipoma is in progress, or conversely a metamorphosis of the lipoma. Then also the myxomas vary very greatly in the proportion of cells, the very cellular ones being called medullary myxomas, and frequently graduating into sarcomas. In fact, with pathologists who take the embryonic nature of the tissue as the criterion of sarcomas, the fact that mucous tissue is the embryonic precursor of adipose 184 SIMPLE-TISSUE TUMORS. tissue induces them to class this form of tumor among the sar- comas. Consistently Math these facts there are some myxomas which show malignant characters, either local or general. In a case recorded by Virchow (Fig. 65) there were tumors on the nerves and in the dura mater of the cord and brain. 4.~THE CARTILAGINOUS TUMOE OE CHONDEOMA. This tumor is composed of cartilaginous tissue. The cartilage may be hyaline or fibrous, generally the latter. The tumor is also intersected with fibrous bands which carry bloodvessels that nourish the tissue. If a cartilaginous tumor grows in connection with and out from cartilage it is called an Ecchondrosis, but if, as in the majority of cases, it grows in connection with other tissues, then it is called an Enchondroma. The term chondroma of course includes both. The ecchondroses are usually small unimportant outgrowths chiefly of the cartilages of the larynx and trachea and ribs. Virchow has described an interesting form of so-called ecchon- drosis at the basilar portion of the occipital and sphenoid bones. The basilar parts of these bones are formed from cartilage, and in adult life they are united, forming a single bone (os tribasilare). The junction takes place irregularly by a kind of toothed union. In this process a little bit of cartilage may be omitted, and this sometimes develops into a little tumor just under the basilar artery, to which it may be adherent. It will be seen that we have here an actual instance of a little piece of embryonic tissue left over to develop afterwards into a tumor. This little tumor sometimes undergoes a remarkable change; the cells swell up and become like those of the chorda dorsalis, but in other cases it ossifies. The cartilaginous loose bodies in joints are sometimes regarded as origi- nally outgrowths from the cartilages or synovial fringes which have been broken ofi^ and grown after their sepa- ration. Enchondromas are mostly met with in ooNNECTioN WITH BoNEs. As bones are developed out of cartilage for the most part, it may be supposed that little bits of the embryonic cartilage are left over and develop into tumors afterwards. The enchondromas of bone may be di- vided into central and peripheral, ac- cording as they originate in the medulla or at the surface. The former are the more common, and they are met with chiefly in early life, occurring especially in the fingers and toes, which mav Pig, Multiple internal enohondromata of fingers. (Cornil and Ranvier.) THE BONY TUMOR OR OSTEOMA. 185 be the seat of multiple tumors as in Fig. 66. These tumors begin inside the phalanges or metacarpal bones, or, less frequently, the analogous bones of the foot. Growing inside the bones they may be for a time unperceived, but afterwards swell up the bones and may even burst through the external shell. These tumors often show a local malignancy, growing by the formation of new nodules in the tissue around. The peripheral chondromas are met with most frequently on the femur and pelvis, and most rarely on the bones of the face and skull. In soft parts chondromas are found occasionally, but are com- monly mixed with fibrous, mucous, glandular, sarcomatous, or cancerous tissue. They are particularly frequent in glands, as the testes, ovaries, mammse, or salivary glands. In these situations they are occasionally found to follow chronic irritations. In their form chondromas are generally rounded tumors and distinctly encapsuled, but if large they are lobulated. It has already been said that the enchondromas are often mixed with other tissue, and it is to be added that secondary changes are not infrequent. They sometimes soften, and this is frequently due to partial transformation into mucous tissue. This is particularly the case vdth the glandular enchondromas. On the other hand, those of bone are liable to ossify. Lastly, chondromas are liable, as has already been said, to show a certain malignancy, forming secondary tumors, especially in the lungs. This is connected with the frequently mixed character of these tumors, and their association especially with sarcomas and cancers. 5.— THE BONY TUilOR OK OSTEOMA. In this class are included tumors composed of bone, not mere new formations due to inflammation, nor tumors in which bone exists as a subordinate element with other tissue. The immense majority of bony tumors grow from bone, and are hence called exostoses. In regard to their structure, some are like spongy bone with the interstices filled Avith ordinary bone- marrow, and some are composed of dense bone such as forms the shaft of a long bone, and are called ivory exostoses. There are even tumors which originate in the teeth. When these are com- posed of cement, they are called dental osteomas, but when formed of dentine, odontomas. Several forms are to be distinguished. (1) The spongy exostosis, or the exostosis cartilaginea (Fig. 67). These tumors occur mostly at the epiphyses of the long bones, and are derived primarily from the epiphyseal cartilage. They grow during childhood, and, just as the cartilage from which they origi- nate ossifies, so do they, and the bony tumor formed is directly continuous with the bone beneath. The tumor begins as a small outgrowth, and so the first bone formed is a narrow piece. The cartilage as it goes on growing enlarges in every direction, and so overhangs its base, the tumor thus becoming larger as it grows 186 SIMPLE-TISSUE TUMORS. outward, and consequently pedunculated. The tumor consists of spongy bone with a thin layer of cartilage on its surface. It is enough to snip through the base in order to remove the tumor. Pig. 67. Cartilaginous spongy exostosis of femur. (ViRCHOW.) (2) The ivory exostosis is mostly met with on the bones of the head, but also on the pelvis, scapula, great toe, etc. The tumors Pig. 68. Internal ivory exostosis of the frontal bone. The surface is tuberoulated, and the tumor has a narrow base. It was situated to the left of the falx (/). Natural size. (ViRCHOW.) are usually rounded in form, and may be tuberculated on the surface. In their favorite seat on the head they may grow from MUSCULAE-TISSUE TUMOR OB MYOMA. 187 the external table and project externally, or from the internal table and project internally ' (as in Fig. 68), in which case they may produce irritation of the brain substance beneath. It sometimes happens that an ivory exostosis grows from corresponding parts of both external and internal tables. These tumors are sometimes multiple, as in Fig. 69. Fig. 69. Multiple exostoses of the frontal bone. Natural size. (Yirchow.) (3) Hyperostosis and periostosis are names applied to growths of bone which are not properly tumors. They are localized thick- enings of bones or portions of bones. This growth of particular parts of the bones of the head may become so independent in its manner that the characters of a tumor are simulated. Osteomas of other parts than bones are rather rare. It is remarkable, however, that bony masses occur sometimes in the central nervous system. They are met with in the arachnoid, where they used to be regarded as evidences of chronic irritation, and are hardly tumors. Actual tumors occur in the dura mater, and even in the brain substance. They are also met with in the eyeball, in the lungs, and, as little bony granules, in the skin. 6.— THE MUSCULAE-TISSUE TUMOR OR MYOMA. These are tumors in which muscular tissue is the essential con- stituent, but just as all muscles have supporting connective tissue so have these, some more, some less. As there are two kinds of muscle, so are there two forms of muscular tumor, those composed of striated, and those of smooth muscle. The Myoma strio-cellulare or labdo-myoma is very rare. Tumors of this structure have been observed in the heart, where they are congenital. They have also been seen in the kidneys, 188 SIMPLE-TISSUE TUMORS. ovaries, and testicles, where the tissue consists usually of spindle- shaped cells, which are transversely striated, and so the tumors are often called myo-sarcomas on account of their cellular character. The SMOOTH-CELLED MYOMA (M. Ifevi-ccllulare or leiomyoma) is an exceedingly common form of tumor, and is met with in almost every part where smooth muscle exists normally. According to the amount and density of the interstitial connective tissue is the consistence of the myoma — it may be very dense and warrant the name fibro-myoraa, or it may be so hard as to resemble cartilage. Myomas are often described as fibrous tumors, and in appear- ance they justify this designation. To the naked eye they appear fibrous on section, and even under the microscope they appear to be formed of fibres. On adding acetic acid to a microscopic section, or staining with cai'mine or other agent, the fibres are seen to be much more abundantly nucleated than ordinary connective tissue. In fact, rod-shaped nuclei (not spindles as in connective tissue) are so closely set as at once to suggest a cellular tissue (see Fig. 70). Pig. 70. ^.f:" "' ' " ' ^oMW^-^fs'^ ^Oy ^ ^-^ ^- Section of a myoma of the uterus stained with carmine. The muscular nuclei are seen in longitudinal and transverse section. X 350. It may here be remarked that in the unimpregnated uterus there is the same difficulty in distinguishing the individual spindle-cells. In both cases, however, the cells may be isolated by macerating the tissue for twenty-four hours in a 20 per cent.' solution of nitric acid, or for twenty to thirty minutes in a 34 per cent, solution of MUSCULAR-TISSUE TUMOR OR MYOMA. 189 caustic potash. This makes the tissue I'otteu, and separates the cells, which are recognized as spindles (as in Fig. 71). Myomas always arise where muscle already exists, and as smooth muscle is most frequent in the walls of mucous canals and cavities, it is there that they usually originate. The tumor may be con- tinuous with the muscular wall, forming an outgrowth from it, or it may be distinctly isolated and encapsuled. It may remain in the substance of the muscular wall (intraparietal or intramural), or it may slip inwards so as to bulge under the mucous membrane Fig. 71. Muscular fibre-cells from a myoma isolated by steeping in nitric acid. X 350. (submucous), or it may pass outward and present under the serous coat (subserous). In the two latter cases the tumors often become polypoid. By far the most frequent seat of the myoma is the female organs OP GENERATION, most frequently the uterus, but also the ligaments and ovaries. The so-called uterine fibroids are myomas, and the most important of these are the submucous which so frequently become polypoid, and give rise to hemorrhage, sloughing, etc. In the PROSTATE the hypertrophy frequently met with in old men is really from the formation of a muscular tumor, and the third lobe which forms a prominent bulging projection at the neck of the bladder is an outgrowth from the muscle of the prostate. Some- times there are even isolated muscular tumors in the midst of the prostate. This form of tumor is to be distinguished from the glandular tumor, which is a much rarer form of hypertrophy and occurs mostly in young men. Myomas of the stomach and intes- tine are infrequent, and are usually submucous. They have also been seen in the urinary bladder. Lastly, they are rarely met 190 SIMPLE-TISSUE TUMORS. with in the skin, one or two cases in connection with the nipple and the scrotum have been observed. The myoma is of slow growth, but many go on as long as thirty or forty years, and many reach a very great weight, as much as sixty pounds. Eetrograde changes may occur, such as fatty degeneration, resulting in shrinking or the formation of cysts. If induration occurs from formation of hard connective tissue, this may calcify, leaving the muscular tissue in the spaces between the calcified trabeculse. In some cases, from derangements of the cir- culation in large tumors, we may have an actual necrosis of a por- tion of the muscular substance.- resulting sometimes in absorption and the formation of a cyst. In other cases, the dead structures become calcified as in Fig. 72, where muscular elements, connec- tive tissue, and walls of bloodvessels were all found impregnated Pig. 72. From a myoma, a portion of which had become calcified, a, muscular fibre-cells impregnated with lime-salts; h, a bloodvessel with wall incrusted. X 350. with lime. As the myomas so readily become polypoid, they are liable to be insufiiciently nourished, as the neck gets thinner; sloughing may even occur, especially if they present on a mucous surface, and are exposed to injury. Such tumors are also liable to bleed, especially as the vessels in them sometimes undergo great dilatation. 7.— THE NERVOUS-TISSUE TUMOK OR NEUROMA. By the name neuroma is often understood a tumor which grows on a nerve-stem, and this use of it may be convenient for surgiqal NERVOUS-TISSUE TUMOB OR NEUROMA. 191 FiQ. 73. purposes. Here we have to consider tumors according to their structure, and if a fatty, mucous, or fibrous tumor grows on a nerve, it is to be embraced in its own class. Tumors on nerves, but not of nervous structure, are designated false neuromas. But there are tumors composed essentially of nervous tissue. As there are two kinds of nerve-tissue, the central or ganglionic and the fibrous or fascicular, it might be expected that we should have two kinds of neuromas. But practically we have no such thing as a tumor composed of ganglionic nerve-tissue, although central nervous tissue does occasionally enter into the composition of a teratoma. The TBUE NEUROMA is composcd of nerve-fibres, which may be either meduUated, as in the ordinary cerebro-spinal nerve, or non- meduUated. One of the most striking forms is the so-called amputation-neuroma (Fig. 73). Sometimes after amputations the cut ends of the nerves produce little knots or knobs which have a hard consis- tence and to the naked eye look fibrous. Under the microscope medullated nerve- fibres are found running in bundles, but there are also many fine fibres which are probably non-medullated nerve-fibres. It is in this case as if the cut end of the nerve had made an attempt at regenera- tion of the lost portion. Allied to this form is the traumatie neuroma, occurring as the result of injury in the course of a nerve. But neuromas occur in the course of nerves spontaneously, and they are often multiple, forming oval swellings, hard and fibrous in appearance. They contain much fibrous tissue, in the midst of which there are medullated nerve-fibres (see Fig. 74) recognizable in the fresh state hj the double contour, especially when the con- nective tissue has been rendered trans- parent by acetic acid or liquor potassge. But usually in addition to these medullated fibres, there are fine nucleated fibres which Yirchow regards as non-medullated nerve- fibres. In some neuromas these are very abundant. Amputation-neuroma. The nerves end in knobbed extremi- ties. The ease was one of am- putation in tbe upper arm. Two-thirds of the natural size. (ViRCHOW.) The PAINFUL SUBCUTANEOUS TUMOR, or "Wood's tumor, is a some- what difiicult growth to classify. It occurs in the form of a small round tumor under the skin, and is commonly the seat of intense pain. The pain indicates some connection with the nerves, and it has been suggested that the tumor may even be a non-medullated neuroma. According to Virchow there are tumors of various 192 SIMPLE-TISSUE TUMORS. structure in this category, myomas, angiomas, neuromas. Re- cently Hoggan has described one which he believes to be an ade- noma of the sweat-glands, but which Yirchow rather takes to be an angioma. In the case from which our figures are taken (Figs. Fig. 74. K'^' ?5^ Transverse section of a neuroma. The medullated nerve-fibres are shown, the appearance being much like that of the section of a nerve. X 80. 75 and 76) the tumor consisted of a dense interlacing network of fibres, very suggestive of the appearance of a myoma (Fig. 74). Fig. 75. Section of a painful subcutaneous tumor (Wood's tumor). The appearance is somewhat like that of a myoma. X 80. On macerating portions in nitric acid the tissue broke up into large spindle-cells, as shown in Fig. 75. This tumor is probably a VASCULAR TUMOE OR ANGIOMA. 193 myoma of the skin, and several others examined by the author had a similar structure. Fig. 76. From same tumor as Fig. 75, after maceration in nitric acid. Large spindles are isolated, probably smooth muscle-cells. X 350. THE VASCULAK TUMOE OE ANGIOMA. "We have here a tumor composed of blood or lymphatic vessels. Several forms are distinguished according to the kind of vessels which form the tumor. The commonest form is (1) the plbxifoem or capillary angioma. This includes most of the vascular nsevi, and consists of capillary Fig. 77. Section of skin in a case of diffuse venous nsevus. The large sinuses (shaded) are seen to lie superficially between the hair-follicles and glands. (Virchow.) and intermediate vessels forming a rich plexus. It is mostly a growth of the skin, and may be very small or cover a large area, forming a flat soft surface of dark or bright hue. It is nearly 13 194 SIMPLE-TISSUE TUMORS. always congenital, although it may increase in size after birth. These capillary nsevi graduate into those consisting of dilated veins, the venous or varicose nsevi (Fig. 77). They have similar situations to the capillary form and similar appearances. (2) The CAVERNOUS ansioma consists of tissue like that of the corpus cavei'nosum of the penis or clitoris, namely a network with meshes which communicate freely and are filled with blood. When empty they are seen to be composed of a pale tissue, in its texture resembling a sponge, with variously thick trabeculse and variously wide spaces. These trabeculse are all accurately lined with endo- thelium, and consist of connective tissue with some muscular fibre- cells in them. These tumors are erectile and sometimes pulsatile. Sometimes the tulnor merges into the neighboring vessels without distinct boundary, but sometimes it has a distinct connective-tissue capsule, which, however, appears to be a secondary formation. Sometimes also they are indurated in the centre, and the indura- tion may gradually lead to the obliteration of the spaces and the destruction of the tumor. These tumors are not so usually con- genital as the former kind, but they come on in childhood at latest, and they may develop out of the other form. The skin is a frequent seat of the cavernous angioma, especially that of the face or head, but also sometimes of the trunk or limbs. They are also met with in the liver, not forming prominent tumors, but simply replacing a piece of liver tissue by cavernous tisssue (see Fig. 78). Fig. 78. Cavernous angioma of liver. The fibrous septa are shown. The spaces between were occupied with blood during life. X 90. (3) Cavernous tumors communicating with the lymphatics and filled with lymphatic fluid have been described, and are designated cavernous lymphangiomas. 9.— THE GLANDULAR TUMOE OE ADENaMA. As there are many glands of different structure, so are there various forms of adenoma. (1) The mammary glandular tumor is a form concerning which there is some difference of opinion. Glandular tissue is frequently GLANDULAR TUMOB OE ADENOMA. 195 present in sarcoma of the mamma, and this is expressed in the name adenoid sarcoma. Again, cancers of the mamma take origin in the glandular tissue, and it may sometimes be doubtful whether we have a cancer or an adenoma before us. But besides these, we meet with distinct isolated growths in the mamma whose tissue imitates that of the gland itself, except that there are no excretory ducts. The tumor occurs in, or over, or under the gland, some- times as if it were a supernumerary breast. It is markedly lobed and varies in consistence according to the predominance of gland tissue or connective tissue. Under the microscope we find lobes, consisting of groups of acini or terminal gland structures lined with glandular epithelium (Fig. 79). Fig. 79. Adenoma of mamma. Glandular structures are seen in the midst of fibrous tissue, but without proper ducts. X 90. (2) In the prostate gland we occasionally have a new formation of gland tissue, leading to enlargement of the gland, but this forms a very small proportion of the hypertrophies of the prostate. (3) Mucous POLYPI are very frequent forms of tumor, and are mostly composed of hypei'trophied mucous glands. The}' form pendulous tumors, generally on mucous membranes which have been the seat of chronic inflammation. There are some polypi of mucous membranes which do not consist of gland tissue, especially those of the ear and of the female urethra (the urethral caruncles). Elsewhere, as in the nose, rectum, stomach, uterus, they are usually composed of masses of mucous gland tissue covered with epi- thelium of the kind existing in the mucous membrane where they grow, cj'lindrical in the stomach and rectum, ciliated in the nose. Very frequently from closure of their ducts, the mucous glands de- velop cysts. These polypi may generally be regarded as evidences of chronic catarrh of the mucous membrane in which they are found. 196 SIMPLE-TISSUE TUMORS. (4) The THYROID ADENOMAS form a large proportion of the GOITRES or BRONCHOCELES. The thyroid gland consists of vesicles lined with epithelium, these vesicles being grouped into lobules. A goitre maj' consist in a simple enlargement of the whole gland, or of a single lobe of it, or it may be due to the formation of isolated tumors consisting of gland tissue. In the case of apparent simple enlargement the vesicles may be found greatly increased in size and many of them filled with colloid material. In the same case the various stages of colloid metamorphosis, as it affects the epithelium, may be observed. These colloid vesicles may coalesce and form considerable cysts. In other cases there is a distinct new formation of glandular tissue, the tumor consisting largely of vesicles of normal size. But the new-formed vesicles are also prone to undergo colloid degeneration. Where distinct isolated tumors exist, there is, of course, a great new formation of gland tissue, and here also there is often colloid change. In all the forms secondary changes are frequent. We have already seen that cysts form. Then blood may be extravasated into cysts or into the interstitial tissue, and though subsequently absorbed the pigment remains. Caseous degeneration may affect the extravasated blood or even the glandular tissue, and calcareous infiltration sometimes ensues, so that great changes may occur in the characters of the tumor. The relation of the colloid goitres to tumors is very dis- tinctly evidenced by the observation of a case by Cohnheim, in which secondary tumors developed by metastasis, the tumors occur- ring in the lungs, lymphatic glands, and elsewhere having the structure of the thyroid with colloid degeneration. (5) Adenomas are of occasional occurrence in the liver, con- sisting of liver tissue. There may be a single tumor or many, and the tumors may be distinctly encapsuled or not. They consist of liver tissue arranged in lobules, but the hepatic cells are larger than normal, and contain more nuclei. They usually show fatty metamorphosis. Similar multiple adenomas of the liver are of frequent occurrence in dogs. In addition to this form, we shall see in the section devoted to diseases of the liver that a form occurs sometimes designated adenoma, in which the tissue follows the type of tubular glands rather than that of the liver. Among the adenomas we might include tumors of lymphatic- gland tissue, but these will be more conveniently considered after- wards under the lymphomas. 10.— THE GLIOMA. This is a tumor with the structure of the connective tissue of the central nervous system, the neuroglia. In examining a section of the brain substance, it is diflacult to tell what is really nervous structure, and what the supporting connective substance, but when we examine the surfaces of the ventricles we find that the ganglion cells and nerve-fibres fall away, and just at the surface or ependyma THE GLIOMA. 197 we have what is presumably a purely connective substance. "When hardened sections are examined, this is seen to consist of a finely reticulated network of fibres and round or slightly elongated cells. In the fresh state the fibres are not obvious, and we have a gran- ular material. This connective substance has some of the charac- ters of mucous tissue, and seems allied to it. The glioma as it occurs in the brain does not usually form an isolated tumor, but, being continuous with the brain substance, has more the appearance of a swelling of part of the brain. It is seen also that the different shades of color of different parts of the brain are lost when a glioma takes their place. Gliomas some- times occur as small granular or warty projections on the surface of the ventricles, but the more important ones involve considerable portions of the brain substance. Under the microscope the glioma is seen to resemble the neu- roglia, but the cells are much more abundant. There is a well- developed fine or coarse network and in it cells with oval nuclei. The cells present considerable variety iji size. Gliomas being soft and somewhat cellular tumors, are liable to secondary changes. Hemorrhage not infrequently occurs, and the blood causing pressure around, the case may end like one of hemorrhagic apoplexy. The tumor may also undergo fatty or caseous meta- morphosis, and if a limited hemorrhage has occurred the clot may change in a similar way. In this manner a tumor which had originally the .appearance of brain substance may change con- siderably. Pig. 80. From a psanimoma of the dura mater. Dark calcareous rods and masses are seen in a fibrous tissue. X 90- Gliomas occur also in the retina, forming soft tumors which fill up the eyeball. The true glioma is an innocent tumor, but sometimes it assumes a sarcomatous chai-acter and malignancy is developed. 198 COMPOUND-TISSUE TUMORS. 11.— THE BKAIN SAND TUMOR OR PSAMMOMA. The pineal gland contains calcareous particles like grains of sand, and tumors are met witli in which similar particles are present. It is necessary, of course, to distinguish these from tumors in which simply a secondary calcareous infiltration has occurred. The psammoma is composed of soft connective tissue in the midst of which there are calcareous masses in the form of irregular globes, rods or spines. (See Fig. 80.) The commonest form is the globe, which has rounded projections on its surface like a berry. The origin and significance of these masses is obscure. The tumors are met with in the pineal gland and choroid plexus — usuallj^ small. They also occur in the dura mater, where they form half globular tumors sometimes as large as a cherry and either smooth or irregular on the surface. B.— COMPOUND-TISSUE TUMOES. 1.— THE CYSTIC TUMOR OR CTSTOilA. A cyst is a cavity having well-defined walls and containing material which is more or less fiuid. Some cysts are formed simply by the transformation of existing structures, and it is clear that according to our definition of tumors these do not come under that designation, as they are not pieces of tissue which grow inde- pendently without regard to the needs of the organism. There are other cysts, however, which do owe their origin to the inde- pendent new formation of tissue, and therefore deserve the name of tumors. The two forms are so similar in appearance that it would be inconvenient to separate them rigidly, and without aiming at logical accuracy we shall here consider the cj'sts as a whole. If necessary, the name Cystoma may be reserved for strictly cystic tumors. Mode of Formation of Ctsxs. — As already indicated, cysts vary greatly in regard to their mode of origin. Some of them arise out of a preexisting cavity, very often by accumulation in it, in the first place, of its normal contents. Thus a gland will become a cyst by its duct becoming obstructed. Cysts arising thus are often designated retention cysts. But the other cysts arise simply by softening of existing tissue, the softened material being absorbed and fluid taking its place. This, as we have seen, often occurs in the brain, resulting in the apoplectic cyst. Again, we may have cysts arising by a distinct new formation; a preliminaiy tissue is formed, generally something like that of a gland, and this is after- wards transformed into a cyst somewhat in the fashion of the retention cyst. Instead of following out these modes of formation it will be more convenient to give some examples of cysts, and THE CYSTIC TUMOB OE CYSTOMA. 199 their mode of origin will come up for discussion as each is con- sidered. Cysts of the skin appear to arise in many cases from sebaceous glands. The duct becomes obstructed by inspissated secretion or adhesion of its walls, and the sebaceous material accumulates behind. Such a cyst may attain some size, and contains mainly fat, cholestearine, and epidermic scales. From the nature of their contents such cysts are often designated atheromatous. Their wall consists of connective tissue with a lining of epidermis, which may present papillary projections. They occur mostly on the head and face, and are often called wens. Besides these we some- times meet with more complex cysts in the skin, and these are congenital in their origin, probably arising by inclusion of a piece of embryonic skin. Their walls are like the skin, containing hairs with hair-follicles and sebaceous glands, and sometimes even sweat glands. These are called dermoid cysts, and they contain a less grumous material than the former ones, their contents consisting of cholestearine and epidermis often with loose hairs. Mucotfs CYSTS, or cysts with mucous contents, arise in situations where mucous glands are present, their chief sites being the nostrils and communicating cavities, the upper surface of the epiglottis, the larynx, the oesophagus, and in connection with the glands of Cowper and Bartolini. Of these a very typical form is the Ranula, whose origin and mode of formation have been carefully studied by Recklinghausen. It has long been taught that these cysts arise by obstruction of ducts and accumulation of the contents behind them, but this Fig. 81. r'-- ^ J -^ ■ 35?-"^ Eormation of mucous cysts; a, the persistent mucous gland tissue ; 6, the dilated duct. X 300. (Recklinghausen.) scarcely explains the continuous enlargement of the cysts after they have been formed. It might be supposed that the epithelium lining the cysts would secrete mucus and so add to the contents. 200 COMPOUND-TISSUE TUMORS. but there is the objection to this that the epithelium loses its gland- ular character, and there are no goblet cells to be found in it. The real state of matters appears to be that the cyst forms, not out of the gland, but from its duct, and, the gland persisting, its secre- tion is thrown into the cjat. This is shown in Fig. 81, copied from Recklinghausen's paper. It would thus appear that the per- sistence of the gland is an essential element in the formation of the cyst. In the enlargement of the cyst the power which mucin has of swelling up and absorbing water is of some consequence. A small amount of mucin formed by the gland and discharged into the cyst will swell up and add considerably to its contents. Before a regular cyst forms, the orifice of the duct is obstructed, usually by an inflammation around it. But on account of the peculiarity of mucin just noticed, a small temporary cyst may form without any considerable obstruction of the duct. If a quantity of mucin is discharged into the duct, it may swell so much as to be unable at once to escape from the orifice and so form a small cyst, which afterwards discharges. In this way cysts often form in the mucous membrane of the mouth. It has already been noted that cysts arise in mucous polypi, and they have a similar mode of formation to that just described. The obstruction of the orifices is here the more likelj'^, as the polypus itself usually originates in connection with a chronic inflammation of the mucous membrane. Cysts of the thykoid gland have been already referred to as taking origin in the vesicles of the gland, but they may also have origin in softening of the tissue of the gland. Sometimes one or more cysts attain very large dimensions in the thyroid. In THE KIDNEY we havc frequent cysts, most of which arise by obstruction, and are to be classed as retention cysts. By obstruc- FiG. 82. Hydronephrosis with granular atrophy of the kidney. The other kidney showed a marked compensatory hypertrophy. (Virchow.) tion of the ureter the condition of hydronephrosis is brought about, in which the whole kidney goes to form a cyst (Fig. 82). Obstruc- CYSTIC TUMOR OR CYSTOMA. 201 tion of the uriniferous tubules by tube-casts, or more commonly by the contraction of new-formed connective tissue, produces cysts in the kidney substance which may be of microscopic size, or large enough to be seen by the naked eye. These cysts are multiple. "We sometimes meet with a single cyst of large size, with a definite lining mem- brane, and obviously of old date. Such cysts are probably congenital, and owe their origin to foetal closure of one or more tubuli uriniferi. Again, the whole kidney may be converted into a con- geries of cysts large and small, filled with serous or bloodj' fluid, the outline of the organ being greatly enlarged (Fig. 83). These also are congenital in their origin, and probably ai'ise by foetal closure of the tubuli uriniferi. In all these cases the cysts contain a serous fluid, although, in some of them at least, urine has been the primary contents; after a time, however, the urinary constituents are absorbed, and serous fluid alone remains. The GALL-BLADDER may be converted into a cyst by obstruction of its duct. It is the secretion of the mucous glands — a mucous material — which accumu- lates and produces the distention ; but after a time this gives way to a serous fluid, and the bladder is converted into a large thin sac full of a watery serum. There may be a formation of cysts in the substance of the liver by obstruction of the hepatic ducts in their finer i-amifieations. Obstruction of the common hepatic duct produces a distention of the ultimate terminations of the duct, but not a proper cystic formation. The VERMIFORM APPENDAGE is somctimcs converted into a cyst by obstruction of its orifice. At first mucus accumulates, and even when the cyst is of large size the con- tents may remain of a gelatinous consist- ence. But here also there is a tendency to simplification of the wall, involving atrophy of the mucous glands, so that there results a thin-walled cyst, consisting of connective tissue with merely a lining of epithelium, and the contents generally cease to have the mucous character. The OVARIES are very frequently the seat of cysts. They may arise by simple accumulation of serous fluid in the Graafian Congenital cystic kidney from a new-born child. Each kidney meas- ured 5^ inches long, 4 inches broad, and 3i inches thick. The entire kidney-tissue was replaced by cysts. (ViRCHOW.} PlQ. 84. Dropsy of Graafian vesicles in ovary of a girl ten years of age. (ViRCHOw.) 202 COMPOUND-TISSUE TUMORS. vesicles, a dropsy of these (Fig. 84), but in the great majority of cases a definite new formation precedes the cystic development. This consists in the production of tubular or gland-like structures out of which cysts develop apparently by closure of their orifices. In this way multitudes of cysts are formed, and as this tissue is continually being produced there is a progressive new formation of cysts. Very often one or more cysts become predominant, and they enlarge by coalescence of others, but there is always evidence in the walls of the cysts that new formation is progressing.^ These cysts contain originally a mucous or colloid material, which may be variously modified by fatty changes, hemorrhage, and inflam- mation. Similar cysts are occasionally, though very rarely, met with in the testicle. , The ovaries are also the seat of cysts which will be referred to afterwards as teratomas. Cysts occur in tumors, and are particularly common in mam- mary tumors, especially the adenoid sarcomas. There is, in fact, a form of sarcoma designated cysto-sarcoma. The cysts here appear to originate from the glandular structures. The glandular acini dilate, much in the manner of retention cysts. When the cyst has formed, the sarcomatous tissue, apparently growing in the direction of least resistance, very often grows into the cyst, and may even fill it up with an intracystic growth. 2.— THE PAPILLARY TUMOE OR PAPILLOMA. By this name is meant a tumor composed of a congeries of ex- aggerated papillae like those of the skin, or like the villi of mucous membranes. A papilla or villus consists of a basis of connective tissue in which there is a loop of capillary bloodvessel, and a covering of epithelium. The epithelium is like that of the surface concerned, and may be stratified or in a single layer. Their commonest situation is the skin, where they form the WART, which is an overgrowth of a group of existing papillae covered with hard epidermis. At the surface of the wart the papillfe may be covered over with a continuous layer of epidermis, or the individual papillae may project independently. The horn is also formed on the basis of a group of papillae, but the hard, horny epidermis is greatly developed, and forms a consistent out- growth of considerable dimensions. The condyloma is a syphilitic outgrowth due to exaggeration of the papillae, with very soft epi- dermis. These occur near the genital organs mostly. On MUCOUS MEMBRANES papillomas may be gathered into a local tumor, or cover a considerable surface, giving it a shaggy, villous appearance. In the larynx (Fig. 85) they often form localized prominent tumors, especially on the vocal cords. They are not uncommon in the rectum. In the urinary bladder they are of con- siderable importance on account of their tendency to hemorrhage. In this situation they may form distinct tumors with long-branched THE PAPILLARY TUMOR OR PAPILLOMA. 203 papillaB, or there may be a large surface which is simply villous in appearance. The papillae are covered with delicate epithelium, and are liable to severe and frequent hemorrhage. ^ The Pacchionian bodies of the encephalon are' really papillary Pig. 85. 11-^^^ ^%5^^ ^*=-;;^-Z^ \ "^ c-ij^" Papilloma of larynx : e, epithelium j A, connective tissue; ^j mucous glands; /, an atrophied gland. X 20. (Coenil and Ranviee.) formations, and Dr. Cleland has described large tumors of this region which seemed to arise by extreme hyperplasia of these papillse. 3.— TERATOMA. This name has been applied by Virchow to tumors in which a number of very different tissues enter into the structure. The name is derived from repaQ, a monster. The tumor contains various structures of the body as if from an ill-arranged foetus. Thus we may have in such tumors skin, bone, muscle, glands, nervous tissue. These tumors probably arise by the abnormal inclusion of a whole embryo or a portion of one. They are most frequently met with in positions where double monsters are usually attached to each other, namely, in the sacral region, or further up the back, and the head and neck. They are also somewhat frequent in the ovary, where they may arise by a kind of equivocal generation, the germinal vesicle endeavoring to develop some of the perfect tissues of the body. The SACRAL TERATOMAS and those of the head and neck are the more typical ones. They frequently contain pieces of bone which simulate the bones of the foetus, also brain substance and muscle. Considering that these tumors develop so frequently in the ordi- rfary places of union of double monsters, they may safely be re- 204 CELLULAR TUMOES. Fm. 86. garded as representing twin pregnancies in which one of the foetuses has grown over and included the other. The teratomas of internal organs do not usually represent such complete systems or so many different tissues as the sacral. They are most frequent in the ovaries, but also occur in the peritoneum, testes, lungs, and so on. In these situations they occur in the form of cysts, approaching in structure to the DERMOID CYSTS of the skin and often grouped along with them as dermoid cysts, but having usually a more complex structure. These cysts, and especially those of the ovary, usu- ally present at some part of their wall a structure similar to that of the skin. There is corium with ejaidermis, and well-developed hair-follicles with hairs in them (Fig. 86). The sebaceous glands are often specially developed, so that a portion of the wall may present little more than open-mouthed glands. Then there is frequently bone in the wall, and in the bone there may be teeth. More rarely are muscle and nervous tissue represented. The contents of these cysts vary according to the structure of the wall. There is usually a great accumulation of fat secreted by the sebaceous glands, so that we may have masses like lumps of butter. These are often mixed with silky hairs, which are regu- larly shed from the hair-follicles just like the normal hairs of the skin. Then there are sometimes teeth mixed with the other con- tents, these being shed also at intervals. As many as three hun- dred teeth have thus been found free in such a cyst. A hair-follicle with hair and sebaceous gland from the wall of a dermoid ovarian cyst. X 50. C— CELLULAR TUMORS. l._SAECOMA. Definition. — Li its literal meaning this term simply means a fleshy tumor, and it was formerly applied in a very indefinite way. In the hands of Yirchow, however, it includes a group of tumors, which, though in certain respects differing in structure, yet present such features in common that they form a consistent class by them- selves. The sarcomas may be defined as tumors which in their structure follow the type of one or other of the connective tissues, but differ in respect of the great preponderance of the cellular elements, and also in respect that the cells are more or less em- bryonic in their character. SAECOMA. 205 Structure and Classification. — The structure of sarcomas has been somewhat aptly compared to that of inflammatory new forma- tions. We have already seen that the tendency of these, as exem- plified in the granulating wound, is to develop into connective tissue. The round cells pass into spindle-cells and then the con- nective tissue develops out of the latter. The round and spindle cells may thus be regarded as the preparatory^, or in a certain sense embryonic stage of connective tissue. In sarcomas we have tumors composed of round cells and tumors composed of spindle cells without any tendency to further development, as if the em- bryonic form had been stereotyped for the whole life of the tumor. Besides these forms sarcomas sometimes contain giant-cells (myelo- plaques). We know that cells of this nature occur normally in growing bones where, as Wegener and Kolliker have shown, they exercise an important function (osteoclasts), and they are not un- known in granulation-tissue, even apart from bone. They also are to be regarded as connective-tissue structures, and as belonging to a developmental stage of connective tissue. In their mode of growth also it may be said that the sarcomas resemble inflammatory new formations. They very often form tumors of considerable size, and may even be encapsuled, as if the tissue simply increased like that of a simple tumor. But they present a peculiar tendency, which has been already mentioned, to incorporate neighboring structures. We have seen that in the disposal of dead animal tissue, such as a thrombus, or a catgut ligature, the inflammatory tissue advances, and, as it were, moulds itself in the first place on the dead structure, copying its general form. So an advancing sarcoma will incorporate the living tissues and mould itself on them, i-epeating their rougher anatomical de- tails in tissue of its own kind. In such cases it sometimes seems as if the sarcoma in advancing were inducing the neighboring tissues of themselves to become sarcomatous in structure, and in the case of connective tissue which is present everywhere, we can easily suppose that by pro- liferation of its cells it might become sarcomatous. It is not impossible that this actually occurs, but it is more probable that the proper tissue of the tumor disposes of and displaces the exist- ing tissues. It has been said already that sarcomas follow in their type the various connective tissues of the body, and it might be possible to divide them according as one or other form is the type. So Vir- ehow indicates the division into fibrosarcoma, myxosarcoma, glio- sarcoma, chondrosarcoma, osteosarcoma, melanosarcoma, to which some would add, myosarcoma and neurosarcoma, if muscle and nerve are regarded as connective tissues, and lymphosarcoma if lymphatic-gland tissue be taken as belonging to this group. It will be convenient to follow a difterent arrangement, however, and we shall desci'ibe sarcomas according to their structure apart from any inferences as to the type which they follow. It is to be added that the structure of the individual tumor is, as a rule, remarkably 206 CELLULAR TUMORS. homogeneous. "We often iind cells heaped on cells without any intersecting bands of connective tissue. In other tumors the BLOODVESSELS are supported and the tumor intersected by a kind of stroma, equivalent to the interstitial connective tissue of muscles, glands, etc., but here there is rarely any fully developed connective tissue, and the bloodvessels are in immediate contact with the cells. Varieties. — (1) The round-cell sarcoma (Fig. 87) is also called the granulation sarcoma and the encephaloid sarcoma. It is com- FiG. 87. Section of a round-celled sarcoma of the brain A thin-walled vein, with blood-corpusoles in it, divides the section. X 175. posed of round or slightly oval cells generally about the size of white blood-corpuscles, but sometimes much larger.* It is an exceedingly soft tumor, often half diffluent, and has usually a gray medullary appearance. Its bloodvessels are in the form mainly of large capillaries whose walls are embryonic in structure and often present varicose or aneurismal dilatations. The vessels are liable to rupture, and so these tumors often present interstitial hemor- rhage. Between the cells there may be some intercellular sub- stance. This is sometimes homogeneous and becomes opaque with acetic acid (myxosarcoma), or it may be somewhat fibrous or reticulated. This form of sarcoma is met with in the skin, where it may origi- nate in a congenital soft wart or mole, in the subcutaneous tissue, in the bones — forming the majority of the so-called medullary cancers — in the muscles, in the glands, especially the mamma and testicle, in the brain and elsewhere. Being a soft tumor with delicate vessels, it more readily produces secondary tumors by metastasis than other sarcomas. It is also usually a tumor of rapid growth and commonly imperfectly delimited from the sur- rounding tissue. SARCOMA. 207 (2) The spindle-cell sarcoma (Fig. 88) is also called the fibro- sarcoma, and corresponds with Paget's class of recurrent fibroids and Lebert's group of fibroplastic tumors. The cells are spindle- shaped like those in the deeper layers of a granulating wound, and there is little or no intercellular substance, the tumor being ■PiQ. Large cells from a spindle-celled sarcoma. X 300. composed of masses of spindle-cells. They are arranged in bun- dles, which, to a certain extent, interlace like the bundles of fibre- cells in the myoma. There are great varieties in the size of the cells, some tumors being composed of very small cells, and these are usually soft, while at the opposite extreme are cases where the spindles are gigantic. When viewed in mass, the individual spin- dles may not be apparent, but they are usually easily isolated, unlike the fibre-cells of the myoma. These tumors are usually EiG. 89. Large fungating spindle-celled sarcoma of the foot. (ViRoaow.) firmer than the round-cell sarcomas, except the small-celled forms, and may even approach the fibroma in hardness. The spindle-cell sarcoma occurs frequently in the periosteum, and in that case is firmly attached to the bone. It is also met with in'or under the skin (see Fig. 89), in muscles, in 'the testicles, etc. 208 OELLULAB TUMORS. It is a frequent tumor in the mamma, and here it not infrequently forms the adenoid sarcoma and the cystic sarcoma, the latter of which deserves more particular notice. In the CYSTIC sarcoma there is, along with the proper sarco- matous tissue, a certain amount of glandular tissue (see Fig. 90). Fig. 90. Pig. 91. Section of an adenoid sarcoma of the mamma. Glandular masses are seen with a very cellular interstitial tissue. X 90. In some cases the gland acini dilate and the sarcomatous tissue projects into the cysts thus formed. In this way the cyst, which has now solid contents, is sometimes enlarged by the intracystic growth. The ingrowing tissue is covered with epithelium which is iisually more or less columnar. When these sarcomas recur the glandular tissue does not reappear, but there is often an appearance of the sarco- matous tissue which suggests an arrange- ment like that around glandular structures. The spindle-cell sarcoma is sometimes a distinctly defined tumor, but often, as in the case of the periosteal form, its bound- aries are not defined, and it advances by incorporating neighboring structures. Although prone to return after removal, it has less tendency than the round-cell form to give rise to secondary tumors by metastasis. (3) Myeloid or giant-cell sarcoma (Fig. 91) is a tumor in which the giant- cell is characteristic, but never forms the only sarcomatous element, there being generally spindle-cells and sometimes round-cells in great abund- ance. The giant-cells are in greater or smaller number in propor- tion to the others, and in the same tumor they may present various Giant-cell sarcoma. X 175. SAECOMA. 209 proportions in different pai'ts. The tumor tissue is soft and very often of a brown color. Cysts not infrequently develop. The myeloid sarcoma occurs in connection with bone, and most frequently' grows from the medulla. This is especially the case with the long bones, where the tumors originate in the cancellated tissue at the extremity — the most usual situation being the lower end of femur or upper end of tibia. As the tumor grows it has a great power of destroying the bone before it, so that by and by it eats through the external layer, and may thus produce fracture of the bone. At the same time there is commonly new formation of bone so that a new external shell is formed continuous with the shaft, and internal septa representing a coarse, cancellated structure. The tumor tissue is thus frequently contained in bony loculi, and after maceration the shell of the tumor looks like a bulbous ex- pansion of the end of the bone with bony septa internally. Having broken through the external laj'cr of the bone, the tumor may proceed into the muscular and other tissues, the tumor tissue being repeated, both the soft myeloid tissue and the bony septa. Myeloid sarcoma is also met with outside bones, growing from the periosteum, especially of the jaws. Many tumors, to which the name epulis is given, are myeloid sarcomas. (4) The OSTEOID sarcoma is a tumor which deserves special notice. It is the form which Paget has very skilfully described under the name of osteoid cancer. The disease occurs most frequently at the lower end of the femur, where it usually develops both within and without the shaft, but sometimes outside alone. The main mass is composed of bone which is usually very dense, but on the surface a tissue is found out of which the bone is being developed. This consists of dense fibres which are very abundantly nucleated. These dense fibres are really cells, and they present varieties of shape often tending to the stellate form. The new bone is devel- oped out of them, and is usually very irregular in structure, the bone-corpuscles often large and with no proper arrangement as in normal bone. The tumor, as it advances, often presents nodules slightly removed from the main mass, and it also forms secondary tumors in the lungs or in the lymphatic glands. These repeat the ossifying tissue. (5) Melanoid or pigmented sarcoma always originates in a situ- ation where pigment already exists, the eye or skin. The cells of which it is composed are usually spindle-shaped, but may be round, and from the first they tend to the aggregation of brown or black pigment in their substance. The pigment aggregates first around the nucleus, but is very irregular in its distribution. In a mela- notic tumor there may be bits unpigmented, and even in the pig- mented parts some cells are free from pigment. The melanotic sarcomas have a great tendency to metastasis, and as the material is conveyed by the blood there are pigmented tu- mors formed in a great variety of organs and tissues where they may grow to great dimensions, though the original tumor may be very small. 14 210 CELLULAR TUMORS. It is necessary to distinguish from these proper melanotic sar- comas those which become pigmented from blood. In the former the pigment is brown or black from the first, being obviously elaborated by the cells. In the latter the pigment is red or yellow, and the pigmentation may be related to a special weakness of the vessels allowing of hemorrhage. (6) Alveolar Sarcoma. — In this form we have round cells, as if packed in spaces or alveoli, and so the tissue resembles that of cancer. But when the structure is carefully examined, two distinct differences can be distinguished. The connective-tissue stroma is very directly related to the cells, and the masses of round-cells seem to be developing out of the connective-tissue stroma. Be- tween the cells there is sometimes a delicate reticulum, but this may be absent, and the tissue may be very like that of cancer. These tumors occur in connection with bone, skin, and muscle. (7) Plexieorm sarcoma or cylindroma is a name applied to a form of tumor whose relations are somewhat obscure, and it probably includes more than one kind. The peculiarity of the tumor is the existence of cylinders and rounded structures having a hyaline character, and like mucous tissue. In the centre of the cylinder there is often a bloodvessel, so that the hyaline material clothes it like a mantle. Then, between the cylinders of hyaline material there are frequently masses of cells which may form long processes so as to give a close resemblance to cancer, to whose cells these may also conform in general appearance. The origin of these cylinders is not perfectly clear. In some cases it may be that we have a combination of sarcoma and myxoma, but this does not account for the peculiar form of the cylinders. A more probable explanation is that the cylinders arise by hyaline or mucous degeneration of the adventitia of the blood- vessels, and this is confirmed by the fact that they are often ar- ranged around the vessels. If this be the proper view, then, in the tumor, the formation of bloodvessels is an important element. In this way we should have a sarcoma in which a peculiar trans- formation occurs in the external coats of the vessels. It is in this view that the name plexiform angiosarcoma is applied to this form of tumor. The tumor as a whole is often of a gelatinous appearance, or it may be that the gelatinous material is seen to be in separate spaces throughout the tumor. It occurs in the orbit and its neighbor- hood, or the upper and lower jaws; it may form part of the con- stituents of tumors of the parotid, and it is also found in the brain and its membranes and the peritoneum, where it may grow to a large size. 2.— CANCER OE CARCINOMA. "We enter here on a class of tumors whose boundaries, when re- garded from a clinical point of view, are rather undefined. In its more general use, the term cancer is applied to any form of malig- CANCEE OR CARCINOMA. 211 nant tumor, altogether irrespective of its finer structure, and in tTiis sense would include most sarcomas. But in the study of Pathology such a general use of the word is not allowable ; the structure must be taken into account, and it will be found that clinical facts are in essential accord with histological and anatomical relations. Definition. — As the sai'comas are tumors whose structure follows the type of the connective tissues, cancers may be defined as tumors whose structure follows the type of the epithelial tissues, but with an excessive production of cells. Structure. — It is well known that epithelial structures are non- vascular, and in order to the nourishment of any considerable mass of epithelium, it is necessary to have bloodvessels supported by connective tissue. This forms the stroma of cancers, and so it is always possible to distinguish in cancers a vascular connective- tissue basis, enclosing and supporting masses of epithelial cells. This stroma may be in whole or part the remains of the preexisting connective tissue of the part, generally giving evidence of the ex- istence of irritation in the presence of large numbers of round- cells, but very often it is as much a new formation as the epithe- lium, and may occur in the form of a delicate network with well- formed meshes (see Fig. 92). Where a cancer produces a well-formed stroma along with the epithelial masses, it will probably grow more readily into a dis- tinct tumor than where the epithelial masses depend for their Fig. 92. Stroma of a soft cancer of the mamma after the cells had been washed out. X 82. nourishment on the existing bloodvessels. In this latter case the cancer will commonly present more the characters of an infiltra- tion of the tissues with epithelial structures, and this infiltration may be associated with such irritation as to lead to considerable new formation of connective tissue, giving sometimes a consider- ably fibrous character to the structure, as in scirrhous cancer. 212 CELLULAR TUMOES. An important question arises here as to the origin of the epi- thelium, which is the essential constituent of a carcinoma. One view is that the epithelium in some cases takes origin in the ex- isting epithelium, and in others develops out of the connective tissue, while another view is that it develops in all cases from the existing epithelium. We have seen in the study of inflammation that, as a precursor of the formation of organized tissue, there is always a rudimentary tissue, of which the granulating wound is a type. ISTow in the development of tumors in general, the forma- tion of such rudimentary' tissue precedes the formation of the ripe tissue, or, in other words, cells of all sorts, when young, have the form of round cells, which, from the fact that they are not distin- guishable from cue another, may be called indifferent or em- bryonic CELLS. In the case of cancers it is supposed by some that indifferent cells may be formed from connective tissue, just as those of the granulating wound are presumed to be, and that these Daay afterwards develop into the epithelium of the cancerous tumor. In the case of inflammation we saw no reason to believe that epithelium is developed out of connective tissue. "When epithelium forms on the surface of a granulating wound, it is always in direct Fig. 93. From the growing margin of an epithelioma of the sliin. The interpapillary processes of epidermis penetrating inwards, a, a small laminated capsule. X 100. continuity with the existing epithelium. In the case of cancers there are certain facts which seem to indicate that here also epi- thelium can only develop from preexisting epithelium, or in other words, that when the differentiation of the tissues is completed, there is no recurrence to the embryonic form in which cells are CANCER OB CARCINOMA. 213 indifferent and have tlie power of developing this or that tissue according to circumstances. The first fact of importance in this regard is, that in some cancers we have the strongest indications that the epithehum of the cancer is actually developing from the existing epithelium. A section of an epithelioma of the skin shows this almost always if the growing marginal parts be examined (see Fig. 93). In the skin the epidermis forms a continuous layer on the surface, and the rete Malpighii, or deep layer, besides covering the papillag also lies between them, forming what may be called interpapillary pro- jections. At the margin of an epithelioma of the lip, we see an elongation of these interpapillary processes, and on passing more and more towards the tumor these processes pass deeper and deeper into the subjacent skin, forming penetrating cylinders. Again, in some cases of cancer of the kidney it can be seen that the tumor is arising as if by transformation of the kidney tissue. The primary cancer of the kidney is not a tumor added on to the kidney, but it is generally a portion of, or sometimes the whole kidney, which has undergone an enormous enlargement while keeping its general shape ; it is in fact the kidney or portion of kidney transformed. And when we examine the marginal parts of such a tumor we find the epithelium of the uriniferous tubules in an active state of germination, the tubules getting distended with new-formed epithelium. The epithelium also is altering its shape in various ways, getting sometimes elongated and tailed (see Fig. 94). In fact the tumor is forming by proliferation of the Fig. 94. From a cancer of the kidney. A tubule is represented in which the epithelium is undergoing alterations in shape. X 300. epithelium, the stroma of the kidney forming the stroma of the tumor. Another fact of consequence in this matter is, that primary cancers in the vast majority of cases occur in situations where epithelium exists. There are some apparent exceptions to this, as where a cancer has been found growing into bone, but these are of the rarest occurrence, and even they can be explained by sup- posing that there has been a connection with the surface which was undiscovered. It is not impossible also that some of these rare cases may be referrible to a foetal inclusion of a bit of em- bryonic epithelium. It is here to be remarked that in a growing cancer there is often great irritation of the connective tissue, so that, say in a case of epithelioma of the lip, the ingrowing processes are, at their deeper 214 CELLULAR TUMORS. extremities, buried in a mass of inflammatory round-cells (Fig. 95). This may obscure the exact new formation of the epithelium, but the fact that the new epithelium is always in connection with the old is of sufficient significance. Fig. 95. From an epithelioma of the skin. Cylinders of epithelium penetrating deeply and causing great irritation, as shown by the presence of abundant round cells. X 200. The growth of cancer happens in various ways. "We have already seen that in some cases there is a transformation of existing tissues and in others a penetration of the epithelium into surround- ing structures. These modes are very common in primary cancers, and so we speak of cancerous infiltration very frequently. In some cases there is a distinct tumor, but even then at the marginal parts there is an infiltration of surrounding tissues, and the tumor is ill-defined. It is laoteworthy that secondary tumors are fre- quently, or indeed commonly much larger and more independent in their growth than the primary ones. Cancers show peculiar relations to the lymphatics. For one thing, the alveoli or spaces containing the epithelial masses seem to be in direct communication with the lymphatics. If a cancerous tumor, before being opened, be punctured with the needle of a hypodermic syringe and a watery solution of Prussian blue, prop- erly prepared, be injected, the material first runs into the allveoli around the puncture, mapping out a series of cavities as it were, and then passes on into the lymphatics, issuingby their extremities divided during the removal of the tumor. Besides, it has been pointed out by Koster that in sending their processes into sur- CANCER OR CAECIjSTOMA. 215 Cells from a cancer, showing fatty degeneration. X 350. rounding parts the lymphatic spaces are often taken advantage of and are largely occupied. From these two circumstances we can understand how cancers so frequently present secondary tumors in lymphatic glands. The secondary tumors in the lymphatic glands reproduce the original tumor, but it has been pointed out by Cornil and Eanvier that at the first there is frequently a simple fibrous transformation of Fig. 96. the gland as if the stroma was being formed in advance of the epithelium. It is further to be remarked that cancers are liable to secondary CHANGES. The epithelium readily dies or undergoes fatty degenera- tion (Fig. 96), and the result may be either that the stroma becomes predominant from the absorption of the fat, or that the whole tissue softens and an ulcer forms. In fact, when a cancer is superficial it very commonly undergoes ulcer- ation. Sometimes, on the other hand, there is from the first a peculiar predominance of the stroma. The epithelial cells of cancers may undergo mucous or colloid metamorphosis, etc. Having entered so fully into general considerations as to cancers, we may be correspondingly brief in regard to the individual forms. (1) Epithelial Cancer or Epithelioma. — According to the description we have given of cancers, it might appear that all cancers are epithelial, but by custom the name has come to be used to designate tumors of the skin and mucous membranes, whose tissue reproduces in its characters to a large extent the sur- face epithelium of these regions. As there are two principal forms of epithelium, the flat and the cylindrical, so the epitheliomas may be divided into two forms, the flat-celled and the cylinder-celled. The FLAT-CELLED EPITHELIOMA occurs in situations where there is normally a flat epithelium, namely the skin, mouth, pharynx, oesophagus, larynx, vagina, and urinary bladder. Here there is an excessive growth of pavement epithelium, generally in the form, as we have seen, of more or less cylindrical processes. In some of the cases the epithelial processes tend to penetrate into the underlying structures so as to produce a more or less dif- fused infiltration and thickening of the part. In other cases the extension is more along the surface so as to form raised, very often circular tumors. The common epithelioma of the lip is a good example of the infiltrating form ; the epithelioma of the skin else- where is usually of the extended flat form. The cylindrical pro- cesses of epithelium, as they grow, exercise pressure which, acting on their own cells, produces closely-compacted epidermic globes 216 CELLULAR TUMORS. in the midst of them (see Fig. 97). These form very commonly a characteristic feature in epitheliomas, and are variously designated epidermic globes, laminated capsules, etc. Fig. 97. ITlat-celled epithelioma : u, isolated cells j 6, a cylinder "with many laminated capsules; e, a laminated capsule opened out so as to show the cells composing it. (Billroth.) ; fAlong v?ith the production of epithelial processes penetrating inwards, there is very commonly the formation of papillae on the surface, and sometimes this is so marked as to give the surface a vparty appearance. This is often seen in the flat extended epithe- liomas of the scrotum and other parts of the skin. It is also very pronounced sometimes in the vagino-uterine epitheliomas, giving rise to the cauliflower appearance. In the urinary bladder there is very frequently such a marked production of elongated villi that the surface is quite shaggy, while the mucous membrane presents inflltration with the epithelial processes. So much is this the case that the name villous cancbb is often given to this form. Like the papilloma of the bladder, this tumor has a marked tendency to hemorrhage. CANCER OH CARCINOMA. 217 The flat-celled epitheliomas are usually of slow growth, and are the least malignant of the cancers. They mostly have a tendency to ulcerate on the surface, especially the infiltrating ones. Cylinder-celled epithelioma. — This is a tumor of parts where cylindrical epithelium normally covers the surface, hence chiefly in the stomach and intestine, and more rarely in the uterus. The tumor takes origin in the mucous membrane, and the tissue has a glandular appearance, forming a congeries of tubes and cavi- ties, lined with cylindrical epithelium (see Fig. 98). Sometimes Fig. 98. wmw From a cylinder-celled epithelioma of the rectum. the glandular appearance is strictly preserved, but frequently the spaces enlarge, and as the epithelial cells accumulate they lose their cylindrical form, although the outer layer of cells next the stroma may still preserve their shape (see figure). The glandular elements are contained in a well-formed stroma, which is new- formed as well as the epithelial elements. In growing, the tumor infiltrates neighboring parts, insinuating itself among the muscular trabeculse very often, and extending further. It may form a considerable tumor, projecting from the surface, and is frequently ulcerated, as it occurs mostly in situa- tions where it is exposed to friction. From the strikingly glandular character of these tumors, many of them are included by some writers among the adenomas. (2) Ordinary cancer or carcinoma is divided into several forms in a somewhat arbitrary way. There are soft cancers and hard cancers; there are pigmented and colloid cancers, and even mucoid. The ordinary cancers consist of epithelial masses contained in 218 CELLULAR TUMORS. meshes, but the epithelium does not conform to that of the surface of the skin or mucous membranes, and is often characterized by great irregularity in form and size. It presents also little tendency to assume a glandular arrangement, and altogether shows less con- formity with normal structures than that of the epitheliomas. Soft cancers or medullary cancers are characterized by the existence of a very delicate stroma in which are abundant cells, usually of small size, and loosely packed in the alveoli with a good deal of fluid. They occur chiefly on mucous membranes, in the ovaries, testicles, kidneys, less commonly in the mamma. Being soft, they tend to bleed, and if originating on a surface or coming to it in their growth, they may undergo ulceration. Sometimes the softened, ulcerating, bleeding tissue projects in a very striking manner from a surface, forming the eungus h^ematodes. The cut surface of such tumors is gray in color, and a somewhat fluid juice can be scraped from it. In this juice will be found cells and free nuclei, the latter large and mainly oval in shape. Many of the cells contain fat-granules, and there may be some in an ad- vanced state of fatty degeneration. Cancers of this kind may grow to a considerable size, as those of the kidney, and they are often of very rapid growth. They are, as a rule, very malignant; the young cells, being loosely at- tached, readily pass away and lead to metastasis. Hard cancer or scirrhus occurs most commonly in the mamma, but also in the stomach, the testicles, ovary, and kidney. It is characterized by the preponderance of connective tissue as com- pared with the epithelial structures. The cancers of this kind have usually a very infiltrating charac- ter, the epithelial processes penetrating among the surrounding structures, and it looks as if these processes, by their irritation, produced an excessive amount of connective tissue. This view is borne out by the fact that the connective tissue is not usually in the form of a well-developed stroma as if planned to support the epithelial structures, but is irregular and even impinges on and destroys the cells. The cells readily undergo fatty degeneration, and sometimes they to a large extent entirely disintegrate, the stroma assuming the upper hand. It therefore happens that dif- ferent parts of such tumors have often very different structures. The more recent parts will show well-marked epithelial masses with stroma (Fig. 99), while in the older parts the cells have almost disappeared, and there is nothing but dense connective tissue. As the scirrhus occurs more as an infiltration than a distinct tumor, the hardening and contraction of the connective tissue causes the organ in which it grows to be sometimes contracted rather than enlarged. It is frequently so in scirrhus of the mamma and of the stomach, its two most frequent seats. On cutting into the organ the tissue is felt to be dense and elastic. The cut surface is grayish and transparent, with opaque yellow markings indicating CANCER OR CARCINOMA. 219 the existence of fatty degeneration in the cells. The juice to be obtained from the cut surface is scarce, and under the microscope Pig. 99. Prom a scirrhus of mamma, recent part showing stroma and epithelial cells. X *^50. Fig. 100. Cells from a cancer of the mamma. Most of them contain several nuclei, and some daughter cells. X 200. it is seen to contain cells, often of large size, and free nuclei (see Fig. 100). The cells vary greatly in size and shape,, and they 220 CELLULAR TUMOES. often contain two nuclei, or even a fully formed cell inside (m other and daughter cells). Fig. 101. Colloid cancer. A finely reticulated stroma is seen with meshes full of colloid material, the cells having disappeared. X 90. These cancers are less malignant than the soft cancers, but they produce somewhat readily secondary tumors in lymphatic glands. Fig. 102. Colloid cancer, m, jf, stroma in whose meshes are cells undergoing colloid det^eneration. X 300. (CoRNiL and Rantiee.) Between the hard and soft cancers there are cases presenting all shades of gradation ; so that it might be possible to form a group CAXCER OR CARCINOMA. 221 of simple or normal cancers. These have mostly a well-developed stroma vs^ith moderately sized cells which lie in the stroma in con- siderable spaces. The mamma presents these varieties, and they will be considered in the section devoted to the diseases of that organ. Colloid or alveolar cancer is a tumor characterized by the occurrence of colloid degeneration of epithelial cells. It is met with chiefly in the stomach and intestines, and in the mamma, more rarely elsewhere. There is here a definite new formation both of stroma and epithelial masses, and the stroma is often produced in the most beautiful and characteristic forms (see Fig. 101). As if it were in the plan of the growth, the cells regularly undergo colloid degeneration (Fig. 102), and finally the masses of cells become converted into masses of colloid material which fill the spaces. In the bulk of the tumor, therefore, there may be nothing visi- ble beyond the regularly' formed stroma whose spaces are filled with clear, transparent material. Occasionally there may be in the centres of the alveoli some remains of the cells visible, while the peripheral cells are already completely converted. Fif!. 103. Colloid cancer in wall of stomach, penetrating among and separating the muscular bundles. X 90. To the naked eye such tumors have a markedly gelatinous appearance, and as the fibrous stroma may in its coarser meshes be visible without the microscope, it may, even to the naked eye, look as if there were nothing but alveoli filled with gelatinous material, hence the name alveolar cancer. The tissue is frequently dense and hard to . the feel. This arises apparently from the fact that the 222 CELLULAR TUMORS. alveoli are tensely packed with the colloid material, and, the fibres being on the stretch, a dense resistance is offered, just as a tightly blown-up bladder is hard. These tumors mostly occur as infiltrations, frequently penetrating among the constituents of the tissues (Fig. 103), and although they very often extend widely by continuity (as in the stomach), they show little tendency to metastasis ; even when they attack the lymphatic glands secondarily they do not usually produce large tumors. Melanotic cancer is a rare form of tumor compared with the melanotic sarcoma. It occurs primarily in similar situations, namely, the skin and eyeball. It is really a soft cancer in which pigment is present in the cells and also sometimes in the stroma. It is usually a very malignant tumor, producing secondary growths by metastasis. Mucous CANCER includes tumors in which the stroma of the cancer assumes the characters of mucous tissue. The cells of the cancer may undergo a similar degeneration. The tumor as a whole is very gelatinous in appearance, and resembles the colloid cancer. These tumors are of rare occurrence, being met with in similar situations to colloid cancer, but attaining the highest development in the ovary. 3.— THE LYMPHATIC GROWTH OE LYMPHOMA. We have already seen that in LEUKiEMiA there is sometimes an enlargement of the lymphatic glands, and that secondary tumors occasionally occur in the liver, kidneys, and elsewhere. "We also saw that in Hodgkin's disease, or adenia, there is an enlargement of the glands and other changes like those in leukaemia, without the peculiar condition of the blood which is the criterion of leuksemia. In TYPHOID EEVER we havc an enlargement of the lymphatic glands of the mesentery, and sometimes secondary lymphatic growths occur in the liver and kidney similar to those in leukaemia. The names ltmphadbnoma and lymphosarcoma are given to tumors of the lymphatic glands, and it will be necessary to con- sider them more in detail. The lymphatic glands of the medias- tinum, for instance, sometimes undergo great enlargement, and get compacted into a bulky mass having the characters of a tumor, and to this condition the name of lymphadenoma has been given. The glands, although greatly enlarged and adherent by their cap- sules, are still individually distinct, and may be seen on section. The enlargement may now proceed to the glands of the neck, or it may originate there and pass downwards. The neck may be enormously enlarged and rendered somewhat rigid. These tumors are of slow growth, do not show any malignant tendencies, and are even amenable to treatment. But in the mediastinum tumors are not infrequent which consist THE LYMPHATIC GROWTH OE LYMPHOMA. 223 of more than a simple enlargement of the glands. The glands do not remain distinct, and the new formation as it were passes through the capsule, and the whole mass becomes one, the indi- vidual glands being no longer distinguishable even on section. The new growth also tends to incorporate neighboring structures. It will envelop a bronchus, and gradually work through its wall, replacing its tissue with its own. It will incorporate the parietal pericardium, and afterwards pass on to the visceral layer, and replace even the wall of the heart by its tissue. It will surround a vein and work its wall up, gradually penetrating to its interior. Before this, thrombosis may have occurred, and the clot is worked up or replaced by the tumor tissue. Such tumors are fitly desig- nated LYMPHO-SARCOMAS, and it will be seen that they possess a high degree of malignancy. They occur also in the mesentery, and may extend to the wall of the intestine, replacing its tube by lymphoid tissue, and forming a bulky tumor through which the calibre of the gut is maintained. They also sometimes develop secondary tumors by metastasis. PAEASITES. Under this designation we include all forms of living creatures, whether vegetable or animal, which exist in or on the human body, and provide themselves with nourishment from the body or its juices. The parasites are beings of the most widely different kinds, and their relations to morbid processes in the body also differ greatly. In the description of parasites we shall begin with the lowest forms, these being the forms also around which most interest at the present moment centres. A.— VEGETABLE PARASITES. jmiceo-obganisms or bactebia. If a fluid containing organic material, such as blood-serum or infusion of flesh, be exposed to the air, it soon becomes putrid, and everyone knows that in such putrid fluid minute forms of organized beings are to be found. All of these, however, are of very minute size, so that they may be classed as micro-organisms. To the entire series of such minute organisms, as we shall see afterwards, the name bacteria is often applied in a general sense, although various forms of such bacteria are distinguishable. With this simple every- day occurrence are connected questions of the highest importance and the greatest difficulty: "Whence come these bacteria? What is their relation to the decomposition of the fluid? and many others of great importance. One of the most important of these questions, and one of the easiest to answer, is that which we have given first: Whence COMB THE BACTERIA? To auswcr this, a very simple experiment is alone necessary. Let a boiled potato be cut in two, and one-half exposed with the cut surface uppermost in an inhabited room, while the other is kept under a bell-jar. After the exposure put the first half along with the other under the jar, and observe the condition of matters for the next few daj^s. In the one which had been exposed, a number of little spots will appear in the course of a day or two, and these will increase in area in a more or less cir- cular manner. These little spots will very likely present consider- able differences in appearance, some yellowish, others whitish or pinkish in tint, and they have all the appearance of plants growing on the nutritious material supplied by the potato. It needs only MICRO-ORGANISMS OR BACTERIA. 225 the most superficial microscopic investigation to prove that some of these spots are due to the growth of fungi, while others are the seat of myriads of bacteria, which are obviously multiplying at an extraordinary rate. It is no less obvious that these micro-organ- isms have arisen from something which has fallen on the potato from the air. The substance which has fallen from the air may be spores of the organism or simply the organisms themselves in a dried state, but we are warranted in inferring that the one or the other is floating in the air, and that the dust, which we know from other sources to be composed largely of organic matter, contains the germs of numerous living micro-organisms. It is only those which will grow on potato that will be rendered visible by their growth in the way mentioned. If different kinds of material suited to their growth be used, more varieties may be obtained. By thus exposing a proper soil to the air we may obtain a garden with several different plants in it. These plants we may propagate as much as we desire. We have only to transplant them with a needle or a knife, which has been recently heated in the flame of a lamp in order to destroy any organisms that may be adherent to it, and we obtain pure cultivations of the various plants. By in- oculating several media we may find out the idiosyncrasies of the different organisms. Some will grow on potatoes, some need an animal diet, and for some a specially prepared soil is necessary. In this way we may cultivate the organisms through successive generations and in different media, and thej' retain their char- acteristics in every case. We may now consider what are the forms and characters of THESE BACTERIA. It is to be uotcd that all of these organisms are of very minute size, being scarcely visible with an ordinary low power of the microscope. It is their extraordinary number that renders them at all readily appreciable even with the microscope,, and, it may be added, it is their extraordinary number that makes their existence of such importance. The extreme minuteness of the individual bacteria renders the classification of them very difficult. In the aggregate, when cultivated, say on the surface of the potato, they often show much more distinctive characters than when examined under the microscope. From this it will be under- stood how it is that considerable divergence exists in the nomen- clature of the bacteria, and differences of opinion as to their specific relations. Bacteria may be defined as minute plants of globular or oblong shape which increase by transverse fission. The whole group of bacteria is included in the family schizomycet^. Individually they are for the most part only slightly colored, although in the aggregate they frequently show some shade of color, by which indeed they may be recognized. They present, like the cells of plants which possess a cellulose membrane, a remarkable resist- ance to the action of caustic alkalies and acids, although it seems that their wall is not actually composed of cellulose. 15 226 PARASITES. According to Cohn's classification there are four fornois of bacteria, namely, the spherical or globular, the small rod-shaped, the larger rod-shaped or thread-like, and the spiral. The first two are closely related, and we may even class them together as Klebs and Billroth do. In that case the globular bacteria and those which form short-beaded rods, as if from the imperfect separation of the globular cells, form one class, and the more definitely rod- shaped or thread-like form another. The first class may be called cocco-BACTBRiA and the other bacilli. There remains the third class of SPIRILLA, whose relations are rather obscure. The COCCO-BACTBRIA are very minute organisms, but they present the peculiarity that they have a great tendency to occur in great Fm. 104. g^-e"o t ,1- l" . .'I' 4 Pia. 105. Swarms of bacteria growing in a nutritive material. X 90. multitudes or swarms together. These swarms are united by a kind of viscous material apparently secreted by the bacteria. Ag- gregated thus in swarms they appear under the microscope as opaque cloudy masses such as those represented in Fig. 104. These are variously named colonies or zoogloea. When thus aggregated to- gether it is difficult to make out whether the bacteria are really globular or formed of fine rods. But if the colonies be flattened out, or if the edge be care- fully observed where they are less thickly set, we may find out their actual struct- ure ; they are probably most frequently formed of globular bacteria. The colo- nies often appear on the surface of de- composing fluids, forming the mem- branous-looking scum which we see so often in such situations. It should be mentioned that these globular bacteria are often called MICROCOCCI (Fig. 105), and that they have no power of spontaneous movement. Two pus-corpuscles containing bacteria. From a preparation wbiGb had been dried and stained with methyl-violet. X 1600. MICRO-ORGANISMS OR BACTERIA. 227 The minute rods, of which colonies are also sometimes formed, are believed by some to develop out of the globular bacteria. Klebs seems to believe that while colonies are often formed of globular bacteria, the peripheral ones frequently elongate into finer rods, and become free in the fluid. Whether this be the case or not, we meet with the fine rod-shaped forms free in fluids more frequently than the micrococci. It may be added that to this form of line rods, which are so common in decomposing fluids, the term bacterium is sometimes applied in a more limited sense. The BACILLUS is a rod-shaped bacterium, but more elongated than those just referred to (Fig. 106). It has also the tendency to elon- gate so as to form threads of some length. Sometimes, as in the tubercular bacillus (Fig. 107) and in the very important bacillus anthracis, the threads produce spores inside themselves, which afterwards may become free. In regard to the cocco-bacteria, there seems no evidence that they bear spores of any kind, but they propagate merely by fission. The remaining form of bacterium is the spiral one or spirillum. This organism is in the form of a fine thread with a cork-screw twist in it. It has already been mentioned that the globular bacterium or micrococcus is incapable of spontaneous movement. In regard to Fig. 106. Fig. 107 Two forms of bacilli which were growing to- gether in the same nutri- tive material. One short and thick, the other long and thin. The short one was much more deeply stained than the long one. Methyl-violet prepara- tion. X 1500. ":'4 ^ f-"'"V"v ,-> d5^ t:^ Tubercular bacillus, consisting of threads beaded with spores. In the preparation the bacilli are red, and the other bodies (pus-oorpuscles) are blue. X 1500. the others, some are motionless and some have locomotive powers. The rod-shaped forms have sometimes a wriggling movement which has caused them to receive sometimes the name of vibrios, although this name is often confined to the bacilli. The spirillar forms sometimes show a corkscrew movement and sometimes are quiescent. It may be said in general that bacteria which have power of motion become still at some period of their development, while others are motionless throughout. 228 PARASITES. Methods of Detection. — It will be obvious that these minute organisms are often very difficult of detection, esjDecially when they are mixed up with other structures or lie in the midst of the tissues. When they are in colonies their opaque clouded appear- ance and their frequent brown color make them often very prom- inent objects. But when more isolated, and even Avhen in sparsely distributed colonies, it may be difficult to distinguish them from the mere granular debris of the tissues. In order to render them more easy of detection, various methods have been devised. The simplest is that originally suggested by Recklinghausen, which is based on the fact already mentioned, that these organisms present a much greater resistance to alkalies and acids than the animal tissues do. The addition of solution of caustic potash to an animal tissue renders it transparent and obscures the structure. If bacteria be present, they Avill be rendered more prominent than before. Dilute acetic acid, which as we know clears up the con- nective tissue especially, ma}- be used in a similar way. This often succeeds in bringing into prominence the zooglcea of bacteria, but is not of much use in detecting isolated ones. Much advance has been made by the introduction of improved methods of staining bacteria devised by Weigert and improved by Koch. Bacteria absorb readily several kinds of dissolved pig- ments, but thej' show a peculiar tendency to become colored with aniline dyes. Many such dyes have been used, but the most suitable seem to be methyl-violet, Bismarck brown, and methyl- blue, of which the first two have been most used. Methyl-violet cannot be used with glycerine, as this agent extracts the color,' and so a strong solution of acetate of potash in water (1 to 2) may be used. Preparations stained with Bismack brown may be mounted in glycerine or Canada balsam. As the observation of bacteria is now of considerable impor- tance, the more usual methods of investigation may be here briefly described. If bacteria be present in a putrid fluid, they can easily be seen by simply placing a drop under the microscope. But if it is desired to observe their characters more particularly, and to preserve them, the fluid may be subjected to the following treat- ment. A microscopic cover-glass is taken, and a small quantity of the fluid smeared on it in a thin layer, which is allowed to dry into a film on the cover-glass. To this film is added a drop of the methyl-violet or other aniline solution (prepared bj' adding a few drops of a strong spirituous solution of the dye to water). This solution should not be too weak, otherwise the viscid material which unites the colonies will be swelled up and the film loosened. The staining agent is allowed to act for a few seconds, and then run off from the cover-glass or sucked up with a pipette or blotting paper. If necessary, the stained film may be washed with a solu- tion of acetate of potash (1 to 10). After this a drop of strong acetate of potash solution is added to the film, and the cover-glass placed on a slide and examined. If aniline-brown be used, then glycerine may be substituted for solution of acetate of potash. In MICRO-ORGANISMS OR BACTERIA. 229 some cases it is desirable to mount the specimen in Canada balsam, and in that case it is only necessary, after staining, to allow the film to dry and then add the balsam. It is sometimes desirable to examine blood or other fluid con- taining albumen in solution. "When that is the case the film obtained by drying contains soluble albumen, and if it be treated as above, then the albumen is dissolved when the staining solution is added, and being afterwards precipitated in the granular form, obscures the appearances. It is necessary, therefore, to fix the albumen. This may be done by simply leaving the film unstained for several days or weeks. It is more quickly done by immersing the cover-glass in spirits for a few days, but it is most quickly effected by exposing the film to a temperature of 120° to 130° C. If the cover-glass be placed for five or ten minutes in an air-bath raised to this temperature the further processes may generally proceed without difficulty, but sometimes it takes longer and some- times shorter, these exceptional cases being determined by experi- ment. A more rapid way of effecting the fixation of the albumen is to pass the cover-glass with the film three or four times through the flame of a spirit or Bnnsen lamp. If the presence of bacteria be suspected in the tissues, then the process of preparation is more detailed. The tissue should be hardened in alcohol. Fine sections are then to be made, and these stained in the aniline solution in the usual way. They are next to be placed for a few seconds in diluted acetic acid, and they can afterwards be mounted in glycerine or acetate of potash solution, according to the staining agent used. If it be desired to mount them in Canada balsam they may be transferred direct from the staining solution to absolute alcohol, where they may be left for a time; they are then cleared up with oil of cloves, and mounted in balsam. Methyl-violet cannot usuallj- be used for this latter pur- pose, and Bismarck brown or gentian violet is perhaps the most useful dye. For the detection of bacteria in the tissues, Koch has introduced the use of a special form of illumination by means of Abbe's con- denser. The use of this piece of apparatus is described in Koch's work on Traumatic Infective Diseases, translated by the Sydenham Society, and thus available to our readers. "When sections stained as above are thus illuminated, the details of the tissues are obscure but all colored objects are rendered visible, and so the oacteria, being the most definitely colored, may be prominently brought out. It is not to be inferred that all bacteria react equally to the aniline dyes. The more ordinary bacteria are stained by most of the colors, but the tubercular bacillus, as we have already seen, the typhoid bacillus, and others, have special aflinities. Influence op Bacteria on the Living Tissues.^Wc have already seen that bacteria are present in fluids which are undergo- ing putrefactive decomposition, and it may now be regarded as demonstrated that the various forms of putrefaction are due to the 230 PARASITES. action of these organisms. The details of these demonstrations need not detain us here, but it is important to consider whether the organisms or their products have any influence on the living body, or are the causes of disease. It is clear that many of these bacteria are perfectly innocuous when merely in contact with the surface of the body or the mucous membranes. The intestinal canal teems with bacteria, and the in- spired air, as we know, contains many kinds of them. These ordinary bacteria are incapable of penetrating the living tissues, but when death occurs they at once begin to swarm into them. Even when directly injected into the blood, few of these bacteria seem capable of surviving, although, as we shall see immediately, some of them undoubtedly are. Although ordinary bacteria and their products are incapable of penetrating into the healthy tissues, or at least work no mischief when they do, yet when they exist in wounds they find a more ready access to the tissues and the blood, and it will be proper here to consider the effects which occur in connection with putre- fying OR SEPTIC WOUNDS. It need hardly be stated that this subject is of vast importance in connection with the treatment of wounds, and that the antiseptic method of treatment is based on the view that the putrid wound is a source of mischief. Of great importance here are the observations of Ogston [British Medical Journal, March 12, 1881). These observations bear chiefly on the connection of micro-organisms with acute inflammations, especially where suppurations occur. The pus from a large number of abscesses was examined, and in all cases where the abscesses were acute, micrococci were found abundantly, whereas in the case of cold abscesses there were no such organisms. "When pus containing these was injected under the skin of animals in small quantity it usually caused acute inflammation ending in abscess, and on examination the micrococci could be seen in the pus as well as invading the tissue around the abscess. A few organisms could also, in these animals, be detected in the blood, and the animal presented signs of general uneasiness. In suppurating wounds also Ogston found micrococci, mixed here with bacteria of various kinds. The number and activity of growth of the organisms were proportionate to the intensity of the suppuration. It would appear therefore from these observations that the active agents in producing inflammations in the tissues are micrococci, while the ordinary bacteria of decomposition are not so distinctly concerned. From his further experiments Ogston inferred that micrococci grow best when not exposed to the air. He cultivated them by introducing a minute portion of pus into an egg, and pro- tecting the latter from the access of air. He found that the or- ganism grew vigorously when kept at the temperature of the body, but that they did not produce ordinary decomposition. The egg albumen in which the micrococci had groAvn produced ab- scesses when iniected under the sMn of animals. MICEO'-OEGANISMS OB BACTERIA. 231 It may be held that these observations of Ogston prove that, of the organisms occurring in ordinary decomposing fluids, the mi- crococci are those which have the greatest power of resisting the living tissues, and propagating themselves inside the body. This is consistent with the fact that in pysemia, septic peritonitis, etc., it is micrococci that are found in connection with the inflammatory processes. It is not to be inferi-ed, however, that in the case of external wounds where decomposition is going on, the chemical products evolved are not concerned in the production of inflam- mation. We know that these products are highly irritating, and they are, doubtless, capable of producing local inflammations as well as giving rise to general symptoms when absorbed into the blood. In the present state of our knowledge it is impossible to say whether there are many or few kinds of micrococci as of other bacteria, but it may be presumed that if there are not different species there are great differences in their state of activity at dif- ferent times. Septicemia. — The absorption of material from putrid wounds or, what is equivalent to that, the injection of putrid material into the blood or under the skin, is followed by certain symptoms, of which the chief are fever, vomiting, and diarrhoea. In some cases there are such general symptoms alone, but in others there are in addition local internal inflammations which have a marked tendency to go rapidly on to suppuration ; the so-called metastatic abscesses. It has become customary to speak of cases where there is simply a general affection of the system, in which, in fact, there is a morbid condition of the blood, binder the designation septicemia, while those other cases in which there are metastatic inflamma- tions, doubtless due to embolism b}- septic material, are called cases of pysemia. We shall speak first of conditions where there are no embolic phenomena, and which are generally included under the term Septicaemia. In considering the phenomena of septicsemia we have two pos- sible conditions to take into account. If putrid material be intro- duced into the blood it may produce symptoms due to the mere poisonous nature of the products of decomposition, namely, the volatile oils which give their odor of putrescence and other chemical principles. But on the other hand it may give rise to symptoms due to the bacteria which may live on in the blood and produce mischief there, multiplying as such organisms do with greater or lesser rapidity. We may thus distinguish a septicasmia due to chemical poisoning, and another due directly to the action of the organism. We shall first take up the former of these, and it will be convenient to refer to it as putrid or septic p>oisomig as dis- tinguished from putrid or septic infection. (German writers use the expression intoxication as equivalent — it is so etymologically — to poisoning, but this use is often rather confusing to English readers, especially when met with in translations.) 232 P A E A S I T E S . (1) Septic Poisoning. — This is produced by the chemical products of decomposition entering the blood. It has been proved by many experiments that these products are capable of producing symptoms of poisoning, and as illustrative of such experiments we may cite those of Puky. The putrid yolk of egg containing free fat and active bacteria as well as the usual products of decomposition was injected into the jugular vein or under the skin. The result was the production of symptoms such as those already mentioned, but in most cases with- out any apparent new formation of organisms in the body. In these observations the organisms introduced may have had some- thing to do with the symptoms, but for the most part they seemed to be nullified by the blood, and the symptoms were due to the poisonous chemical products. That this was so was proved by boiling and filtering the putrid material before injecting it. The effect of boiling would be to kill the organisms, and the filtering would get rid of everything except the dissolved chemical products. "When the filtrate was used similar symptoms were produced, but it required a larger dose on account of some of the poison being carried down with the albumen. These experiments taken along with others seem to show that in putrid material there are chemical products which, if taken into the body in sufficient quantity, act as poisons, and may even prove fatal. These chemical products have not been separated as yet, but it appears from the observations of Panum (Virchow's Archiv, vol. 60, p. 301) that they are soluble in water but not in alcohol. This observer evaporated the putrid material to di'yness and ex- tracted first with alcohol and then with water. The latter solution produced the symptoms of poisoning, the former did not. There are, doubtless, in the human subject many cases in which the chemical products of decomposition are absorbed, the amount of absorption depending on the amount of the material present, and the capability of absorption of the surface exposed. Sub- stances introduced under the skin are very readily absorbed, as the material is introduced directly into the lymphatic channels. In a freshly made wound these channels are laid open, and any putrid material present is absorbed nearly as readily as if it were intro- duced under the skin. The wound fever which occurs so com- monly in septic cases within the first forty-eight hours is doubtless due to septic poisoning, as is shown by its absence in aseptic cases. But, when the surfaces of a wound are covered up with granula- tions, the lymphatic spaces are shut off, and absorption is not so ready. The healthy granulations have a remarkable power of pre- venting absorption, as the most foul substances may be applied to them without any apparent absorption. But in some cases there is much more serious absorption of the products of decomposition in large or irregular wounds, such as those resulting from compound fractures of the bones of the limbs; or in the case of large suppurating and decomposing sur- faces such as those in an opened pleura, or peritoneum, or joint, or MICRO-ORGANISMS OR BACTERIA. 233 chronic abscess. In these cases, the hectic fever so often leading on with diarrhoea to a fatal termination, is no doubt due to septic poisoning. It is to be remarked that the peritoneum and the pleura, being lymphatic sacs, have a very high power of absorp- tion, and decomposing material in contact with them is very readily absorbed. Hence, probably, the rapid fatality of acute peritonitis, which, whether following on an operation, or due to per- foration of the intestines, is usually septic. On post-mortem examination in such cases, little that is definite can be discovered. The blood is dark in color and coagulates im- perfectly, and there are evidences of a tendency to hypersemia and capillary hemorrhage. The hemorrhage is mostly in the form of petechise beneath the pericardium, endocardium, and pleura, and the hypersemia is chiefly of the mucous membrane of the intestines, where it is sometimes very marked. It is a question whether the septic poison may not produce, especially in persons predisposed to it, inflammations in distant parts. The acute inflammation of the pleura, or pericardium, or even of joints, which sometimes occurs in connection with decom- posing wounds, may possibly be due to the septic poison, although more probably caused by organisms which have been absorbed. (2) Septic or Putrid Infection. — This condition differs from septic poisoning in respect that here we have to do with a virus or contagium capable of propagating itself, and multiplying in the body. In septic poisoning the effects, as in the case of other poisons, depend on the dose of the poison. In septic infection a small amount introduced will lead to the disease as well as a larger amount, although it may take a longer time. The term inoculation may be used to designate the application of minimum quantities of a virus to the living body. If we can induce putrid infection by inoculation in animals, we may expect that much light will be thrown on the nature of other diseases which are also capable of production by inoculation, and, indeed, on the nature of contagion in general. ' With this in view, as well as on account of its own inherent importance, it will be well to go more particularly into the subject here. The names of Coze, Feltz, Davaine, Pasteur, and Koch are asso- ciated with the investigation of putrid infection, and it may be said that Koch's observations afford the most recent and strictly accu- rate inforn:iation on this subject. We shall here, therefore, refer more in detail to his researches, especially those contained in his work on Traumatic Infective Diseases, and recent papers by himself and his assistants. If putrid material be injected under the skin of a mouse, the animal will die, as we have already seen, from septic poisoning, if the dose has been large enough. But if a small quantity be used, such as one or at most two drops, the symptoms of poisoning do not appear, and many of the mice recover. A certain number, however (about a third), of the animals become ill in about twenty- four hours, with certain symptoms which are quite constant, and 234 PARASITES. they die in about fifty hours after the inoculation. If now a minute quantity of blood be taken from the body of the dead mouse and inoculated into a living mouse, the same symptoms occur, and the animal dies in about fifty hours. The disease may be propagated from animal to animal without fail for any number of generations, and an exceedinglj' minute quantity of blood is alone required in order to produce the disease. In this disease there are no metastatic abscesses, the only organic lesion being a considerable enlargement of the spleen, and so it is called by Koch SEPTICiEMIA OP MICE. When the blood of such mice is examined, whether the disease was produced by the primary inoculation of putrid material or by the inoculation of the blood of the animal which had died, it is found to contain myriads of minute bacilli. The accompanying figure (Fig. 108, a) from Koch's work, showing the appearances presented by a drop of blood stained with methyl-violet, dried, and mounted in Canada balsam, gives some idea of the appearance of these bacilli. Their size, as compared with that of the anthrax bacillus, is shown by contrast with the other figure (Fig. 108, b). Pig. 108. a, The blood in septicEemia of mice, showing blood-corpuscles and small bacilli, d, Blood from splenic fever, showing blood-corpuscles and large bacilli. X 700. (Koch.) They can be shown also to 'be actually present in the bloodvessels in enormous numbers, as in Fig. 109, in which a vein from the diaphragm, is represented, prepared by Koch's method. In this figure the relation of the bacilli to the white corpuscles is seen. They penetrate into them, multiply in their interior, and finally break them up. Many clusters of bacteria which might be taken for zoogloea have this origin. The bacilli are found not alone in the blood but their path of entrance is discoverable. In the sub- cutaneous tissue in the neighborhood of the inoculated spot they are very numerous, and they may extend widely in the loose con- nective tissue, but do not pass into the lymphatic vessels, although apparently finding access readily to the bloodvessels. The explanation of these facts is obvious. The putrid material originally used contains many forms of bacteria. Many of these are, in relation to mice, innocent, but there is a form usually present (apparently in small numbers) which is capable of multi- plying in the body of this animal. If bacteria of this kind be MICEO-ORGAXISMS OR BACTERIA. 235 present in the fluid inoculated, they multiply in the subcutaneous tissue and pass into the bloodvessels, producing the disease which Koch calls septicgemia of mice. We shall not here follow the further facts in connection with this disease, as they will come up more suitably afterwards. A somewhat similar but even more virulent infective disease has been produced in rabbits, by the injection of putrid material. This Vein of the diaphragm of a septicaamio mouse. The septicemic bacilli are seen in great abundance, some of them attacking the white blood-corpuscles, which are occasionally reduced to masses of bacilli. X TOO. (Koch.) disease has been more particularly studied by Coze and Feltz and Davaine. For the first infection a large quantity of putrid material is required, and it is to be remarked that while different kinds of fluid will produce the disease, such as putrid blood, or peritoneal fluid, or the slime of sewers, yet these materials often fail entirely. "When the disease is produced, the animal begins to sicken in ten to twelve hours, and dies rapidly in about six or eight hours more. While it takes a considerable quantity of the original fluid to 236 PARASITES. produce the disease, a much smaller quantity of blood from the animal killed by the disease suffices to produce it in a fresh animal. Very striking statements have been made, on the ground of Davaine's observations, as to the progressive virulence of this disease when propagated from one animal to another. It has been said that, as generation after generation is infected, a smaller dose is needed till the disease can be certainly produced by a trillionth part of a drop of blood. The observations of Koch, however, seem to show that these statements have arisen largely from mis- apprehension even of Davaine's own observations. It is true that the propagated disease may be produced by such minute doses of blood, but it does not need to be propagated through several generations. In the first or at most the second generation it reaches its maximum of virulence, and a minimum dose is capable of producing the disease as in a later generation. 'Now this septicemia of rabbits is also produced by a bacillus, but one of larger size than that of the septicfemia of mice. Koch succeeded in obtaining a disease which he believes to be identical with Davaine's putrid infection, and the bacteria were rods about one-half larger than those of the septicaemia of mice, and with a clear space in the middle, while the poles were opaque, giving a kind of figure-of-eight appearance. This disease was communi- cable to several other animals, and in the blood of these animals the parasite was found to have multiplied. It is clear from these observations that putrid material contains bacteria which may conveniently be classed into two groups in their relations to the living animal. The members of the one group produce, it may be, chemical mattei'S which are poisonous to the living animal, but they themselves are innocuous, or at least the living tissues are able to resist their action and annul their virulent properties. The other class are able to propagate themselves in the animal body, and, probably by means of the chemical changes which they effect in the blood, they produce symptoms which are rapidly fatal. To the latter class of bacteria the adjective pathogenetic may be conveniently applied, and the class may be conveniently extended to include all bacteria which by propagating themselves inside the body produce morbid condi- tions in it. These pathogenetic organisms are of great importance not only in regard to septic infection, but, as we shall see after- wards, in relation to other diseases. In the case of the pathogenetic bacteria already mentioned efforts have been made to cultivate them in the pure state outside the body. In ordinary putrid fluid they are mixed up with other organisms and may he difficult to distinguish, but by using those developed in the blood of the animals a pure cultivation may be obtained. The bacillus of the septicaemia of mice has been found to grow best in an infusion of flesh to which has been added 1 per cent, of peptone, 0.6 per cent, of common salt, and enough phos- phate of soda to produce a weak alkaline reaction. This fluid MICEO-OEGANISMS OR BACTERIA. 237 may be rendered semi-solid by melting gelatine with it, and in this form it may be spread out on microscopic slides, and the blood containing bacteria sown on it. The bacteria cultivated in this way multiply vigorously, and they retain their pathogenetic character. Koch and his assistants have cultivated them through thirty-live generations, and found them equally virulent through- out. The bacillus of the septicaemia of the rabbit has also been cultivated in liesh-infusion and peptone or blood-serum stiffened with gelatine. They also have been cultivated through nineteen generations and found perfectly infective at the end. We shall return afterwards to the subject of pathogenetic bacteria, and meanwhile the characters of those just described must he borne in mind. PYiEMiA. — AYe have hitherto considered those conditions con- nected with the absorption of putrid material in which the action of the virulent matter is mainly on the blood; we have still to consider those cases in which local inflammations result from the penetration of decomposing material. The name pyemia is now commonly used to designate those conditions in which as a result of the absorption of putrid sub- stances multiple abscesses occur in the body. The occurrence of these multiple inflammations implies that a violent irritant is car- ried inwards and acts on the tissues. It may be said at once tbat these inflammations are always associated with the presence of bacteria, which may at first be carried to the part in small num- bers but afterwards grow into colonies. These organisms will primarily have their seat in the vessels, and the inflammations will therefore havcan embolic origin. Sometimes considerable pieces of broken-down thrombi, arising as we fehall afterwards see, are carried inwards and plug arteries; in other cases it is minute frag- ments which are conveyed, and they stick in the capillaries. As we have seen, however, the bacteria are self-propagating, and even a capillary embolism may set up a considerable inflammation. Let us now trace the course of events in an ordinary case of pysemia. "When putrid material is introduced into the blood from a wound, the active bacteria are usually destroyed by the living blood or vessels, and the result produced is, as we have already seen, a septic poisoning. But under certain circumstances, putrid material passes into the open mouths of veins, and the bacteria contained in the material survive and propagate. The first result produced is thrombosis in the veins. By and by the thrombi begin to soften, and they break down into a yellow material resembling pus. Hence the softening is sometimes called yellow or puriform softening. The material is not pus however, it is composed of the debris of the thrombus, along with the organisms which have been the chief agents in the coagulation and in the subsequent softening. It is easy enough to determine the presence of these bacteria both here in their original seat and in the embolisms which are secondarily produced, but it is much more difllcult to determine 238 PARASITES. their exact nature and relations. It is clear that they are diiFerent from the ordinary bacteria of decomposition, the form called bac- terium termo. The fact that they survive within the body is evi- dence of this, but it is also evidenced by the communicability of the disease. Pygemia when it once occurs in a hospital ward is very apt to spread to other patients who have septic wounds. Puerperal fever, which is often a form of pyaemia, is known to be in the highest degree communicable. The probability is that we have here to do with a specially virulent form of bacterium which occasionally develops in putrid wounds. It does not, like the sep- ticaemia bacterium, propagate to any considerable extent in the circulating blood, but being carried along it fixes itself at partic- ular points and there forms colonies. It is even doubtful whether it is always the same bacterium which is concerned in pyaemia. The form in most, if not all, cases is that of the micrococcus. To return to the softened thrombus, it is clear that when the coagulum has broken down, the soft material and shreds of thrombus will pass up the vein and into the circulation, being carried to the right heart and the lungs. In passing up the veins it soon produces a second thrombosis, which for a time shuts oiF the vein with its softened contents from the rest of the circulation. The soft material at once proclaims its virulent character by setting up an acute inflammation in the walls of the vein, and this inflam- mation, like others produced by this virus, rapidly runs on to sup- puration, so that a suppurative phlebitis is the result. On post- mortem examination the vein or veins are often found full of pus, and this led earlier observers to infer that a phlebitis Avas the origin of the disease. The name pyaemia also is derived from the presence of pus in the veins, and its inferred entrance into the blood. It will be understood that successive coagulation and successive softenings of thrombi will occur, and that on each occasion a fresh series of embolisms will result. The products of the decomposi- tion will also be conveyed into the circulation, and so a septic POISONING will coexist. We have now to trace the efi:ects which those emboli produce in distant organs, and it must be borne in mind that they are infective emboli, containing organisms which in some way produce an in- tense irritation leading to necrosis and inflammations with a ten- dency to develop suppuration very rapidly. The embolisms will occur primarily in the lungs, where we meet most constantly with the characteristic metastatic abscesses. Many times the emboli especially when superficial, lead in the first place to hemorrhagic infarctions having the usual characters, but these soon break down into collections of pus with the slough of lung tissue in the midst. If the embolism does not issue in the infarction, then the first re- sult of the inflammation is a condensation, the air-vesicles being filled up with inflammatory products, a grey hepatization, Avhich rapidly gives way to a purulent inflammation with necrosis of lung tissue. These various stages may be visible side by side in the MICRO-ORGANISMS OR BACTERIA. 239 same lung. If an abscess be neai' the surface, the inflammation spreads to the pleura, and an acute pleurisy having the same sup- purative tendency results. Besides, in the lung we may have abscesses in various other organs. The infective material may pass through the lung capil- laries, or else thrombosis having occurred in the pulmonary veins in connection -with, the abscesses, pieces of the thrombi may be after- wards carried away. In this way abscesses not infrequently occur in the muscular substance of the heart, in the voluntary muscles, in the liver, kidney, etc. Moreover, suppurations occur not infrequently in the joints, and it may be in those far removed from the seat of the original wound. These secondary suppurations in the muscles and kidney are usually small but often very numerous, and we can understand this from the fact that the pieces of thrombus which pass the lung capillaries must be small, and will obstruct either small arteries or capillaries. In the accompanying figure (Fig. 110), the appearances of a Pig. 110. Pyemic abscess of kidney ; a, necrosed central part; i, area of inflammation, the tissue packed with pus-oorpusoles ; c, capillaries filled with micrococci ; d, Malpighian glomeruli ; e, uriniferous tubules. X 16- Rii* ■•«■' pyeemic abscess of the kidney in process of formation are shown. The preparation was stained with aniline-brown. The central part (a) is hardly at all colored; necrosis has occurred in it, and conse- 240 PARASITES. quently the nuclei are no longer stained. In this area a high power showed numerous scattered bacteria. In the zone next the necrosis (b in figure) there are myriads of leucocytes produced by the inflammation. At c, c, c, are seen capillaries filled with bacteria. The artery whose obstruction was the primary lesion is not shown in this section, but many capillaries around are filled with organisms. A capillary containing the organism is shown in Fig. Ill, b, and this figure illustrates another fact. The figure was drawn from a Fig. 111. Capillary bloodvessel h in kidney filled with micrococci, from a ease of pyiemia. There is a tubule on either side (a, a), the nuclei of which are visible except in the neighborhood of the capillary. X 650. preparation stained with aniline-brown, and Abbe's illuminating apparatus was used. As we have seen already, the effect of this is to bring into prominence all colored objects, while those which are unstained are scarcely visible. In this case the nuclei of the uriniferous tubules are stained as well as the . bacteria, and they are represented in the figure at a, a. In the figure a tubule on either side of the capillary is shown, and it will be noticed that the nuclei on the sides of the tubule distal to the capillary are stained, while those next it are not. Here again we have evidence that the first effect of the bacteria is to cause necrosis, it is seen also that necrosis is produced at a certain distance from the bacteria in the uriniferous tubule while the bacteria are in the capillary. The organism here is a micrococcus. In the liver the abscesses are frequently large, and they may be present here while absent in the lungs. There are also not infre- quently considerable collections of pus in the joints. In these cases of the liver and joints it is probable that the phenomena are not so much embolic in the sense that distinct pieces of coagulum with bacteria are carried off", but rather that single bacteria or groups are conveyed by the blood, settle in the part, and propa- gate. The blood-current in the liver is so slow that bacteria may readily lodge in the capillaries, and there multiply. In the case of the joints also, if they once get admission to the interior, thev MJORO-OEGANISMS OR BACTERIA. 241 are likely to multiply in the synovial fluid, and produce a general inflammation. Besides these embolic phenomena, the blood is altered. We have seen that it is poisoned with the products of decomposition, and it may be as a result of this that the red corpuscles are to some extent dissolved, their coloring matter staining the tissues and pro- ducing icterus, called hsematogenous, as the coloring matter is directly derived from the blood. There is also an increase in the proportion of white corpuscles as compared with the red, a leu- cocytosis. Such is the ordinary course of events in pyaemia, but there are cases in which no thrombosis is discoverable in the veins. Putting aside cases in which thrombosis is present, but in such small veins that it is not discovered, there are undoubted cases in which abscesses occur in liver, kidney, spleen, and muscles, and suppura- tion in joints without any preceding thrombosis. These cases are to be accounted for on the supposition that the bacteria are intro- duced from the wound in such small numbers that they do not cause thrombosis in the veins, and consequently in these cases the probability is that they will pass through the lungs and over into the systemic circulation. The frequency of a1)scesses in the liver in such cases will be readily understood from what has gone before. To these we have to add a further class in which multiple ab- scesses occur without any external wound being discoverable. Some of these are associated with ulcerative endocarditis, in which, with an inflammation of the valvular structures, there is an aggregation of organisms, but there are cases in which no such connection can be found, and these are sometimes called cases of SPONTANEOUS PYJEMiA. In tMs couditiou, as well as in ulcerative endocarditis, the mode of entrance of the bacteria is obscure. It is probable that in pyaemia, and in other diseases of a like nature, the bacteria do not of themselves produce the intense irritation manifested. It is the chemical products evolved by them that irritate. Hence the inflammation is frequently present for a considerable distance beyond the seat of the bacteria, the irritant passing out from them and acting on the tissues. Pathogenetic Bacteria in Acute Specific Diseases. — We have now to leave the diseases connected with putrid wounds, and con- sider the question whether pathogenetic bacteria exist apart from these. Much that has been already said will be of assistance here, and it will be necessary to make frequent reference to the facts already adduced. The diseases as they occur in man can only be made the subject of experimentation to a limited extent, and so recourse must be had to the similar diseases in animals. Bacteria have been found in the tissues in a large number of acute diseases in man. and most of these diseases belong to the class of zymotics. Among the diseases in which up to the present 16 242 PARASITES. such organisms have been seen may be mentioned smallpox, scarlet fever, measles, diphtheria, acute rheumatism, erysipelas, typhoid fever, typhus fever, splenic fever, relapsing fever, pneumonia, leprosy, tuberculosis. All that is asserted in the meantime is that bacteria have been observed in these diseases ; it is not meant that each of these diseases depends necessarily on a specific form of micro-organism. Most of these diseases have several things in common with the septicaemias of mice and rabbits, and it may be interesting to con- sider these points as well as some others, and to look at them in the light of ascertained facts. Most of them are communicable or infectious ; that is to say, they are capable of being produced by the introduction of small quantities of their peculiar virus into the body. We have to inquire to what extent this virus is ascertained to be related to micro-organisms. Some of these diseases are appar- ently derived, not from persons already the subjects of them, but rather intermediately from foreign substances taken into the body. "We have to inquire whether there is evidence that the micro- organisms of any of them are capable of cultivation outside the body, and in what kinds of media. Many of these diseases, when once they attack a person, create a complete or comparative im- munity against further attacks. We have to inquire what light can be thrown on this fact. Under these three headings, we shall consider this subject. (1) The Relation of Micro-organisms to Zymotic Diseases. — Although our information in regard to the causation of most of the specific fevers, and other infective diseases, is very imperfect, still there are several in which the evidence is tolerably clear that they are as closely related to bacteria as are the septicaemias of rabbits and mice. Of these, the most fully investigated is the disease now com- monly called splenic pbver, but which has also the names anthrax, charbon, malignant pustule, etc. This is a disease exceedingly prevalent among our domestic animals, especially cattle, and it is sometimes propagated to man from these. The disease is an acute fever, in most cases beginning with shivering, and going on with elevation of temperature to a fatal issue. It sometimes has the characters of a local disease in the form of a malignant boil or pustule, and in many of these cases, as well as occasionally in cases of general infection, it does not prove fatal. Death, how- ever, generally occurs, both in animals and man, in from twenty- four to forty hours after the onset of the first symptoms. Now, in this disease, there is present in the blood, and, if there is a local manifestation in the fluids of the part, a very definite form of bacterium which is called the bacillus anthracis. It is, as compared with most of these organisms, of a large size, as may be seen by comparing Fig. 112, a, in which it is represented, with Fig. 112, h, in which the bacillus of the septicaemia of mice is shown. In its distribution, the bacillus anthracis is very like the last-named form. It is present in quite enormous numbers in the MICKO-OEGANISMS OR BACTERIA. 243 blood of animals which have died of splenic fever. If an organ be hardened in alcohol, and fine sections stained with methyl- violet in the way already indicated, an appearance is presented Fig. 112. Bacillus anthraciSj and of the septicaemia of mice. X ^00. (Koch.) under a low^power as if the capillaries were occupied by a blue injection material. The accompanying figure (Fig. 113) from Pig. 113. Villus of intestine in anthrax, the bacilli visible as minute threads. X 250. (Koch.) Koch's work shows the appearance presented by the villus of the intestine in a rabbit. Under a high power this blue injection resolves into bacilli, as shown in Fig. 114, and it will be seen that these are present in enormous numbers. The bacilli are present in the capillaries, and hardly at all in the arteries and veins, but 244 PARASITES. as they exist in the caxDillaries apparently of every organ they must be in incredible numbers. The smallest quantity of blood from such an animal inoculated into a living animal, such as the mouse, produces the disease, and there is the same enormous reproduction of the organism in the blood. It is clear, therefore, that this disease stands in the same relation to this particular form of bacillus as do the septicaemias of rabbits and mice to theirs. From same preparation as Fig. 113, more highly magnified. The bacilli visible as definite rods. X 700. (Koch.) In the next place, we have one of the acute fevers — eelapsing FEVER — associated with the presence in the blood of a distinct micro-organism of a spiral form. This organism, which is shown in Fig. 115, belongs to the class spirillum, its specific name being Spirochseta Ohermeieri, from its discoverer Obermeier. Spiral organisms have been found in stagnant water, so that this form is not without its analogues in organisms met with outside the body. The spirilla are met with in the blood, and their detection is ren- dered the more easy from the lively movements which they ex- hibit, causing the blood-corpuscles to be moved about to some extent. That the disease depends on this organism seems to be established from the fact that it is always present in the blood during the acute stage of the disease, disappearing, however, in the interval of defervescence, but reappearing when the fever recurs. The disease had not, till recently, been conveyed to MICRO-OEGANISMS OR BACTERIA. 245 Fig. 115. "HC^ animals by inoculation of tlie blood, but now it has been com- municated to monkeys, and the spirillum has been found in these animals just as in that of man. Other animals seem, so far, to present an immunity against this form of organism. A full account of this organism is to be found in an excellent work, recently published by Vandyke Carter, on Spirillum Fever as seen in Western India. Dr. Carter was first to communicate the disease to monkeys by inoculating with the fresh blood of patients with relapsing fever. Typhoid fever is another disease in which a special form of bacillus has been observed. In this refer- ence the observations of Eberth (Virchow's Archiv, vols. 80 and 83) are the most important. He has found a bacillus in the lymphatic organs of the abdomen, namely, in the closed follicles of the intestine, in the mesenteric glands, and in the spleen (Fig. 116). This organism appears to stand Blood from a case of relapsing fever, owing corpuscles and spirillum Ober- aieri. X 750. (Caeteb.) PlQ. 116. i J\ 1 J- ,lll Bacillus from lymphatic gland in a case of typhoid fever. X ISOO. in definite relation to the duration of the disease. At the begin- ning of the disease, and at its height, before the sloughing of the^intestines has occurred, it is present most abundantly, but as the disease becomes prolonged it diminishes and disappears. In the cases investigated it was found in a half, being absent in the more advanced cases. This bacillus does not stain so well as most forms, when sections have been made of organs hardened in alcohol, and it is most readily seen when it happens to be in colonies. But, if a lymphatic gland be laid open in the recent state, and a little of the juice from it spread on a cover-glass, and stained in the way already described after drying, then the rods 246 PARASITES. will stain well, and we obtain an appearance like that shown in the figure. As somewhat less known, it may be mentioned that bacilli have been found in malarial fevers. Klebs and Tomasi Crudeli (Archivf. JEzper. Path., vol. 11) have found in the air of malarial districts, in Italy, a bacillus which they were able to cultivate out of the body and inoculate in animals. They found a similar bacillus in the blood of men who had died of malarial fever. Klebs also states that in the blood in typhus fever there is a form of bacterium present. "We have already seen that tuberculosis is to be added to the list of diseases due to a specific bacillus (see Fig. 54, p. 156). Hansen and iN'eisser have described a bacillus as being univer- sally present in the nodules in the ekin in leprosy. These bacilli lie partly in the round cells of the nodules. Klebs asserts that bacteria which can be cultivated are to be found in the syphilitic CHANCRE, but these observations stand in need of confirmation. Erysipelas is another disease in which bacteria have been found by several observers. The bacteria occur in the lymphatics and lymph spaces, according to some also in the bloodvessels. In the milder cases the organisms, which are in the form of micrococci, are comparatively few in number, but in the more severe forms they fill out the lymph-spaces so as to give almost the appearance of an injection of them Avith finely granular material (see Fig. 117). Pig. 117. Prom the skin in a case of erysipelas. Tlie upper drawing shows a lymphatic vessel at the border of a sebaceous gland filled with micrococci. The lower shows a straight vessel similarly filled. X 350. The organisms are to be found only at the advancing edge of the erysipelas; when the inflammation once becomes pronounced with rich exudation of leucocytes then the organisms disappear. Ulcerative endocarditis is a condition in which with acute inflammation of the valvular structures of the heart there is loss of substance by ulceration. On the inflamed surface there are colonies of bacteria, and these are evidently of a virulent kind MICRO-ORGAATISJIS OR BACTERIA. 247 like, if not identical with, those in pysemia. Pieces of the softened valvular structure with the bacteria are carried off, and produce embolism in various organs. The disease occurs nearly always in the valves of the left side of the heart, mainly the aortic, and so the emboli are carried by the systemic arteries. Wherever they come to rest the emboli produce, like septic emboli, necrosis of the immediately neighboring tissue and acute inflammation, going on to suppuration around. Hence we have multiple abscesses, often with hemorrhage, in the kidneys, muscles, heart, skin, etc. In the midst of these abscesses the micrococci may be found even when the pus-corpuscles are crowded together. It may be added here that in ordinary acute endocarditis micrococci have been asserted by Koster to exist, not on the surface but in the substance of the altered valvular structure, and that by some, acute rheumatism which is the usual cause of acute endocarditis is regarded as due to the presence of bacteria in the blood. Without going further into ]:)articulars, it may be said that in a number of other diseases bacteria have been found in the blood or locally, although the question whether these are specific or are the generators of the, disease must remain in abeyance. In diphtheria they have been found in the exudation on the mucous membranes, and, by some, in their substance. In scarlatina and diphtheria they have been found in the kidneys occupying the capillaries (Fig. 118), and uriniferous tubules. In smallpox they have been i'm. 118. Wit O^X From a section of the kidney in a case of scarlet fever. A capillary bloodvessel distended with bacteria is shown, with uriniferous tubules around. X 350. seen in the capillaries of the kidney and liver. In acute pneu- monia micrococci have been found occupying the lung alveoli at the advancing border of the disease, in this respect resembling those of erysipelas, and they have been seen also in the capillaries of the kidney. It is here to be stated that our knowledge of the organisms in the diseases mentioned in the preceding paragraph is at present 248 PARASITES. exceedingly imperfect. It is remarkable that the organisms are found in the capillaries of the kidneys in so many cases. The explanation of this may be that at the time of death the bacteria are present there in very small numbei'S, and that after death they grow into considerable colonies. There is not usually evidence of considerable inflammation around the colonies, and so they can hardly have existed long before death. The mere fact of their presence, however, is important as connecting these diseases with micro-organisms. (2) Cultivation of Pathogenetic Organisms Outside the Body. — "We have already seen that in the case of the septicsemias of mice and rabbits the micro-organisms are capable of cultivation outside the living body, and, if this can be done in the case of the acute infective diseases of man then much light will be thrown on the origin and extension of these diseases. In the case of infective diseases arising from septic wounds, there is no difficulty in believing that the bacteria develop in the putrid exudations. In decomposing fluids there are numerous micro-organisms, and apparently a considerable variety of kinds. Certain of these seem adapted to one kind of animal and certain to others. But when we come to the acute fevers there are as yet few facts having any considerable degree of certainty. Concerning one disease, how- ever, our knowledge is tolerably complete, and on this account it will be treated of here in some detail. The BACILLUS ANTHRACis cxists, as we have seen, in the blood of animals affected with splenic fever, in the form of minute rods, as in Fig. 113. In the blood it seems incapable of existing in any other form, but it can be readily cultivated outside the body. When placed in a proper mediuna and kept at a proper tempera- ture, the motionless rods elongate into threads, and if there be many bacilli present they form a network. After a short time there appear in the threads glancing oval bodies. By and by the threads disintegrate and leave these oval glancing bodies or spores free in the fluid. It has now been abundantly shown that, while the bacilli themselves do not sur\T.ve long in the dry state, these spores are much more resistant and can be preserved for years in the dry condition. At the end they are as capable of producing the dis- ease as ever. These spores are therefore the fruit or seed of the anthrax bacillus, and may be the means of spreading the disease. This development of spores from the rods which exist in the blood can take place in a large number of media, both vegetable and animal. The bacilli grow and produce these spores very vigorously on the cut surfiice of boiled potatoes. They grow readily in hay infusion which has been rendered neutral or slightly alkaline, and in almost all kinds of vegetable infusions. They grow readily and form their spores in neutralized or weakly alka- line urine and in infusions of animal structures in general. It is quite clear that scattered over the surface of the earth there are abundant media for the propogation of this organism. If an animal with this disease is slaughtered, some of its" blood is shed in the THE QUESTION" OF IMMUNITY. 249 earth. If there is any piece of vegetable tissue lying there, and the conditions are such as to keep it moist and not too cold, and if it has not an acid reaction, then the bacilli will grow and pro- duce their spores. These spores may be carried hither and thither, and if by accident they get into the body of an animal they elongate into the regular rods, multiply with enormous rapidity, and lead to the symptoms of splenic fever. There is evidence to show that there are in certain parts areas of land which are regarded by the people as particularly dangerous as giving origin to anthrax. These are usually marshy places, and the disease is most likely to extend among cattle after inundations in which presumably the water has carried the infective material about. In these marshy places, especially if a chalky substratum keeps the earth more or less alkaline, there may be a continual growth of the bacillus and a continual danger of propagation. Another example of the propogation of a pathogenetic bacterium outside the body is atforded by Pasteur's researches on chicken CHOLERA. This disease of fowls is due to the existence in the blood of a minute bacterium constricted in the middle, so that at first it looks as if formed of two globular bodies. These organisms grow vigorously in chicken soup which has been neutralized and kept at a proper temperature. The organism may be propagated through several generations in the chicken soup, and is as capable of producing the disease as ever. It is interesting that this disease is propagated not only hj inoculation. If a few drops of the fluid in which it has been cultivated be put on bread, and this given to fowls, the animals acquire the disease, the organisms passing in by the alimentary canal. This disease will occupy us again in con- sidering the question of immunity. It has been already mentioned that the tubercular bacillus has been cultivated outside the body through several generations, and has retained its virulence throughout. Regarding the existence of other pathogenetic organisms outside the body, very little is yet known. Most of these have been only recently discovered, and are even now being subjected to observa- tion. It may be said, however, that, as already mentioned, the malarial bacillus seems to exist in the air of malarial districts, and is probably propagated among the decayed vegetable substances there. A bacillus like that of typhoid fever has been described as having been found in the drinking water during an epidemic of typhoid fever. (Brautlecht, Yirchow's Archiv, vol. 84, p. 80.) (3) The question of immunity is the next subject with which we are concerned. We have to consider the fact that, under certain circumstances, an infective disease due to the existence of micro-organisms will certainly reproduce the disease in one animal, and will not produce it in another. There are different kinds of immunity. In some cases there is what may be called a natural immunity, and in others it is acquired or induced, as when an attack of smallpox confers immunity to a fresh attack of the disease. In regard to natural immunity, it seems that the same micro- 250 PARASITES. organism will propagate itself and produce its special disease in one kind of animal and not in another. This has been brought out in a very striking way by Koch in his researches on the sep- ticaemia of mice. This disease which is so highly inoculable_ in the ordinary house mice is not at all inoculable in the nearly-allied field mouse. It is inoculable in the rabbit, but, as we shall see afterwards, it produces a local disease, and the bacillus does not propagate in the blood. The anthrax bacillus seems capable of propagation in every class of animal, and we have seen that it can be cultivated in a great variety of media. But yet, animals even of the same species show remarkable differences in the degree of certainty with which they can be inoculated. Chauveau ( Comptes rendus, 1880, vol. 1. pp. 15-26) has shown that while ordinary sheep are highly susceptible, those from Algiers do not usually acquire the disease from a simple inoculation by a lancet. But when these animals are inoculated with larger quantities of the virus they do succumb. It seems as if they could resist a small number of the bacilli, but that a larger number were able to obtain the upper hand. Again, Pasteur has pointed out that while in ordinary fowls chicken cholera is highly inoculable, yet when inoculated in Cochin China fowls it produces for the most part merely a local inflammation resulting in abscess. The micro-organism which produces the disease is found in the pus, but the pyogenic mem- brane seems to limit the inroads of the organism. But even in the same species of animal there are some individ- uals which show the most remarkable resistance to the attacks of the various organisms. In nearly all the diseases of animals which have been proved to depend on micro-organisms, observation shows that, in the course of a considerable series of experiments, there are some which are proof against the disease, or at least do not acquire it from the same limited inoculation as the generality of their kind. It would seem from these observations that the organisms are not indifferent to the kind of animal which forms their hosts. One form will flourish in one kind of animal and not in another. Besides, there are individual peculiarities among the same species of animal so that one animal will offer much greater resistance to infection than another. These facts are perfectly consistent with what we know in regard to this class of diseases in the human subject. Among men there seem to be extreme differences in the degree of susceptibility to infective diseases. Anthrax itself forms sometimes in the human subject a local disease which is recovered from, while in other cases the bacillus enters the blood and produces a fatal general disease. In the former case the bacillus is found in the tissues which are the seat of local inflammation, in the latter it is present abundantly in the blood. We are familiar also with the fact that when several persons are equally exposed to the infection of small- pox, some may escape while others acquire the disease. It is known that among savage tribes measles may present an extraor- THE QUESTION OF IMMUNITY. 251 dinary malignancy ; in this case it may indeed be that civilized nations have acquired a certain immunity rather than that the others have a special predisposition. A striking illustration of a similar fact is given by Grawitz (Virchow's J.?'cAi(;, vol. 84, p. 110). A troop of Esquimaux visited Berlin, and some were vaccinated with ordinary vaccine lymph. Immediately afterwards three died of an acute fever. Shortly afterwards the remainder were vaccinated in Paris, and thej all perished of what the Parisian physicians called severe smallpox, Here again, it may be, that the European nations generally have acquired immunity from the vaccine virus. "We have now to consider the question of acquired immunity, and from what has gone before it will appear that the line between natural and acquired immunity can hardly be rigidly drawn. In the case of measles it is well known that a degree of immunity is acquired by a single attack of the disease against further attacks, but then it appears that this immunity extends in some degree to the descendants of the person attacked, and so in countries where the disease is common there is not an immunity to the disease, but certainly an immunity to the more severe forms of it. It is the same with vaccination. It confers a degree of immunity against smallpox, and even if this disease occurs it is in a milder form than usual. Without at present attempting any explanation of these facts we have to refer in the first place to certain observa- tions which bear on the question of immunity. In a practical point of view the protection aiForded by vaccina- tion against the attacks of smallpox is the type of acquired im- munity. It is known that in the lymph of smallpox pustules as well as of those of vaccine there are fine globular bodies present, which may be called micrococci, and it has been proved by experi- ment that the virus resides in these solid particles, and not dissolved in the fluid (see Chauveau's researches, confirmed by Burdon Sanderson) ; but the organisms have not been cultivated apart from the body, and it is even possible to suppose that they are not organisms at all. "While our information in regard to smallpox is thus limited, some recent researches on other diseases by Pasteur and other French observers are of great interest as throwing light by analogy on vaccination. The aim in these researches was to obtain what may be called a vaccine of certain diseases, that is to sa.j to obtain the virus in a form in which it would produce the disease in a mild form, and yet be a protection against the virulent form of the disease. Let us take Pasteur'sobservations on chicken cholera to begin with. By cultivating the bacteria of this disease in chicken soup with exposure to the atmospheric air he found that he could pro- duce what he calls an attenuation of the virus. That is to say by letting the organisms grow on in the same medium for several weeks or months before planting them in a fresh medium he found that each successive generation thus produced was less virulent when inoculated than its predecessor. In fact, bj- varying the ex- 252 PARASITES. periment it was possible to procure viruses of varying degrees of intensity. The attenuated virus produces a local disorder rather than a general one, the bacteria being found in the locally affected parts. "But the disease exhausts itseff locally, the micro-organism being after a time nullified by the tissues. And now if animals which have been affected by the attenuated virus are inoculated vnth the virulent form they do not contract the disease, they have acquired an immunity which lasts at least a year. Next, in regard to anthrax, Pasteur has produced most striking results. Proceeding on the same principle as in the case of chicken cholera, his object was by prolonged cultivation of the bacillus with exposure to the oxygen of the air to obtain an attenuated condition of the virus. But here a difficulty occurred. We have already seen that when the bacillus anthracis is cultivated it develops threads and spores in the course of a comparatively short time. Pasteur desired, however, to cultivate the organism in the bacillus form. This was efiected by cultivating it at a comparatively high temperature. It is not possible to grow it at all at 45° C., but coming down to 42° or 43° it does grow but yields no spores. Thus, the bacillus can be grown for days with exposure to oxygen, and as the period extends the virulence of the organism decreases. In this way an attenuated virus can be produced, and when this is inoculated in an animal the disease is acquired in a mild form, and the animal possesses immunity from the virulent form of it. Another instance of acquired immunity is afforded by the experi- ments of Koch. It has been already stated that the septicaemia of mice is not communicable to rabbits, but when the blood of such mice is inoculated into the skin of rabbits, it produces a disease like erysipelas; there is an extending inflammation of the skin, which, however, is recovered from. Similarly, the cornea of rab- bits may be inoculated, with the effect of producing a spreading inflammation, the inflammation in both cases being accompanied by the growth of the bacillus. But when the animal recovers it presents a condition of immunity against further inoculation. It is noteworthy that this immunity does not become complete all at once, but takes in some cases three or four weeks. We have now to endeavor to explain the different kinds op immunity. Here we are met with serious difficulties. Pasteur has suggested that for the growth of each micro-organism there is a certain substance in the blood necessary, and when this is exhausted the micro-organism dies, and till that substance is repro- duced there is no longer any possibility of its growth. There are obvious objections to this. For one thing, the organisms may be cultivated out of the body in the very blood in which they would not grow M'hile it was in the living body. Then such a vie^^- will hardly explain the natural immunity which we have seen to be so closely allied to the acquired. We cannot suppose that those who are naturally indisposed to these diseases have blood which is defective in particular chemical principles. That this is not tlie SARCINA VBNTRICULI. 253 case has been shown by Chauveau, for he found that the Algerine sheep which are not affected by a small dose of anthrax virus do succumb to a larger dose. This points to an unusual degree of resistance to the virus; the bacillus is nullified by the tissues, and must attack in force before it surmounts the opposition. We may suppose that when an animal survives one of these diseases it has in its struggle with it acquired an increased power of resisting and destroying the organisms, and the power lasts a longer or shorter period. It should be stated here that by no means all of these diseases confer immunity by a single attack. Relapsing fever has been proved experimentally to be capable of repetition again and again in the same monkey, and it is well known that ague repeats itself frequently. There are even persons who are liable to repeated attacks of those fevers which usually confer immunity by a single attack. We find, for instance, persons who take scarlatina several times during a limited poriod. The question occurs here, now do these organisms produce THEIR EFFECTS On the living bodj^ ? It is quite clear that some of them produce chemical principles which act injuriously on the living tissues. This is abundantly evident in the case of pyaemia. The organisms here produce a necrosis with inflammation around. But neither the necrosis nor the inflammation occurs in immediate proximity to the bacteria, and it is clear that some chemical pro- ducts passing off from the organisms act as violent irritants. It is so also in erysipelas. The organisms propagate themselves up the lymph spaces and leave behind products which lead to inflamma- tion. And we may suppose it to be the same when the organisms multiply in the blood. It is not they themselves, but the products evolved in the processes of multiplication and growth that are poisonous. Pasteur believes that the drowsiness which occurs in chicken cholera is due to the formation of a narcotic by the organism. SARCINA VENTRICULI. We have here to consider a form of parasite whose position in the vegetable kingdom is rather obscure. This organism occurs in the form of minute cubical bodies, each of which is partially divided by transverse grooves so as to make the cube somewhat like a parcel tied with crossing cord (see Fig. 119). It is as if the individual sarcina were made up by the coalescence of four smaller bodies, and by some methods of preparation the four smaller bodies assume a more nearly globular form, and so still more suggest such an origin. These bodies are found mostly in the stomach where processes of fermentation are proceeding. But they are met with in other situations besides. From the observa- tions of Lostorfer and Ferrier it appears that the sarcina appears spontaneously in the blood when it is kept free from contamina- 254 PAEASITES. Fig. 119. tion at a certain temperature. If, for instance, blood be taken fresh from the vessels into a capillary tube, and preserved in a water-bath at a temperature near that of the body, in almost every case sarcinse will develop in the course of a few days (see Lostorfer, Wiai. Med. Jahrbiicher, 1871, and Ferrier, Brit. Med. Jour., Jan. 27, 1872). The sarcinae first appear as minute glancing globular bodies, and by and by they ag- gregate into the regular cubes. These cubes are much smaller than those of the sarcinae found in the stomach, but when -placed in a proper nourishing fluid such as Pasteur's solution, they grow to the size of these and assume their brownish color. It thus appears ' that, in the blood of man, and also, as ex- periment has shown, in that of animals, there are germs which have the capability of developing the sarcinse. Occurring in the stomach, the germs are probably derived from the blood, the stomach acting as a breeding oven. This explains the fact that sarcinse are met with elsewhere, as in urine, pus from cavities, gangrenous fluid, etc. The exact botanical relations of sarcinae are not determined. Some call them algae. The fact of their appearing in the blood first as minute globular bodies suggests that they may be allied to the bacteria. Sarcinse ventriculi (a), starch granules (6), and fungus spores (c), from vomited matter. X 350. PARASITIC FUNGI. The fungi are defined as consisting of cells devoid of chlorophyll, and occurring in the form of threads (hyphae) and round or oval bodies (spores and conidia). If the spores of ordinary penicillium fall into a fitting medium they soon begin to send out buds which become threads. By elongation and branching of these threads (hyphae) a network is formed, which is designated the mycelium, and is regarded gen- erally as the root structure of the fungus. Under favorable cir- cumstances upright stems (see Fig. 120) arise from this mycelium which bear the fructification of the fungus. These consist of elon- gated cells at the extremity of which rows of round or oval bodies develop in a pencil-like fashion, as seen in Fig. 120. This appear- ance has caused this form of common mould to be called peni- cillium. These round or oval bodies are spores, and each of them when carried off" from the fungus is capable of giving rise to a fresh PARASITIC FUNGI. 255 plant. It is asserted tbat in addition to this mode of fructification which is non-sexual, there is, probably in the case of all fungi, a sexual fructification, and much speculation has arisen as to the powers of the spores thus variously produced. These speculations do not concern us here, but it may be observed that so long as the PiQ. 120. Aerial growth of penieillium, sexual fructification is not determined the exact generic and specific relations of the individual fungi must remain obscure. The mode of production of spores figured above occurs when the fungus is able to send shoots up into the air ; it is an aerial production as distinguished from the mycelium which is in the soil. But a process in some respects similar often takes place in the soil itself This is shown in the case of the same fungus in Fig. 121, where it is seen that instead of forming elongated threads the cells Fig. 121. Formation of conidia in submerged portion of penieillium, are dividing into oval bodies. In many of these the hour-glass shape indicates the process of division actually in progress. In this way spores may be produced which are here called conidia. It is clear that this also is a non-sexual reproduction, and that it is strictly comparable with the aerial reproduction already mentioned. In fact the spores produced in the latter way are also frequently called conidia. It is to be remarked further that, with almost no attempt to 256 PARASITES. produce threads, the spores or conidia may multiply in the medium which forms their soil, and so we may have masses of spores or conidia and little else. This is the condition of the yeast fungus, the torula cerevisiee, and we often find multiplying spores of fungi in the contents of the stomach, as in Fig. 119. In their pathological relations, fungi are of much less conse- quence than the schizomycetfe, and it does not appear that they are capable, to any considerable extent, of producing chemical principles that are seriously injurious to the animal tissues. There are some diseases in which the existence of fungi in the body is rather to be regarded as secondary, the primary diseased condition providing a fitting soil for the growth of the fungus, but there are other conditions in which they act injuriously by their presence and growth. Fungous growth in kidney. To the left of the figure the kidney-tissue has been cleared up by adding solution of soda so as to bring out the fungus (aspergillus). Fat-drops and crystals of tyrosin are present, but no spores. (Grawitz.) It may be well here to inquire whether fungi, like the bacteria are divisible into pathogenetic and innocuous forms. In answer to this, it may be said that there appear to be no fungi capable of PARASITIC FUNGI. 257 actually multiplying in the body, but there are some which possess the capability of growing thei'e. Most fungi, when the spores are injected into the blood, simply die and are destroyed, but, accord- ing to the researches of Grohe, Block, and Grawitz (Virchow's Arehiv, vols. 81 and 84), there are some which may survive and grow inside the body. When spores of such pathogenetic fungi are introduced into the blood, they pass to various parts of the body, where they bud out and grow, by their growth producing numerous local necroses which may cause death in three days, or an inflam- mation which may lead to the death of the fungus and the forma- tion of a capsule around it. In the illustrations to Grawitz's paper, the condition presented to the naked eye by the kidneys is shown, and the resemblance of the multiple necroses to metastatic abscesses in pyaemia is very striking. In each of these a growing fungus is to be found, as shown in Fig. 122, but it does not go on to the formation of spores. If a piece of the tissue be used, however, the fungus may be cultivated outside the body in a suitable medium, and it goes on to the production of spores in the usual fashion. The question occurs here. Are there certain species of fungi which have this special character, or are the ordinary fungi capable of becoming pathogenetic ? This question has been answered in the latter sense by Grawitz. He assei'ts that the ordinary mould fungi, by being cultivated through several generations in alkaline solu- tions of albumen, at a temperature of 38° to 40° C, acquire viru- lent properties as above. Considerable doubt has been thrown on these conclusions by the researches of Koch and his assistants. They have found that the spores of the aspergillus glaucus, without any cultivation in animal fluids, are always pathogenetic, and they seem to assert that in the experiments of Grawitz there has been a contamination with the spores of this common fungus. We are to infer, therefore, that there are some fungi which are naturallj^ able to resist the action of the living tissues, and grow in spite of them. The MADURA FOOT is a disease which occurs in the East, and ■whose relations to fungi have been investigated by Vandyke Carter. In this disease a fungus, called in honor of its discoverer Chionyphe Carteri, penetrates into the substance of the foot, producing canals and cavities among the soft structures and the bones, and giving rise to severe inflammations. In the cavities and canals are masses of fungi of a blackish color, and forming frequent balls. The canals open externally, and discharge a fetid pus containing spores and threads of the fungus. There is great thickening and an appearance resembling that of scrofulous disease, and the condi- tion is a chronic one for which amputation must frequently be performed. In a considerable number of cases a fungus has been found in a:HE EAR. It has its seat in the external meatus and on the mem- 17 258 PARASITES. brana tympani, where it is accompanied by desquamation of the epithelium and other signs of inflammation. It is noteworthy here, in connection with what has gone before, that the fangus met with seems always an aspergillus, although spores of peni- cillium are as abundant in the air, and the two fungi are usually associated in mould. Fungi have also been met with in cavities of the lungs, on ulcers of the skin, etc. Fungi are of frequent occurrence in the skin, and there are three forms of skin disease which are always associated with the Fig. 123. > mmmmmm. ^mmmmmm 1W«W« Hair from a case of ringworm, showing fungus penetrating and breaking up the shaft. X 350. presence of these parasites, namely, Ringworm, Pityriasis versi- color, and Favue. In all of these the fungus appears in the form of multiplying spores or conidia, with irregular production of mycelium, but there is no proper fructification, the nearest ap- proach to that being in the case of pityriasis versicolor. The consideration of these fungi will cotne up for more particular PAEASITIC FUNGI. 259 study under the section on Diseases of the Skin. We have here to refer to the general conditions which they present. The fungus grows chiefly among the epidermic elements, spores and mycelium penetrating among the cells and displacing or breaking up the structures such as the hairs, etc. (Fig. 123). It is usual to describe the fungi of these three diseases as different, and they are named Achorion Schcenleinii (favus), Trichophyton tonsurans (ringworm), and Microsporon furfuri (pityriasis versicolor). Doubts have been raised, however, chiefly at the suggestion of Hebra, whether the fungus is not identical in all the three, and whether it is not one of the common moulds occurring in a special form and locality. It might appear that such a question would be easy of answer by means of observation of the fungus and its cultivation. But there are two difiiculties which are encountered here. In the first place, as the fungus only occurs in the form of multiplying spores and irregular threads, the fructification is not manifested, and the classification of fungi, as we know, is based on the fructification. Then, in the second place, the cultivation of the fungus has, in the hands of different observers, led to apparently contradictory results. Almost all the commoner moulds have been developed from the products of these diseases, and considering the wide prevalence of the spores of fangi in the air, and the probability that many such spores are continually falling on the skin, it is difficult to be certain that accidental contamination has not occurred. In the mouth, fungi are frequently to be found. The white material which lies in the angle between the teeth and the gums always contains multitudinous threads of a fungus or schizomyceta, called Leptothrix buccalis (see Fig. 124). This occurs in the form Fig. 124. Leptothrix buccalis from the gums at edges of teeth : a, the filaments separated; hj masses of filaments. X 350. of fine threads which often hang together in bunches. It has been asserted by Leber and Rottenstein that this organism, by pene- trating into the teeth produces caries ; but, considering its universal ' presence in contact with the teeth, this seems doubtful. There 260 PARASITES. is one circumstance which, however, is in favor of this view, namely, that the organism seems to aggregate lime salts in its nutritive pro- cesses. It usually attracts the lime from the food, and forms with other matters the so-called "tartar" on the teeth, but it is con- ceivable that it may acquire lime from the teeth, and so produce softening of them and caries. There is a disease of the mouth called commonly thrush, de- pendent on a fungus, the Oidium albicans. Here, as in the case of the parasitic skin diseases, the fungus grows am.ong the epithelial cells, detaching them from one another, but binding them together into a kind of soft membrane (Fig. 125). The so-called aphthous condition arising in this way does not develop in healthy persons, Pig. 125. Oidium albicans, from the moutli in a case of thrush. ( Kuchenmeister.) but is met with chiefly in emaciated children, or in adults whose health has been depreciated by tuberculosis, typhus fever, etc. The fungus may extend to oesophagus, stomach, etc., producing the same aphthous patches. B.— ANIMAL PAKASITES. The Animal Parasites are divisil)le into two groups according as they live inside the body (the entozoa), or on the surface (the epizoa). The entozoa are all included among the worms, and are met with in the alimentary canal and in the tissues. ENTOZOA OR INTERNAL PARASITES. or (1) Teematoda. — We have here an order of flat-worms of a more less oval form, and many of them somewhat in the form of a FLAT-WORMS. 261 leaf. The}' possess, on the ventral surface, one or more sucking disks by which the}- attach themselves. They have only one opening of the alimentary canal, which is generally forked. These worms are commonly called flukes from the resemblance in shape of the commonest of them to the fish of that name. The DisTOMA HBPATicuM is the commonest worm of this order. As the name implies, it is met with in the liver, where it inhabits the bile-ducts. The liver fluke is generally about an inch in length (Fig. 126), and rather more than half an inch in greatest breadth. The body is very flat, and anteriorly it ends in an elon- gated process, forming a kind of head. This head bears the mouth, and a short distance behind it comes the sucking disk. Between these lies the opening of the sexual ap- paratus, of which both male and female organs ^i^- 126. exist in each individual. The uterus forms a con- voluted tube behind the sexual opening, and the seminal tubules lie still further back. This para- site is very common in certain of the lower animals, especially sheep. It occurs in enormous numbers in the bile-ducts, which are dilated by it but not otherwise strikingly altered. As many as 1000 have been obtained from a single sheep. It produces in sheep the disease called commonly the rot, which in some years is very fatal. It is said that in 1830-31 between one and two million sheep perished from it. It occurs also in oxen, Distoma hepatioum. where it produces more considerable alterations of (Leuckart.) the ducts. These become greatly dilated, thick- ened by inflammation, and incrusted with lime. It sometimes happens that masses of inspissated bile and lime salts form in the liver where the flukes are present. It is probable that in these cases many of the parasites have died and become themselves the seat of incrustation. This fluke has also been met with in horses and asses, and in some rare cases in man. In man it has not been observed in large numbers, but it may produce serious obstruction of the bile-ducts. The eggs of this parasite are small oval bodies, which, in water, develop into embryos which swim about by the aid of cilia. Their further development is unknown, and also the form in which they pass into the animal which becomes the host of the adult. The DISTOMA siNENSE is a parasite met with in the East, and de- scribed by M'Connell in the Lancet, in 1875, and independently by Macgregor in the Glasgow Medical Journal, in 1877. Although a much smaller worm it is of a more elongated shape than the distoma hepaticum, as will be seen from Fig. 127. It is rather more than half an inch in length, and about an eighth of an inch in greatest breadth. When seen in the bile in the fresh state, the edges show a beautiful, delicate, green color, tinged with yellow, white the centre is of a deep brown. In the accompanying figure 262 PAEASITES. Fig. 127 the position and appearances of the various organs are indicated. The eggs are very small, and each animal possesses thousands. p This parasite has only hitherto been observed in man, and is found in very large numbers — not less than 500, probably more — in the ducts of the liver and in the gall-bladder. In Dr. Macgregor's cases the persons affected with the parasites were Chinese, and they were the victims of a peculiar paralysis of the legs and arms. Dr. M'Connell's case was also in a Chinaman. The DISTOMA LANCEOLATUM is another form of fluke. It is less than three-eighths of an inch in length, and about the fifteenth of an inch in breadth. It is seldom seen in man, and occurs in comparatively small numbers in sheep and i« ^^Pl^l -e cattle, producing little disturbance. I'^^feis St The DISTOMA HiEMATOBiuM, also Called the IDS, I'S^^^ll^l Bilharzia hsematobia, has the male and female organs in different individuals. The male is about half an inch in length, and flat, but rolled up at the edges, especially behind, so as to form a kind of gutter in which the female lodges. The female is about a half longer, but flliform. The eggs are small and furnished with a spine at the end or at the side. The parasite inhabits the bloodvessels of its host, chiefly the portal vein, the splenic and mesenteric veins, and those of the rectum and bladder. The penetration of the eggs in large numbers into the mucous membrane of the rectum and urinar}' bladder produces great irritation, and frequently hemorrhage. Similar irritation may be produced in the pelvis of the Iddney and ureters. This parasite is met with almost solely in Egypt and Abyssinia, is said that in Egypt about half the Distoma sinense, a, oesophagus and stomach tubes ; h, uterus ; c, yolk glands ; rf, ovary ; ti, testes ; f, termination of water-vaseular system. X 5. (After Mac- GREGOR.) and it natives are victims of it. (2) Cbstoda or Tape-worms. — These are in the mature state long flat worms, without mouth or alimentary canal. Anteriorly there is a head furnished with some apparatus for attaching itself to the host. Behind the head and neck the worm forms a series of segments called proglottides, each of which develops a bi- sexual apparatus and is, so far, a complete individual. The adult worm or strobilus is therefore a colonj^ of individuals. The worm inhabits the alimentary canal and apparently occurs only in verte- brate animals. Besides this adult form there is an intermediate immature form, called the scolex, which occurs in the tissues of animals. The scolex has a head like that of the mature worm, and generally possesses a sac or cyst into which it can retire. TAPE-WORMS. 263 There are representatives of two families of this parasite met with in man, namely, the Taenia and Bothriocephalus. The TiENiA SOLIUM is of very common occurrence in this country. The strobilus or mature worm occurs in the alimentary canal, and the head is usually situated in the duodenum or upper part of the jejunum, while the rest of the animal extends downwards in the canal, attaining on an average a length of from ten to twelve feet. As already mentioned, this, like other tapeworms, has no ali- mentary canal, and supports itself by imbibition of nutritious material from the intestine. The head of the worm, which is represented in Fig. 128, is about the size of a pin's head, and of a generally rounded form. In front it is prolonged so as to form a proboscis or rostellum, Avhich is surounded by a circle of twenty-six booklets. The wide part of the head has four large sucking disks. On the head follows a narrow neck, which is so thin that it readily breaks when the worm is handled, rendering it dif&cult to obtain the small head. PiQ. 128. Pig. 129. Head of T. solium. X -ij- (Leuckart.) Unripe proglottis of T. solium, showing sexual organs. The small vesicles scattered throughout are the male organs. The other structures shown are seminal tubes, vagina, globular body, yolk- body, ovaries, and unbranched uterus. X 10. (Leuckart.) The proper neck is about half an inch in length, and it gradually merges in the anterior part of the body, in Avhich fine transverse lines begin to appear as the first indication of the formation of segments. On passing down, the worm increases in breadth, while the segments elongate and become more completely divided. At first the segments or proglottides are homogeneous in appear- ance, but by and by the sexual apparatus begins to appear. The total number of segments in a worm ten feet in length is about 800. The sexual apparatus begins to appear about the 200th seg- ment from the front, and is mature about the 450th; it consists of the male and female organs which are present in each segment. The male organs consist of a large number of vesicles scattered 264 PARASITES. throughout the segment, as shown in Fig. 129, but more abundant anteriorly, as the female organs occupy the space behind. The vesicles are connected with fine seminal tubules which are difficult to make out, and are shown in the figure as fine branching lines. These end in a slightly convoluted tube, the vas deferens which is generally very distinct, and this passes across the segment to the papilla, a slight projection at the side of the segment into which the male and female sexual organs open. At the papilla the vas deferens ends in a projectile penis which is capable of passing into the extremity of the female organ, the first part of which is called the vagina. The vagina forms a canal which passes transversely across the segment towards the middle line and tends also backwards, to end in a somewhat globular dilatation, sometimes called the globular BODY. The connections of this body are difficult to make out, but they may be stated as follows, and understood by the annexed Figs. 129 and 130. In the posterior part of the segment, as shown in Fig. 129, are seen on either side the comparatively large ovaries, forming tree-like expansions, consisting of a congeries of closed tubes. The ovaries have ducts which pass into the globular body. Behind the ovaries and the globular body is the yolk-gland, which is of a somewhat pyramidal shape and spread out laterally. This also communicates with the globular body in front of it. Besides these communications the globular body, which is thus the central part of the female organs, communicates with the uterus in front. At this period of maturity the uterus consists of a simple tube extending longitudinally in the middle of the segment (see Fig. 129). It will thus be observed (Fig. 130) that the globular body has communication with four distinct structures, a with the yolk- sac, b with the ovaries, c with the vagina, and d with the uterus. The eggs pass from the ovaries first into the globular body, where Fig. 130. The globular body, or Mellis's body, and its Proglottis of T. solium, showing branching of connections. See text. X 30. (Leuckart.) uterus. X 5. they receive a covering of yolk, are fertilized, and undergo the beginning of their development. Then they pass into the uterus, which they fill up. As the ova accumulate in the uterus, this begins to throw out lateral branches to the number of seven to ten (see Fig. 131). The lateral branches often show considerable ramifications, in this respect and in their number contrasting with those of the next tapeworm. In the fully mature proglottis only TAPE-WORMS. 265 Fig. 132. the uterus crowded with ova is visible, the remaining organs having disappeared (see Fig. 132). The prominent ova often make the position and shape of the uterus very distinct, especially if the proglottis be spread out on a glass slide and allowed to dry. Besides the sexual organs the proglottides pos- sess EQuscular fibres, and a M^ater-vascular system. The muscle is non-striated and consists of longi- tudinal and transverse bundles. The water-vas- cular or excretorj' sj'stem (shown in Figs. 129 and 131) is in the form of tolerably wide channels, which begin at the head and are continued through the proglottides by two lateral channels right down to the last, ^^'here they open outwards. Near the posterior extremity of each proglottis the tubes form transverse communications (see figures). It is possible to inject these tubes from above down- wards, but not from below upwards. In addition, the proglottides, as well as the head of the worm, possess numerous round or oval calcareous bodies, which are mainly in the superficial layers of the parenchyma. As the proglottides become mature they sever their connection with the worm and drop off" from its lower extremity one by one. They pass down the alimentary canal, and are discharged with the feces, or else work their way out through the anus by virtue of their contractile power. For a short time after discharge they still show a writh- ing movement, but they soon come to rest and die. By the decom- position of the proglottis the ova are set free and are ready under suitable circumstances to develop further. It is mostly in the bodies of swine that the taenia solium passes through the "next phase of its development, although sometimes it occurs in man. It is exceedingly doubtful whether a man who is the host of a mature tape-worm can be affected from it with the form now to be described. The ova (Fig. 133) are surrounded by a dense shell of a brownish color. Inside the shell the egg develops an embryo which acquires six boring spines. When such ova get into the intestinal canal of the pig, the shell bursts, and the embryo with its spines escapes. It proceeds to bore its way outwards, and after piercing the alimentary canal it finds its way to the muscles of the animal where it finds a lodgement. Arrived in its desired seat, the embryo comes to a state of rest, and after a time develops into a vesicle or cyst, which afterwards Two ripe proglot- tides of T. solium, with branches of uterus shown. X 2. (Leuckart.) Fig. 133 Ova of T. solium, a with yolk, i without yolk, as in mature seg- ments. The hard brown shell is indicated. (Leuckart.) 266 PARASITES. forms the proper cysticercus. The appearance of these cysticerci in the muscular tissue is shown in Fig. 134, which is drawn of the natural size. The complete cysticercus or scolex has a head developed in connection with the vesicle, which closely resembles Pig. 134. Cysticerci of tenia solium in muscle. Natural size. (Leuckart.) the head of the mature worm (Fig. 135), and we have now to con- sider how this head forms. The observations of Leuckart and others have thrown much light on this, as they are based on actual experiments in which swine were fed with the ova. Fig. 13-5. Head of cysticercus cellulosaa found in substance of brain. X 90. We have seen that in the muscle a vesicle or cyst is formed. After a time a slight thickening of the wall of the cyst appears. This grows inwards into the cyst, carrying with it, however, the external wall, so that the projection inwards is hollow with an internal canal continuous with the surface of the cyst, and so opens exterjQally; this is shown in Fig. 136, where a portion of the wall of the cyst is preserved, and the projection is shown with its internal cavity communicating with the surface of the cyst. This projection enlarges, and by and by the pecu,liar structures of the TAPE-WORMS. 267 Fig. 186. head, namely, the four sucking disks and the hooklets, show them- selves. But these are formed inside the canal; near its extremity and they are in an inverted position as com- pared with that of the mature tape-worm. The head with its hooklets are thus at the bottom of the canal, and the four suckers, looking towards each other, follow. After a time the head acquires the power of inverting itself outwards, and thus projecting from the vesicle, or again withdrawing itself within the vesicle as before. This is effected by means of muscular fibres. For the comple- tion of this phase of development a period of from three to four months is required from the time of the ova being taken into the ali- mentary canal. It sometimes happens that this scolex of the tsenia solium develops in the human sub- ject, and then it is often spoken of as the cysticercus CELLULOSiE. It occurs chiefly in the brain, in the eyeball, and in muscle. It is to be remarked that in rare cases the scolex assumes in the brain a very peculiar character. The cyst, developing in the membranes on the siirface of the brain, presents pouches and swellings which give it somewhat the character of a bunch of grapes, and so has given rise to the designation cysticercus race- mosus. The cysticercus is usually surrounded by a connective- tissue capsule which is produced from the surrounding tissue and encloses both cyst and head, but not infrequently, especially in the brain and eyeball, it is devoid of this secondary capsule. In Cysticercus with begin- ning of development of head. A portion of the original cyst is shown with the projection inwards of a hollow process which communicates externally. X 25. (Leuckart.) ¥m. 137. Hooks from head of cysticercus cellulosa?. X -^50. 'that case the vesicle sometimes grows to considerable dimens'ions, and the head is able to protrude itself and move about in various directions, perhaps in the venti'icle of the brain or the eyeball. In these parts the scolex may produce considerable disturbance. 268 PARASITES. Although capable of a considerable duration of life, after a time the scolex usually dies, and then it shrinks and becomes, probably, incrusted with lime salts. The booklets are the most resistant parts, and it is of some consequence to observe the size and general appearance of these. In Fig. 137 are represented the booklets of this worm, magnified three hundred and fifty times._ They are to be contrasted with those of the taenia echinococcus (Fig. 138), which are magnified to the same extent. It will be seen that in the taenia solium there are two sizes of booklets, a larger and a smaller, and by comparison with Fig. 135 it will be seen that these are arranged alternately around the rostellum. In this as in other respects, the heads of the scolex and of the mature worm are identical. Fig. 138. Fig. 139. ^ 1/ ^ i^ ^^"^ A single head o£ ta3iiia solium before segmentation has begun. It shows movements of its suckers, etc. X 25. Hooks from taenia echinococcus. X 350. (Leuckart.) We have now to trace the further progress of development where living scolices are taken into the alimentary canal of man. In the first place, the vesicle and everything but the head and neck are lost, and we have a small creature which has considerable power of elongating and moving about its suckers, as shown in Fig. 139/ The head now fixes itself to the wall of the alimentary canal, and the body begins to develop from its posterior extremity. It takes eleven or twelve weeks for the worm to assume its full dimensions, and at the end of that time it begins to show proglottides. The worm is of tolerably long life, and may inhabit the intestine of its host for many years. It not infrequently happens that several coexist in the same person ; as many as thirty or forty have been observed. The T.ffiNiA MEDIOCANBLLATA may be dismissed much more shortly as the various stages in its development and its structure are, in most respects, essentially like those of the taenia solium. Leuckart calls this tapeworm the t^nia saginata. The strobilus is a larger worm than the taenia solium, measuring from. about thirteen feet in the contracted state to about twenty- ' four feet when extended. Fig. 140 shows the head and neck of this worm in the contracted and relaxed conditions. The difference in length and breadth is very striking. The head has no rostellum TAPE-AVOEMS. 269 or circle of hooks, but it possesses four large sucking disks which are usually suiTounded by a zone of pigment. The segments are in the most of the worm broader than they are long, attaining a breadth of about half an inch. But as we come to the fully Fig. 140. ll^iT Head and neok of tsenia mediooanellata ; u, in contracted, and b, uncontraoted state. X §• (Lbuokart.) mature proglottides with embryos in the uterus, then they are considerably elongated and at the same time narrower. The number of segments is greater here than in the taenia solium, reaching as high a figure as thirteen hundred. There are generally about eight discharged from the posterior extremity daily, and these very often find their way outwards, through the anus, by their own movement. . The sexual organs, except the uterus, are essentially the same as in the tsenia solium. The uterus, however, presents in the mature proglottis a much larger number of lateral ofisets, as. many as twenty to thirty, and these mostly branch dichotomously instead of ramifying (see Figs. 141 and 142). The individual segments, like the worm as a whole, possess muscular fibres, and are capable of elongating and contracting. The scolex form of this worm is found chiefly in cattle, and it inhabits mostly the muscles, but is also met with in other organs. The cysticercus measures about the third of an inch, and is of a roundish shape. This worm is nearly equal in frequency to the taenia solium in 270 PARASITES. the human subject. Its cysticercus is not known to occur in man. The worm may live for many years, at least as long as eleven, and, as some assert, up to twenty or even thirty years. Fia. 141. Fig. 142. Immature proglottis of T. mediocanellata. X 5. (Leuckart.) Mature proglottis of T. medio- oanellata. X -• (Leuckart.) Pig. 143. The T^NIA ECHiNOCOflcus in the strobilus form is a comparatively insignificant worm (Fig. 143). It inhabits the dog, and there are generally several individuals present at the same time. The total length of the worm is about an eighth of an inch, and' it consists only of four seg- ments, including that which carries the head. In the fully developed state the last segment exceeds in length the rest of the wori» altogether (see figure). The head is like that of the taenia solium in miniature, being very greatly less in size. It has a rostellum with thirty to forty booklets, and four sucking disks. The last segment develops a large number of eggs, as many as 5000. These eggs develop the usual embryos with six spines, and, if they find their way into the intesti- nal canal of man, they pass out into the tissues. Settling in some organ of the body, they show the most extraoMinary powers of development, pro- ducing the condition commonly called hydatids. It is proper to say here that hydatids occur in the form of large cysts, often of very complex arrangement, and they should be carefully dis- tinguished from the cysticerci, which form small cysts not more than half an inch in size. The hydatids occur in the majority of cases in the liver. E"eisser has collected no less than 986 cases of hydatids in man, and he gives the scale of frequency in the different organs as follows : Liver, 451 ; lungs and pleura, 84 ; kidneys, 80 ; muscle and subcutaneous tissue (including the orbit), 72; brain, 68; spinal cord, 13; female organs of generation (including the mamma), 44 ; male organs. Adult tffinia ech- inocoocus. X 12. (Leuckart.) T A P E - ^vr O R M s . 271 6; pelvis, 36; organs of circulation, 29; spleen and bones, 28 ; eye, 3. When the embryo reaches the liver or other resting place, it soon develops into a cj'st which at iirst is of slow growth. The membrane of the cyst is of considerable thickness, and consists of an external cuticle in several layers and an internal parenchy- matous layer containing muscular fibre and a vascular system. Inside the original vesicle arise very frequently secondary vesicles, and inside these even tertiary ones, the successive vesicles being sometimes spoken of as daughter or granddaughter vesicles. It sometimes happens that the secondary vesicles project outwards, and form a series of external vesicles which may separate from their mother and attain an independent development alongside of her. This latter form is particularly common in the domestic animals, and it is variously designated exogenous hydatids, or echinococcus scolecipariens, or granulosus. There is a third form which has been met with in man, and always in the liver. The parasite develops a congeries of small vesicles, from the size of a grain of wheat to a pea. These are embedded in a gelatinous tissue and sometimes possess gelatinous contents. As the whole is surrounded by a firm fibrous capsule, the tumor is a somewhat solid one, and on section it presents a peculiar alveolar appearance. From this structure it is called the alveolar form, and it should be particularlj' borne in mind, as this condition has been frequently mistaken for a tumor, especially before Virchow demonstrated its true nature. Except in the case of the alveolar form, the vesicles, both pri- mary and secondary, enlarge very much and give rise to tumors of very large dimensions, so as sometimes to produce serious dis- turbance by their mere size. Those of the liver are usually the largest, and they may come to weigh as much as twelve, twenty, or even thirty pounds. The simple ves- icles, in which no daughters develop, ^lo- 144. attain the size of an orange or a fist. In all forms of hydatids the ^^■hole parasite is surrounded by a fibrous cap- sule, developed by the organ in which it has its seat. As the cysts enlarge, this also increases in size. We have now to consider the for- Diagrammatical illustration of mation of the heads_ of the worms, development of eoMnococous heads which differs in certain respects from ;„. brood-oapsuies. «, Waii of cyst. that of the other tSeniaS. In the walls of b l, Brood-capsules, with heads in the vesicles, either primary or secondary, various stages of development. are to be seen when they are perfectly \Leuckart.) fresh, a number of small white points which have their seat in the internal wall. These are what are called BEOOD-CAPSULES, and it is always in connection with them that the heads or scohces develop. The brood-capsules are little vesicles, in the walls of which the echinococcus head grows. The 272 PARASITES. heads begin (see Fig. 144, in which the development of heads in brood-capsules is shown) as projections outwards of the wall of the brood-capsule. The projection is hollow, and communicates with the interior of the brood-capsule. The head develops inside this projection, as in tlie case of the taenia solium, and very soon acquires the power of inverting itself When it does so, it projects into the brood-capsule, so that in this respect the brood-capsule is not like the cyst of the cysticercus as the scolex projects outwards from the latter. A single brood-capsule develops several heads, up to twelve, and they may be found either in the extended or inverted position. All the heads are contained in brood-capsules, but if after death or during removal the brood-capsule bursts, then an appearance may be produced as if the heads were attached to the wall of the cyst itself. If the capsule bursts, its remains may gather round its stalk and the heads stand up from this as in Fig. 145, b b. Heads may also be found lying free if the capsules have Tig. 145. Brood-eapsules in connection with wall of vesicle, a, A capsule in normal unruptured state. 6 bf Ruptured capsule. X 40. (Leuckart.) burst. It is to be added that sometimes the vesicles remain barren, neither brood-capsules nor heads developing in them. The heads are exactly like those of the mature worm. They are very minute objects, measuring about ^n^th of an inch in long diameter, and just visible to the naked eye. They possess a pro- boscis with the ring of booklets, and four suckers. They are also provided with a water-vascular system, and in their parenchyma abundant calcareous particles are to be found. The animal may die spontaneously, or be killed by the fluid which fills the vesicles being drawn off. In that case the vesicles shrink, and their contents become converted into a fatty debris, which afterwards may become infiltrated with lime salts. In this way the hydatid mass may be represented by a cyst filled with an atheromatous material. This may dry-in, and at last we may have nothing left but a stony or mortar-like mass, in which careful search may still discover the booklets (Fig. 138). Besides the distinctive booklets, or even without them, there are usually in these old cysts bits of the membrane of the cyst. The wall of the hydatid cyst consists of two layers, an external (called by Huxley the ectocyst) and an internal (the endocyst). The ectocyst consists of TAPE -wo RMS. 273 a structureless stratified membrane, composed of a chitinous sub- stance, from which circumstance it is often called the cuticle. As this chitinous membrane is very resistant it may be found in the midst of the grumous contents and enable the structure to be rec- ognized. In the case from which Fig. 146 was taken the diagnosis Pig. 1-16. Transverse section of the chitinous membrane from an old hydatid cyst of the kidney, x ^^' was made chiefly by flakes of this membrane being found, the search for booklets being in vain. In regard to the distribution of the echinococcus, it is of pretty frequent occurrence in all known lands, but is particularly common in Iceland where the men, living in close companionship with the dogs, are much exposed to infection. It is also said to be very common in Australia and n-eighboring colonies. The BoTHRiocEPHALUS LATUS bclougs to the family of Bothrio- cephalidse, and is the largest tape-worm which occurs in man. It attains a length of from 16 to 26 feet, and possesses from 3000 to 4000 segments, which are mostly much broader than long, although the last ones (see Fig. 147) become longer and narrower, so as to assume more of a square shape. The breadth at the widest part is about half an inch. The worm is also thick and heavy. The head (Fig. 148) is oval, and about the twenty-fifth of an inch in breadth. It is blunt at the extremity, and possesses neither booklets nor suckers, but fixes itself by means of a slit-like groove on either side of the head (see figure). The sexual organs, and especially the uterus, occupy the middle part of each segment, where they form a rather^ prominent knot or rosette (Fig. 149). The uterus is composed of a convoluted tube which gives the rosette-like appearance just mentioned. The sexual organs open in the middle line near the anterior extremity of the proglottis. The eggs are oval in form and are covered by a brown shell. The scolex form of the worm long eluded observation. It was known that a six-spined embryo formed in the eggs in the usual 18 274 PARASITES. way, but the habitat of the cysticercus was unknown. Lately Braun has demonstrated its existence in the pike and turbot. It Fig. 147. Fig. 148. 53 (sflisfflaai Head and portion of body of Bothriocephalus latus. X 8. (Leuckart.) was found in the muscles, sexual organs, liver, spleen, etc., of these fish. Braun proved that it was the scolex of this animal by feeding dogs with it. A tape- worm identical with the bothriocephalus developed. By this discovery all the tape-worms which occur in Europeans have been traced in their mature and cysticercus forms. This worm is of rather frequent occui'- rence in Switzerland and north-east Euroj)e, but it is not unknown in this country. The frequency of fresh-water lakes in Switzerland explains its fre- quent occurrence there from the use of the fish which form the hosts of the scolex form. Like the other tape-worms the mature worm occurs in the small intestines. The Bothriocephalus latus. Natural size. (Leuckart.) Several other small and infrequent tape-worms have been met with in man. The Taenia nana has only been observed once, and in Egypt. It is very small, scarcely an inch in length, and about the fiftieth of an inch in breadth. It possesses a rostellum with booklets and tour sucking disks. The Taenia flato-puncta has also been ob- served but once, in America. It is about a foot in length, and about one-twentieth of an incli in breadth. The head of this worm is not known, but it is believed to possess booklets. The T.^nia madagascaribnsis has been found in an island on th« Mada- gascar coast. It is about 3 inches long, and the head is not yet known. The T^nia cticumbrina is from 7 to 10 inches long. Its head possesses a rostellum with a quadruple circle of booklets ROUND-WOEMS. 275 to the number of about 60. The proglottides reach a breadth of about the twelfth of an inch. It occurs very frequently in dogs and cats, and is often present in large numbers, especially in dogs. It has been found in several eases in man, and it seems to be not infrequent in children. The scolex form has lately been found in the dog-louse (Trichodectes canis), and it can be readily Pig. l-tfi. 5?«^i Proglottis of Bothriooephalus latus, showing female organs. X 12. (Leuckart.) understood how in the process of licking itself the dog often swallows its host and becomes itself the host of the strobilus. It may be conveyed to children from the tongue of the dog. The T^NiA MARGINATA is a tape-worm of large size, and of common oc- currence in the dog. Its usual length is about 5 feet, but it may be as long as 8 feet. It is very like the Taenia solium, the head possessing a rostellum and booklets of about the same size but more numerous. On the whole, however, the worm is smaller, and so are the proglottides. The scolex form inhabits swine and the ruminants, and as it often develops a large vesicle or set of vesicles, it is liable to be confused with the Taenia echinococcus. The scolex form is called the Cysticercus tenuicollis. Neither ma- ture worm nor cysticercus is met with in man. The dog also frequently contains two other taenia, namely the T. sereata and T. CCENURUS. These also resemble the Taenia solium, and the latter is important, as its scolex form frequently attacks lambs, and, lodging in the brain, is the cause of the very fatal disease " staggers." (3) JSTematoda or Round-worms. — The Trichina spiralis is met with in the muscular substance of man , and occurs there in im- mense numbers, producing the disease trichinosis. We shall see afterwards that this is not the mature form of the W'orm, but it is in this form alone that, for the most part, it is accessible to us, and it will be convenient to begin with its description here. The affected muscles, as seen with the naked eye, seem, for the most part, to be dusted throughout with fine white particles like sawdust. These are most abundant near the places where the muscular fibres are inserted into the tendons. As a rule the par- ticles are most abundant in the muscles of the trunk, the diaphragm, the intercostal muscles, and those of the abdominal wall, but they 276 PARASITES. may extend to all the voluntary muscles of the body, even the most distant ones of the hands and feet. On microscopic examination of the fine particles, they are found to consist each of an oval cyst vrith a tolerably thick wall (see Fig. 150), within which is a small worm coiled up in a spiral manner. Fig. 150. Trichina spiralis in muscle. The elongated shape of the cysts is due to the fact that these were near the insertion of the muscle into its tendon. In the lowest specimen the worm is dead and calcified. X SO. The cyst has very often abundant calcareous particles in its walls, especially at the poles, and, if the case is an old one, the impreg- nation with lime may be so great as to hide the parasite unless the salt be first dissolved out with an acid. "When an acid, such as dilute hydrochloric, is used, the lime dissolves with some evolution of gas, and the whole structure becomes very transparent. Some- times the worm dies in its capsule, and in that case the wall thickens and the cyst collapses to some extent on the remains of the worm, which itself often becomes infiltrated with lime (see lower specimen in figure). It may be said here that the worm in the muscle is in an immature state and quiescent, lying rolled up in this manner for years it may be. It may be present in immense numbers, even in millions, in the same person. "We have now to inquire how these embryos get to the muscles. To begin with, it is to be said that the embryos exist in the mus- cles of swine just as in those of man. If, now, a piece of muscle containing them in their living state — that is to say, not killed by cooking the meat — be eaten, they undergo further development in the intestinal canal. The capsule is dissolved by the gastric juice, and the embryo set free. In the muscle, the embryo, if uncoiled, Avould measure about the twenty-fifth of an inch in length; but now it grows rapidly, and in the course of two and a half days it reaches the adult form, when the female is about one-eighth of an ROUND-WOEMS. 277 inch in length; and the male slightly less. The male possesses a testicle consisting of a convolated tube. The female has an ovary, vagina, and uterus. The adult worms have an intestinal canal from end to end, which is divisible into cesophagus, stoinach, and intestine. The impregnated ova pass into the uterus where they develop into living embryos of minute size. In six or seven days after the female has attained sexual maturity, that is, eight or nine days after the trichinous muscle has been eaten, the birth of living em- bryos begins. The female gives birth to large numbers, and probably continues to do so for some weeks, thus producing as many as 1000 to 1300. The adults do not live longer than five to eight weeks altogether. The minute embryos now begin to penetrate the intestinal canal, and they swarm outwards to the voluntary muscles. The route by which they reach the muscles is not absolutely certain. By most it is thought that they pass outwards into the peritoneal cavity, and thence into the connective tissue around, by which they travel to the muscles. By others it is thought that they pass into the submucous connective tissue, thence into the connective tissue of the mesentery, and so onwards. It is probable that they find their way by both these routes, but it is inconceivable that, as some suppose, they get into the bloodvessels, as the vessels avail- able to them are the portal radicles which would take them to the liver. Swarming outwards from the intestine they reach first the muscles of the trunk, where they are usually most abundant; they then pass to those of the neck and larynx; and, lastly, to those of the limbs. Arrived at the muscles they grow larger, and appar- ently wander about for a time. They penetrate inside the sarco- lemma of the primitive fibre of the muscle, and destroy the sarcous substance. In about fourteen days they have attained their full size, and begin to settle down. As they pass along inside the sar- colemma they are arrested at the insertion of the fibre into the tendon, hence they are particularly numerous near tendons, and here also the cysts, subsequently foi-med, are often much elongated (as in the figure). The sarcolemma collapses as the sarcous sub- stance is destroyed, and as the worm coils itself up spirally the sarcolemma forms for it an oval cyst. The worm itself seems also to add to the cyst a layer of its own. It is not uncommon to find two, or even more, in one cyst. In the muscles the worms assume a quiescent state, as already mentioned, and may remain so for years, the cyst being impregnated with lime. They produce con- siderable destruction by piercing the sarcolemma, and disintegrat- ing the sarcous substance, and there is often to be found a germi- nation of the muscle-nuclei around the worm. During the migration of the embrj^os considerable irritation is produced. There is in the first week intestinal catarrh (diarrhoea)' with fever, and the case may be mistaken for typhoid fever. Later the muscles become stiff and painful, and oedema of the skin, 278 PARASITES. especially of the face, Qiay develop. The symptoms are usually at their height in the fourth or fifth week, and death occasionally ensues. Besides in man, trichinae have been found in the muscles of the pig, cat, rat, mouse, marmot, polecat, fox, marten, badger, hedge- hog, and raccoon. By some it is believed that the rat forms the permanent source of infection, as, vphen one of these animals dies, it is eaten by its neighbors, and so the infection spreads. From their habits, it will be understood how swine sometimes partake of dead rats. The parasite will be communicated to man by eating imperfectly cooked swine's flesh. It is said that a temperature of 50°-55° C. or 120° to 130° F., is enough to kill the embryos, but it is quite conceivable that when large pieces of flesh are cooked rapidly, some parts may escape the thorough penetration of the heat. The search for trichiiise in the muscles of swine before the flesh is sold is compulsory in some countries. For the examination pieces of muscle (preferably from the diaphragm and larynx) are snipped oft' with scissors and spread out in water on a microscopic slide. Some liquor potassfe may be added to make the prepara- tion more transparent. It is then to be examined with low magnifying powers and afterwards with higher. Several speci- mens should be prepared from each animal. The AscABis ltjmbricoides or common round-worm is probably the commonest entozoon in the human subject. It is most common in children, and inhabits chiefly the small intestine. It resembles the common earth worm in its color and general appearance. It measures six to sixteen inches in length, is marked by transverse striae, and tapers to both ends. It possesses an intestinal canal fi-om end to end. The female produces a large number of oval eggs which have a dense shell. The worm mostly occurs singly or in pairs, biit is frequently present in considerable numbers up to one or two hundred. From the intestine it may pass into the stomach and be vomited, or may be discharged per anum. It has been known also to pass up the cesophagus and into the nostrils and sinuses of the head, or by the larynx into the bronchial tubes. Sometimes it penetrates into the bile-ducts, which it maj' obstruct, or through the intestinal wall into the peritoneal cavity. In the intestine they produce catarrh, and by reflex action they are supposed to lead to certain nervous symptoms. "When present in large numbers, they have been observed rolled up in a ball, and so have obstructed the intestine. In cases where they have per- forated into the peritoneum they have given rise usually to local abscesses pointing chiefly near the umbilicus or groin. More rarely they have led to general peritonitis. The AscARis mystax is a small round worm which occurs in the cat, and is said to be always present in the intestine of that animal. KOUND-WORMS. 279 The OxYURis VERMicuLARis 01' THREAD-WORM IS Ell exceedingly common parasite. It is white in color, and the male measures about the eighth of an inch, and the female about three-eighths in length. It possesses an alimentary canal from end to end. The eggs are oval, and have a dense shell. The animal inhabits mostly the large intestine. It is stated by Zenker and Heller that the mature female is in the large intestine, the males and young being in the small. The worm often wanders, especially during the night, to the neighborhood of the anus, where it produces itching. Sometimes it passes over to the vagina, and up into it. It pro- duces catarrh of the bowel, and, as in the case of the ascaris, nervous symptoms are ascribed to it. The Triohocephalus dispar (the whip-shaped worm) is of fre- quent occurrence in the cpecum and neighboring parts of the in- testine. It measures one and a half to two inches in length, and has the peculiarity that the anterior portion is much thinner than the posterior, forming a long thread, like the lash of a whip, which is buried in the mucous membrane. The eggs possess a brown shell. The embryos have been traced in water and moist earth. The Strongylus duodbnalis or Anchylostoma duodenale is not met with in this country, but occurs in Egypt, Italy, and tropical lands. It has been found frequently among the workers at the St. Gothard Tunnel in Switzerland. It is a third to half an inch in length, and it possesses a mouth armed with four strong teeth. Bj' means of these it fixes itself on the mucous membrane, where it sucks the blood. "When present in considerable numbers, as it often is among the valvule conniventes, it may give rise to con- siderable loss of blood and serious angemia. The Strongylus gigas is a large worm, reaching a length of over a yard, and a thickness of about three-eighths of an inch. It has been met with a few times in the pelvis of the kidney in man, and more frequently in the kidney, bladder, lungs, and liver of dogs. The Eilaria or Dracunculus medinbnsis, or Guinea worm, is of frequent occurrence in tropical lands, where it is met with in the tissues of the foot and leg chiefly. The female is a long thin worm from twelve to forty inches in length, and it alone is known as a parasite. The male is much smaller. The worm wanders to some extent in the loose subcutaneous connective tissue, and may give rise to considerable irritation. When mature it presents its extremity at the surface, and a small pustule forms from which the extremity projects. The worm may then be removed gradually by rolling it gently round a quill from day to day as it becomes exposed, care being taken not to bi-eak it, in which case the part left in may give rise to severe inflammation. FiLARiA Sanguinis Hominis. — This name was originally given to a minute thread-like worm which has recently been found to be 280 PARASITES. really the embryo of a larger worm. The embryo, as its name implies, has been found in the blood, although it has also been observed in chylous mine and elsewhere. The adult appears to live in lymphatic vessels, and so the name filaria sanguinis is not strictly applicable to it. Cobbold has given it the name filaria Bancroft!, from the observer who first discovered the adult. As it is inconvenient to give two different names to the adult and embryo forms of the same animal, we shall refer to them under the original designation of Filaria sanguinis. In some respects the two forms of this worm are comparable to those of the Trichina spiralis, which also obtains its name from the embryo form. The adult filaria has the sexes distinct, and as yet the female alone has been fully examined, only a small portion of a male having been discovered. The female is a long hair-like worm, three or four inches in length, and only y^ inch in breadth. It has an opaline appearance, and, as described by Manson {Transac- tions of the Pathological Society of London, 1881), it looks like a delicate thread of catgut animated and wriggling as it lies in the tissues. By the observer just named it was found lying in a lym- phatic vessel while he was removing a scrotum which was affected in a way to be mentioned afterwards, and it appears that this is the usual habitat of the animal. The male is probably much smaller than the female, and they are supposed to live together in the same vessel. The female is believed to live for years in the same position, and gives birth almost continuously to large numbers of embryos. IS^ear the head is the vagina, and behind it the uterus with two Fig. 151. Filaria, sanguinis (embryo) after preservation in weak spirit. The sac is seen at each end of the worm. X 300. (Lewis.) horns is found, stuff'ed with ova, and extending almost to the tail. Manson states that the embryos can be seen escaping fully formed from the vagina, in exactly the same form as they are found in the blood. But the female sometimes gives birth to ova., as these have been found in the lymph and have been supposed to be the principal factors in producing certain local affections to be after- wards mentioned. The living embryo (Figs. 151 and 152) is about ^ inch in length and ixffTT inch in thickness; its breadth therefore nearly corre- sponds with that of a red blood-corpuscle. It is enclosed in a delicate sac, which is rather longer than itself, so that while ROUND-WORMS. 281 moving a portion of the sac extends beyond its extremity. The movements as seen in the blood and lymph are very active and snake-like in character. Pig. ir>2. Filaria sanguinis as they appear in the living state in the blood. From a case of chyluria. X 300. (Lewis.) This embryo is present in the blood of about ten per cent, of the natives where it is endemic, and most of these do not appear to suffer in health from it. A very remarkable circumstance is that, during the day, the parasites are, unless in exceptional cases, absent from the blood, but about six or seven o'clock are so numerous that as many as a hundred may be counted in every drop of blood. As moi'ning approaches they diminish in numbers, and by eight or nine o'clock they disappear entirely. This regular rhythm may apparently go on for years, but'it does not appear to be understood what becomes of the embryos during the day. "We have next to consider how the embryos find their way from the site of the parent worm in the lymphatics to the blood. It is probable that they travel by the way of the lymphatic fluid itself. Being not greater in breadth than a blood-corpuscle, and possess- ing powers of locomotion, they may be supposed to traverse the lymphatic glands with the lymph, and to reach the blood by the thoracic duct. It is also possible that they may get into the blood by penetrating through the bloodvessels. In the blood they will readily circulate with that fluid, and from their size they are capable of passing through the capillaries and repeating the circuit with the blood-corpuscles. They do not pass through any further stage of development in the blood, the embryos found there being exBctly like those which escape from the mother. It is clear also that they do not, either by themselves or their products act in- 282 PARASITES. juriously on the blood or tissues unless by using the nutritious material. It has been stated above that ova are sometimes discharged by the female, and it is probably in connection with this that vai-ious forms of disease are found to occur in connection with this parasite. The sac which has been mentioned as enclosing the embryo is' really the chorional envelope of the ovum stretched and rendered elastic. But ova are sometimes born with the sac confining the embryos which are rolled up inside, and we have then an oval body 5-^ inch to y^^ inch in length. This body is, of course, much thicker than the extended embryo, and when carried by the lymph to the glands it will be unable to traverse these. An in- farction of the fine afferent vessels of the gland will thus occur, and as the vessels leading from the part where the mother is situated are plugged one after another, there will by and by be a complete stasis of the lymph in the vessels of these parts. It is probable that dead embryos though extended will similarly plug the lymphatics. The eflfect of this complete plugging of all the lymphatic channels seems to be an accumulation of lymph in the vessel below the seat of obstruction. The lymph thus distending the vessels often escapes apparently by rupture. The locality of the parent will determine the exact nature of the resulting disease. If it be in the lymphatics of the pelvis or lumbar region, there may be distention of the lymphatics of the kidneys, ureters, or bladder. In that case chylous urine is found, and the embrj'os of the parasite have been observed in the urine. If the adult be in the lymphatics of the leg, there will be gradual plugging of the glands at the groin and accumulation of lymph in the legs and scrotum. The accumulation in the scrotum is of very frequent occurrence, giving rise to the lymph-scrotum, in which vesicles appear on the surface which occasionally discharge lymph. It is to be observed that the condition in these various situations is not a proper osdenia, which we have already seen to consist in overfilling of the serous spaces, but rather an over-distention of the lymphatic vessels with occasional rupture of them. If the explanation given above be the correct one, then as the glands get plugged the embryos, even those born alive, will not get to the blood, and it has actually been observed that in some cases no embryos were found in the blood although i)resent in the urine or lymph from the scrotum. It has been asserted that Elephantiasis is one of the diseases dependent on this parasite, and is to be placed in the same category as lymph-scrotum and chyluria. But there are serious objections to this view. Elephantiasis has the features, as we have seen, rather of a specific inflammation, than a simple stagnation of lymph, and is more neai'ly allied to leprosy. It probably depends on a virus which has a much more active influence on the tissues than the embryo filaria has. In what has gone before the adult and embryo filaria have been EPIZOA OR EXTEKNAL PARASITES. 283 described, but the stages bj which the embryo attains to the adult form have been omitted. The embryo in the human body does not pass beyond the stage which it had reached at birth, and in order to complete the cyclfe of its development it must pass into the body of another animal. The intermediate host has been found to be a species of mosquito (Manson). The female of this animal has a proboscis which she inserts into the skin and through ■which she sucks blood into the stomach. With the blood the embryos are taken in, and they have been found in the stomach even in larger proportional numbers than in the blood of the person from whom they were taken. In the stomach the embryo passes through certain stages of development occupying from four to six days. At this period the mosquito dies, and probably falls into the water, the parasite passing from the stomach. The further stages are not known as yet, but by the time the mosquito dies the parasite has already acquired a boring apparatus fitting it to penetrate the tissues. If it reaches the alimentary canal of man, it will then bore through the tissues till it finds its selected site in the lymphatics. It selects this site just as the trichina selects the muscles or the echinococcus the liver. In its new position it attains to sexual maturity, and being impregnated, gives birth to the embryos as we have seen. The species of mosquito here concerned is, like other mosquitoes, nocturnal in its habits, so that it attacks affected persons at the time when the parasite is present in the blood. The occurrence of the embryos in the blood at night has been regarded as a pro- vision of nature for the propagation of the species. EPIZOA OPv EXTERNAL PARASITES. These do not call for extended treatment here, as they are fully described in works on disease of the skin. Little more than an enumeration of them will be attempted. The AcARUS scabibi, or Sarcoptes hominis, has an oval body just large enough to be visible to the naked eye, the female being one-fiftieth of an inch in length and the male about half that size. The anterior part has a head and four limbs, each of which has a sucker at its extremity. There are also four posteror limbs, all of which in the female have pointed extremities, but in the male two of them have suckers. The female burrows in the epidermis, forming long tunnels in which, as it proceeds, it deposits its eggs ; it is usually to be found at the deepest end of the tunnel and the eggs at intervals. The eggs develop, and, as the epidermis des- quamates, they come to the surface by degrees, the young being born usually as they reach the surface. The irritation of the animal in the epidermis gives rise to a slight infiammation causing the formation of a papule. Usually there is great itching, and the scratching leads to further eruptions, especially in predisposed persons. 284 PARASITES. The AcARUs folliculorum is a long narrow animal provided anteriorly with four pairs of short feet. It is found in the sebaceous follicles, especially of the external meatus of the ear and neighbor- hood of the nose. It seems to produce no special irritation. Pediculi or lice occur in three forms, the pediculus capitis, corporis, and pubis, which hardly require special description. The PuLBX irritans, or common flea, is familiar to every one. The LARViE OF INSECTS Or MAGGOTS are occasionally found in the tissues of man. There are a few cases in which such larvfe have, by migrating under the skin, produced considerable inflammation. There are also cases in which, deposited in neglected wounds, or even in the mouth and nostrils of excessively debilitated persons, they have actually produced considerable destruction by feeding on the tissues. In neglected military hospitals wounds are often abundantly tenanted by maggots. PART II. DISEASES OF THE SPECIAL ORGANS AND SYSTEMS. DISEASES OF THE ORGANS OF CIRCULATION. A.— THE HEART AND PERICARDIUM. .MALFORMATIONS OF THE HEART. For a very full account of the malformations of tlie heart we are indebted to Dr. Peacock, whose work forms the basis of the remarks under this heading. Misplacements of the heart are of rare occurrence, and the more important of them are merely part of a general malformation of the body. The heart maj'' be transposed, that is to say, placed in a position on the right side of the chest corresponding with that which it normally occupies on the left. With this there is usually transposition of .the viscera, but it sometimes occurs alone. Again, the heart may occupy the middle line as it does in early foetal life. It may be placed outside the thorax altogether, but in this case there are other congenital malformations, and that of the heart only forms a part. Absence of the pericardium is a rare congenital malformation, and is mostly associated with misplacement of the heart. It is not to be confused with adhesion of the pericardiup and consequent obliteration of the sac which is so frequent in after-life. True malformations of the heart and great vessels for the most part represent survivals of fcetal conditions. In order to a comprehension of these conditions it will be neeessarj' here to refer briefly to the state of the heart in early foetal life, and the changes which it subsequently undergoes. The heart at an early period consists of two cavities, an auricle and a ventricle. The simple auricle receives the two vense cavse, and the ventricle gives origin to the common arterial trunk. The ventricle, the auricle, and the common arterial trunk subsequently undergo subdivision 286 DISEASES OF THE ORGANS OF CIRCULATION. eacli into two. This separation in the ventricle begins near the apex; the septum gradually rises towards the base, its completion at the base being delayed after the rest of the septum has been formed. The common arterial trunk begins to show signs of divi- sion by a septum about the time that the interventricular septum is approaching the base. A septum passing from both sides of the artery meets and divides the vessel into what are subsequently the pulmonary artery and the aorta. These are so adjusted as to con- nect with the right and left ventricles respectively. The division of the auricles does not begin till the ventricular septum is nearly completed, namely about the ninth week, and after being fully formed the septum remains partially open during the whole of intra-uteriiae life. Some of the malformations met with are survivals from a very early period of foetal life. The heart may consist of only two cavities, an auricle and a ventricle, with a single arterial trunk representing both aorta and pulmonary artery. Then there is the heart with three cavities, an imperfectly divided auricle with two auriculo-ventricular orifices, and a single ventricle with no septum, or a very rudimentary one. Leaving out of view these extreme cases, most instances of im- perfect closure of the septa are directlj^ related to obstruction caused by disease of the pulmonary artery or aorta at or near their orifices. In a way to be presently explained such obstruction leads to imperfect closure and other malformations. It is to be remembered that the part at the base is the last part of the septum to close, and that it is at the base that the great vessels arise. Consequently an imperfect closure will cause both ventricles to communicate more or less with both great arteries, and if one of the latter be larger than the other it will, as it were, overlap the imperfect septum and take origin partly from the other ventricle as well as its own. Let us consider the effect of stenosis of the pulmonary artery occurring at an early period, when the interventricular septum has not yet closed; or let us suppose that the common arterial trunk, instead of dividing into pulmonary artery and aorta, does so im- perfectly, and so there is a large aorta and a small pulmonary artery, or even an entire absence of the latter. In the case last mentioned the blood from the right ventricle, as well as that from the left, would pass into the aorta, and the constant recurrence of this passage of blood at each systole of the ventricle would pre- vent THE CLOSURE OF THE SEPTUM at the base, and cause the aorta to take permanent origin from the right ventricle as well as from the left. The condition would in fact virtually be that of a heart with three cavities, and it is possible that some of the cases in which this is the form of malformation may have such an origin. Short of this complete atresia (or obliteration) of the pulmonary artery, obstruction may occur in varying degrees, and the resu.lt8 will vary correspondingly. The aorta will, in the more serious MALF0R3UATI0NS OF THE HEART. 287 cases, take origin to a greater or lesser extent from tlie right ven- tricle, while in those which are less extreme there will simply be a gap in the septum. It has already been remarked that the last part of the septum to close in the foetus is the basal part, and there is, even in the adult, a small triangular space at the base of the septum, in which there is no muscular tissue, and which is composed only of the two layers of endocardium of the right and left ventricles and some loose connective tissue between. This space is called the UNDEFINED SPACE, and in a considerable proportion of cases a minute aperture persists in adult life at this point. If the septum closes imperfectly the gap has its seat here (see Fig. 153). Pig. 153. Defect of interventricular septum. The gap is situated at the base, in the position of the undefended space in the normal heart. (Peacock.) "We have seen that imperfect closure of the septum and'partial origin of the aorta from the right ventricle are the most direct results of stenosis or atresia of the pulmonary artery, but there are other results which also follow. The septum is bulged to the left, and the right ventricle is generally greatly hypertrophied. This hypertrophy of the right ventricle is probably of the same nature as the hypertrophy of the ventricles in adult life, which occurs so frequently in connection with obstruction of orifices. It is due to the extra-powerful muscular efforts made by the right ventricle to overcome the obstruction of the pulmonary artery. In addition to imperfection of the interventricular septum, there is very often in these cases imperfect closure of the foramen OVALE after birth. This will be a natural consequence of the enlargement of the right ventricle. The obstruction of the pul- 288 DISEASES OF THE ORGANS OF CIECULATIOX. monary artery keeps back the blood, as it were, in the I'ight ventricle and auricle, and the blood, accumulating in the right auricle, continues to pass through the foramen ovale, and prevents its closure. This consequence, however, does not invariably follow. Another consequence of occasional occurrence is the permanent patency of the doctus arteriosus. If the pulmonary artery at its origin is so much obstructed as to prevent the passage of the blood in due amount to the lungs, then the aorta will after birth augment the supply by the ductus arteriosus, through which the blood will pass in the reverse direction to what is normal in the fcetus. We have hitherto considered the case of obstruction of the pulmonary artery at a time when the iuterve'ntricular septum is still incomplete, but it may occur after the completion of the septum. In that case the most direct result will be dilatation and hypertrophy of the right ventricle, and permanent patency of the foramen ovale. Patency of the foramen ovale will be a more constant result here than in the former case, as this orifice will afford the only means of relieving the excessive accumulation of blood in the right side, whereas in the case of imperfect inter- ventricular septum the excess is relieved by this communication. "We have been considering the effects of obstruction of the pulmonary artery, but the aorta is sometimes, though by no means so frequently, the seat of obstruction. In that case the relation of matters is inverted. The septum of the ventricles is imperfect, but it is bulged to the right, and the pulmonary artery takes origin more or less from the left ventricle as well as from the right. The aorta beyond the obstruction often continues after birth to be supplied with blood from the pulmonary artery through the ductus arteriosus. The foramen ovale may remain open. It has been stated above that the pulmonary artery is much more frequently obstructed than the aorta during foetal life, and this leads us to consider what may be the cause Pig. i5i. OP OBSTRUCTION in these cases. The obstruction may be due to disease of the valves or to con- traction of the artery itself We are familiar with inalformation of the valves from adhesion in adult life as a consequence of inflammation, and there is reason to believe that it is due to the same cause in the fcetus. In the annexed figure (Fig. 154), a condition of the pulmonary valve is shown which sion of the curtains ^^ cxactly similar to that which we so often see in of the pulmonary the a-ortic valve m the adult. The three curtains vaire. The valve is are thickened and united by their margins so as viewed from above, to form a diaphragm instead of three mobile folds. (Peacock.) In the adult, inflammation is immensely more common in the valves of the left side than in those of the right, and it is ditficult to understand how it is exactly the reverse in the foetus. MALFOEMATIOlSrS OF TPIE HEART. 289 The proclivity to disease shown by the valves of the left side in the adult is usually ascribed to the fact that these are exposed to greater strain than those of the right side. The blood-pressure in the systemic arteries is much higher, and is exposed to greater variations. But in the fcetus, as Peacock has pointed out, a much larger proportion of the circulation is dependent on the right ventricle than in the adult, the descending aorta and the umbilical arteries being fed by this ventricle. The blood in the umbilical arteries must be exposed to considerable variations in pressure, from obstructions occurring in the umbilical cord and placenta, and these variations vsrill be reflected to the pulmonary artery and right ventricle. On the other hand, the left ventricle and aorta in the foetus are related to a much smaller area of the circulation than in the adult, and the systemic arteries in the quiescent state of the foetus will be little exposed to variations in pressure. In the great majority of cases, the malformations hitherto referred to are connected with and due to obstruction of the pulmonary artery or aorta, but it is to be added that incomplete- ness of the septum and the partial misplacements of the great vessels which go along with it may occur without any such cause being apparent. The same applies to patency of the foramen ovale, but in a much higher degree. Mere patency of the foramen ovale is hardly to be regarded as a serious malformation, especially when we consider that in nearly a half of adult hearts there is a slight degree of incompleteness in the closure of this aperture. In these cases, however, there is no real mixing of the currents in the two auricles, as the remaining aperture is valved by folds in the septum. The imperfect closure becomes important when, through obstruction in the pulmonary artery, the blood-pressure in the right auricle is raised sufficiently to cause the blood to pass through the aperture. Before leaving this part of the subject it will be proper to refer to certain irregularities of the primary vessels. There are cases on record in which the aorta has arisen posteriorly from the right ventricle and the pulmonary artery anteriorly from the left. In this case, the blood from the systemic veins is sent into the systemic arteries without passing through the lungs. Such a con- dition seems hardly compatible with the prolongation of life after birth ; yet several cases of survival are on record, in one case life being prolonged as long as three 3'ears. Another malformation is narro"^^'ness or obliteration of the ISTHMUS OP THE AORTA, Or that portion between the giving oif of the left subclavian and the insertion of the ductus arteriosus. In the foetus this portion is hardly in use, and it may be imperfectly de- veloped and form, after birth, an obstruction. In that case the pulmonary artery will usually supply the abdominal aorta, as in the fcetus, the ductus arteriosus remaining patent. The ductus arteriosus may close, however, in Avhich case tbe descending aorta 19 290 DISEASES OF THE ORGANS OF CIECULATION. must be replenished by circuitous anastomoses through the sub- clavian, mammary, intercostal, and epigastric arteries. In addition to these more serious malformations of the heart and its great vessels, there are certain congenital malformations of THE VALVES which merit some attention. These malformations concern mainly the semilunar valves of the aorta and pulmonary artery. The valve may be in the form of a diaphragm in vphich there are merely indications of a tripartite formation. In this case the diaphragm is often protruded into the vessel in the form of a funnel. Again, we not unfrequently meet with some variety in the size or number of the semilunar folds. There may be only two curtains, usually a large and a normal one. The larger one commonly shows indications of a partial division (see Fig. 165). Fig. 155. Congenital malformation of aortic valve. There are two curtains, but the larger one shows a partial division. (Peacock.) Then with three curtains there may be two large segments and a small rudimentary one between. These malformations are probably to be referred to endocarditis occurring in the foetus. In adult life endocarditis often produces adhesion of the curtains, but there is also very great contortion of the valves. But, in the foetus, the plastic power and adaptability of the structures is much greater, and the three coalesced valves may form a well-shaped diaphragm, or the two a single larger semilunar fold. In either case there are still indications of the coalescence in the form of thickenings along the line of union. It is obvious that these malformations will frequently interfere with the functions of the valves. In the extreme cases of complete union of the three curtains (as in Fig. 154) there will be great obstruction as well as imperfect closure. When there are only two curtains the middle part, where coalescence has occurred, is thicker, and the curtain will be more rigid at this point. This, itself, will interfere with the curtains falling back against the aortic wall during the systole of the ventricle, and so there will be a certain degree of obstruction. But, again, during the process of growth, the thickened line of junction being unduly rigid will not probably expand sufficiently, and the middle of the curtain will thus be held back. During the closure of the valve there will thus MALFOKMATIOJSrS OF THE HEART. 291 be an aperture left, allowing of regurgitation. The tendency to regurgitation is increased by the imperfect support which the large curtain receives from the smaller one. During closure the edge of the large one must partially double up in order to adapt itself to the small one, and so a gap may occur. We have seen that these adhesions of the curtains are probably due to intra-utcrine endocarditis, and there is apt to be a recur- rence of the disease after birth. It may be said that the previous existence of inflammation renders the structures liable to a recur- rence or possibly a prolongation from the foetal period. But, in addition, the imperfect adaptation of the valves will itself afford a certain irritation and predispose the structures to inflammation. So it happens that valv«s malformed in this way are peculiarly prone to disease in after-life, even though their function is not at first imperfect. Besides the variations already noted the curtains of the aortic and pulmonary valves are sometimes abnormally numerous, espe- cially those of the latter. There may be four curtains instead of three, and they may present all varieties of size relative to one another. The semilunar valves sometimes present a condition somewhat APPROACHING that of THE AURICULO-VBNTRIOULAR VALVES, wMch are of the cuspid form. It is to be noted that during the closure of a semilunar valve the curtains do not come in contact by their free margins, but that the line of contact is somewhat removed from Fenestration of the marginal parts of the aortic valve. There is an appearance of chordae tendinese, and the bands from two proximal curtains are inserted into a projection from the aorta. the margin. During closure, therefore, when the artery is full, a certain portion of the curtain floats free in the blood. Now the portion between the line of contact and the free margin is frequently the seat of apertures or fenestrations, and that without affecting the function of the valve. This fenestration may be very extreme and may graduate towards a condition in which (see Fig. 156), instead 292 DISEASES OF THE ORGANS OF CIRCULATION. of a piece of tissue, there are merely a series of tendinous bands passing from the curtain, near the line of contact,, to the wall of the vessel at the point of insertion of the curtain. These tendinous bands resemble the chordae tendinese of the cuspid valves, and the resemblance maj- be increased by the neighboring edges of the curtains being joined, and the tendinous bands from the adjacent borders of two curtains passing together to the wall of the vessel (see figure). There may be even on the wall of the vessel an elongated prominence into which the bands are inserted, and resembling a musculus papillaris. These hands may have a con- siderable free course from the middle of the curtain to the wall of the vessel. A certain indication of such conditions is very frequent in both the aortic and pulmonary valves. It may be asked. Does such a malformation interfere with the function of the valve ? Probably not much, but still to a certain extent. Each form of valve is appropriate to its own place. The cuspid form is adapted to an aperture between two cavities, the semilunar to the orifice or course of a vessel. The latter takes up less room, and by reason of the complete separation of the curtains it falls back completely when the blood rushes past it. But if the valve approaches to the cuspid form, especially if the margins of the curtains are united, and the tendinous bands from two have a common insertion, then there can hardly be that complete falling back which occurs when the function is perfect. This will probably cause a trivial obstruction, and the curtains being unduly exposed to the force of the wave of blood may be specially liable to inflam- mation. Cyanosis. — Before leaving the subject of malformations of the heart, we have to consider this condition which is so often associated with certain forms. Children born with malformations of the heart are usualty liable to symptoms connected with the respiration and circulation, which are in many respects comparable with those from valvular disease acquired in after-life, and consist chiefly in attacks of dyspnoea and lividity. These symptoms may occur at birth or soon after it, but they may be postponed even for years, and develop apparently by some extra stress laid on the circulation. Occurring at first intermittently the dyspnoea and lividity very often, to some extent, become permanent, and this is particularly true of the lividity. This generally becomes such a marked characteristic of such persons that they are visibly the subjects of Cyanosis or morbus osiruleus. The lips and finger-nails are blue, and there is, perhaps, a deep lividity of hands, feet, and cheeks as well. Two explanations of this symptom have been offered. The first is that, as in these cases, the septa of the heart are mostly imper- fect, the lividity results from the mixing of the currents, venous blood being mixed with the arterial in the systemic vessels. This looks a very likely explanation, but there are two serious objections to it. Cyanosis has been found in cases where the currents did not MALFORMATIONS OF THE HEAET. 293 mix, and it has been absent -where they undoubtedly did. Besides this, it is found that the degree of cyanosis is not at all propor- tionate to the mixing of the currents. The other explanation is that the cyanosis is due to venous engorgement, just as lividity oc- curring in valvular disease in the adult. In nearly all the cases there is obstruction of the pulmonary artery which we have seen to be at the basis of most malformations, and this has the effect of bringing about a general venous engorgement. Duiing the early periods of life the bloodvessels are more yielding and plastic, and so the permanent congestion tells much more on them than it does in adult life. Cyanosis developed in after-life sometimes ap- proaches in intensity to that from malformation, but it rarely reaches it. It may be interesting to refer to the duration of life in persons affected with malformation of the heart. If there is merely slight imperfection of the septa, the defect is of little importance, and we have already seen that there is imperfect closure of the foramen ovale in a large proportion of the cases met with in the ordinarj- course of post-mortem examination. If there is moderate con- traction of the pulmonary artei-y while the heart is otherwise well formed, the right ventricle will probably hypertrophy, and this may almost completely compensate, so that life is scarcely shortened. If the foramen ovale is distinctly patent, this generally implies a greater degree of obstruction of the pulmonary artery, and life is usually abbreviated. Peacock has collected twent}^ cases of this kind, and only eleven of these lived to the age of 15 and upwards, but some lived as long as 34, 40, and .)7. In three cases the ductus arteriosus was also open, and these died at the ages of 10 months, 15 months, and 29 years. If the interventricular septum is imperfect, this implies an obstruction at an earlier period of fcBtal life, and the duration of life is shorter. Of sixty-four cases, only fourteen survived the age of 15, but still three lived as long as 25, and one to 39 years. Where the pulmonary artery is entirely impervious, the duration of life is still shorter ; of twenty-eight such cases only seven lived over a year, and the longest duration was 12 years. "Where there is still greater arrest of development, and the heart consists of but one ventricle, with one or two auricles, the period of survival is usually very limited, but it is interesting to find that four persons thus affected have lived to the ages of 11, 16, 23, and 24 years. Transposition of the pulmonary artery and aorta might appear to be a malformation almost incompatible with life, and yet of twenty-one such cases, four lived between 2 and 3 years. When the aorta is obstructed at its isthmus, and the descending aorta is supplied, wholly or partially, by the pulmonary artery, the duration of life is usually very limited. The lungs seem to be deprived of blood, because it passes to the abdominal aorta, and the children die with symptoms of dyspncea and syncope. If the obstruction, however, be only slight, the person may survive to adult or middle life, even though the ductus arteriosus 294 DISEASES OF THE OEGAKS OF CIRCULATION. remains pervious; thus there are cases of survival to 24, 32, and 43 years of age. If the constriction be so slight that the ductus arteriosus closes, it may yet become much more considerable after- wards, or the aorta may even be obliterated at the point indicated. Yet such patients may survive long, as even with obliteration the ages of 45, 50, and 57 have been attained. ATEOPHY OF THE HEAKT. This condition is one of comparatively frequent occurrence, but is for the most part merely a part of general atrophy, or emaciation of the body. In emaciating diseases such as phthisis pulmonalis, stricture of the cesophagus, "cancer of the stomach, etc., where the muscular system as a whole has undergone great reduction in bulk, the heart is found to take part in the same process. Taking the normal weight of the heart as nine ounces for the female, and ten or eleven ounces for. the male, we may find it reduced to six or even five ounces. The heart as a whole is obviously smaller, and it has a darker color than normal, while the coronary arteries stand out unduly, often as somewhat prominent tubes. This change of color and the prominence of the arteries are largely due to the loss of the sub-pericardial fat, which normally covers the greater part of the surface and accompanies the coronary arteries, partially embedding them in the adipose tissue. The muscular tissue itself is darker in color, presenting a dirty-brown hue instead of the normal robust red. It is also tougher and di'yer. The deepening of the color is probably due to a concentration of the normal pigment from the diminution of the contractile substance without any loss of the pigment, just as red blood-corpuscles become much deeper in tint when they shrink by drying in. There is little doubt that the muscular fibres in this condition undergo an actual diminution in thickness, although from the great variety in diameter which the muscular fibres of the heart present this is very difficult to prove. The shrinking of the muscular fibres causes the connective tissue to be unduly promi- nent, and gives the muscle its undue toughness. HYPERTROPHY OE THE HEART. In entering on this subject it is necessary in the first place to consider under what circumstances such a condition may be brought about. It will be understood that the term is applied to hypertrophy of the muscular substance of the heart, giving rise according to circumstances to enlargement of particular ventricles or auricles, or of the heart as a whole. "We have already seen that hypertrophy of muscle occurs as a result of repeated forcible contraction of the muscle, and apparently from no other cause, hence in each case of cardiac hypertrophy we have to look for HYPEETBOPHY OF THE HEART. 295 some cause producing increased vigor of the .contractions of the cardiac muscle. The cardiac contractions are regulated by the wants of the system. When we lie quiet in bed they are com- paratively infrequent and deficient in force. "When we exert ourselves by walking or climbing up a hill, they increase, it may be greatly, in frequency and force. The needs of the tissues assert themselves by the nervous connections of the body on the cardiac ganglia, and the contractions become more forcible. Within the limits of health, and without any increase of the volume of the cardiac muscle, there are great variations possible in the force of the cardiac contractions. But where the heart is for a prolonged period impelled to unusually violent exertion, it may become hypertrophied. Thus, in soldiers who have had to execute a series of long marches, hypertrophy has been found to develop; in such a case it is comparable with that of the muscles of a blacksmith's arm, and is hardly pathological. ISTow, anything which interferes with the due carrying on of the circulation will be likely to lead to increased vigor of the cardiac contractions, and, if prolonged, to hypertrophy. If the arteries are not duly tilled at each systole, if the blood does not reach the capillaries with a sufiiciently rapid current, then the heart replies to certain reflex impulses and con- tracts more vigorously. Conditions leading thus directly to im- poverishment of the circulation, may be situated in the heart itself or outside it, and it will be understood that the hypertrophy will be COMPENSATORY, and may be sufficient to overcome the difficulty. In many of these conditions there is a mechanical interference with the flow of the blood either in the heart itself or in the arteries, and as a consequence the heart is overloaded with blood. In such cases the cavities will be dilated and the dilatation may indeed be the primary condition, the hypertrophy occurring as a secondary consequence. It is usual, therefore, to consider dilatation and hypertrophy together, there being commonly some dilatation along with the hypertrophy, although it is rare to find dilatation without hypertrophy. For the sake of illustration we shall here consider some cases of cardiac hypertrophy. One of the commonest forms is that which occurs in adhesion of the pericardium. In this condition as we shall see afterwards, the sac of the pericardium is obliterated and the parietal pericardium has coalesced with the visceral. In some cases there is very little hypertrophy, but in others it is very great. It is to be remembered that adhesion of the pericardium takes origin in inflammation, and from this circumstance it results that in several ways the action of the heart is interfered with. During the acute stage of the inflammation there is fluid in the sac of the pericardium, and by the mere mechanical pressure of this fluid the cardiac contractions are interfered with; in order to overcome this obstacle the heart may hypertrophy, and if the eft'usion con- tinue long enough there may be hypertrophy from this cause alone. But again, the inflammation extends a certain distance into the 296 DISKASES OP THE OEGAXS OF CIECULATIOX. muscular wall of the heai't beneath the pericardium. A certain portion of muscle is thus interfered with in its action and more vigorous contraction is required of the rest. There may even be considerable thickening of the pericardium by development of connective tissue, and this extending some distance in the connec- tive tissue between the muscular iibres may seriously compromise them. But further, when adhesion is complete, the heart in con- tracting must drag in with it the parietal as well as the visceral pericardium. In the normal state the parietal pericardium lies against the visceral, and there is no cavity left, but then the two surfaces slide on one another, and the parietal layer accommodates itself to the movements of the heart. If there is adhesion, how- ever, unless the adhesion be vei'y loose, there can be no such sliding, and there must be some loss of force in dragging the visceral layer inwards. But there is a further very important element in the problem. The inflammation of the pericardium does not confine itself exactly to the sac, but extends somewhat outside it, so that when recovery occurs the visceral layer is united more firmly by new-formed connective tissue to parts around, to the ribs and intercostal spaces, the sternum, the pleura, and the roots of the lungs. This being the case, the heart will meet with greatly increased resistance in contracting, as it will have to drag in these adhesions in order to empty itself. In order, therefore, to send a normal amount of blood out of the ventricles, an excessive amount of muscular force will be required, and the continuance of this will lead to hypertrophy. It will be seen that these causes vary to a considerable extent, and the amount of hypertrophy varies in proportion. As the causes also act nearly uniformly on the heart, the hypertrophy is general, that is, it usually affects all the cavities of the heart. Such a hypertrophy may almost com- pletely compensate, so that a person with adherent pericardium and a very large heart may have no cardiac symptoms. As other illustrations of cardiac hypertrophy we might refer to cases of valvular disease of the heart. In these the force of the cardiac contractions is to some extent ^^'asted, and the heart is spurred to increased exertion to supply the wants of the system. In studying the various forms of valvular disease we shall have sufficient illustration of this. Outside the heart itself there may be causes interfering with the circulation and leading to cardiac hypertrophy. These causes, like disease of the valves, will mostly act primarily on one cavity, and so we shall have partial hypertrophies. One of the most obvious illustrations of this is afibrded by diseases in which the circulation in the lungs is obstructed. In emphysema there is great obliteration of the pulmonary vessels, and as the needs of the organism require a certain amount of blood to pass through the pulmonary vessels in a given time, the right ventricle is stirred to more vigorous contraction in order to force the due amount through the smaller number of vessels, and through time it hypertrophies. HYPERTROPHY OF THE HEART. 297 In the case of the systemic circulation, aneurisms and rigidity of the arteries are frequent causes of hypertrophy of the left ventricle. We come now. to a form of hypertrophy of the left ventricle which it is somewhat difficult to explain, namely, that which occurs IN Bright's disease. It M'ould carry us too far at the present stage were we fully to discuss the causes of this hypertrophy of the heart, which will be taken up again in considering the path- ology of affections of the kidney. In the mean time it may be noted that the hypertrophy is purely of the left ventricle, and its cause is to be looked for in something which increases the force of its contractions, or, in other words, some obstruction in the sys- temic arterial circulation. It is natural to look for this obstruction in the kidneys where, in chronic Bright's disease, there is often great contraction and obstruction of the capillaries. There are serious objections to the acceptance of this view (which was that of Traube), at least in its simplest form, and we shall return to this point afterwards. In the mean time it may be stated that this form of Brighfs disease is associated with an increased blood- pressure (increased tension) in the systemic arteries, and that this is sufficient to account for the hypertrophy of the heart. An in- crease of the general blood-pressure is caused most effectually b}' a general narrowing of the smaller arteries throughout the body, and this would seriously stress the heart, if it had not sufficient force in its existing muscular fibre. In the case of Bright's dis- ease increased arterial tension first develops, and this is followed by hypertrophy of the heart. Even when we have enumerated all the cases of hypertrophy of the heart, and especially of the left ventricle, in which a definite cause can be assigned, there still remains a residuum to which no mechanical explanation is discoverable. In these cases it may be presumed that there is some peripheral obstruction to the circula- tion, perhaps a habitual contraction of the arteries and consequent increased tension. Such persons are often liable to palpitation, and sometimes to other signs of heart disease, but without any val- vular lesion or other mechanical hindrance. Forms of Cardiac Hypertrophy. — From what has gone before, it will be apparent that hypertrophies of the heart vary greatly in amount and in the distribution of the enlargement. The total increase in weight is greatest in cases where both ventricles are enlarged, and the weight of the heart in such cases not uncom- monly reaches from twenty-seven to thirty ounces. It is least where the right ventricle alone is enlarged, because this ventricle, as a whole, weighs much less than the left, but in pure right ven- tricle hypertrophy a weight up to seventeen ounces is not infre- quent. In hypertrophy of the left ventricle, as in Bright's disease, the weight is frequently over twenty ounces. In GENERAL HYPERTROPHY the general shape of the heart is not 298 DISEASES OF THE ORGANS OF CIRCULATION. much altered. The heart is enlarged in all its parts, the ven- tricles and auricles are increased in capacity, and their walls are thickened. The heart is like that of a bullock in size, so that the name cor bovis is often applied to it. "When the right ventricle is mainly affected, the heart assumes a somewhat quadrilateral form (see Fig. 157). On examining the normal heart as it lies on its posterior surface, after removal fi'om the body, the right ventricle is seen to occupy the greater part of the anterior aspect. The position of the septum, as shown in the accompanying figure, is slightly to the right of the left border, and it reaches the apex region slightly to the right of the true apex. In the heart the position of the septum is always indicated on the surface by the coronary artery which, with its padding of fat, occupies a groove corresponding with the anterior border of the I'^i'i. 157. Pig. I'lH. Hypertrophy of right ventricle. The Hypertrophy of left ventricle. The alter- alteration in shape is indicated by the dot- ation in shape indicated by dotted line; g, ted line; a, superior vena cava; i, aorta: the hypertrophied ventricle. (Rindfleisch.) c, conus arteriosus; d, right auricle; e, left auricle; /, left ventricle. (Rindfleisch.) septum. In hypertrophy of the right ventricle, as shown bv the dotted line in the figure, the apex is unduly obtuse, and it is often difficult to determine what is its exact seat. The septum is nearer the left border than usual, and it reaches the apex region rather to the left than the right of the most projecting point. The right ventricle also monopolizes the anterior aspect of the heart still more than in the normal condition. When the heart is laid open, the undue thickness of the right ventricle, as well as the enlarge- ment of its cavity, becomes apparent. In HYPERTROPHY OP THE LEFT VENTRICLE the relations are very different, as shown in Fig. 158. The heart as a whole is more elongated and pointed than normal, and this is often very striking. The apex part especially appears greatly prolonged. When the heart is viewed on its anterior aspect tlae septum is seen to lie more to the right, and the true apex is much further to the left of FATTY INFILTRATION OF THE HEART. 299 the point at which the septum reaches the apex region. On laj'ing open the heart, the thickening of the wall of the left ventricle is very obvious, and the septum is often greatly thickened. The septum belongs partly to the left and partly to the right ventricle, but as the left ventricle is much thicker than the right, the septum belongs more to the left. It will partake in the hypertrophy of either ventricle, and, in the case we are considering, the thickening is often very striking. The thickened septum frequently bulges into the right ventricle, sometimes diminishing its capacity greatly, and even producing actual obstruction of the conus arteriosus. The hypertrophied heart often presents a peculiarly firm condi- tion of its wall, and this has been ascribed by Sir "William Jenner {Med.-Chir. Trans., 1860, p. 199) to a passive congestion op the HEART. Cases of cardiac hypertrophy are very frequently such (as in the more common forms of valvular disease) as to lead to a general venous engorgement, in which the heart itself, being re- lated to the general venous system, partakes. l!Tow, prolonged venous hyperemia produces in organs, as we have seen already, a certain hypertrophy and increased density of the connective tissue. Some part of the hypertrophy in such cases may even be due to increase of the insterstitial connective tissue. Hence the result is that the walls of the heart are more rigid than normal, and when the cavities are laid open they do not collapse, but stand out with their outline retained, the walls having a tough leathery character. The muscular substance also is frequently of a very red color, this being largely due to the excess of blood in the vessels. FATTY INFILTRATION OF THE HEART. The normal heart is well known to present on its surface a cer- tain amount of adipose tissue. This fat is beneath the pericardium, lying between it and the muscular substance of the wall. It is normally most abundant along the course of the coronary arteries, along the inferior border of the right ventricle, at the apex and at the origins of the great vessels. In different individuals the amount of the adipose tissue and the extent to which it covers the muscular substance so as to conceal it from view, vary greatly, but it may be said generally that a considerable part of the surface of the right ventricle and the greater part of that of the left are usually free of fat. Sometimes this fat increases greatly, both in superficial area and in thickness. We know that adipose tissue in any part of the body is formed out of loose connective tissue by the infiltration of fat into its cells, and so the subpericardial con- nective tissue may become extensively converted into adipose tissue. In this way the entire right ventricle may be covered while a por- tion of the left is still free; or, the whole heart may be coated with a thick mantle of fat. The conversion does not always confine itself to the pericardium, 300 DISEASES OF THE ORGANS OF CIECULATIOX. but frequently extends into the connective tissue in the proper muscular wall of the heart, lyin^ between the muscular fasciculi. In such cases if we make a section of the ventricle we find streaks of adipose tissue extending in from the surface. In this way the superficial layers of the muscular wall may be largely replaced by adipose tissue, which may even appear in isolated patches imme- diately beneath the endocardium. Informally there is more fat on the surface of the right ventricle than on that of the left, and here also the pathological increase occurs to the greatest extent. It is not uncommon to find the proper muscular substance of the right ventricle largely replaced by adipose tissue, only a thin layer of red muscle appearing inside the thick layer of fat. Of course, in this case, there is great loss of the muscular power of the heart; the right ventricle is much moi-e liable to this than the left. In some cases the increase of the external fat is merely part of a general obesity, in which the fat in all its various localities throughout the body takes part. But sometimes its significance is much more serious, and this applies especially to the cases in which adipose tissue forms between the muscular bundles. The space occupied by the fat must be obtained at the expense of the proper muscular substance, and the question arises whether the atrophy of the muscle is the primary condition or the fatty infil- tration. We are to take into consideration the fact that a fatty infiltration of an exactly similar character occurs, as we have already seen, in voluntary muscle, and is there associated with loss of function of the muscle. The muscle may have lost its function by fixation of the joints -which it has to move, or by reason of pai-alysis of a nervous origin. In either case the loss of function is the primary condition and the fatty infiltration is secondary. And so in the case of the heart, we meet with fatty infiltration in cases where there is no general obesity, often in old debilitated persons, or even in those who have been subject to some emaci- ating disease such as cancer. In that case we may infer that the weakening and atrophy of the muscle has been primary and the infiltration of fat secondary. FATTY DEGENERATION. From our former study of fatty degeneration as a whole, it will be understood that there is here meant an actual transformation of the muscular substance. This condition is of exceedingly frequent occurrence in the heart, especially in its minor degrees. Any dis- ease which causes a serious deterioration of the blood will produce it, and it is seen in its most pronounced form in the various kinds of ansemia, in leuksemia, and in the acute fevers. It is also brought about in a very pronounced form in poisoning by phosphorus and arsenic. In a minor degree it is seen in debilitating diseases, and is often the more immediate cause of death in hypei'trophy of the heart. FATTY DEG-EXEF.ATIOX. 301 It is remarkalile that, though the determining cause is a de- teriorated state of the blood, yet the fatt}^ degeneration frequently shows itself in patches, so that the muscular tissue is seen to he, as it were, flecked with pale spots or streaks. This is best seen on examining the muscular tissue from within, as the endocardium generally produces but little obscuration of these markings, and they are most abundant in the inner layers of the muscular sub- stance. This flecked appearance is not always present, and it would be a mistake to infer the absence of fatty degeneration from its absence. The heart again is generall}- flabb}', friable, and pale in color, but a very flabby heart may be very little fatty, and fatty degeneration may coexist Avith a comparatively firm muscular tissue. Microscopic examination should therefore always be resorted to. Under the microscope in those cases in which the degeneration is in patches, the transparent muscular tissue is seen with a low power to be interrupted by opaque patches, as in Fig. l.'')9. The Fig. 1-59. Fatty degeneration of the heart. The occurrence of the lesion in patches is indicated by the dark appearance of the fibres, X 9*^. general outline of the muscular cylinders is preserved, but thej are evidently replaced by some foreign material. Under a high power, as in Fig. 160, the individual fat-drops become apparent. Pig. IfiO. Fatty degeneration of the heart. A single fibre with oil-drops in it, as seen in the fresh state. X 3511. These fat-granules are frequently seen to be in rows, representing the original muscular fibrillse, and the contractile substance is obviously lost or converted into oil. In minor degrees the de- generation is, as a rule, more uniformly distributed in the muscular 302 DISEASES OF THE ORGAJSTS OF CIECULATION. substance, and we can see that the fat-granules generally appear first in the neighborhood of the nuclei of the muscular fibres, forming elongated collections extending from either pole of the nucleus. It is clear that muscular fibres which have undergone this trans- formation' in its extreme form, are incapable of recovering their original condition. The sarcous substance has undergone trans- formation. It is to be inferred, therefore, that when such a heart recovers there is an absorption of the fat and an actual new forma- tion of muscular tissue. This process must be a comparatively frequent one when we consider how common fatty degeneration is in severe ansemias and in acute fevers. The fatty heart is usually a dilated one, even where there is no dilatation to begin with. On recovery the ventricles will resume their former dimensions. CALCAREOUS INFILTEATION OF THE ilUSCULAR SUBSTANCE OF THE HEART. In this place we have to consider calcareous impregnation of the muscular substance of the heart, which is a somewhat rare occur- rence. But it is necessary, in the first place, to refer to certain other forms of calcareous impregnation in order to clear the ground for that more immediately before us. In connection with pericarditis it is not very uncommon to meet with calcareous in- filtration of old fibrine or dried-in pus which may remain on the surface. Again, where in the pericardium there has been great new formation of dense connective tissue from prolonged pericar- ditis, lime salts may be deposited in the hard tissue. In this wav Calcareous infiltration of the muscular tissue of the heart. The branching muscular cylinders are shown in a petrified condition with transverse fractures. From a case of pyaemia. X 350. we may have the heart almost enclosed in a firm shell. But, further, in the muscular substance, old connective tissue may calcify, or an abscess may dry in and become impregnated with lime salts. In this way we may have stony masses developed in the muscular wall, these being actually in the connective tissue ot the wall. But there is a true calcareous infiltration of the muscular tissue INJURIES AND RUPTUEE OF THE HEART. 303 and although recorded cases are few, the author is able to refer to two cases in which lie has met with it, the condition, however, being somewhat different in each. In the one there were pale patches seen with the naked eye in the muscular substance, some- what like those of fatty degeneration, but larger and situated in the superficial layers just under the pericardium. These patches had, even to the naked eye, a streaked appearance, the streaks following the direction of the muscular fibres and indicating that the condition affected the muscular substance. On cutting into the patches a gritty feeling was experienced, and under the micro- scope the appearances shown in Fig. 161 were seen. The muscular fibres were converted into solid cylinders which had a markedly crystalline appearance. Many of the cylinders were fractured transversely. On adding hydrochloric acid to these patches, there was an abundant evolution of gas and a solution of the lime salts. After the lime salts were dissolved the muscular fibres were restored i,-i,j, iPj^. so far as their outline was con- ^^a!Ss«p<- cerned, but their transverse strise ^s^^^^^f^^^^^^^^^^^ were gone. The case in which -^^^^^^^^^^^^^^^^^^ this occurred Avas one of pyaemia, ^^^^^^^^^^^^^^^^^^S and it is probable that the arteries ^^^^^^^^^^^^^^^^^^^ had been obstructed, causing a i^^^^^^^^^^^^^^^^^^ft was very different. A certain '--'^^.ri.^s.i^Lsiskafcsas^®'^^**'^^" portion of the muscular sub- calcareous infiltration of the muscular stance of the left ventricle was fibre of the heart. Fine granules occupy found of a pale color suggesting the muscular fibres. X 300. fatty degeneration, but the color was continuous, and it was the external layers that were affected, and that mainly towards the apex. On microscopic examination the muscular fibres were found clouded with fine granules not unlike fat-granules (Fig. 162). The granules, however, were dis- solved by hydrochloric acid, but without evolution of gas. Koster has met with a somewhat similar case, and he believes that the salt here is, in part at least, sulphate of lime. In this case the true pathology of the condition was obscure. I]Sr.JUKIBS AND RUPTURE OF THE HEART. Wounds of the heart are not by any means necessarily fatal, although, of course, commonly so. A needle or similar small in- strument may be passed into it without obvious injury. In most cases of penetrating v?ound of the heart there will be fatal hemor- rhage, but such wounds, especially if they do not divide the 304 DISEASES OF THE ORGANS OF CIRCULATIOX. muscular fibres transversely, may heal, and be finally closed by connective tissue. There are even cases in which the point of a knife or a rifle-ball has lodged in the heart and become surrounded by a connective-tissue capsule. Spontaneous rupture of the heart is of very rare occurrence, and the conditions which bring it about are by no means clear. It is natural to suppose that fatty degeneration, especially when asso- ciated with a lesion which increases the blood-pressure in the heart, as, for example, stenosis of the aortic orifice, will be the most frequent cause, but it is by no means fully proved that fatty degeneration is always present. The rupture mostly occurs in the left ventricle, and near the apex, or towards the aortic orifice. There is usually a large escape of blood into the sac of the peri- cardium, and the patient dies rapidly. Rupture of the heart may be the consequence of the bursting of an aneurism of the heart, but, as this subject comes up for consideration afterwards, it Avill not be further dwelt on here. 3rY0CAEDITIS. It is to be understood that here we include inflammations occur- ring in the muscular substance of the heart, although not neces- sarily originating in the muscular tissue proper. It is doubtful whether a true inflammation of the muscular tissue of the heart occurs, a true parenchymatous myocarditis. Eindfleiseh describes a case in which he supposes that this condition was the cause of sudden death. He found the muscular substance of a pale violet color, and with ecchymoses under the pericardium and endocar- dium. Under the microscope the muscular fibres presented a granular appearance, especially around the nuclei. We can well understand that an inflammation affecting the proper muscular fibre will destroy its function, and in the case of the heart cause death almost immediately. The designation interstitial myocar- ditis is applied to infiammations which occur in the muscular substance, but affect the interstitial connective tissue. These in- flammations are mostly secondary, and are chiefly due either to propagation from the endocardium or pericardium, or to septic embolism. In the course of acute endocarditis the inflammation may spread into the muscular substance, causing, it may be, softening of it. This is particularly the case with ulcerative endocarditis, to be afterwards described. In this disease virulent bacteria are present in the endocardium, and these may invade the muscular substance, causing a suppurative inflammation of it, or a kind of abscess. As we shall afterwards see, there may, in ulcerative endocarditis be abscesses in the substance of the heart from another cause. Again, chronic endocarditis not infrequently extends to the mus- cular substance. Like other forms of chronic inflammation, this is associated with great new formation of connective tissue. For MYOCAEDITIS. 305 the most part it is the valvular structures which are involved, and they, as we shall afterwards see, are greatly thickened, but the inflammation frequently extends beyond the immediate valvular structures. This is most frequently seen in the case of the mitral valve. Here, along with thickening of the chordse tendineee, we often see a partial conversion of the musculi papillares into dense fibrous tissue ; in fact, an interstitial inflammation with destruction of the muscular tissue. The muscular substance is not so imme- diately continuous with the aortic valve, but we sometimes see, just beneath the valve, a tendon-like thickening of the endocar- dium with extension to the muscular tissue beneath. But chronic endocarditis sometimes attacks the endocardium at a distance from the valves, and in that case it is very liable to extend to the muscular substance. This form occurs perhaps most frequently towards the . apex of the left ventricle, where a considerable area may be converted into dense connective tissue. By the distention of this altered wall of the heart aneurisms of the heart may take origin. There has recently been described, especially by Fagge and Charlewood Turner, a more independent fibroid myocarditis. This may occur in patches, so that there are tendinous areas in the muscular substance in the midst of which the muscular fibres may be calcareous. But in other cases it is generalized, so that a condition is brought about in which the interstitial connective tissue is greatly increased, and the muscular fibres correspondingly separated from each other, a condition corresponding to cirrhosis of the liver or kidney. In the localized form the cause is prob- ably some interference -with the circulation, perhaps an obstruction of the coronary arteries by atheroma or syphilis. In the more generalized form the cause must be one which affects the whole heart, and as it occiirs mostly in dilated or hypertrophied hearts, the strain or over-distention may have to do with it. The hyper- trophy of the left ventricle in Bright's disease is stated to be associated with this fibroid change, but the author has failed to convince himself that this is the case. It is possible that in some obscure oases of hypertrophy and dilatation of the heart this lesion may be the primary one. Abscess of the heart is a form of inflammation which probably occurs only by the transplantation of septic material in pygemia, ulcerative endocarditis, etc. In about a third of the cases of pyaemia there are abscesses in the heart. In connection with these abscesses, colonies of micrococci are to be found in the midst of the pus in the abscess or in the fine arteries and capil- laries. These metastatic abscesses first appear as small pale yellow spots or streaks which rapidly soften and enlarge. The abscesses contain a brownish material composed of pus and the debris of muscular fibre. They are usually elongated in shape, and, while numerous, are individually of small size. If situated near the surface, they may burst into the pericardium, producing a septic 20 306 DISEASES OF THE ORGANS OF CIRCULATION. pericarditis, but even without actual rupture they may, apparently by irritating material passing from them, give rise to pericarditis. When situated near the internal surface, they may communicate with one of the cavities, and it is said that an aneurism of the heart may occur in this way, and may even lead to rupture of the heart. It will be understood that these abscesses rarely have the oppor- tunity of healing, as the patient dies from the general disease, but it is asserted that survival may occur, and the abscess dry-in to a caseous mass, which may afterwards calcify. ENDOCARDITIS. It will be necessary, in considering the subject of inflammation of the endocardium, to subdivide it. "We shall consider in the first place simple acute endocarditis, then chronic endocarditis, and lastly the special form, ulcerative endocarditis. {a) Simple acute endocarditis is, in the great majority of cases, related to acute rheumatism, and, according to Bamberger, it occurs in twenty per cent, of the cases of that disease. Whatever view we iake of the origin and nature of acute articular rheuma- tism, it must be admitted that in it the blood is in some way altered. The blood is in itself of an unusually irritating nature, or else it carries an irritant. The occurrence of acute inflam- mations in several joints often removed considerably from one another, and the frequent supervention of inflammation in the pericardium and endocardium, are sufficient evidence of this. The irritant, whatever be its nature, seems to act specially on connec- tive-tissue membranes, and on such as are exposed to friction of their surfaces. It afi:ects the joints where the synovial membranes lie against each other, and in the movements of the joints are moved on one another. It attacks the pericardium where the movements of the heart cause continuous rubbing, and when it attacks the endocardium it aftects exactly the localities where the surfaces come in contact. It is as if in addition to the irritant in the blood, the mechanical irritation of friction were necessary to the occurrence of inflammation, and it may be added that in the adult the inflammation is almost limited to the valves of the left side of the heart, where the higher tension of the blood and greater force of the heart make the mechanical force of friction greater than on the right side. We shall see afterwards how this fact bears on the localization of the endocarditis. The most characteristic effects produced in acute endocarditis are the so-called warty vegetations, which are irregular projections from the surface of the endocardium, generally of small size and somewhat shaggy in appearance. On their first occurrence these are limited to the parts of the valves which come against each other in the closure of the valves, and this localization continues more or less throughout. It is therefore important to know what ENDOCARDITIS. 307 are the lines of contact in the aortic and mitral valves, because it is there chiefly that we are to look for these endocarditic vegeta- tions. "When after removal of the heart a stream of water is sent into the aorta cut transversely a short distance above the valve, we can look down on the valve closed by the force of the water. It will then be seen that the curtains are not in contact by their margins, but that the line of contact is slightly removed from their edges, and a certain portion of the valve floats free in the water, taking no direct part in the closure of the orifice. The line of contact is nearest the edge of the curtain at the middle of each segment or the corpus Arantii, and forms on either side of this a curved line with the convexity downwards. Between the line of contact and the edge of the curtain the valve is often perforated, and it may even, as we have seen before (p. 291, Fig. 156), be partially re- solved into tendinous cords, without interfering with the closure of the valve. It is by the modification of this portion that we may have the aortic valve showing approaches to the construction of a cuspid valve, as seen in considering malformations of the heart. In the mitral valve the line of contact is also removed from the edges of the curtains. In the case of the aortic valve the line of contact is of course on the ventricular side of the curtains, but in the mitral it is on the auricular side, and in order to see the vege- tation in acute endocarditis it is usually necessary to examine the orifice by looking in from the auricle. Acute endocarditis of the mitral often escapes notice from this not being done. In acute endocarditis the warty vegetations frequently demarcate very accurately the lines of contact of the aortic and mitral valves, and the appearances produced in the former case are indicated in Fig. 163. When the inflammation extends to the valves of the Pig. 163. The aortie yalve in acute endocarditis. The warty vegetations, occupying the line of contact, are shown. right side, the same principles apply. In the case of the pul- monary valve the vegetations appear along the line of contact on the ventricular aspect of the curtains, and in the tricuspid] they are to be seen by looking down through the auricle. 308 DISEASES OF THE ORGANS OF CIBCULATION. We now turn to the consideration of the actual changes and the structure of these warty vegetations. The inflammation ati'ecting the connective tissue of the valve leads to formation of round cells or granulation tissue. The structures by this change are increased in bulk and rendered more friable, and in this waj' irregular pro- jections are produced. But the warty projections are not formed entirely or even chiefly by the granulation tissue. The blood de- posits fibrine on the inflamed irregular surface, and this covers up the granulation tissue and forms the principal part of the warty vegetations. Several authors have described micrococci as oc- curring in these vegetations, chiefly Klebs, Koster, and Osier, and some are inclined to associate these organisms with the essential pathology of acute rheumatism. But these micrococci are not of the virulent sort found in ulcerative endocarditis, and they are probably of subordinate importance. The occurrence of these changes in the tissue renders it unduly brittle, and it is not surprising to And that bits of the vegetations are frequently broken off and carried by the arteries to distant parts, to produce embolism there. These broken-off pieces are mostly small, and, beyond the ordinary phenomena of embolism in small arteries and capillaries, they do not by their own nature produce much disturbance, in this respect contrasting with the emboli of ulcerative endocarditis. There is not usually any serious loss of substance of the valvular structures, but the softening of the tissue not uncommonly leads to the formation of valvular aneurisms, which we shall consider more fully further on. (b) Chronic endocarditis commonly follows on the acute form, and, like it, is related to acute rheumatism. It appears as if the irritation were prolonged in a less intense form, and the changes in the valvular structures extend beyond the localities which we have seen to be mainly affected in acute endocarditis. In the chronic form there is great new formation of connective tissue. The granulation tissue of the acute stage develops into connective tissue, and the process extends slowly to the remaining structures of the valves. In this way arise great thickenings of the valves (Fig. 164), and, as the connective tissue is of that dense nature common in chronic inflammations, the thickened valvular struct- ures are often exceedingly rigid. The new-formed tissue also contracts, and in this way we may have great retractions of the valves leading to serious deformities, as we shall see in studying valvular diseases. Again, it frequently happens that two opposed inflamed surfaces coalesce, and we may have still further deformity from this. We have already seen that the inflammation may ex- tend from the endocardium to the muscular substance, leading to cicatricial transformation of it. In the great majority of cases, the endocarditis is limited to, or has its centre in, the valvular structures, but it sometimes happens that in other parts of the heart an apparently independent endo- carditis is set up. This may be along with valvular endocarditis. •ENDOCARDITIS. 309 but separated from it by sound tissue, or it may be without any valvular lesion. We may find an isolated patch of thickening on the surface of the left ventricle, and we have already seen that the disease may penetrate into the muscular substance. The thickened and rigid connective tissue frequently becomes the seat of secondary changes. Fafty degeneration may occur. Fig. 104. Great thickening of the ohordce tendinecc of the mitral valve, the result of chronic endocarditis. But this is much less frequent than calcareous impregnation, which may be taken as evidence that the hard, dense, cicatricial connective tissue has, to a great extent, lost its vitality. This condition is of such frequent occurrence that it may be regarded as the normal termination of chronic endocarditis. It sometimes occurs with a very moderate degree of thickening, and its extent and the date of its occurrence are doubtless determined by individual peculiarities. It may occur in the form of a moderate calcification in the deeper parts of the thickened tissue, or the lime salts may be deposited in .a more bulky form, so as to give the feeling of considerable stony masses. This occurrence is often of serious import. The valvular structures are rendered still more rigid, and there enters the new element of brittleness. The calcified portion of the valve is exposed very often to mechanical violence in the closure of the valve, and it is common to find that the valve has been broken and a piece of calcareous matter carried off. So far as the valve is con- cerned, this is not usually very serious, but as the piece carried oif is usually of some size, the resulting embolism is frequently of great consequence. Embolism of the cerebral arteries leading to extensive softening is much more frequent in chronic than in acute endocarditis, and probably the same applies to aneurisms of the larger cerebral arteries, which, as we shall afterwards see, may have their origin in embolism. Embolism of the spleen and kid- neys is also a frequent result. The rough surface left by the breaking-off of the calcareous piece gets coated with fibrine, and 310 DISEASES OF THE ORGANS OF CIRCULATION. here again it is said that micro-organisms may be present. The fibrine may, by getting detached, form a fresh source of embolism. Besides the form of chronic endocarditis hitherto considered, which is the most frequent and most iinportant in its results, there is a form which deserves some notice. This form is closely allied to the disease of arteries commonly designated atheroma, and it occurs most frequently in the aortic valve, being here continuous with atheroma of that vessel. In its causation, therefore, it has nothing to do with rheumatism, but is rather related to the degen- erative tendencies of old age. It produces thickenings and indu- rations of the endocardium, with fatty and calcareous changes just as in ordinary endocarditis, but the processes are more chronic, and produce less considerable deformity of the valvular structures, although from calcareous deposition there may be great rigidity. Besides this, and still more removed from inflammatory pro- cesses, we sometimes have simply opaque patches on the valves with very little thickening. In this case there is little more than a fatty degeneration of the endocardium. Such patches are not uncommon on the mitral valve, and are often erroneously regarded as due to endocarditis. " (c) Ulcerative endocarditis, also called malignant and diph- theritic endocarditis, is regarded by some as merely a form of acute endocarditis, but it presents such diflerences that it seems necessary to place it in a class by itself The special features in the disease are the activity of the destructive process in the heart, its connection with the existence of micrococci, and the virulence of the metastatic processes when emboli are carried to distant parts. In its local manifestations this form presents some resemblance to simple acute endocarditis. The disease affects, usually, the val- vular structures, and produces an enlargement and roughening of them. But there is not the same localization along the lines of contact, the process generally developing in a defined area, and sometimes removed from the valve. Again, the disease, as the name implies, is a much more destructive one. the parts concerned breaking down more readily. In this way perforation or aneurism of the valve may occur. Sometimes an actual suppuration mani- fests itself in the valvular structures, but the frequent passage of the blood prevents any considerable accumulation of pus. The ulceration sometimes passes to the muscular wall of the heart, especially when the patch of ulceration is away from the valves. The destructive process spreads rapidly in the myocardium, and a distinct abscess may be the result. In this way also an acute aneurism of the heart may supervene. In their more intimate characters, also, the conditions in ulcer- ative endocarditis differ from those in the ordinary simple form. As the accompanying figure shows, there is a very marked infiltra- tion of the valvular structures with round cells, almost a suppur- ative condition. This is immediately overlaid by a fibrinous coagulum, as in the case of simple endocarditis, but mixed with ENDOCARDITIS. 311 the fibrine there are colonies of micrococci which give quite a striking character to the layer. The appearances in distant parts are evidence that pieces are frequently carried ofl:' from the valves, Fig. 165. f-. Portion of valve in ulcerative endocarditis, u, fibrine with colonies of micrococci j the colonies are indicated by the roundish clumps; i, endocardium becoming raised by inflam- matory infiltration; e, elastic layer of endocardium ; c, round cells infiltrating endocardium, at d, passing into superficial layer of fibrine and micrococci. X 22. and looking to the soft character of the superficial parts we are not surprised at the occurrence of multiple embolism. Perhaps the most striking feature in this disease is the occurrence of metastatic abscesses in distant parts. These are found in the heart itself, in the spleen, in the kidneys, in the skin, etc. They are everywhere of small size, and usually in large numbers. These abscesses are obviously related to emboli carried ofi" from the endo- cardial lesion, and lodged in the finer arteries or capillaries. The accompanying figure represents a small artery in the midst of an incipient abscess in the kidney. It is seen that its calibre is plugged by a material in which are occasional masses of micro- cocci. At the distal part the wall of the artery is obscure, appar- ently from necrosis, and the vessel is buried in an enormous aggregation of inflammation cells. The peculiar virulence of this process is surely to be associated with the presence of the micro- cocci, yet it seems to be not the micrococci themselves, but rather the chemical products evolved by them, which set up the intense inflammation. For, in the illustration given, the micrococci are confined to the calibre of the artery, yet there is necrosis of the wall, and an intense inflammation around. Then, again, the micrococci are frequent in the capillaries and Malpighian vessels, but not generally with obvious inflammation; apparently they are in that case of recent development, possibly to some extent post- mortem, and their products have not had time to produce inflam- mation. A very important question remains for consideration, namely, the origin of the micrococci which give such special characters to 312 DISEASES OF THE ORGAjSTS OF CIBCULATIOX the disease. The disease has been observed to occur in the course of a number of acute febrile affections. It is met with in pyaemia, Fig. 166. From the kidney in ulcerative endocarditis. An artery is shown, plugged with a dark material containing micrococci. Around these are myriads of leucocytes which are infil- trating the necrosed wall of the vessel and the kidney tissue around. X 90. puerperal fever, acute rheumatism, smallpox, etc., and Osier has recently pointed out that in a large proportion of cases acute pneu- monia has been the primary disease. There are, however, cases in which no definite connection with any other disease can be traced. In the case of pyaemia and puerperal fever the source of the micro-organisms is not far to seek. For the rest we are hardly warranted in going further than merely calling attention to the occasional association of this apparently septic disease with these specific febrile conditions. It may be added that the micrococci removed from the valvular lesion soon after death have been found capaible of propagation in the tissues of living animals, where they produce intense inflammation. Inoculated into the cornea of a rabbit they produced panophthalmitis with rapid growth of the organism. "We have seen that the micrococci present, locally, an intensely irritating action, and that necrosis of the tissue attacked is a com- PERJCARDITIS. 313 mon result. It is probable that they also produce changes in the constitution of the blood. Patients afl'ected with this disease fre- quently present, like those in pyfemia, a yellow color of the skin appi^oaching to that of jaundice. The probable explanation of this is, that the blood-corpuscles undergo solution, and the coloring matter stains the skin. But, besides that, we often have little eechymoses of the skin, and small hemorrhages in the pia mater, and even in the brain substance. These have been found asso- ciated with the presence of colonies of micrococci in the capillaries, and are to be ascribed to the action of these in weakening the wall, and allowing escape of blood. PEEICAEDITIS. The pericardium is comparable in its anatomical and path- ological relations to the serous sacs, and, to a certain extent, to the synovial. The pleura, peritoneum, and pericardium are to be re- garded, as we previously found in studying oedema and dropsy, as large lymphatic spaces. These sacs are composed of connective tissue, and lined with a single layer of flat endothelium. By means of numerous stomata they are in communication with the lymphatic vessels, and to some extent with one another. The pericardium is in less direct communication with the pleura and peritoneum than these are with each other, but by circuitous routes there is some communication, especially with the pleura. It is to be remembered also that through each serous cavity there is a certain circulation of serous fluid. This fluid does not accumulate in the sac, because it is carried off as quickly as it is transuded from the vessels, but if the transudation increases greatly there may be an accumulation and consequent dropsy. (a) Acute Pericarditis. — In considering the causes of this disease it is of some consequence to note that the inflammation usually affects the whole surface at once. This seems to indicate that an irritant has found admission to the pericardial sac, and bjj^ the motions of the heart and the natural currents of the fluid in the sac, has been carried hither and thither throughout it. There are many cases in which the tubercular virus is the irritant; we find tubercles mixed up with the inflammatory products. The appearances in this case, however, are so peculiar, and the course of the disease differs to such an extent from that in ordinary cases that it will be proper afterwards to refer more particularly to tubercular pericarditis. The great majority of cases of pericarditis are associated with acute rheumatism. It is to be presumed that the irritant here is the same as that which produces the acute in- flammation of the joints of the endocardium. The irritant circu- lates in the blood, but we do not know its nature and form, nor why it settles in the pericardium and synovial sacs. The irritant, whatever it may be, having been conveyed to the sac by the blood 314 DISEASES OF THE ORGANS OF CIRCULATION. is carried throughout the latter, and acts on its whole surface. There are some cases in which the disease appears t6 be of spon- taneous origin ; it is ascribed to cold. It is altogethei obscure in what way such inflammations are brought about. We have now to consider the phenomena which manifest them- selves at the onset of an acute pericarditis. We may presume that the irritant induces the changes in the vessels which have been described in treating of inflammation in general, but opportunities are wanting for observing the consequent redness, as patients survive this early stage. Exudation from the vessels soon follows, and serous fluid begins to accumulate in the sac. As the inflam- mation afiects the surface of the sac, the endothelial lining is very directly involved. The flat endothelial cells are to a considerable extent shed, being apparently killed by the irritant, but they may also be found showing signs of germination. The exudation con- sists primarily of exuded liquor sanguinis with contractile cells, but soon fibrine is deposited on the inflamed surface. The de- tachment of the endothelium seems to be the circumstance which determines the coagulation, on principles already explained. The deposition of fibrine occurs on both visceral and parietal layers of the sac, but it is usually thickest on the visceral surface, where it may present shaggy masses on the surface of the heart. It is whitish in color, and of soft, almost gelatinous consistence. The fibrinous layers on the opposed surfaces of the pericardium are usually separated by serous fiuid which occupies the sac, but an appearance is often presented which suggests the application and withdrawal of the layers while still in a soft plastic condition. This appearance is variously described as the honeycomb or pine-apple condition, and it has been aptly compared to that presented when two pieces of bread thickly buttered are stuck loosely together and then separated. This honeycomb appearance, it will be understood, is most markedly present on those parts of the peri- cardium where the heart in its movement comes most frequently against the parietes. It will be most extensive and characteristic when there is little serous exudation, and may be taken roughly as an indication of the extent to which the soft fibrine of the op- posite layers has been able to come in contact. The exuded fibrine has the usual characters, as seen under the microscope, forming a fine reticulum ; and in its meshes are leuco- cytes, and sometimes red corpuscles, whose origin we have already considered in studying infiammation in general. If the inflammation has been slight and transient, there may be little beyond a small serous and fibrinous exudation, which is gradually absorbed. But as a general rule further changes de- velop, and these are mainly in the connective tissue of the peri- cardial sac. This shows evidence of inflammation in the presence of innumerable cells, so that by degrees it is converted into what is equivalent to granulation tissue. This inflammatory transforma- tion does not confine itself to the superficial layers of the sac, but, according to the intensity of the irritation, penetrates more and PERICARDITIS. 315 more deeply, even extending frequently to the interstitial connective tissue in the muscular substance of the heart. A layer of granula- tions thus forms beneath the fibrinous exudation, and like other such layers, it is abundantly supplied by thin-walled bloodvessels. The formation of this granulation tissue implies here, as elsewhere, that the acuteness of the inflammation has somewhat subsided, or at least that a considerable interval has elapsed since its onset. The layer of granulations has the general tendencies as well as the structure of granulation tissue elsewhere, it tends to develop into connective tissue as soon as the inflammatory irritation becomes sufllciently mild. "With the subsidence of the inflammation there will be a reduction of the serous exudation. The fibrine is also disposed of, partly undergoing fatty degeneration and so becoming absorbed, and partly eaten into from beneath by the granulation tissue. The result of this is that the granulations are, as it were, laid bare, and a vascular layer occupies the place of the former fibrinous deposit. Looking to this substitution of the fibrinous layer by the vas- cular granulations, it is easy to understand how the inference was formerly drawn that an actual transformation occurs. The fibrine was regarded as plastic lymph which had the power of developing into the vascular tissue, first granulations and then fibrous tissue. The soft fibrine is still sometimes called soft lymph, and the name is even applied to shreds of connective tissue which have been formed from the granulations. With the absorption of the exudation the two layers of the peri- cardium come in contact, and a coalescence of the granulating surfaces, more or less complete, occurs. The vessels intei'com- municate, and the two layers so far as they are in contact become virtually one. As the granulation tissue passes on in its develop- ment into connective tissue the pericardial sac undergoes partial or complete obliteration, the uniting agent being vascular con- nective tissue. The connection will at first be delicate, and may be torn through, but as time goes on it gets firmer, and a condi- tion results in which the two layers are absolutely inseparable. Under certain circumstances the coalescence of the two layers is not complete, and there is only a partial adhesion ; in that case the adhesions are sometimes greatly stretched by the movements of the heart so that tags or ligaments may unite the surface of the heart to the peripheral layer. This, which may be regarded as the normal course of pericar- ditis, is sometimes departed from, chiefly when the inflammation remains too intense to allow of the formation of proper connective tissue. Instead of progressing in this direction, suppuration oc- curs, and the serous exudation in the pericardium gives place to pus. The inflammation in that case is usually very prolonged, and even when it subsides there are obstacles to the adhesion of the layers. On the subsidence of the inflammation the pus dries in by the absorption of its fluid. The pus-corpuscles undergo fatty degeneration and die, but the surface not being well adapted for 316 DISEASES OF THE ORGANS OF CIRCULATION. absorption, the debris remains as dead matter. In this way caseous material is produced, which subsequently gets infiltrated with lime salts. At first the lime forms a pultaceous layer on the surface of the heart, but it may afterwards become consolidated so as to form calcareous plates in the midst of thick adhesions. It is to be added that septic inflammations, such as those which occur in jDysemia when an abscess in the substance of the heart ex- tends to the surface and bursts into the pericardium or gives off septic organisms, or in the rarer case of perforation of an ulcer of the stomach or oesophagus into the pericardium, are purulent from the outset. The septic irritant acts so intense!}' that leucocytes are at once exuded in such numbers as to give a purulent character to the exudation. In considering hypertrophy of the heart in a previous page, it was pointed out that this condition may be caused by complete synechia of the pericardium, and an endeavor was made to explain the mode of its production. It may here be stated that hyper- trophy may occur even in the stage of pericarditis associated with fibrinous and serous exudation, but these conditions must have persisted long in order to induce it; the mode in which they bring it about has been already explained. It should be borne in mind, however, that, as pericarditis is often associated with endocarditis, we may have hypertrophy from valvular disease associated with adherent pericardium, and it may be difiicult sometimes to assign the exact proportion of one or other agent in bringing about the I'esult. Tubercular pericarditis has commonly a subacute or chronic course. It is very often associated with tuberculosis of the pleura, and the conditions in that sac have similar characters. Occasion- ally we meet with an acute fibrinous pericarditis in which, when we remove the fibrine, numerous small white fresh tubercles are to be seen on the pericardium. More frequently, however, the two layers of the pericardium are firmly united by connective tissue, and it is impossible to separate them. In the 'midst of the thickened layers are to be seen yellow caseous masses, sometimes of considerable size. These represent old tubercles, and the whole process is a more or less chronic one, even from the outset. Under the microscope there will be found large masses having the indefi- nite characters of caseous necrosis with occasional fresh tubercles, in the midst of tissue which presents in some parts evidences of recent inflammation and in others merely dense connective tissue. White spots, milk spots, or soldier's spots, on the pericardium. — These are very common pathological conditions and warrant a passing notice. They occur in about half the cases examined post- mortem, and their frequency seems nearly in direct proportion to age. They are in the form of well-defined, whitish, opaque areas on the surface of the heart, of very various size, sometimes very small, at other times so large as almost to cover the anterior sur- ANEURISMS OF THE HEART AND VALVES. 317 face. Their edges are usually abrupt and well-deiined, but they may merge gradually in the pericardium. They have often a bril- liant white tendinous appearance, but may be more dull. They are most frequently situated on the anterior surface of the right ventricle, and next on that of the left ventricle, especially near the apex. They are also met with on the posterior surface, especially near the base of the heart, and on the intra-pericardial portions of the great vessels. They are more uncommon on the parietal layer of the sac. These spots actually consist in a thickening of the pericardium, presenting merely dense connective tissue covered with endothelium (see Fig. 167). The thickening is due to a chronic irritation, and Fig. 167. Soldier's spot on pericardium, b, muscular wall of heart; «, pericardium; c, thickeniug so as to form spot. X 25. the condition is really a chronic pericarditis. The cause of the ir- ritation is not at first very clear. We have here a circumscribed inflammation afllecting by preference certain districts, and the cause must be a local one. It seems to be due to the irritation resulting from the projection of the heart against its surroundings. The commonest seat is where the anterior surface of the right ventricle comes against the sternum at the place where the edges of the lungs turn aside and expose the pericardium. The sternum is less yielding than most surrounding parts, and so the irritation is greater here. The spot where the left ventricle near the apex strikes against the fifth rib, is the next most frequent site. ANEURISMS OF THE HEART AND VALVES. Although these aneurisms are not usually of independent origin or significance, we give them here a special treatment because of their frequency and importance. By ANEURISMS OP THE HEART are meant aneurisms which, in the form of sacs or diverticula, communicate with one of the cavities of the heart. These aneurisms are almost confined to the left ventricle, and they may be divided into two forms. In one form the aneurism projects out from the heart, so as to be visible externally as a protrusion ; in the other form the aneurism burrows 318 DISEASES OF THE ORGANS OF CIECUL ATION. in the wall of the heart, and is not visible externally. The first form usually has its seat at the apex or the base, and in the latter case it may project up between the great vessels. These aneurisms mostly arise as a consequence of chronic endocarditis, or chronic myocarditis. The latter, especially when it produces a localized fibroid condition, or cirrhosis of the muscular wall, may allow of partial dilatation in the form of a pouch. In the second form, the dimensions and outline of the aneurism may be very complicated. The blood, getting into the muscular substance, may dissect a path for itself for a considerable distance from the original aperture. In this way it may almost form a girdle round the heart. Or it may undermine the pericardium, dissecting it largely ii'om the sur- face of the heart, so as to form a kind of blood-filled sac around the heart. For the most part these aneurisms originate in soften- ing of the endocardium, admitting of penetration of the blood into the muscular substance. It need hardly be added that, in both forms, rupture of the aneurism is liable to occur, usually into the sac of the pericardium, and with fatal results. Aneurism of the valves is the condition in which a pouch exists, projecting from a valve and with a narrow neck. This form of aneurism results from acute endocarditis, either simple or ulcerative. "With the aid of the accompanying diagram, the mode Pig. 168. Diagram of mode of formation of aneurism of aortic valve. The curtain (o) formed of two layers. At b, its outer layer roughened and softened. At c, the aneurism, which has burst at (Z, so as to perforate the valve. of formation of the aneurism may be illustrated in the case of the aortic valve, which is its most frequent seat. The semilunar curtains which form the valve are each composed of a double fold of endocardium, as represented at a. From what has already been stated, it will be known that in acute endocarditis it is the ven- tricular layer which is principally involved along the line of contact, as indicated at h. The aortic layer is usually smooth and unaltered to the naked eye. At the aflected part of the ventricular layer the tissue is softened, and during the closure of the valve, the single aortic_ layer may be unable to support the full pressure of the blood. In this way it may be pushed towards the ventricle, carrying before it the softened ventricular layer, as at c. It will be apparent that, in the case of the aortic valve, the aneurism will always pro- ject into the ventricle. In the case of the mitral valve, on the VALVULAR DISEASE OF THE HEART. 819 other hand, the softened layer is on the auricular surface of the valve, and the pressure of the blood during closure of the valve will he exercised towards the auricle, and the aneurism consequently projects towards that cavity. As the aneurism owes its origin to acute endocarditis, its surface is usually covered with vegetations, which are often very abundant, and may so conceal the aneurism as to lead to its being overlooked. The aneurism, again, may rupture, and so produce a perforation of the valve. It is sometimes as if the bottom had been blown out of the aneurism and a short tube left, surrounded by shaggy vege- tations (as at d in figure). Even in that case, however, if the neck of the aneurism be examined, it is often found that the endocar- dium, as it passes into it, is smooth and unaltered. VALVULAR DISEASE OP THE HEAET. In studying endocarditis, we have seen that the valves are fre- quently altered in their structure; we have now to consider these alterations more specifically, and their effects on the heart and cir- culation. It is not usual to designate anything as valvular disease unless it interferes with the function of a valve or orifice. The function of a A^alve is to close an orifice under certain circum- stances, and we speak of valvular disease when the alterations are such as either to obstruct the orifice or to interfere with its closure by the valve. Hence valvular lesions may be divided into two kinds, namely, narrowing or stenosis of the orifice, and insuffi- ciency of the valve. In referring to these same lesions, as they affect the current of blood in the heart, we speak of obstruction of an orifice and of regurgitation through the orifice or incompetency of the valve. Of course, it would be a very incorrect use of language to speak of obstruction of a valve, or insufficiency of an orifice. Valvular disease occurs much more frequently in the valves of the left side than in those of the right, and hence we have chiefly to do with the mitral and aortic valves. We have already seen that in the fcetus it is the valves of the right side which are most frequently affected, and we have connected this with the fact that these valves are more liable to variations of pressure in the foetus than in the adult. Insufficiency or Incompetency op the Mitral Valve. — This is a condition in which, during the systole of the heart, some portion of the blood passes back into the left auricle instead of the whole being forced into the aorta. The actual physical conditions are somewhat various, but most of them m-e related to chronic endocarditis. The commonest is that in which the valvular structures are thickened by the new- formed connective tissue and retracted and shortened from its con- traction. This applies to the curtains themselves, but still more 320 DISEASES OF THE ORGANS OF CIRCULATION. to the chordffi tendiness, which become thickened and shortened, and frequently grow together, so that they hold the curtains rigidly drawn down and do not allow them to go together during the sys- tole of the ventricle (see Fig. 164, p. 309). Again, much more rarely, in acute endocarditis, the valve may be perforated, as in the case of valvular aneurism, or the chordse tendinese torn so as to allow a portion of the valve to flap upwards through the orifice. Lastly, without much alteration of the curtains, there may be a relative insufficiency of the valve. That is to say, the cavity of the ventricles sometimes enlarges greatly, and produces enlargement of the orifice, which the valve is no longer able to cover. There are some cases of permanent hypertrophy and dilatation of the left' ventricle where this occurs, but it may be met with where the dilatation is temporary, as in the flabby fatty heart of typhus fever and anaemia. It is not to be supposed that the so-called ansemic murmurs are usually due to this cause, but there is in some cases an actual mitral regurgitation. When recovery occurs, and the heart resumes its former vigor, the valve will again cover the orifice. We have now to consider what results ensue from insufficient closure of the valve. At each ventricular systole blood regurgi- tates into the left auricle, and the most direct result is over-disten- tion of this auricle occurring at successive intervals. The wall of the auricle is weak, and does not ofier much resistance to the dis- tensile force. There is another result which often follows, appar- ently from the unduly forcible impact of the blood against the endocardium, and the over-stretching of this membrane, namely, a thickening of the endocardium. We may find it generally thickened and opaque, or there may be patches of opacity. But the results do not confine themselves to the auricle — the abnormal blood-pressure is reflected to the pulmonary veins which feed the auricle, and they become distended. The distention is further reflected to the capillaries and the pulmonary arteries, and finally to the right ventricle. The right ventricle is overdistended, and unless it acts more vigorously than usual, so as to empty itself into the pulmonary artery at every systole with greater force, the overfilling is reflected to the systemic venous system. We have already seen, however, that when necessity arises the heart is stimulated to increased action. The rhythmical contrac- tions of the heart are referrible to its intrinsic ganglia, and the heart of a frog will beat for a time when empty of blood. But it beats much more vigorously when full, and the more its cavities are distended, up to a certain point, the more vigorous are its con- tractions. It is as if the stretching of the fibres supplied the reflex stimulus to increased vigor in the contraction of the muscle. In the case we are considering, the increase in the amount and pressure of the blood in the right ventricle, as well as the neces- sities of the pulmonary circulation, act as a spur to more vigorous contraction, and we have already seen that this increased action when prolonged leads to hypertrophy. Hypertrophy ot the right VALVULAB DISEASE OF THE HEART. 321 ventricle is, therefore, a very constant result of the lesion we are considering. Returning now to the left side of the heart, it is clear that, as part of the blood in the left ventricle passes at each systole into the auiicle, too little will go into the aorta, and the systemic cir- culation will be partially starved. But when the right ventricle acts with increased vigor, the blood passes into the left ventricle with increased force and in larger amount than normally. The result will be increased action and consequent hypertrophy of the left ventricle. We can see here again a double action such as we found in the case of the right ventricle. The systemic circulation, being starved, calls for increased supply of blood, and on the other hand the distention of the ventricle induces increase in the force of the contractions. The hypertrophy of the left ventricle is usually small in amount and quite subordinate to that of the right, which with the distention of the left auricle is the most prominent appearance. The heart presents the more globular or quadrilateral shape already referred to as characteristic of hypertrophy of the right ventricle. These changes may completely compensate for the incompetence of the valve, that is to say, the circulation may be restored to its normal efficiency ; but it may not be so, or, even when established, the restored efficiency may be impaired from some further inter- ference with the pulmonary circulation or weakness of the heart. So there is apt, after a time, to be overdistention of the systemic venous circulation, and the train of changes which are usually more fully developed in mitral obstruction, and will be described under that heading. The pulmonary circulation suffers even more than the systemic from any insufficient compensation on the part of the right ventricle. The pulmonary vessels are permanently overdistended, and oedema and hemorrhage are frequent results. The hemorrhage is in the form of slight oozing from the pul- monary capillaries, so that the sputum is streaked with blood. It is not to be confused with that which occurs in consequence of embolism of the pulmonary artery, forming the hemorrhagic infarction, which is of frequent occurrence in disease of the mitral valve, but from a cause to be afterwards considered. Obstruction of the Mitral Orifice. Mitral Stenosis. — This name is applied to the condition in which the mitral orifice is not large enough to allow of the usual quantity of blood passing from the auricle to the ventricle. The normal width of the mitral orifice may be roughly estimated with the fingers ; in the adult it should allow the index and middle fingers to pass freely through as far as the first joint. The contraction may be very slight, or it may be to such an extent that hardly a crow-quill can be admitted into the orifice. In the case of stenosis of the mitral as well as in that of the aortic orifice, the obstruction is usually caused by the curtains of the valves becoming thickened and rigid, and especially by their coalescence. The thickened valves grow 21 322 DISEASES OF THE OEGAXS OF CIEGULATIOX Fig. 169. together by tlieir edges, and so tlie valve is converted into a funnel with its apex turned down into the ventricle. The normal orifice is at the base of the curtains. But when the valves coalesce, the orifice while becoming con- tracted is moved down^vards, and comes to have its site at the apex of the funnel. This will be understood from the accompanying simple dia- gram (Fig. 169), in which black lines represent the orifice and cur- tains in their normal condition dur- ing the diastole of the ventricle, the curtains lying back against the wall of the ventricle, and the orifice at their base. The dotted lines repre- sent the coalesced, funnel-shaped valve ; the contraction of the orifice and its removal downwards being shown. The chordse tendinese are commonlj' thickened and often partly incorporated in the funnel (see Fig. 164, p. 309). On laying open the ventricle, this thick, rigid, funnel-shaped deformity is often strikingly prominent. These con- ditions result from chronic endo- carditis, and it will be readily understood that the rigid valve is frequently incompetent, so that this condition is often combined with the one before. There are also not infrequently changes in the aortic valve. It might be supposed that the vegetations occurring in acute en- docarditis would obstruct the orifice, but although these rough projections undoubtedly interrupt the even fiow of blood, and may produce during life what is technically a murmur of mitral obstruc- tion, yet their actual influence on the function of the orifice must be very slight, and we are not to look for any definite evidences of their influence on the circulation. Obstruction is occasionally produced by thrombi growing on the valve, or having their seat in the auricle and projecting into the orifice. This is a rare cause of obstruction, and a still rarer is the presence of tumors growing in such a way as to obstruct the orifice. We have now to consider the results to the circulation of mitral obstruction. The most direct eflJect will be dilatation of the left auricle, as the blood is, to a certain extent, hindered in its passage into the ventricle. As a consequence, the whole pulmonary vessels will be loaded and the right ventricle distended with the accumu- lated blood. On the principles already laid down there will be increased action and consequent hypertrophy of the right ventricle, and this is commonly more extreme than in mitral insufficiency. Diagram of funnel-shaped deformity of mitral valve. The dotted lines indi- cate the coalesced curtains forming a funnel projecting into the ventricle with a reduced aperture at the apex. VALVULAR DISEASE OF THE HEART. 323 The contraction of the orifice interferes with the passage of blood into the left ventricle, which, in extreme cases, is, as it were, starved of blood. The increased force of the right ventricle may in great part make up for this deficiency, and sometimes there is also aortic insufiiciency, so that the ventricle is fed from the aorta as well. According to these various circumstances will be the state of the left ventricle. It may be actually atrophied and appear as a small appendage to the enlarged right ventricle, or it maj"- be normal in size or even hypertrophied. In any case the hypertrophy of the right ventricle is the predominating condition. The shape of the heart is more quadrilateral, the apex is blunt and formed by the right ventricle. During life, instead of the defined apex beat of the left ventricle, there is the more diffused heaving of the right. Passing from the heart, we have a permanent passive hyperasmia of the pulmonary circulation, with consequent brown induration of the lungs. There Avill also be the tendency to slight hemor- rhages, showing itself in the sputa. (Edema of the lungs readily develops. The dilatation of the right ventricle, especially when followed by thrombosis, also frequently leads to embolism of the pulmonary artery and the hemorrhagic infarction. The hypersemia is reflected to the systemic venous circulation, especially if the dilatation of the right ventricle lead to relative insufiiciency of the tricuspid valve, and we find evidences of passive hypersemia of the liver (nutmeg liver), kidneys and other organs. Not infre- quently serious oedema of the skin and dropsy of the serous cavities develop. Thrombosis in the veins of the legs often complicates the condition, and this again may be a source of pulmonary embolism. Insufficiency of the Aortic Valve. — This is the condition in which, after the completion of the ventricular systole, a portion of the blood regurgitates into the left ventricle through the imper- PiG. 170. Diagram of aortic insufficiency, a, the normal valve closed, o.s seen from above; h, the valve with curtains shortened and leaving a triangular space. fectly closed semilunar valve. This condition is usually brought about by chronic endocarditis. The individual semilunar folds are thickened and shortened, the actual length of free margin being reduced. The consequence is that, during the closure of the valve. 324 DISEASES OF THE ORGANS OF CIECULATION. the edges have not sufficient length to meet perfectly and so a tri- angular aperture is left. This is illustrated diagrammatically in the accompanying figure. The contraction may reach such an extent as to leave only a nodulation on the waM of the aorta in place of the curtains. These changes are very commonly accompanied by adhesion of the adjacent folds of the curtains, and this necessarily causes contraction of the orifice ; indeed, the curtains as such may disappear, leaving only a diaphragm with a permanent aperture in its middle, the condition being similar to that illustrated in Figure 154, p. 288. An unusual cause of aortic insufficiency is perforation of the curtains as a result of acute endocarditis or the bursting of a valvular aneurism. Of course, the perforation of the curtains beyond the line of contact already referred to is not to be mistaken for a pathological perforation. A rare cause of aortic insufficiency is the tearing of one of the curtains. During severe exertion the blood-pressure in the aorta may be so much raised as to rupture a curiain, and such a wound will hardly unite as it Avill be torn aside at each closure. It may be added here that aortic disease is often accompanied by mitral disease, chronic endocarditis, having its oiigin in rheu- matism, attacking both; Chronic endocarditis of the aortic valve again is often covinected, as we have seen, with endarteritis or atheroma of the aorta, and in that case it is not so likely to be associated with mitral disease. It may be interesting here to observe that the origin of the endocarditis has an important bearing on the age at which these valvular lesions occur. Acute rheumatism is a disease of youth and manhood, and most cases of valvular disease take origin in it. Accordingly, diseases of the valves are most common, at least in their inception, between the ages of ten and thirty. But there are some cases of aortic disease which, as we have seen, stand in a diflerent category. Chronic endarteritis or atheroma is a dis- ease mostly of advanced life, and so it is more common in old persons to meet with aortic disease than with mitral. We have now to consider the effect of this insufficiency of the aortic valve on the circulation. In the normal state during the diastole of the ventricle, the blood flows from the auricle into the ventricle. But just at the close of the diastole the auricle con- tracts and forces the blood more vigorously into the ventricle, so as to distend it, and perhaps give it the impulse to contract. "When the ventricle contracts, the blood passes into the aorta, and the wave is propagated forwards, and at the same time partly distends that vessel. At the end of the systole the semilunar valve closes, and on the recoil of the distended aorta the blood is forqed onwards in the systemic arteries. But now, suppose that the semilunar valve does not close completely, then the aorta in its recoil will force blood back into the ventricle as well as foi-ward into the systemic arteries. This extra mass of blood driven with considerable force into the left ventricle Avill overfill it and forcibly digtend it, while the systemic circulation will be proportionately VALVULAR DISEASE OF THE HEART. 325 starved. The left ventricle is called on to make increased exer- tions to get rid of the excess of blood and fulfil the wants of the system, and we may suppose that the stimulus to increased action is afforded by the stretching of the fibres by the excess of blood. The natural result is dilatation and hypertrophy of the left ven- tricle, which may almost completely compensate. In this disease, therefore, the primary and prominent fact is the enlargement of the left ventricle. As previously mentioned, the heart becomes more conical in shape ; the septum takes part in the hypertrophy and bulges into the right ventricle. This may exist to such an extent that the right ventricle is seen on transverse section as a mere crescentic appendage of the left, and there may even be, to some extent, obstruction of the right auriculo-ventricular orifice by the bulging of the septum, inducing general venous hyperaemia. As the ventricle propels a much larger amount of blood into the aorta, and with abnormal force, there is sometimes a resulting dilatation of the arch and great vessels. In this way there may even be an actual aneurism of the arch. It is to be added that, as hypertrophy of the left ventricle is associated with dilatation of that cavity, there is frequently a con- sequent widening of the mitral orifice. As a result of this, we may have a relative incompetency of the mitral valve, which is incapable of completely covering the dilated orifice. In this way, the consequences already considered of mitral insufficiency may be brought about; but they are usually much less pronounced, and of late occurrence. It is to be remembered, also, that mitral disease often coexists with aoi'tic. Obstruction of the Aortic Orifice. Aortic Stenosis. — In this lesion the passage of blood from the left ventricle into the aorta is interfered with. It is, in the great majority of cases, caused bj'' chronic endocarditis. The conditions already described as leading to insufiiciency of the valve by causing rigidity of the curtains, mostly produce obstruction of the orifice, and this is all the more marked when calcareous infiltration ensues. Where the valve is, in the way already mentioned, converted into a rigid diaphragm, then there must be great obstruction of the orifice as well as insuf- ficiency of the valve. These two forms of lesion are, therefore, usually found associated. In acute endocarditis the roughening of the curtains may to some extent obstruct the flow of blood, but the interference is trivial, and will hardly lead to any of the secondary results of aortic stenosis. The obstruction at the orifice prevents the blood getting away fully during the systole of the ventricle, and there comes to be an overfilling of the ventricle. The ventricle, as in the previous case, is stimulated to increased exertion, and the distensile force of the blood may again be supposed to afford the necessary stimulus. Increased action induces hypertrophy as before, and so here, as in the previous case, the primary phenomenon is hypertrophy of the left ventricle. This may completely compensate for the obstruc- 326 DISEASES OF THE ORGAXS OF CIRCDLATIOX. tion, and pei'sons may go about comparatively well with an ob- structed orifice and enlarged left ventricle. But this is not so likely as in the previous case, and any extra need for exertion on the part of the heart, or weakness of its muscle, may lead to in- complete compensation. In such a case the ventricle will get abnormally dilated, and the auricle will not be able to empty itself fully into the dilated ventricle. The pulmonary circulation will become engorged and the right ventricle overloaded, and so we may have all the evil consequences of mitral disease. It will be observed, however, that, as the left ventricle is much more capable of undertaking additional work than the right, it succeeds much more frequently in bringing about a complete compensation. The hypertrophied left ventricle having to dispose of an increased mass of blood, generally does so slowly, and the pulse is consequently slow and regular. It will have become apparent that in many cases aortic disease is associated with mitral, and that there is frequently combination and complication of the resulting changes in the heart and circulation-. Valvular Disease op the Eight Heart. — We have already seen that, except in the fcetus, this form of disease is uncommon. In cases of acute or chronic endocarditis with well-marked lesions on the left side, however, there are very often slight indications of inflammation in the valves of the right heart. There is one condition of the tricuspid valve which, although secondary, is often of considerable consequence on account of the effects to which it leads, and that is relative insufficiency op THE TRICUSPID VALVE. We have seen that in mitral disease the right ventricle usually dilates and hypertrophies, and with this change in the ventricle the orifice widens. The valve may thus be unable to cover the enlarged orifice, and become insufficient. In other forms of dilatation and hypertrophy of the left ventricle as in that due to obstruction to the pulmonary circulation, the same thing may occur. The tricuspid orifice normally admits readily three fingers up to the first joints, and when enlarged it is not uncommon to meet with cases in which it admits four, five, six, or even seven fingers. If the valve is thus incompetent to close the enlarged orifice the blood will, during the systole of the ventricle, regurgitate into the auricle. The wave will be propa- gated into the veins of the neck, and there will probably be an aggravation of existing congestion of the systemic veins. It need only be added that, if chronic endocarditis attacks the tricuspid or pulmonary valves, it may produce results similar to those effected in the mitral and aortic. The tissue here, however, is less substantial to begin with, and the inflammation is usually much less intense, and so the changes are rarely of any great consequence. COAGULA IN THE HEART. 327 COAGULA IN THE HEART. Simple Clots. — It is very common to meet with clots in the heart at post-mortem examinations, and very important to dis- tinguish those that are of pathological significance. In a great majority of cases we meet with soft gelatinous clots occupying auricles and ventricles, and sometimes extending from them into the aorta and pulmonary artery. These clots are produced just about the period of death. It cannot be said that they are always in the strictest sense post-mortem, because the fact that they are sometimes decolorized shows that the blood-corpuscles have been in these cases removed from them. Yet they are to all intents and purposes post-mortem. During the last minutes of life the heart may give irregular and imperfect contractions, not sufficient to forward the circulation, but having the effect of churning the blood. Coagula may thus be formed somewhat in the way that the fibrine is separated in whipping blood. In that case the clot is apt to be stringy and slightly opaque in appearance. Again, the absence of the red corpuscles in a clot may be brought about in a different way. ~\An.ien blood is shed it coagulates quickly, and in human blood it is rare for the coagulation to be long enough delayed to allow of the sinking of the corpuscles so as to leave a buffy coat on the surface. In the heart, however, the coagulation, unless it be induced by the churning action just referred to, is delayed, because the tissiie does not immediately lose all vitality. Time is often thus afforded for the sinking of the red corpuscles, and so we may find some parts of the clot deeply red and others colorless or yellow. For practical purposes all this class of coagula may be designated simply clots, the term thrombi being applied to those occurring during life. The clots have more or less the shape of the cavity in which they are found. They sometimes extend into the great vessels, and show a constriction where they have taken the mould of the valve. They adhere very little to the endocardium, although the}' may have a deceptive appearance of adhesion from being entangled among the chordpe tendinepe and musculi papillares. The gelatinous character, transparent appearance, and smooth surface of these clots are other indications. They are also as a rule much more bulky than thrombi. Thrombi are of various kinds and different significance, and it may be said that coagulation of blood within the heart during life is of frequent occurrence. We have already incidentally considered most of these forms of thrombi, and it will be necessary here to do little more than enumerate them. Thrombi are frequently desig- nated vegetations, but it is not advisable to use this word in place of the more accurate one thrombi. We may distinguish three forms of thrombi: warty, globular, and polypoid. Warty thrombi we have already seen to occur in acute endocar- 328 DISEASES OF THE ORGANS OP CIRCULATION. ditis, owing to the coagulation of tlie fibrine on the inflamed and roughened surfaces. G-LOBTJLAE THROMBI have been described in the section on throm- bosis (see page 41) in the first part of this work, and are represented in Fig. 171. It is to be remembered that they are of fi'e<|uent occur- FiG. 171. Globular thrombi near the apex of the left ventricle. Several of these are seen to project from between the musculi papillares. rence in dilated and hypertrophied hearts, and that thej- are prone to soften in the central parts and finally to break down, so that they may give rise to embolism. These thrombi are sometimes very loosely adherent to the endocardium and may be detached bodily and carried into the pulmonary artery or aorta — most fre- quently into the former, as they are more common in the right ventricle and auricle than in the left. The POLYPOID THROMBI are much more uncommon than the other two forms. It sometimes happens that a thrombus is formed on a valve or on the internal surface of the heart and from this point grows out by successive deposition to a considerable size. The author has met with a case in which the left ventricle was filled with massive festoons thus formed, and great hypertrophy and dilatation had occurred. In this case also the coagula had under- gone a partial impregnation with lime. He has also seen a case in which a thromlDus, formed of firm fibrine and attached to the wall of the right auricle, hung free in the auricle and assumed a THE BLOODVESSELS. 329 nearly globular form. It Avas so placed as to hang down into the tricuspid orifice, which it greatly obstructed, like a ball-valve. TUMORS OF THE HEART. Primary tumors are exceedingly rare, but a primary sarcoma of the endocardium has been described, as also primary fibroma, myoma, and lipoma. Secondary tumors are not uncommon, and they are either malignant or infective tumors. Miliary tubercles are sometimes met with in cases of acute general tuberculosis, occupying the endocardium, or the pericardium, or even the muscular substance. Syphilitic gummata are occasionally met with in the muscular substance, and as usual they are accompanied by interstitial infiammation. The gumma has the usual indefinite and varied structure, in the more recent stage softer and more cellular, in the more advanced stage largely composed of dense connective tissue, with probably a caseous centre. There may be a single tumor replacing a portion of the wall, and surrounded by the cicatricial tissue of chronic infiammation, in which the endocardium or the pericardium maybe involved. In the latter case there is adhesion of the two layers of the sac. Or the gummata maj be multiple, in which case there is a more difliused interstitial inflammation. Sarcomas occurring in the neighborhood may spread to the heart, and especially those of the mediastinum, involving first the parietal and then the visceral pericardium. Sometimes also a cancer of the oesophagus extends to the pericardium. Cancers when they become genei'alized very often occur in the heart, in the form of round pale tumors. Of PARASITES, the echiuococcus and the eysticercus cellulose have been found in the heart. B.— THE BLOODVJvSSELS. The bloodvessels are to be regarded as tubes of which the essen- tial constituent is the intima. According to circumstances the intima becomes clothed with external and middle coats, and so we have arteries and veins. We have already seen that, in neaz'ly all new formations, bloodvessels are produced as well as tlie proper tissue, and it is first a tube composed of intima which is formed, or a capillary. This primary vessel is capable of enlargement and farther complication in the way just indicated, so that a transfor- mation of the primary capillaries into arteries and veins may take place. This process of formation of vessels and their further de- velopment according to the requirements of the tissues is an ex- ceedingly common one, and may be regarded as equivalent to that 330 DISEASES OF THE ORGANS OF OIRCULATIOX. which occurs in tlie formation of the tissues during the period of growth of the body as a wliole. A process of a similar nature is sometimes seen when the obstruction of an arterj- causes the cur- rent to be in great part diverted into other channels. We know that in this case the anastomosing vessels enlarge, small arteries becoming converted into large ones, and perhaps even capillaries into arteries. The vascular system is thus an exceedingly plastic one, and possesses great powers of new formation and development according to the needs of the tissues. INPLAMilATION OF THE VESSELS. We have already seen that the bloodvessels bear an important, perhaps an essential, part in the inflammatory process, but apart from this we have to consider inflammations aftecting the tissues composing the walls of the vessels, and some of these also have been already referred to incidentally. Acute Inflammation. — Considei-ing the close analogy between the endocardium and the intima of bloodvessels it might be sup- posed that the latter would be prone to acute inflammation under similar circumstances to the former. But this is not the case, and an acute endarteritis scarcely ever occurs. Sometimes an acute endocarditis affecting the aortic valve extends to the neighboring portions of the aorta, resulting in the formation of iiTegular pro- jections, generally on the surface of a chronic thickening, but even this is rare. The acute inflammations of the vessels are nearly always secondary. A typical instance of acute inflammation is afforded by that which occurs in the veins in pypemia (Phlebitis). The conditions here have been already considered, and we saw that the inflamma- tion depends on the action of a septic irritant. In the metastatic abscesses of pysemia we have also a septic inflammation of the arteries. Vessels which communicate with wounds are liable to inflammations at their mouths, especially when the wounds are septic. The arteries and veins in stumps are thus often inflamed. In all cases of acute inflammation of bloodvessels, thrombi form in them, the blood coagulating on the inflamed surface. But the formation of thrombi may be the primary phenomenon, they by their presence inducing inflammation. This is sometimes because they are septic thrombi, as in the case we have already referred to of suppurative phlebitis in pyemia; but a simple thrombus by its mere presence irritates the wall of the vessel, and induces inflam- mation. This is an essential factor in the organization of the thrombus itself, as we have already seen. Again, inflammation is induced in vessels by injurj' to them. When an artery is ligatured, for instance, the internal and middle coats, as shown in Fig. 172, are torn through, and the result of this injury as well as of the continued action of the ligature is to induce inflammation. IXFLAMMATIOX OF THE VESSELS. 331 The condition of the coats of the inflamed vessel varies consider- abh', according to the nature of the case. In septic inflammations they are infiltrated with pus, softened and opened out, or even necrotic. Where the inflammation is less intense the coats are Fig. 172. l)^-^* -- — Longitudinal section of an artery at seat of ligature. ■', u, apertures in which the silk- ligature was found. The external coat is drawn in at this place, while the middle and in- ternal coats are absent, being absolutely disjoined. These coats are seen above at b and below at c. X 3'>- infiltrated with inflammatory cells, and so thickened and rendered more rigid than normal. In this way a vein may assume the appearance of an artery. If tlie inflammation be prolonged there will be a partial organization of the contained thrombus. A similar new formation of tissue occurs externally, and the thickened vessel is adherent to its sheath, and to parts around. In this way there is often considerable matting of the structures around the veins of the legs which are the seat of thrombosis. In the regular progress of the inflammation, the whole new- formed tissue, including that in the wall of the vessel, and that which replaces the thrombus, develops into connective tissue 332 DISEASES OF THE ORGANS OF CIRCULATION". having the usual tendency to contraction. The common result is that the vessel and thrombus are replaced by a fibrous cord, but sometimes the contraction of the new-formed tissue causes, in the way already described at p. 44, the formation of a cavernous tissue through which the circulation may be restored. CHRONIC EN DARTBlilTIS— ATHEKOilA. These names are applied to a disease of very frequent occurrence in arteries, the nature of which has been differently regarded at different times. Besides the common name atheroma, it is variously designated chronic endarteritis, sclerosis of arteries, etc. According to the former of these names the disease is an inflam- mation of the internal coat, and this view is so far a correct one; but degenerative processes play such an important part in the course of the disease that it would be a mistake to regard it as merely an ordinary chronic inflammation. The fact that the dis- ease is peculiarly one of advanced life is another indication of its degenerative nature, and it may almost be said that a weakness of the wall of the vessel must be regarded as one of the principal agents in the causation of the disease. While there is this predis- position the actual supervention of the disease is apparently caused by mechanical irritation. Its principal seat is the arch of the aorta, and this is doubtless due to the fact that this part is more exposed to the force of the wave of blood during the systole of the heart than any other portion of the arterial system. The disease is fre- quently met with in the arteries of the brain, and here it is more difficult to account for its occurrence on the theory of mechanical irritation, but the atheromatous patch is often situated just at a bifurcation, where, presumably, the vessel-wall is more exposed to the force of the current. Again, it is met with in the pulmonarj^ artery in cases of hypertrophy of the right ventricle, the excessive impulse of the blood from the hypertrophied ventricle apparently determining its occurrence. As we shall see afterwards, syphilis produces a disease of arteries in many ways similar to atheroma, and it is matter of uncertainty how far ordinary atheroma may be due to syphilis. The disease consists in a more or less localized thickening of the internal coat. The thickening is nearly always distinctly limited in area, so that we speak of atheromatous patches. When we examine the aorta in the earlier stages we see elevated areas with tolerably abrupt edges, and usually of a dead- white color as com- pared with the surrounding intima. These patches are hard, and cut like cartilage. They have the appearance at first sight of deposits on the surface of the intima, and so they were long regarded, but on making a section through patch and vessel, it is seen that the intima is continuous with the raised patch. In the arteries of the brain the diseased parts are seen as white opaque patches, and the vessel is more rigid than normal, so that it does CHKONIC EXDARTEEITIS — ATHEROMA. 333 not collapse; the calibre also is diminished by the inward projec- tion of the patch. On cutting into the patch, either in the aorta or cerebral artery, there is often an opaque yellow color revealed in the deeper parts, and this is an indication of fatty degeneration. Very often, too, there is, especially in the aorta, calcareous infiltra- tion of the deeper parts of the patch, but these two conditions will be more fully discussed further on. In considering more particularly the details of the process, it is instructive to examine microscopic sections including the edge of the patch and the neighboring parts of the vessel (see Figs. 173, 174, and 176). In well-preserved recent cases it can be seen that Pig. 173. Atheroma of aorta. The internal coat (a) is seen to be thicltened. In its deeper layers there are darker markings indicating the commencement of fatty degeneration, b, middle, and e, external coat. X --• the endothelium of the intima is continued over the patch, and in nearly all cases there is little difficulty in observing that the patch is really a thickening of the internal coat, as shown in the figures. The thickened intima is composed of a dense connective tissue, which in the early stages contain many round, oval, and stellate cells. In a fully formed patch the structure is often exceedingly indefinite, and there are few cells that are at all prominent even when staining agents are used. The structure is indeed half obsolete, and, as already indicated, fatty degeneration readily occurs. The fatty degeneration begins usually in the deeper layers of the patch, so that on making a section one generally finds in the portion of the patch bordering on the middle coat an opaque yellow streak. (See also Fig. 178.) The fatty degeneration at first affects the cells of the intima, but as time goes on the intercellular substance gives way, and the tissue breaks down so that a cavity containing fatty debris and cholestearine is formed. From the character of this fatty debris the name atheroma is derived, and the cavity thus formed is sometimes called an atheromatous 334 DISEASES OF THE ORGANS OF CIRCULATIOX. ABSCESS. (See Fig. 174.) The tissue superficial to the cavity may ultimately give way, and so expose the cavity, thus forming an ATHEROMATOUS ULCER. The ulcer sometimes presents calcareous masses in its walls, and in any case it may induce the deposition of librine on its surface. The fatty material may, on the other hand, be absorbed without forming an actual ulcer, and in that Pig. 174, Atheroma of femoral artery. The greatly thickened internal coat (a) is shown. In the midst of it, towards the right, are dark masses consisting mainly of fatty debris, and repre- senting the atheromatous abscess. At one part the middle coat (i) is considerably en- croached on from within. X 22. case there will be produced depressions and irregular foldings and puckerings of the internal coat. These depressions and foldings have often a kind of cicatricial appearance. Calcareous infiltration is a frequent result of the disease under consideration. It is generally stated that the calcareous salts are deposited in the fatty degenerated structure. But this is not always the case. The dense tissue of the patch may become infiltrated with lime salts without a preceding fatty degeneration, This is peculiarly the case when the tissue is very hard and dry. We shall see, in studying calcareous infiltration of the middle coat, that some individuals present a very great tendency to the deposi- tion of lime salts in the walls of their arteries, and there are cases of atheroma in which this tendency is very marked, so that with comparatively little atheromatous thickening there may be very extensive calcareous deposition. The peculiar tendency presented in some cases to the deposition of lime salts is a strong indication of the degenerative nature of the process. At first the salts are deposited in fine granules, and in the deeper layers of the patch, but as time goes on these aggregate into consistent masses which, from the lateral extension of the afifected parts, have the form of plates. Thus we have calcareous plates of various forms and sizes, sometimes attaining to a square inch in area. These plates, having abrupt edges, not infrequently tear through the remaining layers of the intima, and present an edge or angle inside the vessel. They may even become to a considerable extent separated, and CHRONIC ENDAETERITIS — ATHEROMA. 335 hang into the calibre attached only by a strip of intima like a hinge. The rough calcareous edge very commonly induces a deposition of librine, and the thrombus thus formed may subse- quently get detached, and form an embolus. The determination of the preponderance of the fatty or calcareous change appears to depend on individual peculiarities. Both forms are very frequent in the aorta. The fatty change preponderates greatly in the cerebral arteries. It is to be noted here that there are some cases in which the atheroma has a much more distinctly inflammatory course than that described above. The thickened intima is infiltrated with round cells, and there is also inflammatory infiltration of the middle and external coats, the round cells aggregating specially around the bloodvessels, so that the whole wall of the vessel is aifected. Such cases are perhaps hardly to be placed in the same category as ordinary atheroma, but as this condition occurs like the other, mainly in the aorta, and the result is a thickening of the internal coat in patches, it is diflicult to draw a distinct line of demarcation between them. By some, this condition has been specially distinguished under the designation acute aortitis. It is important to consider what changes the atheromatous pro- cess produces in the middle and external coats. At first the middle coat is hardly at all affected, but if the process advances far, and especially if the degen- eration of the patch causes much Fig. 17o. deformity of the internal coat, then the middle coat becomes softened and loosened. It also becomes aflfected with fatty de- generation, the muscular fibre- cells being first involved (see Fig. 175). In advanced cases, especi- ally in the cerebral arteries, we may even find, along with fat- granules, crystals of cholestearine and margarine and pigment, so that through time the middle coat maybe considerably broken up. patty degeneration in atheroma. «,from This process may be present in internal coat; b, muscle-oells from middle the middle coat while the hard coat, x 350. thickening of the internal coat is still present, and we may find a localized dilatation of the vessel occurring, into which the thickened intima dips. The external coat is much less seriously affected than the middle; if at all in- volved it presents increased thickening and vascularization. We have now to consider the effect of atheroma on the circula- tion. There are three alterations which it produces, each of which may, according to circumstances, have important effects on the circulation. The disease causes narrowing of the calibre., loss of 336 BISKASKS O. THK OKa.NS O. CIKC.L.VTXO. elusMty and rigiM, of the wall, and Merference contractility of the vessel. Fig. 170. un th the musc-ular .tw thickened internal coat is seen. In its sub- Atheroma of cerebral artery. The Sr^^^'^f^sUH were found. On the surface is a ing calibre. X 34. • r. nf thP vessel will be of little consequence in such Jgr»SrS°f 'Xbtt inthe ca» of tb. ce,,b,a. vessel. Pig 177 cerebral artery to contrast with Fig. 176. X 34. Transverse section of normal ce the interference with the circulation may be considerable (see Fig. 176). and those of the legs, t^^.r'Thirirsoniesimes peculiarly the case CHEONIG ENDARTEBITIS ATHEROMA. 337 in the coronary arteries of the heart, where an atheromatous patch, originating perhaps in the aorta, may cause very great narrowing and even complete obstruction. The disturbance of the circula- tion in the substance of the heart sometimes produces severe angina, and may lead to sudden death. If by reason of the rough- ness of the surface or the formation of the atheromatous ulcer fibrine is deposited, then the narrowing may be very serious, and may even amount to complete occlusion. The interference with the muscular contractility will also affect mainly the arteries of smaller dimensions, and in the case of the arteries of the brain, the absence of that control of the circulation which is afforded by their varying calibre may lead to serious consequences. But of all the consequences of atheroma the rigidity and weak- ening of the wall are the most important. These consequences are most serious in the aorta, where they are probably the chief factors in the causation of aneurism. The immediate consequence of rigidity of the aorta is that during the systole of the heart the vessel does not dilate, and at the end of the systole it does not re- coil, so that the force of the elastic recoil is lost to the circulation, and in distant parts there is apt to be more or less stagnation. As a result of this we have hypertrophy of the left ventricle, which is often very marked in cases where much calcareous infiltration exists. The hypertrophied ventricle sending the blood forcibly into the rigid aorta produces commonly a diffuse dilatation of the arch. The influence of atheroma in producing aneurism will be considered subsequently. The time of life at which atheroma is most frequent is a point of some importance in relation to the causation of aneurism. Ac- 5'ig. 17«. cording to Rokitansky, it is commonest between the ages of forty and sixty. It is still pretty Miji.pii, ; ..■■.( frequent down to thirty years Pf[i]pf^|,ljji,v''|| of age, but rapidly diminishes Sjll'fr^^lj'fsl in frequency from that age If j(- "u'jiijjl downwards. It is extremely If^t^ifH: /^ rare under twenty years, and %§r Wi§i ^ ^ y'' when it does occur it is mostly B^^^^^0, °- ^ in connection with congenital .'''.r^ --*',;,!..,! , i a J, anomalies of the great vessels pMKmSi!^^ 'vi;V - ' J \ or heart, such as stenosis of a /S{l|'|SP');flfJj'l \ ~ ' i stem with defect of the septum, ' ^m ■- '■ , __^ ^^^' Endarteritis obliterans in arteries of kidney, a, thickened and fibrous internal coat ; h, As an addendum to the sub- middle coat. ject of ajtheroma, mention has to be made of a condition sometimes designated Endarteritis OBLITERANS (Fig. 178). This is not an independent disease, but is frequently of considerable importance as a part of the phenomena 22 338 DISEASES OF THE OEGAXS OF CIRCULATION. of other conditions. It affects the finer vessels of certain organs, and consists, lilce atheroma, in a thickening of the internal coat which, in these fine arteries, frequently leads to complete ob- literation. This form of lesion is seen especiallj- in interstitial inflammations of organs, and is particularly frequent in chronic interstitial nephritis, where it will be again referred to. Faxxy Degeneration of the Intima of Arteries. — This is a condition which we consider here because it is apt to be mistaken for atheroma. We frequently see, especially in the aorta, yellow markings on the internal surface. These markings are onlj' slightly raised above the surface, and have the appearance of superficial figurings. They are to be found in the aorta, pul- monary artery, and other parts of the arterial system. If a portion of such a patch be examined under the microscope by removing a thin layer by a section parallel to the surface, it will be found that the condition consists in a fatty degeneration of the cells of the intima. The flat-branched cells are demarcated by the presence in them of abundant fat-drops. If the fatty degeneration is much advanced then the intercellular substance becomes also the seat of fat-drops, and the cells are no longer demarcated. It sometimes happens that when the degeneration is very advanced the little patch softens and an erosion forms. This erosion is verj' super- ficial, and is not to be mistaken for the atheromatous ulcer. This condition is sometimes met with in the bodies of com- paratively healthy persons, but we have already seen that in anaemia and in emaciated persons it is frequent, and is to be classed in the same category as fatt}^ degeneration of the muscular tissue of the heart. CALCAEEOUS IKFILTEATION OF AETERIES. We have already seen that in atheroma there is verj- frequentlv a calcareous infiltration of the affected structures, and it has been stated that individual peculiarities appear to play an important part here. In some cases a more independent calcareous deposition occurs, and here individual peculiarities are of still greater con- sequence. Calcification of the middle coat is the most frequent and important form. This is very frequently associated with atheroma, but it is noteworthy that the atheroma and calcareous deposition very often affect different arteries or different parts of the same. We may have, for instance, an atheroma of the aorta and calcification of the middle coat in the femoral and smaller vessels ; or there is atheroma as well as calcification in the femoral, but in their extreme degrees the two are present at separate parts of the artery. For instance, Figs. 174 and 180 are from the same femoral artery, and from parts near each other ; but the one shows atheroma with fatty degeneration, while the other exhibits very advanced calcareous infiltration of the middle coat. It may here CALCAREOUS IXFILTEATIOX OF ARTERIES. 339 be remarked that calcification affects by preference the arteries of medium and smaller size. It is often very pronounced in the femoral and brachial, and extends to those of smaller size, but not to the finest arteries. The deposition occurs primarily into the muscular fibre-cells of the middle coat, and at first marks these out by the presence of fine opaque granules (see Fig. 179). The granules flow together till a Pig. 179. Calcareous infiltration of the middle coat (6) in an artery, early stage, with atheroma (a). At the edges of the affected part, the general outline of the muscle fibre-cells can be made out. X 60. patch is formed of an opaque appearance, but confined to the middle coat. As the calcareous deposition increases, the patch sometimes assumes a crystalline appearance, and the material may become broken and irregular, as in Fig. 180. This condition Fig. 180. Calcareous infiltration of the middle coat in an artery. The lime salts have aggregated together so as to produce a crystalline appearance. This was taken from the same artery as Fig. 174. X 22. necessaril}' gives greatly increased rigidity to the walls of the arteries, and the feeling of rigidity so often felt in the radial and other small arteries is mostly due to this cause, and not to atheroma. The fact, however, that calcification of the middle coat is so often associated with atheroma renders this rigidity to some extent an indication of the existence of atheroma in the larger arteries. To the naked eye the calcified parts frequently manifest themselves by 340 DISKA.SES OF THE ORGANS OF CIKCULATION. the appearance of a circular opaque striation, visible especially when the artery is laid open and viewed from within. The ap- pearance is better seen if the artery be allowed to dry partially, as then the normal tissue becomes more transparent and the chalky structures more prominent. In that case complete or partial rings are seen, not unlike the irregular cartilaginous rings of the bronchi, but smaller. Another method of rendering the calcilication prom- inent is to tear oft" the internal coat, which is usuallj' somewhat loosely attached. The calcareous infiltration of the middle coat renders the artery peculiarly rigid, and, when extensive, induces hypertrophy of the left ventricle just as rigidity of the aorta does. The rigid vessels are also liable to dilatation, as in the case of the aorta. But besides that, the calcified middle coat is brittle and affords a much less effective resistance to the distensile wave of blood. An addi- tional strain on the circulation, or some special movement of the body, may break the brittle coat and directly lead to aneurismal dilatation of the artery. It is not unlikely that peripheral aneu- risms are frequently induced in this way, and especially those of the popliteal region, where the artery is peculiarly liable to mechanical injury from the movements of the limb. A peculiar calcification of arteries has been described as a result of metastasis. We have already seen that when great destruction of bone is occurring the lime salts may be deposited in distant parts, the lungs and mucous membrane of the alimentary canal being the chief seats. Kuttner has described a case in which the incrustation occurred in the arteries. The deposition increased in amount the further the arteries were removed from the heart, and it was especially manifest where the current was permanently impeded, as where a small branch issued from a comparatively large stem. In this case it was the intima that was incrusted, and it was peculiar that the veins were not in the least affected. Apart from the incrustation, the arterial coats were apparently normal. The source of the lime salts was an acute caries of the vertebral column from the first dorsal to the last lumbar. In relation to the pathology of the case, it is to be added that there was a purulent interstitial nephritis, so that the excretion of lime salts was presumably obstructed. It is remarkable that in this case the metastasis was to the arteries, and that the lungs and mucous membrane of the intestine were entirely free. SYPHILITIC DISEASE OF ARTERIES. The condition met with in syphilis in many respects resembles atheroma, and it is sometimes difficult to say definitely which of these processes is present. In fact it is not safe to call a lesion syphilitic unless there be other evidences of syphilis. The condi- tion has been most frequently seen in the arteries of the brain, but it has also been observed in the pulmonary artery, and it probably SYPHILITIC DISEASE OF ARTERIES. 341 occurs in other vessels. It is asserted by some that a large pro- portion of cases of atheroma of the aorta have a syphilitic origin, but this is exceedingly doubtful. Like atheroma it occurs in patches, but these are more frequently single and isolated than is the case in atheroma. Thickening of the "internal coat is the most characteristic appearance, and it may be so great as almost to close the artery. The patch is dense, almost cartilaginous or fibrous to the feeling. The thickening is sometimes not confined to the intima but extends to the other coats, and this is especially the case when the patch is in the neighborhood of a gumma or syphilitic inflammation. The disease begins with a cellular formation in the internal coat (Fig. 181), so that it comes to have the characteristics Fig. 181. Syphilitic arteritis. The internal coat (a) thickened and infaltrated with cells. The external {d) and middle (c) coats also somewhat infiltrated. To the left the membrana fenestrata [b] is interrupted. X l-'"- {Zikgleti.) of granulation tissue, and this cellular character is most manifest when the lesion is in the neighborhood of a gumma. The new formation extends outwards as well as inwards, and very often the middle and external coats become involved. There is little ten- dency to fatty degeneration or calcareous infiltration in this disease. The new-formed tissue follows more commonly the regular course of granulation tissue. Capillaries by and by form in it, and the coats of the vessel may be, to a considerable extent, restored with some narrowing. On the other hand there may be great cicatricial contraction, the new-formed tissue developing into a dense fibrous tissue with great narrowing of the vessel, or even complete ob- struction if the vessel be a small one. It sometimes happens that a thrombus is formed on the patch, and the organization of this may aid or complete the obstruction of the vessel. As already indicated, the distinction of syphilitic disease from atheroma is sometimes difiicult, and the main points of difference 342 DISEASES OF THE ORGANS OF CIRCULATION. may be here indicated. Atheroma is a disease of advanced life, while syphilis occurs mostly in comparatively young people. Both are very common in the cerebral arteries, but in the case of athe- roma the aorta is usually simultaneously affected, whereas in the case of syphilis it has frequently been specially noted that theaorta was normal. In the syphilitic disease again the new formation is more cellular and tends more to extend to the other coats of the vessel. It has also been noticed that fatty degeneration and calci- fication are much less frequent. In spite of these difiEerences there are many cases in which the distinction is impossible and the existence of syphilitic disease should never be absolutely concluded unless there are other evidences of the disease present. It is evident that syphilitic disease will induce secondary changes similar to those produced by atheroma. As it affects the arteries of the brain with peculiar frequency, and leads to obstruction of them, it may induce softening of the brain. The narrowing may also induce dilatation of the artery on the proximal side, and, in this reference, it is stated that aneurism of the cerebral vessels is not infrequently present in syphilitic persons. ANEURISMS. An aneurism is a localized dilatation of an artery. Taking this as the definition it will follow that in forming the aneurism the coats of the artery are stretched, and, to some extent, retained as the covering of it. We shall afterwards see that there are aneu- risms in which this is hardly the case, in which the coats rather give way and rupture. Such aneurisms are often designated spurious aneurisms, of which it will be necessary afterwards to describe several varieties. Even of the aneurisms which come under the above definition there are several varieties, but we have to consider here, in the first jjlace, those which arise by a limited dilatation of an artery. The artery may be dilated in its whole circumference, thus forming a spindle-shaped or fusiform aneu- rism, or the dilatation may be at a limited point and we have then a SACCULATED ANEURISM. Causation of Aneurisms. — It may be said that permanent un- due dilatation of an artery can hardly occur unless the wall of the vessel be weakened. It is perhaps conceivable that the blood- pressure might be so increased as to dilate an artery unduly, but such increased pressure would, in its extreme form, be temporary, and unless there were some weakness of the vessel-wall it would hardly produce a permanent dilatation. "\Ye shall see reason to believe that in the actual production of the ordinary aneurism, both of these conditions, namely, weakness of the wall and in- creased blood-pressure are nearly always to be traced. The more important of the two conditions is weakness of the wall of the artery. By far the most frequent cause of this weak- ANEURISMS. 343 ness is atheroma. We have already seen how atheroma with great calcareous deposition maj lead to dilatation of the arch of the aorta. But aneurism is even more frequent in cases where the ordinary fatty change takes place in the patches, causing irregu- larity in the internal coat. By the formation of the atheromatous abscess and ulcer, or still more frequently by the absorption of the fat and consequent shrinking, depressions and furrows are formed in the internal coat. It is to be remembered also that the athero- matous part is rendered unduly rigid by the thickening of the in- ternal coat, and that any extra distending force will act specially on parts which have been weakened. Another element of equal importance is the weakening of the middle coat, which we have seen to be a frequent consequence of atheroma. Fatty degenera- tion is of frequent occurrence in the media under the atheroma- tous patch. In the case of the peripheral arteries calcareous infiltration of the media may occur with or without atheroma, and the calcification may be such as to render the media exceedingly brittle. It is true that, according to old experiments of John Hunter and Home, destruction of the external or even external and middle coats of arteries in animals is not sufficient to cause dilatation of these vessels, but with a seriously weakened middle coat any considerable increase of the blood-pressure may be suffi- cient to cause dilatation. "While atheroma, especially when associated with weakening of the middle coat, is concerned in the causation of aneurisms, there are certain circumstances which indicate that this of itself is not a sufficient cause. One of these is the age at which aneurisms occur. We have seen that atheroma is a disease of advanced life, being most frequent after forty, altliough still very common be- tween thirty and forty. IsTow aneurisms are most common between the ages of thirty and forty. Another circumstance is the great preponderance of aneurisms in the male. It is true that atheroma is commonest in the male, but not to anything like the same ex- tent as aneui'ism. Bizot found in 189 cases of the latter, 171 in males and 18 in females, and Hodgson found in 63 cases, 56 in in males and 7 in females. It is noteworthy further that in some localities aneurisms are uncommon, while atheroma is by no means so rare. The great frequency of aneurism in the army as com- pared with civil life is another circumstance requiring explanation. All these circumstances are to be explained on the view that, in addition to weakening of the vessel-wall increase of blood-pressure is needed to produce aneurisms. In severe continued exertion we find the most frequent cause of increased blood-pressure. The engineer who has to manipulate a piece of hot iron while wielding a heavy hammer, or the soldier who has to perform long marches with heavy accoutrements, must put a strain on his heart and larger vessels which ordinary persons are not liable to. It will be apparent that men are much more exposed than women to such excessive stress on their vascular systems. It is again between the ages of twenty and forty that men are mostly exposed in this way. 344 DISEASES OF THE ORGANS ^4 __j. J — -, e, greatly thickened epithelium ; 7», connective tissue; ^r, mucous lands; /, a gland at base of tumor atrophied by its pressure. X 20. (Cornil and Papilloma of larynx, glands; Rantier Fig. 223). The epithelium may be thick, and the connective tissue dense, so that the tumor is like a hard wart, or the epithelium may be thin and the connective tissue soft, sometimes richly infiltrated with round cells, and so the growth is soft like a soft wart or condyloma. The growth may occupy a small surface of the cord, being partially pedunculated, but it often has a considerable base, forming a shaggy, irregular outgrowth. Sometimes, after extirpa- tion, these tumors take on a sarcomatous character, or even develop a cancerous growth. A kind of false papilloma occurs, as we have already seen, in some cases of tubercular or syphilitic ulceration of the larynx. Sometimes, also, the surface of an epithelioma has a papillary character. Next to the papillomas the fibromas are the commonest tumors in the larynx. Morell Mackenzie has found in one hundred cases of non-malignant tumors, sixty-seven papillomas and sixteen fibromas. They are tumors of slow growth, mostly seated on the THE BRONCHIAL TUBES. 465 cords or at the base of the epiglottis. They consist of firm or soft connective tissue, those of firm consistence being the commoner. They are usually more or less pedunculated, and their surface is generally smooth, although it may be irregular or even furnished with papillse. They are usually small tumors, from the size of a split pea to that of an acorn. Mucous Polypi occasionally occur, taking origin in the mucous glands. They very commonly undergo transformation into cysts, and their most frequent seats are the epiglottis and the ventricles of Morgagni. Other forms of simple tumors are uncommon, but cases of LIPOMA, MYXOMA, and ANGIOMA have been met with. Cartila- ginous TUMORS formed by outgrowth from the normal cartilages have been found. They are usually multiple and sessile. They may project considerably into the larynx, and being covered with mucous membrane may be mistaken for one of the commoner tumors mentioned above. As these tumors are firmly connected with the cartilage beneath, they cannot be removed by forceps, and so it is important to distinguish them from the others. Sarcomas of the larynx are of occasional occurrence. They are usually of the spindle-celled form, but may be round-celled. They may grow to a considerable size, and are, of course, prone to recur unless the whole larynx be removed along with the tumor. Cancer of the larynx develops in the form of flat-celled epithl- LiOMA.' It is not infrequently a primary tumor, growing usually from the ventricular bands, but also originating in other parts. An epithelioma may also extend from a neighboring part, particu- larly from the tongue. There is first an infiltration of a limited part which extends in area, involving more and more in an indis- criminate advance. Very commonly there is an abundant papillary growth on the surface, so that there is a resemblance to the cauli- flower cancer or to the papilloma. The central parts of the growth undergo ulceration while the disease is extending circumferentially. In this way great destruction of tissue may result, and the parts present great deformity. Tumors are of very rare occurrence in the trachea, but we may have similar growths to those in the larynx. THE BRONCHIAL TUBES. The diseases of the bronchi stand in close relation on the one hand to those of the larynx and trachea, and on the other to those of the lungs, and it is impossible to draw an absolute line of dis- tinction on either side. The affections of the larger and middle bronchi are essentially like those of the larynx and trachea, and this is consistent with the fact that in structure they are similar. As we pass down the bronchial tree, however, the structure changes considerably. The cartilaginous plates become irregular and smaller, and finally disappear; the elastic tissue becomes 30 466 DISEASES OF THE ORGANS OF RESPIRATION. more completely incorporated with the mucous membrane, so as to form a single layer which becomes thinner as the tube diminishes in calibre ; the bronchial glands altogether disappear in the finer tubes. The bronchial tube thus becomes more simple in structure, and approximates to that of the lung alveoli. So it happens that in their diseases the finer bronchi are more allied to the lungs, and are often involved with them. We shall afterwards see that in acute catarrhal inflammation of the lung the disease often begins in a capillary bronchitis, and is sometimes described under that name. Bronchiectasis. — By this name is meant dilatation of bronchial tubes, a condition of somewhat frequent occurrence, but depending on a considerable variety of circumstances. The normal bronchial tube offers resistance to the dilating force of the air, chiefly by virtue of its elastic or dense walls, and the support which it receives from the pulmonary tissue around. If the walls be weakened or the support of the pulmonary parenchyma withdrawn, or if the distensile force of the air or other contents be considerably in- creased, then we may have bronchiectasis. It will be seen that one or other of these predisposing conditions may occur under very various circumstances. A prolonged catarrh may cause atrophy of the elastic tissue of the bronchial wall, and so reduce the resistance. On the other hand, obliteration of the finer bronchi and lung alveoli in a district will cause the pressure of the air in inspiration to act especially on the bronchial tubes, the dilatation being here similar in its origin to compensatory em- physema. Lastly, we may have the bronchi dilated from accumu- lation of secretion. This will occur chiefly when a small bronchus has been obstructed, and the condition may be compared to a re- tention cyst. The various forms of bronchiectasis may be divided into two, namely, cylindrical and sacculated dilatations. The former occurs mainly where the causal condition has been more or less of a general one, such as a prolonged bronchitis. The bronchi, especially the middle-sized ones, are unduly wide, and their walls are thinned. The dilatation may be quite regular, but ver^^ often there are little bulgings or pouches. In the sacculated form there has usually been a more local agent at work. The most typical sacculated dilatations are found in fibroid phthisis, under which heading they will be treated of more fully. They may be pro- duced also by any cause which induces shrinking of the lung tissue. The wall of the bronchus is thinned, but it still presents a distinct membrane lining the sac. When cavities in the lung have a distinct lining membrane, they are generally of this origin, and they are especially so when the membrane is surrounded by lung tissue which approaches to the normal condition. As the secretion stagnates in the sacculated dilatation, and may decompose, there may be ulceration of its internal wall. BRONCHIAL CATAREH BRONCHITIS. 467 Bronchial Catarrh or Ordinary Bronchitis. — This is an inflammation affecting the larger and middle-sized tubes, but not extending to any considerable degree into the finer ones. As to the conditions giving rise to it, much that has been said under nasal catarrh is again applicable here. It is to be added, however, that in many persons there is a special proclivity to recurrent attacks of bronchitis. This may be due to an inherited weakness in this direction, but is perhaps more frequently occasioned by an acute bronchitis which has left the bronchi considerably altered in structure, has rendered them, in fact, the least resistant part of the body. In such persons, cold may set up a bronchitis, or it may be set up by disorder of the stomach, or hy some other trivial cause. Valvular disease of the heart frequently gives rise to bronchitis, but we shall consider this when the results of cardiac disease in regard to the lung are under review. In the slighter forms of bronchitis, the larger bronchi and the trachea are mainly affected. In fact, it frequently happens that along with a slight laryngitis there is a tracheitis and a bronchitis of the larger stems, without the name bronchitis being given. In the more definite cases of bronchial catarrh, it is the middle-sized tubes that are chiefiy involved. In order to appreciate the changes which occur in bronchitis, it is necessary to refer to some points in the structure of the tubes. The mucous membrane is covered with epithelium whose super- ficial layer is c^'lindrical and ciliated. Beneath the epithelium there is a basement membrane which is separate from the proper mucosa under it. The mucosa is composed of connective tissue, and presents externally a muscular layer, chiefly of circular fibres, but with some longitudinal ones. Outside this we have the sub- mucosa or adventitia, which is continuous with and really forms a part of the general interstitial connective tissue of the lung. In this loose adventitia the cartilages are embedded, and there are abundant serous and lymphatic spaces, which are in communica- tion with those throughout the lung, the perivascular and others. According to the careful description of Hamilton, acute bron- chitis is accompanied first by great congestion, chiefly of the vessels in the proper mucosa. OEdema of the basement membrane follows, and this structure becomes greatly thickened. The superficial layer of columnar epithelium is shed, but vigorous germination of the deeper layers occurs, abundant embryonic cells being produced. At the same time there is great infiltration of the mucosa, muscular layer, and adventitia, with round cells of inflammation. This infiltration may be very great, and, as the adventitia communicates with the general interstitial tissue of the lungs, there may be a wide distribution of these cells, which pass on by the lymphatic channels to the lymphatic glands. If the disease becomes chronic, the inflammatory infiltration of the layers beneath the basement membrane continues, and there is the usual new formation of connective tissue producing an induration of the tissue. As in other productive inflammations. 468 DISEASES OF THE ORGANS OF EESPIRATIOIS . the new-formed tissue often causes atrophy of the proper structures. In many cases the muscular coat is to some extent atrophied, although sometimes it is hypertrophied. The mucous glands are often considerably destroyed, and even the cartilages may be partially atrophied. These alterations in the walls of the tubes no doubt weaken them, and, as they occur especially in long-con- tinued cases of bronchitis, we can understand how in such cases the bronchial tubes sometimes undergo dilatation. Dilatation of bronchial tubes is not, however, a very prominent feature of ordi- nary bronchitis. The exudation in bronchitis is important, as it forms the sputum, and gives its characters to the latter. In the normal condition the mucous glands secrete enough mucus to keep the membrane moist, the secretion consisting of a glairy fluid containing a few leuco- cytes which are here called mucous corpuscles. The fluid owes its glairy or sticky character to the fact that it contains mucin, a chemical substance allied to albumen and secreted by the mucous glands. This normal secretion catches and holds the minute particles forming the dust which we inhale with the air, and the vibratile cilia of the epithelium acting towards the outlets carry mucus and dust outwards, to be swallowed or expectorated. In bronchitis there is at first very little increase of the secretion, and what there is is chiefly concentrated mucus, tough and scanty. As the disease progresses it becomes more abundant but less tough and less transparent, and this is brought about by the increase of the inflammatory exudation consisting of serous fluid and inflammatory cells. The degree of toughness depends on the proportion of mucin, and the degree of opacity on the quantity of cells. As the disease advances the leucocytes go on increasing, and so the fluid on the surface of the mucous membrane becomes more and more opaque. The SPUTUM coctum, or ripe sputum met with at the acme of the disease, is yellowish-white or greenish and opaque. It is not homogeneous, but has more opaque and less opaque portions according as it has got mixed and coated with mucus from less affected parts of the tubes. The sputum as seen in a vessel appears at first sight like pus, but it is much more tenacious. Under the microscope it also resembles pus, the field being crowded with multitudes of leucocytes. But the tenacity of the fluid is often shown by the manner in which the plastic leucocytes are altered in shape, being drawn out into oval or more elongated forms according as the tough mucus is drawn out., On adding acetic acid the usual development of nuclei occurs in the cells, and the intermediate fluid becomes markedly opaque from the precipita- tion of the mucin which can be seen now in fine granules. With acetic acid the sputum assumes to the naked eye a whitish opaque, and almost membranous character. In chronic bronchitis the sputum is often very abundant, and is usually sero-mucous with comparatively few leucocytes, and hence DISEASES OF THE LUNGS. 469 transparent. There is a comparatively rich serous exudation with very little increase in the secretion of mucus. The sputum is not so tough as in more acute cases, and is often very frothy. In some very chronic cases there is a very abundant cellular exudation — the sputum is almost like pus and has not the toughness of the sputum coctum. Large quantities of pus may thus be expectorated. In these cases it may be supposed that leucocytes are present in the walls and outside the bronchi as well as in the expectoration, and it is in them that we may look especially for dilatation of the tubes. Fibrinous Bronchitis. — -This name, as well as that of plastic BRONCHITIS or BRONCHIAL CROUP, is givcu to a Condition of very rare occurrence and of rather obscure pathology, but yet of great interest. We have seen that in laryngeal and tracheal croup the fibrinous exudation sometimes extends down into the bronchial tubes, and that casts of these are formed occasionally. Taking the other end of the bronchial tree we find that in acute pneumonia the fibrinous exudation which forms in the lung aveoli commonly extends some distance into the finer bronchi, and so we find easts in them. But there are cases in which fibrinous casts form in the bronchial tubes independently, without any disease of the trachea on the one hand, or of the lung proper on the other. These cases are somewhat chronic in character, and the expectoration of casts occurs at intervals during months or even years. The casts are of a whitish-gray color and represent the bronchi of, it may be, a single lobe, with their ramifications, as we can see very beautifully by floating them out in water. Sometimes the fine ends of the casts are swollen out as if they had come from the alveoli. The casts sometimes present on section a stratified arrangement as if the fibrine had been deposited in layers. They show under the microscope fibrine with leucocytes. The exact pathology and the source of this exudation are some- what obscure. In some cases, where death has occurred shortly after the expectoration of the casts, or where they have been found in situ, there has been little preceptible alteration of the mucous membrane. This has led some to suppose that the fibrine comes from the lung alveoli, and in many cases the lung tissue is con- siderably altered, for there may be phthisis, or pneumonia, or collapse. But it is not apparent to what extent these may be secondary to the bronchitis. A possible indication of the pathol- ogy may be afforded by the fact that in a considerable proportion of the cases there has been hemorrhage from the lungs. B.— THE LUNGS. In examining the lungs after death we seldom meet with them in a perfectly normal condition. They may be abnormally ad- herent to the wall of the thorax, or unduly pigmented, or there 470 DISEASES OF THE ORGANS OF RESPIRATION. may be cicatrices in them, or oedema, and so on. The explanation of this is, perhaps, that the lungs are peculiarly exposed to deleteri- ous influences in two directions. The air passing into them is apt to carry irritating materials with it, and the blood circulating so richly through their tissue is liable to variations in its constitution and degree of pressure. We have already seen, for instance, that organic disease of the heart has serious effects on the pulmonary circulation, but apart from that, simple weakness of the heart may, as we shall afterwards see, have important effects on the lung. It must not be forgotten also that there is no organ of the body whose tissue is so intimately related to its bloodvessels as the lungs. These organs are little more than a congeries of blood- vessels with a suthcient supporting stroma. Any deleterious sub- stance circulating in the blood, therefore, is very prone to affect the lungs, especially if there be any special weakness in this direc- tion. We have abundant illustrations of this in the frequency of lung complications in the acute fevers. There are one or two points in the anatomical relations of the lung which should be kept in mind. It is supplied with two different sets of bloodvessels, the pulmonary artery on the one hand, and the bronchial artery on the other. We should remember the distribution of these, and not confuse effects due to obstruction of the one with those due to obstruction of the other. Then we speak of diseases affecting the respiratory surface on the one hand, and the supporting structures on the other ; that is to say, there are some diseases which affect the surfaces of the finer bronchi and of the alveoli, while others involve the walls of the alveoli and of the bronchi. It is true that these two are generally in- volved together, but in different cases the one or the other is primaril}' concerned, and usually retains the lead. It is obvious that to a certain extent the determining cause of the disease will have something to do with this. An agent which acts by being carried into the lungs with the air will mostly affect the surface of the alveoli and bronchi in the first place, whereas an agent arriving by the blood will be more apt to attack the walls. We shall see, however, that to this there are important exceptions, because, on the one hand, the capillary vessels have such a close relation to the surface of the alveoli, and, on the other hand, substances arriving from without very readily penetrate into the substance of the lung. A more important consideration arising from the anatomical relations has reference to the distribution of a lesion in larger or smaller districts of the lung. When a disease is caused by something arriving by the blood then we should expect it to be distributed over a large extent of lung tissue or over the whole ; the disease will occupy whole lobes. If it arrives by the bronchial tubes, we should expect it to extend to the proper lung tissue more irregularly, here and there an extension corresponding with a particular minute bronchus; the disease at first involves lobules. In this way we may distinguish roughly diseases which ATELECTASIS AND COLLAPSE OF THE LUNG. 471 are lobar as due to alterations in the blood, and those that are lobular as related to the bronchial stem. MALFORMATIONS OP THE LUNG. These are not frequent, and are of minor importance. Apart from absence or exceeding sraallness of one or both lungs, which occurs as part of general malformations, there are cases where single lobes have been wanting, and their place taken by cicatricial tissue. These have probably their origin in obliteration of a bronchus in early foetal life. Again, the lungs may be normal in form, but very small in size. In such cases the whole body, and especially the circulatory system, will remain ill-developed. It is not uncommon to meet with abnormal lobulation of the lungs, the regular lobes being divided by the formation of deep fissures. Rokitansky has described a case in which an accessory lobe existed between the base of the left lung and the diaphragm, and quite separate from the lung. It had no bronchus, however. ATELECTASIS AND COLLAPSE OP THE LUNG. These names designate conditions in which the lung alveoli and finer bronchi contain no air, but are in a condition similar to that of the foetal lung before inflation, the internal surfaces of the alveoli being applied to each other. It may be a survival of the fcetal state, or it may be subsequently produced by the alveoli being, in some way, emptied of their air. As this condition occurs under a considerable variety of circumstances we shall give no general description, but refer to the individual forms. Atelectasis is frequently found in new-born children, being, indeed, a survival of the foetal state. The lungs have to a greater or less extent remained uninflated. The non-infiation may be due to some obstruction in the bronchi, by meconium or mucus, but in most cases it is merely due to the weakness of the respiratory efforts. The new-born child usually cries lustily, and in the deep inspiratory gasps between the cries the lungs are fully infiated. But if the child be weak or has not cried freely, certain parts of the lungs are apt to remain devoid of air. The atelectasis of the new-born is most frequent in the lower lobe, and in the posterior parts of this lobe. It may be only in small areas in the midst of the inflated lung tissue, or the greater part of a lobe, or the whole lobe may be atfected. In any case the non-inflated part usually shows by its shape that it is the district supplied by one or more bronchi. The atelectasis shows itself by the smaller volume of the part. If it is in the midst of inflated lung it is depressed below the surface. Like the fcetal lung, it is redder than the normal, firmer to the touch, and non-crepitant when handled. It 472 DISEASES OP THE ORGANS OF RESPIRATION. is important to distinguish this condition from condensation of the ' lung, for which it is liable to be mistaken. In both the lung is devoid of air, but in the case of condensation it is so because the air-spaces are filled up with solid material, usually inflammatory exudation. The atelectatic portion is capable of inflation by blowing air into the lung by the bronchi, at least it is so at the outset, while the condensed part is not inflatable. There is no doubt that a lung which was partly atelectatic immediately after birth may subsequently become perfectly inflated. On the other hand there is reason to believe that, if the atelectasis presist long, the lung becomes incapable of inflation. If the child survive, the applied walls of the lung alveoli adhere and an actual obliteration of the latter occurs. The part gradually atrophies, and it has been supposed that cicatrices sometimes seen in the adult lung and without any obvious cause may have this origin. The question arises here whether, after inflation of the lung, portions or the whole may again collapse. We shall see immedi- ately that collapse occurs in the adult, and there is no reason to suppose that it does not occur in the new-born infant. There are undoubted cases of children who have lived over twenty-fours and have cried, in whose bodies the lungs have been found with only one island here and there of inflated lung. Collapse op the Lung is of frequent occurrence. In some cases it is due to direct compression of the lung; the air is simply squeezed out of it. Usually this arises from the presence of fluid or air in the pleural cavity. In that case the collapse is not unlikely to be only partial, that is to say, the air-vesicles are only partly emptied and readily recover. But if the exudation is great and remains long, then the lung may be pressed upwards and backwards and come to tbrm merely a red fleshy layer flattened against the chest wall. This condition is often called carnipica- TiON, and in it the tissue appears darkly pigmented, the absence of blood and the packing together of the lung tissue exaggerating the existing carbonaceous pigmentation. The cause mentioned above is by far the most frequent in producing collapse by pressure, but there are others. Curvature of the spine sometimes causes such a hai-rowing of a part of the chest that the lung is squeezed or collapsed. Aneurisms or tumors may also compress the lung, but they more frequently cause collapse by obstructing the bronchi. Even distention of the abdomen, by pressing the diaphragm upwards and limiting the chest space, may cause a partial collapse. A great distention of the pericardium may have a similar eflfect. A very important cause of collapse is obstruction of bronchi. To a limited extent collapse is exceedingly frequent in bronchitis, much more frequent than is usually supposed. The collapse very often appears in the form of small wedge-shaped depressions at the edges of the lungs, and may be almost concealed by neighboring emphysematous lung. But sometimes, especially in children, the collapse may be much more extensive. The mode in which this HYPEETEOPHY OF THE LUNG. 473 collapse occurs has been well described by Gairdner. If a pellet of mucus obstructs a bronchus it generally does so at a bifurcation. The bronchus is partially obstructed, and the pellet of mucus being movable, acts to a certain extent like a valve; it is pushed out into the larger tube during expiration, and being drawn back against the bifui'cation in inspiration stops the tube. In this way the escape of air during expiration is allowed, but the entrance of air during inspiration prevented. The respiratory movements will thus act, to a certain extent, like an air pump, and the portion of lung tissue concerned will be gradually emptied of air. There is another way in which collapse probably occurs when a bronchus is obstructed. It is to be i-emembered that the lung tissue is elastic, and that left to themselves the alveoli collapse and their walls apply themselves together. If a bronchus be obstructed, therefore, and communication with the external air withdrawn, the absorption of oxygen will soon reduce the bulk of the contained air, and cause a reduction of its elastic pressure. The elasticity of the lung tissue, again, will cause pressure to be exercised on the air, and absorption of the gases of the air will be thus promoted. It has been proved that such absorption actually occurs, first of the oxygen, then of the carbonic acid, the nitrogen being slowest of absorption. The lung of course collapses as the air is absorbed. [t has just been stated that collapse from bronchial obstruction is most common in the bronchitis of children, but it is necessary to observe that in children, in whom the form called capillary bronchitis is common, it is often accompanied by a condition which is apt to be mistaken for collapse, namely, lobular condensation. The catarrhal process in the bronchi readily passes in children to the lung alveoli, and the catarrhal products fill these up, causing condensation of a portion of the tissue which has a wedge-shaped configuration similar to that of the collapsed portion. Of course, these two conditions may coexist in the same lung, or we may even have a combination of them, the collapsed lung becoming the seat of catarrh, and so passing into the condition of condensation. HYPEETEOPHY OP THE LUNG. A case occurred recently to the author which distinctly mani- fested th*e characters of compensatory hypertrophy of the lung. The left lung was of very small dimensions, especially the upper lobe, which appeared merely as a membranous structure in which dilated bronchi would be felt. There was no pigment in this lobe, and not a trace of lung parenchyma. The lower lobe contained the ordinary carbonaceous pigment in limited amount, but was greatly reduced in size. The right lung was of very unusual volume, extending across the middle line, so that its edge reached beyond the left nipple. The enlargement seemed to be due to an addition of lung tissue 474 DISEASES OF THE ORGANS OF RESPIRATION. at the anterior parts. The supra-clavicular part of the apex of the lung had the normal form and size, and its anterior border indi- cated the position of the normal anterior margin. What should have been the anterior margin was indicated by this. Beyond this, however, a bulky piece of lung extended into the other half of the chest. This part of the lung had not the appearances of emphysema, at least in any considerable degree. The right ven- tricle of the heart was greatly enlarged, and the pulmonary artery showed a remarkable thickening of its wall, there being scarcely any diflerence between it and the aorta. The absence of pulmonary tissue in the upper lobe of the left lung indicated that the collapse had been of long standing,^ while the entire absence of pigment showed that, if not congenital, it had occurred in very early life. The enlargement of the right lung was thus compensatory, dating from a period when the organ was in a state of growth. The compensation seems to have been somewhat effective, as the person lived to the age of 46, and it was only during the later months of his life that he suffered from serious dyspnoea, followed by signs of venous engorgement. The remarkable thickening of the pulmonary artery without any ap- pearance of atheroma, also seems to point to a compensatory hypertrophy of the right ventricle during the period of growth, the vessel in its growth accommodating itself to the increased blood-pressure. It may be added that the left pulmonary artery had only about a third of the calibre of the right, but the main bronchus was of equal size on the two sides. PULMONARY EMPHYSEMA. This name includes two distinct lesions, in one of which air escapes into the connective tissue of the lungs and distends the connective-tissue spaces, while in the other the alveoli are over- distended and various other changes result, but the air does not escape from its natural chambers. It will be seen that the first form is comparable with surgical or cutaneous emphysema, while the second is essentially difierent. The one form is called inter- lobular or interstitial emphysema : the other, which is much com- moner, is named vesicular emphysema or simply emphysema. Intbelobulak Emphysema occurs when the air-vesicles are rup- tured and the air escapes into the interstitial tissue. The air- vesicles may be actually torn open by a broken rib coming against the lung, or by the lung being directly wounded. On the other hand, it occasionally happens that the air-vesicles rupture from acute over-distention. We shall see afterwards that over-disten- tion usually produces the other form of emphysema, but, if very acute and very extreme, it may lead to an actual rupture of the air-vesicles. A sudden obstruction of a considerable hronchus, causing imperfect inflation of a portion of lung, may cause such VESICULAR EMPHYSEMA. 475 serious over-distention of other parts as to lead to actual rupture of the air-vesicles. More commonly it is the result of very violent expiratory efforts, generally with, hut sometimes without, obstruc- tion of the air-passages. It has been met with in whooping-cough, in diphtheria, and in violent coughing from the inhalation of irritating material. The violent efforts Avith closed glottis cause such compression of the air in the alveoli, that at some place the vesicles rupture. As seen after death, the air appears in the form of minute rows of bead-like bubbles, visible through the pleura. These rows of beads demarcate the lobules. Occasionally there are larger bullee, which have been known to rupture externally, and so lead to pneumothorax. The air sometimes travels along the connective tissue for some distance, just as we find in the case of subcutaneous emphysema. It may pass to the root of the lung, and from there up along the trachea and out to the subcutaneous tissue of the neck, and so lead to a surgical emphysema. This has led in some cases to a mistake in diagnosis, as Virchow has pointed out. Interlobular emphysema sometimes occurs in diph- theria, and may lead to subcutaneous emphysema in the way just mentioned. But, if tracheotomy has been performed, it may be thought that the emphysema has taken origin in the wound. Vesicular Emphysema. — In this condition the air-vesicles are over-distended, and, by partial atrophy of their walls, to some extent coalesced, but without any actual tearing of them. It will be clear that the distention must be frequently repeated or per- manent, and we have to consider to what it may be due. Of course the distensile force is in the air within the air-vesicles, and it may be exercised either in inspiration or expiration. Wben the glottis is closed, and expiration violently performed, then the air in the vesicles will be at an increased pressure. The expiratory effort is produced by the muscles causing the movable walls of the chest to be pressed against the lung. The contraction of the abdominal muscles presses the diaphragm upwards, while the ribs are depressed. The lung is thus compressed, but at the same time it is supported by the structures which compress it, and the same force that increases the pressure helps the lung tissue to resist it by increasing the support. When the glottis is closed, the whole lung may be regarded as one cavity, and the pressure will be universally diffused. It may be expected, there- fore, that if any part of the lung be insutficiently supported, the distensile force will tell especially there. The question therefore arises. Are there any parts where the lung is not fully supported by the chest walls ? If a deep breath be taken, the glottis closed, and the act of expiration vigorously performed for a few seconds, we find in our own feelings" indications that the lungs are over- distended, mainly at the anterior parts and the parts above the clavicles. We can easily understand how this should be. The anterior part of the chest, by reason of the flexibility of the costal cartilages, is more movable than the rest of it, aud the anterior 476 DISEASES OF THE ORGANS OF RESPIRATION. edges of the lungs, as we can see in an animal whose chest is laid open while artificial respiration is carried on, have very free play. Then, above the clavicle the lung is obviously less supported than where the chest has bony walls. We shall see afterwards that these, with one or two other parts, are those in which emphysema, when due to frequent expiratory efforts, occurs most typically. _ It will be obvious that if the lung tissue has lost in elasticity, the permanent dilatation of the air-vesicles will occur more easily, and will readily extend to parts more fully supported than those mentioned. In the form to be afterwards referred to under the name of Senile Emphysema, there is a loss of elasticity from the atrophy of old age. But there seems to be in some cases a general loss of elasticity, and it appears as if such a condition were heredi- tary to some extent. It is true that frequent over-distention will cause atrophy of the elastic tissue of itself, but it is quite apparent that in many individuals there is, to begin with, less elastic tissue, or it is less resistant, and so we have a predisposition to emphysema, sometimes inherited. We have still to inquire under what circumstances frequent or violent expiratory efforts are made with closed glottis. Coughing implies such efforts, and it is in diseases where coughing is a prominent feature that we are to look for emphysema from this cause, It is met with preeminently in bronchitis. It also occurs in whooping-cough, occasionally in croup, and even in the violent expiratory efforts of parturition, although in the last two cases interlobular emphysema is more likely to occur from the sudden and violent nature of the distention. As chronic bronchitis is peculiarly a disease of more advanced life, we may expect that a preliminary atrophy of the lung tissue, implying a loss of elastic tissue, plays an important part in the production of emphysema in a large number of eases. We turn now to cases in which the air-vesicles are over-distended during inspiration. A large number of cases of what is called COMPENSATORY or VICARIOUS EMPHYSEMA belong to this class. If a part of the lung does not distend fully in inspiration, there must either be a falling in of the chest to a corresponding extent, or else an over-distention of another part of the lung in order to fill up the space. To what extent one or other or both of these will occur is determined by circumstances, chiefly by the situation of the insufficiently distended part and the time occupied in the oc- currence of the lesion. There are many different circumstances under which compensatory emphysema may occur. If a portion of the lung is collapsed, the neighboring part often undergoes emphysematous distention. It occurs thus in bronchitis, and the wedges of collapse, already referred to, are often fringed with emphysema. We see it also around cicatrices in phthisis, or along with bronchiectasis in fibroid phthisis. Emphysema occurs some- times to a remarkable extent in connection with general adhesions of the lung, and the emphysema is often very marked at the VESICULAR EMPHYSEMA. 477 anterior parts. In order to explain this it is to be remembered that the lungs have a considerable play in the thorax. They come well forward in inspiration and retreat during expiration. We see this in the opened thorax during artificial respiration, but in the closed thorax the greater mobility of the anterior wall of the thorax and the elevation of the sternum produce a similar shifting of the lung. But now if one lung is bound down by firm general adhe- sions, this play of the lung is prevented, and the distention of the lung as a whole is hindered. There may be as a result deficient movement of that side of the chest as a whole. The sternum will continue to rise during inspiration, however, and, in order to fill up the space, one of two things will happen — either the other lung, if not also adherent, will be over-distended and project beyond the middle line, or else an emphysema will occur at the anterior parts of the adherent lung ; this latter is very frequently seen. It is sometimes stated that emphysema occurs in cases of con- densation of the lungs, as in pneumonia and especially in phthisis. We have here to do with conditions in which the air-vesicles are filled up with solid material and air does not get in ; the finer bronchi are at the same time plugged. The air-vesicles are not necessarily distended with the material, but, being plugged, they do not expand during inspiration. For this reason the chest in phthisis is often immobile in its upper part, and it may fall in somewhat even without the formation and collapse of a cavity. On the other hand, this deficient expansion may lead to a com- pensatory emphysema. There is still another way in which it is asserted emphysema occurs in the inspiratory phase. If the bronchi be partially obstructed, the more powerful inspiratory muscles may be able to overcome the obstruction, while the expiratory forces, which nor- mally depend mainly on the elasticity of the lung, may do so much less efficiently. At each inspiration, therefore, the air-vesicles are over-distended, and are only partially relieved in expiration, so that there is an almost continuous condition of dilatation, which readily passes into emphysema. This applies chiefly to the case of bronchitis, and especially where the smaller bronchi are partially obstructed by swelling of the mucous membrane. This view does not now meet with very general acceptance, especially as in bron- chitis the coughing gives frequent violent expiratory acts. We have next to consider the anatomical changes which occur in the lung tissue in emphysema. We have to do with air-spaces of irregular shape and separated by partial partitions, and as the distensile force acts from within, its tendency is to distend equally and so render the spaces globular. The ultimate bronchial tubes terminate in the elongated passages called from their shape infun- dibula. From these passages open by wide apertures the air- vesicles, which therefore cluster around the infundibula and are mere pouches out from them. The distensile force will act first on the infundibulum with its system of air-vesicles, causing disten- 478 DISEASES OF THE ORGANS OF RESPIRATION. tion. The tendency will be to render the outline more globular and the cavity simpler. The partitions separating the alveoli atrophy, and the infundibulum expands into a simpler cavity (a a in Fig. 224). Thus while more space is occupied there is less res- "PlG. 1224. Section of the lung in emphysema, early stage. The infundibula, u, i^, w, are dilated. X 100. (Uindfleisch.) piratory surface. The infundibulum continues to expand and meets with other infundibula undergoing a similar process. By mutual pressure the adjoining tissue atrophies, and the two com- municate by such rounded apertures as are shown in Fig. 225. The larger cavity tends to become simpler by atrophy of all parti- tions and septa, and so the process goes on by coalescence of neighboring spaces and atrophy of the partitions. The enlarged air-spaces thus produced are of various sizes, up to considerable vesicles or bullae. With this atrophy there is great loss of tissue and of bloodvessels. Before the actual destruction of the blood- vessels the pressure seems to cause obstruction of them so that they are not able to be injected and appear as white cords. It is stated that this obstruction is effected by the formation of white thrombi. The epithelium for the most part persists in the dis- tended air-spaces, but it is frequently in a state of fatt}' degenera- tion. It may happen that, as in Fig. 225, the wall of the alveolus has atrophied except the epithelium, and the actual apertures are formed by its being shed. Of most importance is the atrophy of the elastic tissue, because on this account the lung tissue will be prevented from collapsing as it normally does. The changes in the lungs visibl6 to the naked eye are in ac- cordance with these alterations in the finer structure. In the first place the changes described cause the affected lung tissue to take VESICULAR EMPHYSEMA. 479 up more room, and there will, therefore, be enlargement of the lung varying in extent and situation according to circumstances. If the emphysema be at all extensive the lungs as a whole appear more bulky, and when the chest is laid open they may appear as if Fig. 225. 'V^^''^ Emphysema of lung, portion of the wall of an alveolus. There are several rounded apertures. In some parts, and especially at right-hand corner, an aperture seems to be forming by the separation of epithelium which has come to form the entire thickness of the alveolar wall. X <)00. (TniERrEr.DER.) bulging out at the aperture. This appearance is not altogether due to enlargement, but to a certain extent it is related to the fact that as the elastic tissue is largely lost the lungs do not retract in the normal fashion. The increase of bulk is usually most manifest at the anterior margins which, in bronchitis at least, are the most frequent seats of the lesion. The margins are unduly voluminous and the edges rounded. It not infrequently happens that certain portions of the anterior margins undergo special enlargement, a projecting piece of lung becoming by its increase in bulk partially isolated. The tongue-shaped projection at the edge of the left lung corresponding with the lower part of the heart, often presents considerable elongation and partial separation. Another locality where emphysema is often very manifest is the base. Here they are frequently rounded prominences projecting against the diaphragm, and the diaphragmatic surface of the lung as a whole may be convex instead of concave. This is especially the case in the left lung where the diaphragm is not supported by a solid organ as it is on the right side by the liver. Again the en- largement is very frequent at the apices. It has been pointed out by Jenner that the right lung often presents a special bulging pos- teriorly at a place corresponding to the space behind the trachea. The localization will be more various where the emphysema is compensatory, and in that case will depend greatly on the locality of the cause. Thus we see it around cicatrices or contracted 480 DISEASES OF THE ORGANS OF EBSPIKATION. pieces of lung, but in nearly all cases there is a tendency to affect especially the anterior parts. In all these places, with increase of bulk in general there is, even to the naked eye, a visible enlargement of the air-spaces. Nor- mally, the individual air-vesicles are scarcely visible, but in emphysema the abnormal air-spaces are plainly seen through the pleura, often giving a frothy appearance from the size of the vesi- cles and the delicacy of the partitions. Beyond this we may have all degrees of visible enlargement of the air-spaces up to consid- erable bladders as large as an egg. The emphysematous portion is unduly pale, and gives a soft downy feeling to the touch. On cutting into it there is often a creaking, crisp sound, and if the vesicles are large they collapse markedly. We have still to consider some of the effects of emphysema on other parts. The lungs are permanently increased in bulk, and the capacity of the chest is correspondingly increased. The chest is kept more or less in the condition of deep inspiration, the dia- phragm depressed and flattened, the shoulders elevated, the sternum pushed forwards and outwards, and the chest more or less barrel- shaped. The heart is depressed along with the diaphragm and placed more horizontally, while it is overlaid by the edges of the lung. The liver is pushed downwards by the flattened diaphragm. The emphj'sema has a serious effect on the circulation. We have seen that there is obstruction and destruction of the bloodvessels in the lung, and this reacting on the pulmonary artery causes engorgement of the right ventricle. The right ventricle is induced to hypertrophy by reason of the increased strain thrown on it, and by more vigorous efibrts it may to a great extent compensate for the obstruction and send enough blood through the reduced channels. But the compensation may, as the disease advances, be insufficient, and so we have insufiicient aeration of the blood and dilatation of the right ventricle without corresponding hypertrophy. On this follow all the serious results of venous engorgement already referred to. The dilatation of the heart is more apt to ensue if, from imperfect nutrition of the heart, the muscular fibre under- goes fatty degeneration, and as a matter of fact the actual fatal result is often traceable to fatty degeneration allowing of very severe venous engorgement. Senile Emphysema is primarily an atrophy of the lung tissue along with atrophy of the other tissues of the body. The lung in this form does not become more voluminous, but rather retracts and becomes softer and more pliable. On opening the chest the lungs are found much reduced in bulk and collapsed against the posterior wall of the chest. The normal weight of the lungs is about 44J ounces in the male and 35 ounces in the female, but in senile emphysema they may be only two-thirds of this weight. The air-vesicles undergo changes similar in appearance to those in ordinary vesicular emphysema; their walls atrophy and the infun- ACTIVE HYPEEJEMIA OF THE LUNGS. 481 dibula coalesce so as to form larger cavities, but this is by a simple process of atrophy. On examining the lung the increased size of the air spaces may be invisible at first, but if the lung be distended, or if after laying it open by incision it be floated in water, the large vesicles become visible. Of course old people are subject to bronchitis, and senile atrophy may strongly predispose to the more ordinary form of emphysema. DISOBDEES OP THE CIRCULATION IN THE LUNGS. It is to be remembered that the pulmonary arteries are thin- walled, and that their muscular coat is comparatively insufficient. Any increase of blood-pressure, therefore, will tell with full force on the pulmonary circulation. The capillaries are abundant and closely set, and are capable of great distention. Their dilatation will cause them to project into the air-vesicles, and it is not im- probable that they sometimes interfere seriously with the inflation of the air-vesicles. Active Hyperemia. — This is a condition which we have few opportunities of actually observing, but which is to be inferred as existing under certain circumstances. It has been a matter of question whether an increase in the strength of the cardiac con- tractions is capable by itself of producing active congestion of the lungs. But, to take a simple example, the feeling of breathlessness which one experiences in going up a hill, accompanied as it is with severe palpitation and a feeling of oppression in the chest, is probably due to an active hypersemia of the lungs from this cause. The exertion of the body sends more blood to the right ventricle and also stimulates the heart to increased exertion. A larger amount of blood is forced into the pulmonary artery, and at a greater pressure. Thus the feeling of oppression and breathless- ness may be due to the overloading of the vessels, and perhaps to some extent to the insufficient inflation of the alveoli. In some persons this condition is brought about by very slight exertion, their hearts being peculiarly excitable; or it may occur without any exertion at all. In persons with damaged hearts, in whom the pulmonary circulation is already somewhat engorged, a very slight increase in the force of the heart may bring on a further hypersemia such as to lead to severe dyspncea. Thus we know that persons suffering from mitral disease find great difficulty even in ascending a stair. An acute hypersemia sometimes develops as a collateral hyper- iEMiA. Cases have been recorded in which a person while heated has drunk large quantities of cold water, and has immediately been attacked by great dyspnoea, which has even been fatal. Hertz has related a case in which a workman, while much heated, went into a vault and drank a quantity of water which he had cooled with ice. He was immediately seized with the most intense dyspnoea, 31 482 DISEASES OF THE OBGAlSrS OF RESPIRATION. and soon began to expectorate a bright red sputum. In this case there was evidently an acute hypersemia, which would probably have proved fatal but for timely venesection. The exact mode of occurrence of such severe hypersemia has been made the subject of experimental investigation. Quantities of ice-cold water have been introduced into the stomach in animals, while the blood- pressure was registered by a kymograph connected with the carotid. The result was an immediate and very marked increase of blood-pressure. The cause of increase in pressure was not the absorption into the blood of an excess of fluid, because an equal quantity of warm water injected directly into the veins produced no such rise. The explanation is that the cold water reduces the temperature not only in the stomach but in the organs around. The result of this application of cold is contraction of arteries, and as in this neighborhood there are a large number of arteries — those of the stomach itself, the splenic, the hepatic, and the mesenteries, with their numerous tine ramifications in the mesentery and in- testine — their sudden contraction at once raises the blood-pressure, and this acts most readily backwards on the lungs. On similar grounds, we may explain the breathlessness which one experiences in plunging into cold water. Here the arteries of the skin contract, and the risk of pulmonary congestion is greater if the cutaneous arteries have been peculiarly relaxed, as when the person has been much heated beforehand. A simple active hyperaemia of the lungs seldom gives rise to cedema. We have already seen this to be the case in regard to active hypersemia in general, and it especially applies here. In the case which we have cited from Hertz there was curvature of the spine, and some contraction of the thorax, and this may have had to do with the severity of the hypersemia and the occurrence of oedema as evidenced by the rSles in the chest and the expectoration. Passive HypbrjEmia and Pulmonary OEdema.- — Passive hyper- semia is of much more frequent occurrence than that just considered. In the regular course of post-mortem examinations, we very fre- quently find that the dependent parts of the lungs present a dark- blue color due to the vessels being overfilled with blood. This condition is commonly called hypostatic engorgement, and to a certain extent it is really of post-mortem occurrence, the blood gravitating to the dependent parts of the lungs. In many cases, however, it has existed, at least partly, during life, especially when it is associated, as it commonly is, with cedema. This condition arises most frequently in persons whose hearts are weakened by debilitating diseases, and it frequently develops not long before death. In a large number of cases of all kinds of debilitating diseases we find just before death the chest full of rSles and the breathing much obstructed, and it is in these cases that we find hypersemia and csdema after death. Or the engorgement and cedema may occur in the midst of a debilitating disease, such as typhus fever, when they are regarded as of a very serious import. PASSIVE HYPEK^MIA AND PULMONARY (EDEMA. 483 Sometimes an oedema develops with remarkable suddenness, and seriously endangers life. It has been stated above that the hypersemia and oedema in these cases are connected with weakening of the heart, but it is not easy to see how this should produce such results, especially when they are of sudden occurrence. When the blood is already deteriorated, as in typhus fever, and when by reason of the weakness of the heart the circulation is very sluggish in the capil- laries of the lung, we can understand the occurrence of engorge- ment and oedema, just as in these diseases we may have gangrene of the toes. Here the absence of the proper renewal of the blood causes the vessels to lose their natural vigor and allow of transu- dation. In the more ordinary cases of hypostatic oedema occurring just before death, we have also, as a consequence of some debilitating disease, not only weakness of the heart, but the deterioration of the blood, and these together may account for the occurrence of the engorgement and oedema. But there are some cases in which oedema occurs suddenly, and without any previous anaemia or morbid condition of the blood. Some of these are cases of Bright's disease, and the oedema here is of similar import to that of the skin in that disease. There are cases, however, chiefly of heart disease, in which a sudden oedema occurs and is sometimes fatal. These cases can hardly be accounted for by a simple weakening of the heart as a whole, or else we should have oedema in cases of syncope in which there is simple failure of the heart. An endeavor has been made to account for it by sup- posing increase of blood-pressure in the pulmonary circulation. It has been shown by Cohnheim, from experiments on animals, that in oi'der to produce pulmonary oedema the blood-pressure must be enormously increased, much more than is ever likely to happen from simple mechanical interruption to the circulation in the ordinary way. This author has found, however, that if the left ventricle be paralyzed while the right keeps beating vigorously, we may have such an increase of blood-pressure as to cause oedema of the lungs. The weakened left ventricle does not empty itself, and acts as an obstruction to the return of blood from the lungs, and the obstruction is so great that the right ventricle cannot overcome it. It might be objected to this that if the left ventricle is thus paralyzed the systemic circulation will be at a standstill, and very little blood will find its way to the right ventricle. But we have to consider that in such patients there is urgent dyspnoea with violent inspiratory efibrts which have the effect of sucking the blood into the chest. The diastole of the right heart also acts in the way of drawing blood towards it. These cases then of sudden oedema may be accounted for by weakening of the left ventricle while the right remains vigorous. Any special over- straining of the left ventricle may cause sudden paralysis of it. It is not improbable also that immediately before death the pulsations of the left ventricle may, in many cases, cease before those of the 484 DISEASES OF THE OEGANS OF RESPIK ATION . right, and that the ordinary oedema at the end of debilitating diseases may have partly a similar origin. When the lungs are examined after death in cases of passive hypersemia, they present a dark-blue color which is often limited to the posterior parts and those towards the base. If oedema co- exists, as it so often does, the tissue is bulkier and inore solid. If the lung be divided with the knife and the organ squeezed, a frothy fluid mixed with blood issues from the cut surface. If the oedema exists without much hypersemia the lung is pale, but bulky and heavy, and a watery fluid exudes from the cut surface. The con- dition of hypersemia with oedema is sometimes called splenization, because the tissue is like that of the spleen in its naked-eye characters. Examined minutely, it is found that the capillaries are distended and the air-vesicles filled with serous fluid in which leucocytes and red corpuscles are present. If this condition persists, it usually passes gradually into an in- flammatoi'y condition. Fibrine is exuded into the air-vesicles, but it is mixed with serous fluid, and does not give that extreme solidi- fication to the lung which we find in acute pneumonia. The lung is more solid than in splenization, however, and the color is not so deep. In some cases we find a close approximation to actual hepatization, and there may even be breaking down of the inflam- matory products, as in the later stages of a pneumonia, so that on squeezing the lung a grumous fluid exudes from the cut surface. Passive Hyperemia of the Lungs prom Heart Disease. — This subject has to a large extent been treated of in previous para- graphs, but some special points remain to be considered. In mitral disease especially, there is a constant obstruction to the return of blood from the lungs, which, in many cases, is largely compensated by hypertrophy of the right ventricle, but even when it is so the pulmonary circulation will be constantly at an increased pressure, and there will be, consequently, a more or less permanent passive hypersemia. This passive hypersemia has various secondary re- sults. The most prominent of these during life is bronchitis, a more or less persistent catarrh of the bronchial mucous membrane. Another result is the condition designated brown induration. In this, as in other cases of prolonged passive hypersemia, the con- nective tissue of the lung is thickened and increased in density, so much so that the condition was described by Rokitansky as an in- flammatory hypertrophy of the connective tissue. At the same time the capillaries are distended and rendered tortuous. This condition of the capillaries is rendered obvious by separating a piece pf lung tissue by a ligature, placing it in nitric acid, and then in spirit. Sections will show the enlarged and varicose capillaries as a brownish-red network. The larger vessels are also dilated and their supporting connective tissue hypertrophied. The dilated capillaries are apt to allow of the leakage of blood- corpuscles into the interior of th^ alveoli, and these give the sputum a bloody appearance. Hemorrhage occurs also into the THE HEMORRHAGIC INFARCTION. 485 connective tissue, and the result is a pigmentation, the coloring matter existing in the form of granules contained in the connec- tive-tissue corpuscles. The blood in some of the capillaries may stagnate altogether, and in that case the capillaries will come to be represented by a network of brown pigment. The general appearance of the lung corresponds to the finer characters. As a whole the lung is more consistent, and does not retract so fully as usual when the chest is laid open. The color is brownish, but it varies considerably both in different cases and in different parts of the same lung. There may be a general brownish color, or there may be lighter and darker pieces, accord- ing as local hemorrhages have occurred more or less recently. We must remember that the hemorrhagic infarction occurs mainly in cases of heart disease, but has a different origin as ap- pears in the next section. The Hemorrhagic Infarction. — This condition has already been the subject of studj' when treating of embolism at p. 49. We there saw that the pulmonary artery and its branches are end- arteries, and that obstruction of one of them is likely to produce the hemorrhagic infarction. We saw, however, that two circum- stances render this result less uniform in the lungs; in the first place, the wide capillaries may act as anastomosing vessels, and so the circulation may be kept up sufiiciently to prevent diapedesis; and, in the second place, the bronchial artery keeps the lung tissue, to a certain extent, nourished. We saw that when the infarction occurs it is likely to form at the periphery of the lung, especially towards the edges where the lung substance is covered on more than one side with pleura. The infarction forms by the blood taking a backward course from the veins into the capillaries. The capillaries become engorged, and the red corpuscles pass through their walls into the lung alveoli, which they fill to the exclusion of the air. But the hemorrhagic infarction appears to form sometimes as a result rather of thrombosis than of embolism of the pulmonary artery. In cases, especially of mitral disease, there may be, from the great obstruction of the circulation in the lungs, an actual stasis in the capillaries, and if the stasis extends backwards to the pulmonary artery, it may induce coagulation there. If thrombosis occurs in the pulmonary artery, then the blood in the correspond- ing veins will take a backward course as before, and the previous engorgement of the vessels from the mitral disease will render this all the more likely; the capillaries will pe distended, and diapedesis will result. A hemorrhagic infarction occurring in this way will closely resemble one having an embolic origin, and the thrombus may be itself hardly distinguishable from an embolus. The infarction will, like the other, have a wedge-shape, with its blunt end towards the surface. It may be added that this mode of origin is much less common than the other, but that an embolus 486 DISEASES OF THE ORGANS OF RESPIRATION. is often increased in size by thrombosis, and may not obstruct till added to by thrombosis. The appearances of the hemorrhagic infarction are such as result from distention of the air-spaces with blood. If quite recent, it is of a dark-blue color, dense to the feeling, and more or less wedge- shaped, with the apex inwards. It may present all varieties of size up to half the lung. As the infarction is mostly peripheral, it may be often recognized by the dark color seen through the pleura, but it is more easily discovered by handling the lung, when the solid mass is readily detected. At first it looks, on section, like a recent blood-clot, and has almost a similar smooth surface, but, as time goes on, the color merges into brown, and the appearance may come to resemble that of red hepatization. As blood fills the air-spaces, the piece of lung is more bulky than that surrounding it. The infarction, therefore, is often seen as a rounded bulging beneath the pleura, or, when the lung is divided, it stands at a Fig. 226. tfiW From a hemorrhagic infarction of the lung. The alveolus is filled with red blood-cor- puscles, with one or two large catarrhal cells. In the wall of the alveolus the capillaries are greatly distended with blood. X 350. higher level than the surrounding tissue. The pleura over the infarction is usually covered with a layer of fibrinous exudation of a yellow color, and the pleural cavity contains fluid, often in considerable quantity. & EMBOLISM OF THE PULMONARY ARTERY. 487 Under the microscope, as shown in Figure 226, we have simply an enormous aggregation of red corpuscles in the lung alveoli and finer bronchial tubes, with distention of the pulmonary capil- laries. There is usually hardly a trace of fibrine to be seen, merely red corpuscles which have escaped by diapedesis, and perhaps a few catarrhal cells. If the patient live for some time after the occurrence of the infarction certain changes occur in it, but there are few actual observations bearing on this point. It is very probable that in some eases the infarction clears away ; the blood is discharged by expectoration, and the circulation is reestablished, but the portion of lung is unduly pigmented. In other cases the portion of lung gradually shrinks, and the ultimate result is a pigmented indura- tion. Indurations, probably of this origin, are not infrequently met with in cases of valvular disease. In still other cases the portion of lung tissue dies and sloughs, so that a cavitj' forms. This condition has probably been often mistaken for phthisis, especially as it has probably been preceded by hfemoptysis. Some- times the slough decomposes, and we have all the features of gan- grene of the lungs. It may seem strange that necrosis, which is the regular result in other organs, is not of more constant occur- rence in the lungs. It is to be remembered, however, that the lung tissue in the midst of the infarction is still nourished by the bronchial artery, and that, while the capillaries and actual walls of the alveoli may die, the interlobular connective tissue may survive, and may even use the necrosed tissue as pabulum. Embolism of the Pulmonary Artery has been referred to in its relations to the hemorrhagic infarction, but we have already seen that it by no means uniformly leads to that result. If the main artery of a lung be obstructed the infarction cannot occur, because by the obstruction of the artery the lung is deprived of blood. But even when smaller branches are occluded the infarction may be absent. Cases of sudden death after parturition occur from embolic obstruction of the lungs without any infarction. The suddenness of death in some of these cases seems to indicate that it is not due entirely to the obstruction in the lungs and consequent non-aeration of the blood. It seems rather due in great measure to the fact that, as the blood is prevented from reaching the left ventricle in sufficient amount, the brain and medulla oblongata are deprived of their proper nourishment. In such cases the right ventricle will be found dilated, while the lungs are pale and probably over-inflated by the violent but ineffectual respiratory efforts. These sudden deaths after confinement used to be ex- plained as cases of shock before Virchow pointed out their true significance. Reference has already been made to the special form of oil EMBOLISM. "When the subcutaneous fat has been much torn by injury, or when in fracture of a bone the marrow is much broken up, then fat is apt to find its way into the veins, and this is espe- 488 DISEASES OF THE ORGANS OF RESPIRATION. daily the case when the open mouths of the veins in the broken bone come in contact with the fluid fat rendered free by the tearing of the adipose tissue. The fat is carried by the veins to the right heart and thence to the lungs. It floats in the blood as larger or smaller drops, and it may obstruct branches of the pulmonary artery of not inconsiderable size, and frequently pro- duces extensive injection of the capillaries (see Fig. 227). If the Fig. 227. Wq^, ^j,^r/ ^>>/ i; ^ ^~ -^--rg :.v m Tr^£m¥^ Oil or fat embolism of the lung. The fat occupies the smaller arteries and extends into the capillaries, which, towards the right, form a network injected with oil. X 90* (Thierfelder.) obstruction be extensive, even though the capillaries are the vessels mainly affected, and then serious results may follow. We may have diapedesis and condensation, but in a scattered irregular form. When the lungs are laid open by incision, the fat drops may sometimes be detected with the naked eye by their glancing character as they have issued on the cut surface. Pulmonary Hemorrhage. — -We have still to refer to certain forms besides the hemorrhagic infarction. The hemorrhage which occurs in heart disease, and which leads on to brown induration, has been considered already. That which so frequently occurs in phthisis will be taken up afterwards. Then there is hemorrhage in consequence of tearing of the lung by a broken rib or otherwise. It is asserted also that there may be rupture of a branch of the pulmonary artery from fatty degeneration of its walls, as we may have hemorrhage in the brain from atheroma, but this is excessively rare. In the case of tearing or rupture there is a massive hemorrhage, ACUTE PNEUMONIA. 489 and the blood forms a cavity for itself just as it does in a cerebral hemorrhage. To such conditions some would apply the name pulmonary apoplexy, but as this is more frequently used to desig- nate the hemorrhagic infarction, it is perhaps better to discontinue its use. According to Eokitansky, blood thus effused may become encapsuled and subsequently become infiltrated with lime salts like a foreign body. When the hemorrhage is from the bronchial mucous membrane or the lung alveoli, then it appears in the sputum. To some extent, however, the blood remains in the air-passages, and if it be in considerable quantity it may even be carried in considerable quantity into the lung alveoli. The blood, in this case, is mixed with air, and there is no such condensation as that which occurs in the hemorrhagic infarction. In the lung alveoli the blood acting as a foreign body irritates the tissue and a catarrhal inflam- mation may result. In such cases large catarrhal cells may occupy the alveoli wherever the blood has penetrated, and these cells may be deeply stained with the coloring matter of the blood. It is stated that blood insufllated in large quantities may even cause necrosis of the lung tissue in which it lies, and so give rise to a condition like that of the infarction. This may, perhaps, occur when the lung is already seriously damaged, as in phthisis pulmonalis, but hardly in an otherwise healthy lung. It is also possible that blood may be drawn into cavities and form fibrinous plugs there. INFLAMMATIONS OF THE LUNGS. Acute Pneumonia. — This is a disease essentially of the lung alveoli, and as the most prominent feature is the exudation of fibrine into the alveoli, it is frequently called croupous pneumonia. Its causation is somewhat obscure. In considering the causation of inflammations in general, we have already referred to the fact that an irritant, such as carbolic acid, conveyed by the blood to the lungs may produce pneumonia. The fact that the disease afiects whole lobes of the lung is also in favor of the view that the irritant is conveyed by the blood. Many physicians regard it as belonging to the group of zymotic diseases, and in favor of this is the fact that, while usually endemic, it sometimes assumes an epidemic prevalence. Lately Koch and others have asserted that a bacillus is present in the lung tissue. Koch finds it in the alveoli, but only in places where the disease is advancing, the condition in this respect resembling that in erysipelas. The disease is an acute inflammation, and as the lung alveoli possesses merely a single layer of pavement epithelium the inflam- mation resembles that of serous rather than of mucous membranes. As in the former we have here a fibrinous exudation, and though this occurs primarily and mainly in the alveoli, the fibrine, as we shall see, generally extends to the finer bronchi, forming casts of them. 490 DISEASES OF THE OEGANS OF EESPIEATION". Pneumonia has been divided into three stages, a preliminary one of engorgement, a second one of hepatization, which is divided into two divisions, red and gray hepatization, and lastly the stage of resolution. By separating the second stage into its two divisions we shall have four stages, under which arrangement it will be con- sidered here, namely, engorgement, red hepatization, gray hepati- zation, and finally purulent infiltration and resolution. In the first stage, that of engorgement, the lung-capillaries are highly injected, and there is an exudation of serious fluid into the air-vesicles. To the naked eye the affected portion of lung is of a dark-red color, to the touch it is inelastic, and the finger applied to the surface leaves a pit behind. On section a reddish serum flows out, and the tissue does not crepitate under the knife so much as in the natural state. Though heavier than usual, the dis- eased portion of lung still contains some air and therefore usually floats in water. This state, from the resemblance of the cut surface of the diseased lung to the spleen, has been called SPLBNiZATiON. So far as the merely anatomical condition is con- cerned, the lung is very much in the same state as in passive hypersemia and oedema, such as we see in the ordinary hypostatic engorgement, and we have seen that the same term splenization is applied there. In the present case, however, the splenization is not localized in the dependent parts as in the other, but it affects a definite region of lung, generally the lower lobe as a whole, along with, perhaps, a portion of the upper. The hj'persemia and CBdema are, of course, inflammatory in character, and the serum is the inflammatory exudation. Like other inflammatory exudations, this fluid contains leucocytes and also red blood-corpuscles, some- times in large numbers. As the alveoli are filled with serous fluid, the air bubbling in and out among them during respiration produces the fine crepitation which is the characteristic auscultatory sign of this stage. In the second stage, that of red hepatiza- iiON, we have fibrine exuded from the over- filled capillary vessels. In consequence a coagulum (Fig. 228) comes to occupy the lumen of the vesicles and infundibula, instead of the mixture of serous fiuid and air which is present in the first stage. But the coagulum is not entirely composed of the fibrine effused from the vessels; it contains, in addition, abundant leucocytes and red corpuscles which are often so abundant as almost to conceal the fibrine. The fibrine may be detected as a coarse network with interlacing fibres (Tig. 229). The capillaries of the lung are in much the same state of over-distention as in the first stage, and the lung-parenchyma is likewise little -altered. The red corpuscles are present in the alveoli in very varying proportion. They are never entirely absent, Pig. 228. Cast of small l)ronchLis infundibula and air-vesi- cles in pneumonia. X 40. (CoRNiL and Ranvier.) ACUTE PNEUMONIA. 491 but in general form the minority of the total cells present; in some cases they are equal to the white ones, in some more abundant. In very rare cases they are so abundant that the exudation has more the character of an ordinary clot than of a fibrinous exudation. In Pig. 229. Alveolus filled with fibrine and a few leucocytes, from a case of pneumonia in stage of red hepatization. X 350. these latter cases, which may be described as hemorrhagic pneu- monia, the lung itself has a deep-red color. These are mostly very severe cases, and imply a previous state of debility in the patient, very commonly referrible to alcoholic excess. In accordance with this exudation of red blood-corpuscles we have in this and in the preceding stage, the rusty tinge of the sputum which is character- istic of pneumonia. The appearance of the lung in this stage is somewhat different from that in the first. It retains its red color, both from the continuance of the congestion of the capillaries and from the red corpuscles in the exudation. But it is now much firmer and heavier — it does not crepitate under the knife or finger, and it sinks in water — no air being any longer contained in the vesicles. On section from a sound part into a hepatized part, it is observed that the latter remains on a level while the sound part sinks away so that the diseased part appears enlarged. Even on 492 DISEASES OF THE ORGAN'S OF "RESPIRATION. external examination the affected part of the lung looks bulky. On more close examination, the cut surface has not the homo- geneous velvety appearance of the lung in splenization, but a coarse granular appearance, and this will be more readily seen on tearing the tissue and examining the torn surface vpith a lens. The red granulations thus brought out are undoubtedly the plugs of fibrine with corpuscles which fill the air-vesicles. If you stroke a surface so cut with the blade of the knife, you may succeed in getting one or two casts of the vesicles and infuudibula which, under the microscope, have the appearance shown in Fig. 228. If the bronchial tubes be cut open with scissors, the finer ones will generally be found to contain fine casts of soft fibrine, as if the exudation had overflowed from the alveoli into them. The appear- ance of a section of such a lung has been compared, from its solid character, granxilar surface and color, to that of the liver, hence the name hepatization applied to the second stage. The solidified lung is a much better conductor of sounds than that filled with air; hence, during life, we hear the sounds of the trachea and bronchi much more distinctly than usual; it is as if you put the stethoscope over the trachea itself. The third stage, that of gray hepatization, develops naturally out of the second (Fig. 230). In the earlier periods red corpuscles Pig. 230. Section of lung in gray hepatization. Tlie alveoli filled with plugs in which are multitudes of round cells. In the stroma the usual carbonaceous pigmentation of the lung is seen at lower part of figure. X 90. are exuded largely, but except in cases of a hemorrhagic kind the white very much preponderate in the later periods. The leucocytes ACUTE PNEUMONIA. 493 swarming into the alveoli cover up the red corpuscles. The addi- tional material in the vesicles also causes pressure to be exercised on the capillaries, which are thereby emptied. In this way we have, instead of the previous hypersemia, an ansemia of the tissue. In accordance with the much less abundance of red blood, and the presence of an additional number of colorless cells, the color of the tissue is changed. It retains the firm character, and the granular appearance of the previous stage, but the color is gray. The pig- ment of the lung intermixed with the white color of the multitu- dinous cells gives the appearance which has been aptly described as marbled. In the last stage, that of resolution and purulent infiltration, the lung returns to its normal condition. In some cases the cells and fibrine in the air-vesicles undergo fattj" degeneration, and the plugs soften. The fat is partly absorbed, but to a large extent the degenerated corpuscles are expectorated. In other cases the leucocytes go on accumulating in the air-vesicles, and as the fibrine degenerates and softens the alveoli come to contain what is virtu- ally pus. The appearance of the lung in these two conditions is not very different, as the emulsion-like fatty material is not unlike pus. The lung is still solid, still sinks in water, but its firmness is gone, its surface is pale, yellowish, or grayish-red, it has lost the granular appearance, and a grayish, dirty fluid oozes out, which makes the surface so slippery that a small portion is with difficulty lifted or held in the fingers. The tissue is also extremely soft, and tears under the mere pressure of the fingers. In removing such a lung from the body, unless care is exercised, pressure of the fingers may rupture the tissue, and as the pus or emulsion flows into the cavity it may give rise to the appearance of abscesses in the midst of the lung. This stage may be looked on as the prepa- ration for the removal of the exudation, which takes place by the degeneration and absorption of the young cells, and by their ex- pectoration. The exudation must have very thoroughly softened before it can make its way through the narrow neck of the in- fundibulum into the bronchus. After the infundibula and vesicles are emptied the blood returns in full force into the capillaries. Instead of the anaemia we have indeed a hyperemia, for the tissue has been weakened by the inflammation, and is less able to resist the blood-pressure than formerly. It should be remembered in practice that the lungs of a pneumonic patient take some time to recover from the effects of the inflammation, and great exertion during convalescence should be warned against, till the tissue has recovered its tone. While the above is the most common termination of pneumonia sometimes it does not issue so fortunately. The purulent infiltra- tion may involve the lung tissue, and by its sloughing an abscess may be formed. In this way we may have one or several abscesses of various sizes, or several may coalesce into one of larger dimen- sions. In the wall of the abscess a consideraole vessel may rupture. 494 DISEASES OF THE ORGANS OF RESPIRATION". and so we may have profuse hemorrhage. The abscess may sub- sequently burst into a bronchus or the pleura, in the latter case producing empyema and perhaps pneumothorax. Another unfortunate result which sometimes occurs is gangrene of the lung. This is mostly met with in the hemorrhagic form and in drunkards, but it may occur where there is a bronchiectatic cavity with decomposing contents. There are some cases of pneumonia which end in phthisis PXJLMONALis, and that either in the indurative or caseous form. This outcome is rare, and only occurs in persons predisposed to phthisis. Another rare result is chronic pneumonia, whose de- scription follows below. It is more common than the termination in phthisis, and is probably mistaken for the latter not infrequently. The PLEURA always takes part more or less in the inflammation of the lung. The pleural surface of the inflamed portion of lung is coated with a white fibrinous exudation, which is sometimes of considerable thickness. There is rarely any considerable serous exudation in the pleura, probably because the lung is distended with the solid exudation, fills the cavity, and by its pressure pre- vents the accumulation of fluid. Sometimes the pleural exudation takes on a purulent character, and an empyema may remain after the resolution of the pneumonia. In some cases the inflammation extends to the pericardium, on the surface of which there may be a slight flbrinous exudation. Pneumonia is an acute febrile disease, and so produces secondary changes in the organs of the body, generally comparable with those in acute specific fevers. There is commonly, but not always, enlargement of the spleen. The liver is usually enlarged, and shows parenchymatous infiltration. Chronic Pneumonia. — This name is one whose significance is somewhat ambiguous, and it will be necessary in the first place to define the meaning attached to it here. We include those condi- tions in which the lung tissue is the seat of a simple chronic in- flammation, without anything of a tubercular or otherwise specific nature. The simplest cases are those in which an acute pneumonia, instead of resolving, passes into a chronic condition. In addition to that we may have a chronic inflammation set up by the inhala- tion of irritating particles, as among potters, stone-hewers, etc. In old persons ordinary pneumonia is apt to be chronic, and it may therefore be said that senile pneumonia is included under the present head. To a certain extent the same is true of pneumonia in drunkards, and in debilitated persons, especially when it affects the apex of the lung. The chronic inflammation here, as in other organs, is chiefly characterized by a new-formation of connective tissue, so that induration of the lung is the result. In this view of it the terms chronic interstitial pneumonia, cirrhosis, sclerosis, fibroid phthisis, are sometimes used as being virtually of the same meaning as CHRONIC PjSTEUMONIA. 495 chronic pneumonia. But here it is necessary to distinguish very carefully. "We shall see afterwards that there is a form of phthisis pulmonalis in which a great new formation of connective tissue occurs, but the inflammation in that case is due to the tubercular virus. In the disease at present under consideration there is no such irritant present, and the inflammation is simple. The proper tubercular fibroid phthisis is a much commoner condition than the simple chronic induration. The appearances presented by the lung in cases of acute pneu- monia which had a prolonged course and have become chronic are not unlike those of the lung in the stage of gray hepatization. The disease is generally confined to one lung, and may aflfect only a portion of it. The lung is bulky and dense, and feels solid to the touch. When cut into, the solid lung has usually a gray color, although sometimes with a tint of red, but it has a smoother cut surface than that in hepatization, and the tissue is also tougher. To this condition the name iron-gray induration may be aptly applied. Under the microscope the conditions are such as are indicated in Fig. 231. The walls of the alveoli are greatly thickened by fibrous tissue, which largely encroaches on the alveoli, the epi- Pig. 231. Chronic pneumonia. The connective tissue is greatly increased, and the alveoli (a, a, a,) are represented by contracted spaces lined with well-formed epithelium. The epithelium here is much more distinct than in the normal alveoli. X 350. thelium of which is preserved, and sometimes occupies their interior. "When it is considered that the lung as a whole is not reduced in bulk, and that the alveoli are in great part empty, then the overgrowth of connective tissue will be understood to be very 496 DISEASES OF THE ORGANS OF EESPIRATION . great. Along with the interstitial new-formation there are commonly thickening and adhesion of the pleura. In the con- dition hitherto described, there is no considerable obliteration of the air-vesicles except in so far as they are encroached on from without. If the disease progresses, however, the new-formed connective tissue takes on a cicatricial character and by its contraction destroys and contorts the proper lung tissue. Just as in the case of cirrhosis of the liver, there is here an atrophy of the normal structure and a tendency in the organ to shrink. This leads to dilatation of the bronchi on principles already enunciated, so that bronchiectasis is a prominent feature in advanced cases of this kind. The bronchial secretion may stagnate in the dilated bronchi and de- compose ; the irritation of the decomposing juices sometimes causes ulceration, and ragged cavities may thus form, so that the condition closely resembles that of phthisis. Acute Catarrhal Pneumonia [Broncho-Pneumonia, Capillary Bronchitis). — This disease occurs most frequently in children, and is in them, as in adults, associated with catarrh of the liner bronchi. So close is the connection between the pulmonary catarrh and that of the bronchi that the disease may very properly be called broncho- pneumonia. The bronchi are first affected, and so it may be said that the pneumonia springs out of a capillary bronchitis, the tubes affected being those of the finest calibre. In a large pro- portion of cases the bronchitis originates in measles, or it may occur in diphtheria, or smallpox, or whooping-cough. In adults it may follow typhoid or other infectious fever, or it may be the result of the inhalation of irritating gases, or of the presence of decomposing material or foreign bodies. It is to be noted that an ordinary bronchial catarrh, such as was described in the section on bronchitis, seldom goes on to a catarrhal pneumonia, but that for the most part the latter is due to the existence of some special irritant such as the virus of measles or decomposing juices in the bronchial tubes. We have already seen that the presence of blood in the alveoli may cause it, and this is a good instance of the action of a foreign substance in its production. In this regard it is interesting that a catarrhal pneumonia maj' be produced in animals by division of the pneumogastric nerves. The pneumonia here seems due to stagnation of the secretion which is no longer expelled, and to the irritation which this produces. As the disease begins in the bronchial tubes and is propagated to the lung tissue, it follows in its distribution the arrangement of the bronchial tubes; that is to say, it occurs in a lobular form. Although the disease is thus primarily lobular, it is clear that it will often occur in several neighboring lobules, and so a considerable tract of lung may be involved. This will be more particularly the case when it is due to the insufflation of irritating substances, which may be distributed in almost all the lobules of the lung. ACUTE CATARRHAL PNEUMONIA. 497 As the disease begins in a catarrh of the finer bronchi, there is often COLLAPSE of the corresponding portion of lung before any actual inflammatory processes occur in it. The obstruction of the tubes with tough secretion sufficiently accounts for this collapse. It is a lobular collapse, and as seen from the surface areas of larger or smaller size are depressed and of a bluish-red color. These are mostly to be found in the first instance at the posterior and inferior parts of the lung. In other parts, and especially in the upper lobes, we may have emphysema. With or without a previous stage of collapse, the inflammation by and by extends to the lung alveoli. There is a rich production of catarrhal cells, which fill the alveoli and cause condensation of the lung. The afliected pieces of lung tissue are firm and pale, and again present more or less of the lobular arrangement. This condensation of the lung tissue may be more or less extensive, and as it springs very often out of col- lapse there may be various gradations visible in the same lung. The inflammatory products in the air-vesieles may after a time undergo fatty degeneration, break down, and be discharged, some part of them being probably absorbed by the lymphatics. In some cases, however, the result is not in every part of the lung so fortunate. For one thing, the collapse may never go on to a proper condensation, and when recovery takes place the collapsed portion remains uninflated. Or, again, the catarrh may become chronic, and, being associated with an interstitial inflammation, result in a permanent induration, the alveoli being encroached on by the growing connective tissue, as in the case of chronic pneumonia. In this way, the person, though recovering, emerges from the disease with a damaged lung ; according to the extent of the permanent damage will be the shrinking of the lung and possible displacement of organs. Again, phthisis pulmonalis may develop out of an acute catarrhal pneumonia, but this is fortunately an unusual result. The inflammatory products in this disease deserve particular notice. In the acute capillary bronchitis we have a muco-purulent material produced, and on section of the lung little yellow drops appear on the cut surface. In the alveoli themselves the secretion is more apt to contain large cells of epithelial origin and character^ but here also pus-corpuscles or leucocytes often predominate largely. These leucocytes are very often not by any means confined to the surface of the mucous membrane and the alveoli, but are often present abundantly in the connective tissue around the bronchi and between the lobules. In fact the lung tissue may be largely over-run by leucocytes, and the characters of an acute INTERSTITIAL PNEUMONIA may be added to those of catarrhal inflammation. It has already been mentioned that the disease begins in the bronchi, and it has been asserted by Buhl that, throughout, the inflammation remains confined to the bronchi, the inflammatory products found in the alveoli being simply insufflated from the bronchi. This view, however, can hardly be maintained, as 32 498 DI.SEASES OF THE ORGANS OP EESPIRATIOK' . evidence of acute changes can actually be observed in the epithe- lium of the alveoli. GANGKENE OP THE LUNGS. In this condition necrosis of a definite piece of lung tissue occurs. The necrosis is always accompanied or followed hy de- composition, and the irritating character of the decomposing material plays an important part in the processes concerned. The gangrene may itself arise by the action of decomposing material. If a foreign substance, such as a piece of solid food, gets into the bronchi, it may induce a bronchitis with putrescence of the secretion, and the irritation of the putrid juices may induce gangrene of the lung. Similarly, putrid juices inspired from ulcers and wounds of the mouth and air-passages, or perforation of abscesses or ulcers into the trachea or bronchi may set it up. Again, the juices in cavities, especially in those arising by dilatation of bronchi, may stagnate and decompose, and lead to gangrene. "Wounds and con- tusions may cause necrosis directly. -Sometimes the lung tissue dies in severe cases of typhoid fever or other zymotic diseases. "We have also seen that gangrene may occasionally follow the hemorrhagic infarction or acute pneumonia, and that it is a constant feature of the metastatic abscess. Lastly, there are some cases in which the cause of the gangrene is obscure, but these cases, as well as those with more definite cause, are somewhat common in persons given to alcoholic excess. It is customary to divide gangrene of the lung into a circum- scribed and a diifuse form. In both the lung tissue dies and decomposes, ultimately becoming separated, if the patient survive, as a shreddy slough, which occupies the cavity formed by the loss of tissue. In the diffuse form there are gangrenous patches throughout the lung, or a considerable portion of it, and there is much less probability of the effects becoming limited by reactive inflammation in the neighborhood. The diffuse form not infre- quently develops from the circumscribed, the decomposing juices from the slough causing still further necrosis. The various changes which occur around a gangrenous piece of lung, and in more distant parts of the organ, are related to the irritating character of the slough. These changes are mainly in- flammatory. The immediately neighboring lung tissue is acutely inflamed, and there is thus a zone of condensation around having the usual features of acute pneumonia, often with a specially hemorrhagic character. In this inflammatory zone the gangrene may advance. On the other hand the slough may be detached by the inflammatory process, and through time, a more chronic in- flammation having occurred, the slough may be separated from the lung tissue by a layer of granulation tissue which produces pus abundantly into the interior of the cavity. If the slough be small enough the cavity may, after the discharge of the slough. PHTHISIS PULMONALIS. 499 ultimately contract and form a cicatrix, but in the case of larger sloughs a suppurating cavity may long remain. The effect on the bronchial mucous membrane is of importance. The decomposing juices from the slough and from the inflamed lung tissue find their way into the bronchial tubes, where they set up an acute inflammation of a highly suppurative character. A rich secretion of putrid pus is the result. This secretion carried to the bronchi in other parts of the lung may set up gangrene in numerous small isolated patches, and in this way multiple small abscesses may occur. If the gangrene be near the surface an acute pleurisy is the result with fibrinous exudation. Sometimes the cavity opens into the pleura, and we have a suppurative pleurisy, perhaps with pneumothorax. An occasional complication of gan- grene is hemorrhage. As the slough separates from the living tissue the more resistant tissues retain their connection longest. The bronchi and larger vessels sometimes remain as rigid trabeculse in the midst of the soft slough. The arteries remain longest in connection, but they are usually filled with thrombi and ob- literated. Occasionally, however, the gangrene advances around an artery which is still pervious, and in that case hemorrhage of a serious or even fatal character may result. Sometimes the gan- grene leads to a definite septicsemia, or metastatic inflammations result, having their seats especially in the brain. In these cases the decomposing material gets into the pulmonary veins, having first caused thrombosis of them. A peculiar feature in gangrene of the lung is the very abundant and highly putrid sputum. The decomposing juices from the slough set up, wherever they are carried, acute suppurative in- flammations, and the abundant inflammatory products also undergo decomposition. The bronchial tubes being weakened by the severe inflammation often undergo dilatation, and the material stagnates in them all the more, and decomposes. So it happens that in the cavity itself, and in the dilated bronchi there are usually large quantities of putrid secretion. This is expectorated at intervals, and sometimes so abundantly that it pours out of the nose and mouth. The sputum is extraordinarily fetid, and if allowed to stand deposits ti'iple phosphates, crystals of margarin, etc. It also contains abundant pus-corpuscles, many of them broken down by decomposition, pieces of lung tissue, and bacteria isolated and in colonies. Sometimes the sputum contains also spirilla. PHTHISIS PULMONALIS. Under this designation are included conditions in which there is disease of the lungs, accompanied by destruction of the lung tissue and wasting of the body. The disease is usually progressive, but it presents all degrees of acuteness and the greatest variety in its duration. When we look at the lung removed from a case of phthisis, and observe the various appearances, the cavities, the 500 DISEASES OF THE ORGANS OF BESPIRATIOX. solidifications, the indurations, the yellow caseous appearances, and so on, we seem to see nothing but inextricable confusion. And when we subject the phthisical lung to microscopic examina- tion, the confusion is hardly reduced. We see evidences of inflam- mation aftecting bronchi, alveoli, and interstitial tissue ; we see the inflammatory products undergoing processes of degeneration and organization ; we see tubercles, also variously modified ; but the interrelation of the various conditions is by no means apparent. It is clear that there is some serious disturbing cause present, but the connection of the various phenomena with this cause is not clear. In accordance with our usual method it will be proper here to inquire what is the cause of phthisis pulmonalis. We shall put aside in the mean time the true tubercles which are of almost constant occurrence in most forms of phthisis, and, looking merely at the anatomical changes in the lung tissue, we shall find them comprised under the two processes — namely, inflammation and necrosis. The inflammation manifests itself in the interstitial connective tissue, in the alveoli, and in the bronchi; and the necrosis involves inflammatory products and lung tissue. We shall see afterwards that in ditt'erent cases the difterent structures of the lungs are involved to a varying degree, but in a large pro- portion we have both catarrhal and interstitial inflammations to some extent. Now, we have seen that inflammations arise as the result of the action of some irritant, and that necrosis frequently goes along with inflammation if the irritant be a severe one. We have to inquire here what may be the nature of the irritant, and what may be the cause of the necrosis which is such a frequent concurrent. There are some cases of phthisis which owe their origin to syphilis. The syphilitic virus here, as in other organs, gives rise mainly to an interstitial inflammation. Along with this we find, in some cases, at intervals that more pronounced new formation of granulation-tissue which is designated the gumma. In the gumma we have caseous necrosis, so that in this disease we may have, as in ordinary phthisis, the combination of inflammation and necrosis. But syphilitic phthisis is a rare disease, and in the vast majority of cases of phthisis, syphilis has nothing to do with it. There can now be little doubt that in the ordinary forms of phthisis there is a virus present, and that this is related to the micro-organism already referred to and described at p. 161. It is not to be asserted that the existence of this organism explains everything. We must presume a previous state of susceptibility in the individual, but when this exists the virus takes possession, and all the progressive lesions are apt to follow. It may be well here to refer briefly to the various phases through which the views as to the pathology op phthisis have gone since the time of Lsennec, especially as many of the terms PHTHISIS PULMONALIS. 501 in common use in connection with ihe disease are related to some of these views. Lsennec believed that there was a particular tubercular matter which was liable to be deposited in the lungs or elsewhere. It might be deposited in isolated places, forming miliary tubercles, or infiltrated into a considerable portion of lung, forming infil- trated tubercle. In both cases the deposit usually begins as a gray, transparent structure, which, however, is prone to change into a yellow or whitish material which is drier and harder. This yellow material was called yellow or crude tubercle, whether occurring in the isolated or in the infiltrated form. All cases were regarded as tubercular in ^A'hich there were either isolated nodules or exten- sive infiltrations, whether these were gray or yellow. By and by it came to be seen, however, that many of the con- ditions in phthisis are simply inflammatory. The minute histo- logical characters of what we now call the tubercle were discrimi- nated, and the essentially inflammatory processes were sought to be separated from the tubercular. It was shown that the existence of caseous material is no evidence of tuberculosis, since the ordi- nary products of inflammation and other new formations, such as tumors, may undergo this change, which, in its essence, is really a necrosis with degeneration of the structures concerned. In phthisis, then, the process is largely an inflammatory one, with the special tendency in the products of inflammation to undergo a caseous metamorphosis. In this way arose Virchow's designation CASEOUS PNEUMONIA — namely, an inflammation with a caseous ten- dency in its products, just as scrofulous disease of the glands is an adenitis with a similar tendency. When the lungs in phthisis were more particularly examined, however, it was found that the condition is not such a purely inflammatory one as Virchow's position would indicate. In all stages of the disease, tubercles are to be found alongside the inflammatory products. The tubercles undergo changes similar to these, and it is often difl&cult to discriminate between the two, especially when caseous metamorphosis has occurred. But in nearly all cases where the disease is advancing proper tubercles are to be found along with the inflammatory conditions. The more modern ^Dosition brings us back more nearly to that of Lsennec. Again we regard phthisis as a tubercular disease, but not merely in the general sense of Lsennec. "We are to ob- serve carefully the inflammatory processes and distinguish their effects on the lung tissue. Our position differs also from Lsen- nec's in respect that he regarded a particular state of the constitu- tion as the essential cause of the tuberculosis. It is not to be denied that the lungs must be in a state of susceptibility before they can be affected by the tubercular virus, but the same may be said concerning any form of tuberculosis, and, indeed, concerning ordinary inflammatory processes. We know that different per- sons, or the same person at different times, are very variously sus- ceptible to catarrhs, and to inflammations of all sorts. 502 DISEASES OF TllE ORGANS OF EESPIR ATION. "We are to regard phthisis puhnonalis as a local tuberculosis, in which chronic inflammatory processes and the actual formation of tubercles play their parts, and both lead on to tiecrosis and ulceration. It is necessary here to observe that phthisis pulmonalis has nothing to do with acute miliary tuberculosis of the lungs. This condition is merely part of a general tuberculosis in which the virus is in the blood. Phthisis may indeed give origin to general tuberculosis by the virus getting into the blood in sufficient quantity, but it does so very rarely, and the great majority of cases of general tuberculosis are not even associated with phthisis pul- monalis. We have still to consider the conditions of the lungs which PREDISPOSE to the occurrence of phthisis, and the path by which the tubercular virus finds access to the lungs. All authors seem agreed that phthisis is in many cases hereditary. That is to say, persons are born with a condition of lungs which renders them peculiarly susceptible to the changes which are to be described below. Taking the view that these changes are due to the tuber- cular virus it seems that persons are born with constitutions peculiarly incapable of resisting the action of the virus. It need hardly be said that this is perfectly consistent with what we know concerning other diseases. There are families in which diphtheria and scarlet fever make the most serious ravages, and there are others which they never attack. There are persons who are attacked by every form of fever in turn, there are others equally exposed who take none. But, besides an inherited liability, there is an acquired tendency to phthisis. This occurs principally in persons placed in circumstances in which the general health is reduced, and where especially the respiratory functions do not get justice. Persons living in close dwellings, especially when at their work, in factories and otherwise, are in the habit of breathing vitiated air, in which, it may be, finely divided dust is abundantly suspended, and thus frequently acquire a tendency to phthisis although originally free from it. We have now to inquire as to the path of entrance of the irri- tant to the lungs. In the study of the lesions met with we shall find that they all start at the finer bronchi. A catarrh of the finest bronchial tubes, usually occurring in a number of these simultane- ously, is the starting-point of a variety of lesions, which, however, for a considerable time remain related to the bronchi in their dis- tribution. This is a sufficient indication that the agent finds access to the lungs by the inspired air. Before leaving the etiology of phthisis, we may consider its almost uniform localization at the apex of the lungs, at least at the outset. The cause of this localization is generally regarded as obscure, but as has been hinted it has probably to do with the fact that the apices of the lungs are the least expansile portions. The first rib even in women is very little raised in inspiration, and in PHTHISIS PULMONALIS. 503 persons witli weak respiratory movements the air is apt to stagnate at the apex. This view receives some confirmation from the fact that phthisis so frequently improves when the patients go to reside in high altitudes where the rarefied air requires more vigorous respiratory efforts. In such persons the size of the chest as a whole generally undergoes an increase. If the localization of the disease at the apices is due to imperfect expansion of the lungs, then this will fall in perfectly with the view that the disease orginates in a virus inhaled from without. If the air stagnates the virus will remain lying in the lung, and will have time to develop and begin its disastrous effects. Koch found that the bacillus is of slow development, at least at first, so that the absence of disturbance will greatly favor its growth. Anatomical Changes in Phthisis. — -In studying the changes in the lung it will be necessary to give descriptions of the various processes separately, and to a certain extent these processes are separable, but at the same time it will be understood that many of them go together and by their simultaneous occurrence fre- quently mask each other. It may be said in general that the disease, beginning in the finer bronchi, tends to spread in one of two directions, or in both of them at once, namely, from the bronchus to the surrounding connective tissue and on into the general connective tissue of the lungs, or else along the bronchus to the lung alveoli. In both cases we find tubercles developed in all stages of the process, and in both there is inflammation, but of different kinds according to the structures involved. In the case of the connective tissue the inflammation produces new formation of connective tissue and consequent induration. In the case of the alveoli it is a catarrh, although the alveolar wall may be at the same time involved. It is exceedingly difficult to say what de- termines the one or the other mode of extension, but it is probable that it depends on individual peculiarities. Some persons are peculiarly liable to catarrh of the alveoli, and some are not. It is important to observe that the tubercles which occur in both cases partake, to a considerable extent, of the peculiarities of the in- flammations. In the case of extension to the connective tissue the tubercles tend to undergo fibrous transformation. In the other case they are liable rather to caseous metamorphosis. As the morbid changes begin in the bronchial tubes we shall begin our description by the processes met with there. Condition op the Bronchi. — The most constant primary change is catarrh, but it is a much more chronic catarrh than that of ordinary bronchitis. Whether catarrh occurs without the forma- tion of tubercles or not, it is impossible to say, but certainly tubercles are to be found at a comparatively early period. The catarrhal products sometimes dry in and become caseous, especially when the phthisis passes on to catarrh of the alveoli. This change may also occur in the other form of extension, and we may find a 504 DISEASES OF THE ORGANS OF RESPIRATION. bronchus plugged with a white mass and surrounded by indurated connective tissue. The catarrh is not infrequently accompanied by ulceration of the bronchial mucous membrane, and little cavities frequently arise in this way, the cavity appearing to the naked eye to form a sacculated dilatation of a small bronchial tube. These ulcers are surrounded by inflamed and indurated connective tissue, in the midst of which numerous tubercles are to be found (see Fig. 232). The ulcer here is essentially like the tubercular ulcer Fig. 232. Tubercular ulcer of bronchus; u, mucous membrane; b, muscular coat. At rf there is a small ulcer on the summit of a swelling. In the latter are several tubercles indicated by the concentric shading. The muscular coat is broken up by the tubercles. X 60. (Rindfleisch.) of the intestine or the urino-genital canals. We shall next consider the appearances presented when the irritation extends from the bronchi to the surrounding connective tissue, in which case the re- sulting inflammation may be designated peribronchitis. Acute Peribronchitis. — In some very rapid cases the peribron- chitis is acute, and may even be purulent. Suppuration occurs in the bronchial wall as well as in the surrounding tissue, and, these structures being broken up, a kind of acute abscess is formed. Some of these abscesses may be near the surface and by rapidly "undermining the pleura cause it to slough. By the separation of the sloughs the cavity of the abscess may come to communicate with the pleural cavity and so pneumothorax may result. The peribronchitis, however, is very rarely the only prominent condition. Along with it there is inflammation of the alveoli, but here too it is an acute inflammation, and the products are small round cells rather than the larger epithelioid elements of catarrhal inflamma- tion. This inflammatory condition of the alveoli existing in the neighborhood of the suppurating bronchi assists in the formation of the abscesses. Sometimes there is even a gangrenous condition developed, and actual sloughing of pieces of lung tissue occurs. Acute cases such as these bespeak a peculiar virulence of the morbid agent or a peculiar susceptibility of the patient. They usually pass rapidly on to a fatal issue with high fever. In some cases recovery takes place, the pus dries in or is discharged, and PHTHISIS PULMONALIS. 505 the abscesses become surrounded by indurated connective tissue and contract. iPiBRous Peribbonchitis. Fibroid Phthisis. — This is a chronic process, and is more common than the acute condition just de- scribed. In an early stage of this disease the lung, especially in the upper lobes, may be found dotted over with hard masses, often nearly black in color. These are small in size and isolated. On examination they are found to consist each of a small bronchus surrounded by indurated and pigmented connective tissue in which tubercles are to be found. The disease has begun in a set of bronchi of nearly the same size and has produced similar results in all. The appearances of inflammation here ai'e similar to those in other parts. The mucous membrane and the connective tissue outside are infiltrated with round cells, which as usual develop dense con- nective tissue. Sometimes tlaere are tubercular ulcers of the bronchi having the characters already described. It has been stated above that these nodules are often nearly black in color. This coloration is derived from the blood-pigment, and may be an indication of the existence of minute hemorrhages, or else of occlusion of the vessels by the contracting tissue and staining of the tissue with the coloring matter dissolved out from the blood left in the obstructed vessels. It is to be noted that in this stage considerable hemorrhage may take place into the bronchi. The hemorrhage from each spot may be trifling, but from many together a severe hsemoptysis may occur. Some cases of haemop- tysis before any clinical signs of phthisis have manifested them- selves are of this kind. The blood may to some extent come from the tubercular ulcers, but apparently this is not necessary. In many cases this tendency to pigmentation is manifest throughout the disease, and the extensive formations of connective tissue which occur are frequently of a slaty color. The new formation of connective tissue may limit itself for a considerable time to the neighborhood of the bronchial tubes, and the nodules may enlarge. But as a rule it slowlj' extends outwards to the interstitial tissue of the lungs generally. An extensive new formation of dense connective tissue thus occurs throughout the lungs. The normal connective tissue of the lungs lies mainly around the bronchi and vessels, and between the lobules, and it forms one system with the subpleural layer, the tissue in these three situations being in intimate connection hj means of the lym- phatics. Hamilton has pointed out very instructively how foreign material, such as dust, when inhaled and conveyed into the lung tissue is carried about the lung and deposited in these three situa- tions. In similar fashion the irritant in the condition under con- sideration seems to be conveyed and produces inflammatory indura- tion everywhere. The new-formed connective tissue may be found in different stages of development, according to the particular part examined. We may find mainly round cells, spindle cells, or a dense tissue like that of the cicatrix, in which only small spindle 506 DISEASES OF THE ORGANS OF EESPIE ATIO^" . cells are to be found. In all these stages tubercles can be seen, and they also, as they undergo fibroid transformation, present various appearances. In the latter stage the tubercles are repre- sented merely by a concentric arrangement of the dense connec- tive tissue at intervals, this concentric appearance being sometimes emphasized by the existence of pigment. If the lung be examined when this disease is fully developed, there will be found, to begin with, a very firm adhesion of the pleura over the diseased part. The pleura often undergoes a very remarkable thickening reaching sometimes half an inch, and the thickened portion may form a kind of hard cap at the apex of the lung. When cut into there are trabeculse of firm tissue traversing the lung, and frequently retaining something of the interlobular arrangement in respect that the trabeculse tend to pass towards the root of the lung. The lung tissue which remains in the midst of these masses of connective tissue is often emphysematous, but the dilated alveoli present also thickening of their walls. Besides all this there are commonly cavities, and sometimes these are of very large dimensions. The cavities have as a rule the characters of bronchiectasis. The bronchiectatic cavity has a distinct lining membrane which may limit it from surrounding lung tissue. This lining membrane is sometimes directly con- tinuous with the bronchial membrane, and the cavity may be obviously continuous with the bronchus, having sometimes an elongated shape with sacculated dilatations. But the cavities are often much more than mere dilatations of the bronchi. We may find almost the entire upper lobe forming one cavity M'ith a dis- tinct lining membrane, and with partial septa radiating from the neighborhood of the root of the lung. The occurrence of emphysema and cavities in this form of phthisis merits more particular consideration. The emphysema is largely compensatory. By the formation and contraction of the connective tissue large numbers of alveoli are destroyed and the remaining ones dilate to fill up the space. The cavities are obviously formed in connection with the bronchial tubes. To a certain extent the dilatation is compensatory like the emphj'seraa, and the inflammatory infiltration of the wall may allow more readily of dilatation. It is to be remembered also that tubercular ulceration often accompanies the process, and where this exists dilatation will more readily occur ; besides that, a gap caused by ulceration may, as we have seen, have much the appearance of a dilatation. There is another way in which dilatation of the bronchi occurs, and this has been well described by Hamilton. There are agents at work which may directly pull out the bronchial wall. We have seen that there is usually thickening and adhesion of the pleura on the one hand, and the peribronchial induration on the other. BetM^een these there is the indurated interlobular con- nective tissue, which by its contraction tends to approximate the two. As the pleura is fixed to the chest wall by firm adhesions there is a dragging in of this wall, producing the flattening of the PHTHISJS PULMONALIS. 507 apex which is sometimes so very marked in this disease. But the bronchial wall is also drawn outwards, at first unequally, so that the cavity is an irregular one. _ There is still another method by which cavities form in this disease ; it has been already referred to and compared to that of the formation of the retention-cyst. The peribronchial connective tissue may contract concentrically and obstruct small bronchial tubes, or the obstruction may be assisted by the drying-in of the catarrhal products in the lumen of the tube. If a small tube be thus obstructed, the secretion may accumulate behind and cause dilatation of the tube, this occurring the more readily that these fine tubes are thin-walled. In this way we may have sacculated dilatations of the tubes, and the communications with the bronchi from which they took origin may even be obscured or cut off. In cavities thus formed the lining membrane is very commonly directly in contact with sound lung tissue, and although the wall is composed largely of round-celled tissue of an inflammatory kind, yet here, as in other bronchiectatic cavities, ciliated epi- thelial cells are usually to be found. The cavity frequently con- tains pus, and if it be near the surface and of rapid formation it may so undermine the pleura as to caiise necrosis and render pneumothorax imminent. It is to be remembered that, although these processes may occur by themselves, and in their aggravated form warrant the special designation of fibroid phthisis or cirrhosis of the lung, yet many of them occur along with the changes next to be described. This applies especially to the peribronchitis and the induration of the connective tissue around the individual lobules, as distinguished from an induration of the general connective tissue of the lungs. Catarrhal or Caseous Form. — We have now to consider the other mode of extension, namely, from the finer bi'onchi along to the alveoli. In studying acute catarrhal pneumonia we have seen that the disease begins with a capillary bronchitis which runs into a proper pneumonia. In the present case there is a similar ex- tension, so that the condition is sometimes called chronic catar- rhal PNEUJioNiA, or broncho pneumonia. But there are cei'tain important differences which from the first should be borne in mind. In the first place the affection of the finer bronchi is not a simple catarrh, but is accompanied by the formation of tubercles. These tubercles form most readily, according to Kindfleisch, just where the bronchial tubes pass into the lung alveoli, attacking the projecting angles at the points where bronchi give place to in- fundibula. Another distinction is that, as the tubercles are in the connective tissue forming the bronchial wall, so there is always some inflammatory inflltration of the wall with more or less peri- bronchitis. In like manner, when the disease passes into the alveoli it does not, like the acute catarrhal pneumonia, conflne itself to the surface, but here again we have it extending into the alveolar wall and producing thickening and induration there. 508 DISEASES OF THE OEGANS OF RESPIRATION". Lastly, there is a marked tendency for the products of inflamma- tion to undergo caseous necrosis. This process occurs not only in the material accumulated in the alveoli, but also in the alveolar wall and the wall of the bronchus. So characteristic is. this con- dition in many cases that as we have seen the name CASEOUS PNEUMONIA has been sometimes applied. The disease beginning in a catarrh with infiltra- tion of the bronchus passes on to catarrh of the alveoli. The inflammation leads to the filling up of the alveoli with cells which are mostly of the large epithelioid character, such as are shown in Fig. 233. With these may be mingled small round cells such as exist in ordinary acute pneumonia, but there is rarely a filling up of the alveoli with small round cells and fibrine such as we see in hepatization, although in very acute cases this may occur. The alveolar wall, as has already been noticed, is infiltrated with inflammatory round cells, and it is very often diflicult to distinguish the exact boundaries of the alveoli, the swollen wall being ill-defined from the products inside. The re- sult of all this is a conden sation of the lung tissue, and according to the extent of the affected areas will there be larger or smaller solidification s of the lung. These will always in their distribution bear a relation to the bronchial stems, having usually in this early stage a ■ distinctly lobular arrangement, like bunches of fruit in clusters. . These condensations will Lung in ciseous form of] hth s s, the cap llaries injected (shown black). At A there are catarrhal cells (6) in alveoli, and the capillaries are well filled. At B, the capillaries are less injected. At 0, caseous necrosis has begun; and at i>, it is complete, the structure being here quite obscured in a general granular opacity. X 350. (Hamilton.) PHTHISIS PULMONALIS. 509 have a gray color, but soon caseous necrosis occurs, and it is rare to find many of them purely gray. The caseous necrosis has been ascribed to the infiltration of the alveolar wall, causing compression of the bloodvessels, and consequent ansemia, resulting in degenera- tion and death. It is true that in a caseating condensation the vessels do become obstructed, as may be proved by injection (see Fig. 233), but this is just as likely to be the result of the necrosis as the cause. In the swelling and induration of connective tissue produced in ordinary inflammations we never have such obstruction of the vessels or a caseous process. Moreover, the inflammatory infiltration is derived from the blood, and it seems strange that the bloodvessels should yield material to such an extent as to cause their own obstruction. The process of caseation so characteristic of the condition we are describing must be set down to a different cause. It is analogous to the caseation of syphilitic and tubercular formations, and due to the virulence of the agent which produces the primary changes. In the present case the caseous necrosis attacks indiscriminately the whole structures concerned. Begin- ning in the central parts of each small condensation, it involves the products within the alveoli, the altered alveolar wall, the tubercles, and the fine bronchus. The caseous area presents under the microscope a finely granular homogeneous appearance as in Fig. 288, £>, in which it is very often impossible to recognize any structure at all. Sometimes the outlines of the alveoli can be made out, but even these may be obscured. As seen with the naked eye, the caseous condition is recognized by the opaque yellow or white appearance presented, this usually beginning in the central parts of the gray condensations. As confirmatory of the view that the caseous necrosis is due directly to the action of the original irritant, it is to be noted that in very acute cases necrosis may occur almost directly and without caseation. An acute condensation takes place not unlike that of pneumonia but with the lobular distribution, and goes straight on to sloughing of the lung tissue, perhaps with a purulent peri- bronchitis. The caseous material is of course dead, and in any further changes it is merely passive. In some cases, which unfortunately are not very common, the disease makes pauses. The caseous mass becomes encapsuled and dries in more and more. By and by it becomes infiltrated with lime salts, and may thus be converted into a putty-like material, or condensed into a stony mass, which may lie for years in the lung tissue. More frequently the caseous material softens and partially liquefies, so that a cavity forms. It may be that, as Hamilton suggests, this may be due to a chemical change analogous to that which occurs in the ripening of cheese, in which, according to M. Duclaux, certain insoluble albuminates become soluble in water. The softening affects the whole caseous material, and the piece of lung concerned breaks down and liquefies, so that a small cavity results. The broken-down caseous material forms a grumous 510 DISEASES OF THE OEGAXS OE RESPIEATION. turbid fluid, in which the more resisting elastic tissue of the lung may be found still retaining to some extent the form of the alveoli. This elastic tissue may be frequently recognized in the sputum of such patients by proper methods of search (see Fig. 234). At first the cavity formed is small, but by extension of the process and Pig. 234. Lung tissue from the sputum in phthisis. The sputum was digested in caustic soda according to Fenwick's method, and then subjected to microscopic examination. X 350. coalescence of neighboring softenings, larger cavities result. These cavities are very irregular, and their walls at first ragged and ill-defined. After all the caseous material has been cleared out there may be a smoothing of the walls of the cavities by the formation of connective tissue, but there is not the regular lining membrane of the bronchiectatic cavity, nor the same relation to the bronchi. The cavity sooner or later opens into one or more bronchi, and its contents are discharged. When the caseous material is cleared out the wall assumes an inflammatory character and secretes pus more or less abundantly. In the walls of such cavities, and in the mucous membrane of the bronchi with which they are in communication, tubercular ulcers may usually be dis- tinguished. It may be well here to consider the general appearances pre- sented by the lung on post-mortem examination of an advanced case of the kind we are considering. The lung will be found firmly adherent over the upper lobe or more extensively. There will not, however, be the same thickening of the pleura as is met with so commonly in the indurative form. In removing the lung, it will generally be found that there are cavities at the apices, often PHTHISIS PULMONALIS.. 511 of very large size, and in separating the lung from the pleura there is great risk of opening into some of these cavities. If the lung after removal be divided from apex to base, various appear- ances will be presented, many of which are sometimes difficult of interpretation. There are cavities filled mostly with a grumous yellow material. These are exceedingly irregular in shape, and traversed by partial septa or by completely isolated trabeculse. These trabeculse represent branches of the pulmonary artery which have survived the general necrosis, and although the arteries are mostly obstructed, some of them remain partially pervious, and we may find aneurismal dilatations on these. The cavities have frequently no proper lining membrane, but if they are large and of some duration there is a red layer having the appearance of granulation tissue. Looking away from the cavities, the lung tissue is found condensed and frequently caseous. In the imme- diate neighborhood of the cavities the condensation is probably continuous, and is frequently accompanied with great induration of the lung tissue. But farther oflf, and especially' in the lower lobe, there are usually more isolated patches of condensation. These on section very commonly have a circular form, or they present the appearance already mentioned of clusters of fruit. By the coalescence of these we may have more continuous condensa- tions, but at the marginal parts there are usually indications of the lobular extension of the lesion. The condensed portions are usually very firm, and in each we find the opaque appearance of the caseous necrosis. In the central parts there may be softening and incipient cavities. After examining the cut surface, the bronchial tubes may be opened up with the scissors. Those which pass towards the cavities are nearly always the seat of tubercular ulceration. The mucous membrane is irregularly destroyed, and the ulcers have commonly a rather ragged appearance, but are usually superficial. The ulceration is very often prolonged into the main bronchus of the affected lung, and even to the lower part of the trachea. In the larynx there is also frequently ulceration as already desciibed, but it is not usually continuous with that in the bronchi or lower trachea, there being mostly an interval be- tween in which the mucous membrane of the trachea is normal or only red from inflammation. It is to be understood that these appearances will vary greatly according to circumstances, the chief cause of variation being the different degrees in which, along with the caseous catarrhal pneu- monia, there is induration of the connective tissue of the lung. We have seen how this induration so often starts from the bronchi, but after the extension of the catarrh to the alveoli we may have a very pronounced inflammation of the connective tissue, causing induration of the alveolar wall and extending to the general con- nective tissue. This will cause the condensation to have a much firmer character to begin with, and if the induration predominate over the caseous catarrh we may have the features of fibrous phthisis becoming pronounced in the older parts of the lesion. 512 DISEASES OP THE ORGANS OP EESPIEATION. while the more recent parts show rather those of lobular broncho- pneumonia. It may be useful here, before leaving the subject, to refer to the various modes in which cavities form and extend. We have seen that in the indurative form of fibrous phthisis, cavities form by dilatation of the bronchial tubes, tubercular ulceration often playing an important part in the process. Then we have cavities formed by the softening of the caseous material. Around such softening there is frequently a reactive inflammation, resulting in the formation of granulation tissue which finally forms the lining of the cavities. Such cavities commonly enlarge by the coales- cence of neighboring softenings, and in their walls also tubercular ulceration often progresses. Then there is the more direct destruc- tion of the lung tissue occurring in very acute cases, associated, as we have seen, with purulent peribronchitis, acute inflammation of the alveoli, and such a rapid necrosis of the tissue as to appi'oach to the characters of gangrene of the lung. The SPUTUM in phthisis pulmonalis is variously composed. In the earlier stages the expectoration has the usual characters of that in catarrh, consisting of mucus, with more or less abundant leuco- cytes. In the sputum in this early stage are often found large epithelioid cells with one or more nuclei such as we find in the lung alveoli in the catarrhal form of phthisis. These cells fre- quently present fatty degeneration. Considerable weight has sometimes been attached to the presence of such cells as evidence of the existence of the disease in its early stage, and their discovery may be useftil in this regard; but as they may exist in simple catarrhs their diagnostic value may be overrated. The sputum in phthisis often contains elastic tissue from the breaking down of the lung. In very rapid cases we may find this by a simple exam- ination of the sputum, but the search is often a difficult one because the thick mucus and pus hold the pieces of lung tissue suspended and isolated. By Fenwick's method of digestion in soda solution, pieces of lung tissue, such as that shown in Pig. 234, will frequently be found in the deposit. This method is also applicable to the sputum in gangrene of the lungs. The tubercular bacillus is usually to be found in the sputum, especially in advanced cases. The characters are shown in Fig. 56, p. 161, and have been already described. The sputum often contains blood in phthisis, and it will be proper here to inquire as to the source of hemorrhage. Bleeding sometimes occurs in early stages before cavities have formed, arising from the mucous membrane of the finer bronchial tubes. "We have already seen that this frequently occurs in the early stages of the indurative form of phthisis, and we saw reason to believe that it is sometimes related to tubercular ulceration of these bronchi, although the hypersemia coincident with the process PHTHISIS PULMONALIS. 513 probably plays the principal part. In the other form of phthisis the finer bronchi are also the source of the early hemorrhage, and here, too, the inflammatory hypereemia appears to be the principal cause, although it may be complicated with tubercular ulceration as well. In late stages after cavities have formed hemorrhage may occur from their walls. In the process of extension of cavities, whether by caseous necrosis or tubercular ulceration, the more resisting walls of the pulmonary arteries are able to persist longer than the rest of the tissues, and these form prominent elongated projections on the walls of the cavities or isolated cylindrical trabe- culse traversing them. The calibre of the artery is frequently obliterated, and the structure consists of granulation tissue in which some remains of elastic tissue may be found. But some- times the calibre persists, at least partially. At the same time the wall is infiltrated and consists essentially of soft granulation tissue. This soft tissue frequently allows of dilatation of the artery, and we have aneurisms whose walls are similarly soft and friable. Rupture of the softened wall of the artery or aneurism would occur more readily were it not that the blood-pressure is already reduced by the narrowing of the calibre, but it does occur not infrequently, and it appears that in a large proportion of cases the blood comes from aneurisms. The resulting hemorrhage is com- monly very severe, and often fatal, either by obstruction of the air- passages with the blood or from the general collapse resulting from loss of blood. The condition of the pleura in phthisis has already several times been incidentally referred to. As the pulmonary layer of the pleura or at least the subpleural tissue is part of the system of the interstitial connective tissue, it takes part in the inflammatory new-formation in the indurative form of phthisis, and we have seen that it is sometimes greatly thickened. In the other form of phthisis when the disease approaches the pleura there is always inflammation with new-formation of connective tissue, and adhe- sion of the two layers. This adhesion occurs in the way that will be described in considering the diseases of the pleura, and consists of an actual coalescence of the two layers with communication of the bloodvessels. The adhesion is often so firm that it is easier to strip off the parietal pleura from the internal surface of the thorax than to separate the layers. Sometimes it happens that the inflam- matory condition extends beyond the parietal pleura and causes adhesion of this layer to the periosteum of the ribs and intercostal tissue. In that case the separation of the lung from the chest-wall is very difficult, and sometimes cannot be accomplished without cutting. Ca^dties in the lung very often come close up to the pleura and undermine it. If the cavity be at all large, it cuts off a portion of pleura from its vascular supply from the lung. But, as a general rule, adhesion has already taken place between the two layers of pleura, and, the vessels being in communication, the portion over 33 514 DISEASES OP THE ORGANS OF RESPIRATION. the cavity is kept supplied with blood from the parietal layer. We may even suppose that the blood passing from the branches of the bronchial artery out into the parietal pleura may be conveyed along over the cavity and return in part to nourish the visceral layer. But if a cavity comes to the surface at a place vrhere vas- cular adhesion has not taken place, then necrosis of the pleura will probably result. The portion of pleura is of a dead-white color, and by and by it becomes abruptly demarcated from the neighboring parts. The line of demarcation becomes more and more distinct, and an actual separation often occurs, the result of which is communication between the cavity and the pleural sac, leading to pneumothorax. This is nearly always the manner in which pneumothorax occurs. It will happen mostly in acute cases, where the cavities form rapidly without affording time for the formation of vascular adhesions. More especially is this the case where cavities form by purulent peribronchitis with or with- out sloughing of the lung tissue. It will be seen that the occur- rence of the pneumothorax depends on the absence of adhesions, hence it happens that it so frequently occurs in the lung which is least advanced in the disease, because in that lung adhesions are less likely to be present. The pneumothorax, being associated with the passage into the sac of foreign material from the pulmo- nary cavity, generally results in an acute pleurisy, so that the layers of the pleura may be glued together by recent fibrinous exudation. It very frequently happens in a case of pneumothorax that there are several places in which necrosis of the pleura exists, one of these having given way, but the others being in a condition in which they might readily have done so. The bronchial glands are nearly always more or less effected in phthisis. They are frequently enlarged and caseous, exactly- like scrofulous glands. Like them, they contain tubercles. These caseous glands are sometimes found in a state of softening. Not infrequently the caseous material becomes impregnated with lime salts, and we may find the gland represented by a capsule filled with a material like mortar, or more nearly of a stony consistence. In the indurative form of phthisis, the tubercles in the glands undergo fibrous transformation like those in the lung tissue, and we meet with dense, hard, pigmented glands with an almost cica- tricial appearance. We have already noted the existence of tubercular ulceration of the mucous membrane of the bronchi, and of the trachea and larynx. These are to be explained by the passage of the virulent material from the broken-down lung substance, over the struct- ures concerned and its action on them. Of similar import is the ULCERATION OE THE INTESTINES, which occurs in the later stages of about two-thirds of the cases of phthisis. The material from the cavities is partly swallowed, and, containing the virus, it produces a tuberculosis in the parts of the intestine which afibrd a fitting ACUTE MILIART TUBERCULOSIS. 515 soil. These ulcers are most common in the caseating form of phthisis, and we may associate this with the fact that the debris of the lung is much greater in that form. Besides the tuberculosis of the bronchial glands and intestine, we find sometimes a tuberculosis of the ukino-genital organs, but this is comparatively rare. Then we sometimes find miliary tubercles in the liver and kidneys, scattered through these organs as in acute general tuberculosis. There are usually, however, but few tubercles compared with what we find in the latter disease. When tubercles exist scattered throughout the liver or in the kidney, we must regard that as evidence that the virus has got into the blood, although present only in small quantity there. ACUTE MILIARY TUBEECULOSIS. This condition we have already seen to be that in which the tubercular virus is contained in the blood, apparently in consider- able abundance, giving origin to miliary tubercles in many organs. The lungs are aflected in almost all cases. Acute miliary tuber- culosis is very common in children, being nearly always the fund- amental condition in acute hydrocephalus, but it also occurs in adults. If the patient die in the earlier stages, the lungs are found beset from apex to base with minute tubercles which are often very closely placed. The tubercles may be so small as to be only distinguishable as such with the microscope, but they present the typical structure of miliary tubercles. In the early stages this, with general hypersemia of the lungs, is all that can be seen. But if the case be one of rather longer duration, we find around the individual tubercles processes which can be strictly compared with those in phthisis pulmonalis. The air-vesicles are filled with catarrhal cells, and the alveolar walls infiltrated with inflammatory round cells. The tubercles appear larger, but this is because each of them is surrounded by a zone of condensed lung tissue which cannot with the naked eye be distinguished from the tubercle. By and by caseous necrosis occurs, beginning in the centres of the tubercles. As in the case of phthisis, the caseous process extends to the lung tissue and inflammatory products, and the whole is involved in an indiscriminate necrosis. The caseous material may also soften, and numerous minute cavities form, but the patient rarely survives till this has occurred to any considerable extent. The disease of animals, called by the Germans perlsucht, pre- sents many analogies to tuberculosis, and, according to the obser- vations of Koch, it depends on the same form of organism. This relation is expressed in the term bovine tuberculosis which is sometimes applied to it. We have already seen that cases of what looks like general tuberculosis occur which are probably actual cases of bovine tuberculosis transmitted to the human subject. There are also cases in which the lung is the seat of a more local 516 DISEASES OF THE ORGANS OF RESPIRATION. destructive process which may be mistaken for ordinary phthisis, especially as there may be considerable cavities produced. This subject has received notice, however, at an earlier part of this work (see p. 164). SYPHILITIC DISEASE OF THE LUNGS. This is somewhat rare, at least in the adult, although more fre- quent in the newly-born. We have here similar lesions to those in other organs, consisting of inflammatory changes with the occa- sional formation of gummata. The inflammation affects mainly, but not alone, the connective tissue, so that a condition sometimes ensues like that of fibrous phthisis. In syphilis, however, the virus coming by the blood is more generally difi"used, and we have not that relation to the bronchi which we saw in ordinary phthisis. An extensive tract of lung is involved, and we have a rich forma- tion of connective tissue so that the alveoli are compressed, while they also contain catarrhal products. In this way is produced what is called a white pneumonia. If gummata occur, they are as usual surrounded by a connective-tissue formation, so that cicatri- cial depressions and corresponding deformities of the lung may result. The gummata are often distinguishable by the caseous necrosis which they present, and if the caseous material soften we may have cavities resembling those in ordinary phthisis. TUMOKS OF THE LUNGS. Tumors of the lungs are much more frequently secondary than primary growths, but there are some forms of primary tumor. Little pieces of bone have been met with in the interstitial connec- tive tissue, also little cartilaginous tumors in connection with the cartilages of the bronchi. Secondary tumors of various kinds are met with. We have most frequently lympho-sarcomas originating in the bronchial glands and extending into the lung. The new-formation follows the connective tissue of the lung, and we find it penetrating in a radiating manner from the root, often burying the bronchial tubes in a sheath of new-formed tissue and partially or completely obstructing them. Other forms of sarcoma originating in the mediastinum may spread in a similar fashion. Secondary tumors may arise by embolism, the tumor having its origin in something conveyed to the lungs by the pulmonary artery, and being thus metastatic. Sarcomas, as we know, sometimes penetrate directly into the veins, and portions being carried to the right heart are caught in the branches of the pulmonary artery or capillaries. The secondary tumors in the lung are multiple and they repeat exactly the structure of the primary one. Thus we have giant-celled, TUMOES OF THE LUNGS. 517 round-celled, and spindle-celled sarcomas. A tolerably frequent form is the pigmented sarcoma. The enchondroma also not infre- quently undergoes secondary development, like the sarcoma, by penetrating into veins, and the embolic origin of these secondary tumors has been directly demonstrated. Cancers, as we have seen, do not readily penetrate into the veins directly. Finding an easier path by the lymphatics, they nearly always first develop in the lymphatic glands. After a time the cancerous tissue may penetrate from the lymphatic sinuses in the gland into the veins, or they may possibly in a few cases penetrate Fig. 235. Embolic cancer of lung. Two branches of the pulmonary artery («, a) are obstructed. Around them are various spaces {d, b) filled with epithelial cells, e, c, normal lung alreoli. X16. directly into the latter, and the material is carried on to the lungs. As the cancer is usually arrested for a considerable time at the lymphatic glands, it happens that in all forms of cancer secondary tumors in the lungs are of late development. As the secondary tumors are in the lymphatic glands, we may regard these in the lungs as of a tertiary order. Further, the material which produces these tumors often passes to some extent through the wide capil- laries' of the lung and on into the systemic arteries, so that we may have tertiary tumors occurring at the same time in a variety of organs. The tumors in the lung are multiple, and they repeat the structure of the primary tumor whatever lae the variety of cancer which has formed it. That these tertiary cancers form by embolism was readily seen in a case which occurred to the author, and which may here be 518 DISEASES OF THE ORGANS OF RESPIRATION. briefly related. It illustrates as well the tendency, which turners even of this order show, of the cancerous masses to penetrate into existing spaces and canals. The primary tumor was a cancer of the stomach, and secondary growths had occurred in the preverte- bral glands. One of these glands was adherent to thevena cava, and several radicles of this vein emerged from the midst of can- cerous glands. Actual cancerous thrombi of some of these veins were detected by the naked eye, and under the microscope it was seen that the cancerous masses had partially penetrated into the venous radicles in the glands. In the lungs the finer branches of Fig. 236. Embolic cancer of lung. One of the spaces filled with epithelial cells (6 in preceding figure) under a high power. There is a larger space with two branches into which the epithelial cells have extended. X 90. the pulmonary artery were found frequently obstructed (see Fig. 235). The obstructing material was not entirely cancerous in structure. There was often a round-cell formation with now and again a distinctly cancerous appearance. In most cases the ob- struction was complete. Outside the obstructed arteries there were spaces and canals filled with cancerous growths, as shown in Figs. 235 and 236. These were obviously the lymphatic channels of the sheath of the vessels into which the cancerous formation had penetrated. INHALATION OF FOREIGN SUBSTANCES. The lungs of all adults have more or less of a gray color from the existence of a black pigment in the lung tissue. This pigment is absent from the lungs of childi'en, and is undoubtedly the dust of the air inhaled with the respired air. It need hardly be said that the air of all confined spaces, such as rooms, is loaded with finely divided particles. This is particularly the case in cities ANTHEACOSIS. 519 where coal is burnt extensively, and it attains its maximum in the black fogs of such cities as London and Glasgow. The particles of dust inhaled with the air are for the most part caught by the mucus with which the surface of the bronchial tubes is moistened, and, as the ciliated epithelium plays in the direction towards the , larynx, the dust-laden mucus is carried upM^ards to the larynx, where it is either expectorated or swallowed. ISTo doubt when the .air is unusually laden Avith dust the mucous secretion is increased, and those who live in cities know that, when the weather is thick, a considerable mass of black mucus is brought up from the larynx in the morning, the busy cilia having swept it thither during the hours of sleep. But some of the dust penetrates beyond the reach of those scavengers and passes into the lung alveoli, where it lodges. From the lung alveoli it penetrates into the lung tissue. It is to be remembered that the structure of the alveolus is some- what like that of a serous membrane. There is a single layer of epithelium, and some have even described stomata or pseudo- stomata as existing. At any rate, the dust particles penetrate through or between the epithelial cells, and emerge into the lymph-spaces of the alveolar wall. Having entered the lymphatic system of the lung, the dust is carried into all the communi- cating channels of that system, and is partially deposited and retained as it goes by the connective-tissue cells. In this way a kind of pigmentation of the entire lymphatic system of the lung is obtained which for demonstration may serve the purposes of an injection of that system. In this conveyance of the dust par- ticles the leucocytes which are always present in the lymphatic spaces probably play an important part. The parts pigmented are, the walls of the alveoli, the interstitial connective tissue, especially that around the pulmonary artery and the bronchi, and the subpleural tissue, which is often definitely demarcated from the pleura proper by the pigmentation. The pigment is also carried to the bronchial glands at the root of the lung, which are more or less blackened. This pigment is a carbonaceous material consisting mostly of round particles, and is to a great extent the soot of coal. Persons who live in a very dusty atmosphere are liable to a very excessive pigmentation of the lungs, to which the name anthracosis is applied. This is seen most typically in the coal-miner's lung. Here the path by which the dust gets in, and its permanent locality, are the same as those indicated above, but the amount is greatly increased. The material also is essentially the same. It is some- times asserted that in the coal-miner's lung the pigment consists of coal dust, each minute particle having the irregular crystalline character of a piece of broken coal. But this is not entirely the case. The particles are largely spherical and smooth, and these consist of the soot from the lamps that are burnt in the mines with imperfect combustion. The pigment in this case, as in the ordinary pigmentation of the lungs, is in the lymphatics and 520 DISEASES OF THE OEGANS OF RESPIRATION. follows the distribution of the connective tissue. It is often seen in excessive quantity around the branches of the pulmonary artery, where it occupies the perivascular lymphatic spaces. It is not present in the proper walls of the bronchi, but exists to some extent in the lymphatic spaces of their adventitia. The inter- lobular and subpleural connective tissue is deeply pigmented. The inhaled dust seems a comparatively innocuous substance. In the bronchial tubes and in the alveoli it may induce, or be associated with, a catarrh, and in that case the inflammatory pro- ducts contain abuudant pigment, giving rise Fig. 237. to the well-known black spit of miners. ff;;^~x The pigment is found abundantly in cells r3^' V'''-**) as in Fig. 237. \S^t , • fs-ij^* cases of anthracosis there may be merely a ,— rf«\\, ^ " But in the lung tissue itself there is usu- ■.•>,%,'^/' " .^* ally little disturbance, and even in severe r ■ V-^ *'^ moderate induration of the connective tissue. ^^,fil '.\.' •* -' It is to be noted that in persons whose lungs • - ~^ ' ■ are the seat of excessive pigment, a catarrh Part of the eoDtents of a ig often associatcd with a recurrence of the lung alveolus in anthracopis. u ijjack spit," although the persous may have Black particles are seen, j^^ ^^^ -^ ^^^ j,g_ j^ ^^^^ ^^^^ ^^^ ^^^^]^ some angular, and others ., .t,^ , ^ n ,i • n j.- ,,%,,, , spit Will not occur unless the inflammation rounded. The large catar- .^ i , . • n i rhai cells contain many par- mvolvcs the Connective tissuc as wcll as the tides. X 360. epithelial layers of the bronchi and alveoli, and it is to be presumed that the pigment passes out of the lungs in the same way as it has passed into them, namely, from the connective tissue into the alveoli and thence outwards. As mentioned above, there is no pigmentation of the bronchial mucous membrane, and it does not seem probable that pigment will penetrate from without through the bronchial wall into the interior of the tube. This indicates that in catarrhs the connective tissue is active, and that the pigment is conveyed by leucocytes into the alveoli or bronchi. There are some persons exposed to the inhalation of particles of a more irritating nature. It has long been known that masons are peculiarly liable to bronchitis and phthisis. The particles of sandstone are inhaled just as are the particles of dust. From their shape and the sharp angles which the particles of rock crystal present, they are much more irritating than the dust par- ticles. They irritate the bronchial mucous membrane. When they pass into the interstitial tissue of the lungs they irritate it, and in this case there is frequently a very marked induration of the connective tissue. This induration, along with the bronchitis, may go on to the formation of cavities by bronchiectasis. The indurations in this disease often have special centres of greatest intensity' in the form of hard nodules, in the centres of which a collection of glistening particles may be found. Other kinds of dust may be inhaled, and give rise to inflamma- PLEURISY. 521 tory conditions in the lungs. They seem to irritate more or less according to the mechanical qualities of the particles. Particles which are hard, heavy, and angular, like the siliceous particles of sandstone, or like the steel dust to which file-cutters are exposed, irritate more than those which are light and rounded like those in the miner's lung. The color of the inhaled dust communicates itself to the lungs, and so we have various pigmentations, but in all the forms there is a tendency to the occurrence of black pig- ment along with the other colored substances. C— THE PLEUEA. Pleurisy. — The pleural sac in its structure and in many of its relations is comparable to the pericardial and peritoneal sacs, and much that has already been stated above regarding inflammation of the pericardium is applicable to inflammation of the pleura. There are two circumstances, however, that place the pleura in its pathological relations in a somewhat different position from the pericardium, and these are its connections with the lung on the one hand, and with the peritoneum on the other. In studying diseases of the lung, we have seen that whenever any form of inflammation comes to the surface of the lung it causes inflam- matory changes in the pleura; there is acute pleurisy in acute pneumonia, and chronic pleurisy is a nearly constant accompani- ment of phthisis pulmonalis. On the other hand, the pleura seems to have intimate connections with the peritoneum, as there are lymphatic channels passing through the diaphragm which form communications between the two sacs. These channels are doubt- less intricate and narrow, so that the diaphragm acts to a certain extent as a barrier between the two sacs, but it is not sutEcient to prevent the passage, for instance, of the tubercular virus from the one to the other. A tubercular peritonitis is nearly always accompanied by a tubercular pleurisy, perhaps limited to the lower parts of the sac. Similarly a septic peritonitis has usually a de- pendent pleurisy. Tumors of the peritoneum also frequently lead to similar formations in the pleura. In the above cases the pleurisy is secondary to inflammation in some other part, but there are also cases of primary pleurisy. Persons take pleurisy from catching cold, as it is said, whatever be the exact mode in which the cold produces its effects. There is very often a localized pleurisy occurring in a limited area, just where the pleura is most directly exposed to the effects of cold, namely, in the left lower lateral region. In this position the chest is not covered by any considerable mass of muscles, as the fleshy masses of the latissimus dorsi and pectoralis major passing upwards to the arm leave, as it were, an unprotected space covered by the eomparatively thin origins of the serratus magnus and external oblique muscle of the abdomen. This part is also removed from 522 DISEASES OP THE ORGANS OF RESPIEATION. the centre of heat in the heart, and on the left side instead of the liver there is the hollow stomach. On the right side the liver is a source of heat, and renders the corresponding part on this side less exposed to cold than that on the left, but still more exposed than most other parts of the chest. It is probable that, in these locali- ties especially, cold, acting directly on the chest wall, may cause an inflammation of the pleura by depressing the _ temperature. But cold may produce a general pleurisy just as it is said to pro- duce a general pneumonia, the fact of the general character of the inflammation indicating that some irritant is present in the fluid which exists in the pleural sac. It is here proper to state that a considerable number of cases appearing to be simple pleurisy are really cases of tubercular pleurisy. The tubercular virus sometimes finds its way into the pleura independently of neighboring organs, being apparently carried by the blood to the pleural sac. The lymphatic system of the lungs is not in direct communication with that of the pleura, and so it does not usually happen that a tubercular pleurisy de- velops from phthisis pulmonalis except in its later stages. The true tubercular pleurisy develops independently of lung disease, although it may be present along with tuberculosis of the lungs in acute miliary tuberculosis, where the virus is undoubtedly con- veyed by the blood. Tubercular pleurisy is usually an acute dis- ease, and is often associated with tubercular pericarditis, or, more rarely, with tubercular peritonitis. In its ANATOMICAL DETAILS, acute pleurisy is closely analogous to acute pericarditis. There is hypersemia, soon followed by a thin, fibrinous deposit. This fibrinous exudation, forming a soft, yellow layer, often attains to a considerable thickness, forming shaggy projections from the pleural surface, especially in the region of the lower lobe. Serous fiuid is also exuded, sometimes in considerable abundance. If the fluid in the pleura is not too abundant, the two surfaces of the membrane come in contact, and there is adhe- sion of the two layers of fibrine. This adhesion prevents further deposition of fibrine, which is often very thin over the upper lobe. If the inflammation goes on, there is a new formation of vascular granulation tissue which may come to replace the fibrine. If two such surfaces are in contact, by absorption of the serous fluid or otherwise, coalescence occurs and complete union of the surfaces, the granulation tissue afterwards developing into connective tissue. "We have already seen that the fluid accumulated in the pleural sac frequently compresses the lung greatlj^, producing collapse of it. An ordinary pleurisy may go on to suppuration (empyema) if the inflammation be very acute, or it may be suppurative from the outset. In the latter case there has usually been some specially virulent irritant present in the pleura, as where a metastatic ab- scess in the lung has approached the pleura, or where the pleurisy is one of the phenomena of septicaemia. In these cases the disease PNEUMOTHOEAX. 523 is generally rapidly fatal, and we may find remains of the fibrinous exudation mixed with abundant pus. Where the suppuration has come on in the course of a simple pleurisy the disease is often greatly prolonged, and the pleura undergoes great thickening, being converted into a bulky layer of granulation tissue like the wall of an abscess. The granulation tissue may undergo partial transformations into connective tissue with occasional adhesion, and as the lung has been compressed by the exudation we may have drawing together of the chest to an extreme degree should the pus be discharged or partially absorbed. Reference has already been made to tubbrcdlae pleurisy. The tubercles occur in the form of comparatively small white nodules which are present in the substance of the pleura, but near the surface. They are very commonly hidden by fibrinous exudation, and are therefore most easily seen on separating the lobes, the contact of which has prevented any thick fibrinous deposit. The pleurisy is usually prolonged, and we have at once fibrinous exudation with a certain amount of serum and chronic thickening of the membrane. Pleural Adhesions. — We have already seen that an acute pleurisy may result in adhesion of the sac, the process of adhesion resulting from coalescence of the surfaces which have become like granulation tissue from the inflammation. Such adhesion will not occur so long as fibrine is present on the surface, and is to be care- fully distinguished from the mere gluing which may occur in the earlier stages from the adhesion of the fibrinous exudation on opposed surfaces. But we have also seen that in the frequent chronic pleurisy of phthisis a similar adhesion occurs, and the method of its occurrence is similar. "Without any fibrinous or serous exudation (hence called dry pleurisy) the surfaces come to have the characters of granulation tissue and coalescence with vascular communication occurs. Hydrothorax is a dropsy of the pleural sac. The serous exuda- tion of acute pleurisy is not to be placed in this category, which only includes cases in which the transudation is increased without infiammation. Most frequently it is part of a general dropsy, as in Bright's disease, cardiac disease, or ansemia. Malignant tumors, especially secondary cancers, produce hydrothorax just as they produce accumulation in the peritoneal sac. As cancers spread along the lymphatic spaces it may possibly be that the dropsy results from obstruction of these. Pneumothorax has been referred to in connection with phthisis pulmonalis, and the mode of origin there indicated is that in the great majority of cases. Of the remainder there are some in which it is due to empyema — the visceral pleura has softened and the lung has become ulcerated so as to communicate with the pleura, or to gangrene of the lung, or to metastatic abscesses, or to the 524 DISEASES OF THE OBGAjSTS OF KESPIRATION . bursting of emphysematous vesicles, or to a traumatic cause. The air in the pleural cavity is usually at a high pressure and the cavity is much distended, so that when the chest is opened the air rushes out with some force. The pleural cavity as exposed presents a remarkably empty appearance, the lung being compressed except where there are adhesions, which may form tense bridges across from parietal to visceral layer or may limit the pneumothorax con- siderably. If the patient live there is nearly always an acute suppurative pleurisy, so that the condition may be designated pyo- pneumothorax. Experimental observation seems to show that the air may be absorbed, and this is confirmed by actual clinical observation. In the great majority of cases, however, the pneumothorax being followed by suppurative pleurisy, the aperture does not close and the condition persists till death, which is not generally long de- layed. Tumors of the pleura are rarely primary, but osteomas and lipomas have been seen. Cases have also been described of primary cancer of the pleura in which the tumor appeared to take origin in the endothelium of the sac or of its lymphatics. Secondary tumors are not infrequent. A sarcoma of the medi- astinum, originating in the bronchial glands, may result in an erup- tion of secondary tumors in the pleura, or a cancer originating in connection with the bronchi at the root of the lung may have a similar consequence. In cancer of the mamma the secondary tumors sometimes involve the chest-wall and are propagated to the pleura, where they produce an eruption, and may pass on to the lungs. Cancers of the peritoneum also frequently cause cancer of the pleura. In all these cases the tumors form pale soft masses which are usually flat and sessile, but may show considerable prominence. As already mentioned, the cancers are usually asso- ciated with dropsical exudation. DISEASES OF THE ALIMENTAEY CANAL. INTRODUCTOEY OBSERVATIONS. In studying the diseases of the alimentary canal certain facts as to its structure and functions are to be borne in mind. The canal is lined throughout by a mucous membrane, which consists of loose connective tissue covered with epithelium in one or several layers. In the mucous membrane and to some extent beneath it are glands which in difterent parts have different structures, but everywhere secrete materials that pass into the calibre of the canal. In addition to these there are in many parts closed follicles of a lymphatic structure which usually lie near the surface and fre- quently take part in changes going on there. Beneath the mucous membrane is the submucous tissue which, for the most part, is loose, and so allows the mucous membrane to go into folds or be stretched out flat according to the state of dilatation or contraction of the canal. Outside this there is a muscular coat, generallj^ in two layers, by means of which movements and variations in calibre are effected. In most parts of the intestinal canal there is a serous coat outside of all. In the diseases of the alimentary canal it is chiefly the mucous membrane that we have to deal with, the subjacent structures being usually subordinate to and affected secondarily to it. The serous coat, it is true, is often affected independently ; its diseases, however, do not belong specially to the alimentary canal, but to the peritoneum as a whole. The mucous membrane on account of its exposure to a variety of influences derived from the varying contents of the canal is specially liable to inflammations, and the great majority of the diseases to be considered here are inflam- matory ones. It will be necessary for convenience to subdivide the alimentary canal into different sections and to consider each of these separately. A.— THE MOUTH. As the mouth is exposed in an especial manner to external influences, so its mucous membrane possesses an epithelium in many layers, and it is not nearly so liable to inflammations as most other parts of the alimentary canal. 526 DISEASES OF THE ALIMENTARY CANAL. INFLAMMATIONS OF THE MOUTH. Catarrh. — If we leave out of view the catarrhs of the fauces and pharynx which we consider aftei'wards, simple catarrh of the mouth is exceedingly rare as a primary disease. It is not infre- quent, however, as a secondary affection, arising from the imitation of carious teeth, from the use of mercury, the presence of ulcers, etc. It is also of frequent occurrence in the acute fevers, especially typhus, scarlet fever, smallpox and measles. In these fevers there is also a catarrh of the stomach, and the inflammation in both seems due to the action of the poison in the blood. The mucous membrane is swollen and red and there is greatly increased desquamation of the epithelium, especially inside the cheeks and on the tongue. The desquamated epithelium is mixed with leucocytes, serous exudation, and mucus in varying proportions, and on that account it has varying characters. On the tongue there is usually much epithelium which lies on the surface, and so a tolerably thick layer is formed mostly of a whitish or yellowish color (furred tongue). On the cheeks and gums there is more fluid and less epithelium. In the midst of the epithelium and leucocytes bacteria and leptothrix threads are to be found. If the patient is feverish and lies with the mouth open, the catarrhal products dry in and form a dirty brownish coating of the tongue and gums which goes under the name of sordbs. Sometimes the inflammation centres especially around the mucous glands, and they may form prominent nodules or vesicles. To this form the name follicular stomatitis has been given, and it is frequently seen in children during dentition or after measles, and is often associated with catarrh of the stomach or intestine. The vesicles or small prominences frequently burst and leave multiple small ulcers covered by a dirty exudation. Catarrh of the mouth rarely assumes a phlegmonous character, in this respect contrasting with inflammation of the fauces. Thrush or Aphthous Stomatitis or Soor. — This condition has already been mentioned as connected with the presence of a fungus. It occurs in the mouths of young unhealthy children, but is also occasionally seen in emaciated adults, as in diabetes. The normal secretion of the mouth is alkaline, but in this disease it becomes acid, which may perhaps be the reason that the fungus develops. If the mouth be examined it will be found beset with small white spots, which look like little bits of white curd on the surface of the mucous membrane. These patches are, however, adherent, and in removing them the mucous membrane beneath will be found red and bleeding. The white patch consists of epithelium united into a membrane by a fungus, the o'idium albicans (Fig. 238). It consists of branching threads composed of elongated cells placed end to end and sometimes losing themselves in masses GANGRENOUS STOMATITIS. 527 of spores. The aphthous patches frequently extend from the mouth downwards to the pharynx and cesophagus. The condition of the mucous membrane in certain special FORMS OF INFLAMMATION deserves particular mention. In smallpox, besides a general catarrh there are vesicles or pustules analogous to those on the skin. We have first whitish patches consisting of raised and desquamating epithelium. The epithelium is soon Pig. 238. 'isf — — --' e- Oidium albicans or thrush-fungus. The constituents of the fungus are associated with flat epithelium. X 450. (Kuchenmeister.) discharged and superficial ulcers result. In scorvy there is great swelling and oedema of the mucous membrane of the gums around the teeth. The gums bleed and, apparently as a consequence of this, ulcers form at the edges of the teeth and may extend down to the bone, which may undergo necrosis. Very often the teeth are loosened. As a consequence of the use of mercury we sometimes have a considerable stomatitis. It occurs after the medicinal use of mercury and also among workmen who employ it in their occu- pations. The mucous membrane is swollen, especially that of the gums and cheeks, and there is severe salivation. Ulcers frequently form, especially on the internal surface of the cheeks and lips, and on the edges of the tongue. They may be in the form of flat excoriations or deeper ulcers with a membranous covering. Gangrenous Stomatitis or Cancrum Oris or IN'oma. — This dis- ease, which is fortunately a rare one, occurs in badly nourished children, particularly when reduced by severe illness such as scarlet fever or measles. It presents itself first as a diffuse swelling of the cheek which is seen to be tense, red, and glistening, with one spot in the centre usually redder than the rest. On examining the inside of the mouth there is already an excavated ulcer oppo- 528 DISEASES OF THE ALIMENTARY CANAL. site the red spot on the cheek, and the gums opposite may also be ulcerated. As the disease progresses, more and more of the mucous membrane of the mouth is ulcerated away. At the same time the red spot on the cheek gets black in the centre, and after- wards extends in area. By and by a slough of various sizes sepa- rates and a communication forms through the cheek with the inside of the mouth. If the patient survive still further destruction occurs, the necrosis passing on to the surrounding skin of the jaws, even to the ear and eyelids. There may be necrosis of the jaws. Not infrequently this disease is associated with a gangrenous pneu- monia and there are general symptoms of septic poisoning. The exact nature of this disease is not known, but it must be suspected from the rapid necrosis that a specific virus has to do with it. Inflammation of the tongue deserves a brief special notice. "We have seen that the tongue takes part in most of the inflammations of the mucous membrane, but sometimes it becomes the seat of a special inflammation of its substance, a true glossitis. This may occur as a result of wounds or irritations from without, or in the course of such diseases as erysipelas and smallpox. The tongue swells greatly in consequence of the inflammatory infiltration of the interstitial connective tissue, and this sometimes, though rarely, goes on to the formation of abscesses. The muscular fibres are swollen, pale and brittle. Usually the infiammation ends in resolution, but sometimes it becomes chronic, and there may be great increase of connective tissue with permanent induration of the tongue. INFECTIVE TITJIOES OE THE MOUTH. Syphilis.— We have various syphilitic lesions in the mouth, from slight inflammation to deep ulceration. It is not uncommon to meet with a primary chancre on the lips. In that case there is a prominent tumor which has, in more than one case, been taken for an epithelioma. On microscopic examination the tumor is found to consist of immense aggregations of round cells (Fig. 239). The catarrh which accompanies the secondary stage is often very slight, but it may be accompanied by superficial ulceration of con- siderable extent. Flat condylomata are particularly frequent in the mouth, and they often break down and form superficial ulcers, especially on the lower lip and angle of the mouth. The deeper ulcers arise in connection with gummata, which form in the sub- stance of the mucous membrane, and may lead to very serious loss of substance. If healing occurs a cicatrix forms, but cicatrices sometimes occur without ulceration having taken place, the gumma itself giving place to a cicatrix. The gummata not infre- quently have their S3at deep in the substance of the tongue, and the resulting cicatrices, with or without ulceration, may produce very marked deformity of this organ. TUMORS OF THE MOUTH. 629 Lupus not infrequently extends from the neighboring skin into the mouth and may produce considerable destruction. Lepeosy also aflects the mucous membrane of the mouth sometimes. ¥iG. 239. Section of a chancre of the lip which was exc sed under the bel cf that t was an epithe- lioma. There are multitudes of round cells beneath the epithelium, which is encroached on towards the left. X 90. Glanders occasionally manifests itself here, are exceedingly rare. Tubercular ulcers TUMOES OP THE MOUTH. These are of somewhat frequent occurrence and considerable variety. We rarely meet with fibromas, lipomas, and enchon- dromas. Rather more common are adenoid tumors of the lips. These take origin in the mucous glands of the lips, and frequently become converted into mucous or colloid cysts. They form promi- nent rounded tumors sometimes as large as a hazel-nut, and are readily enucleated. Vascular tumors, mostly congenital nsevi, are not infrequent on the lips, forming either flat elevations or, more rarely, prominent tumors with limited base. Vascular tumors are also met with on the tongue. Warts occur on the lips, espe- cially at the edges. In that situation they are mostly hard, while those on the proper mucous membrane are soft. Not infrequently the wart ulcerates, and, it is said, may give origin to a cancerous tumor. Warty outgrowths also occur on the tongue. The papillse of the tongue sometimes undergo great elongation, especially their epithelial "layers, and we may have a condition as of hairs on the tongue. Sarcomas rarely develop in the mouth itself, although they have been met with in the tongue. On the other hand, it is not uncom- mon to iind a sarcoma of the jaws growing from the periosteum and projecting into the mouth. This applies especially to the form of tumor called epulis. This name is given generally to tumors 34 530 DISEASES OF THE ALIMENTARY CANAL. which arise from the alveolar processes of the jaws, growing mainly from the periosteum. These are mostly sarcomas, and composed of spindle-cells, but they nearly always contain giant-cells, and sometimes these are in large numbers. Osseous trabeculse pass into them frequently from the bone beneath. As these tumors grow they push the mucous membrane of the gums before them, and so form red prominences of a rounded form, behind, in front of, or between the teeth, and generally hard to the feel. The teeth are often considerably displaced by them as they grow, especially when they assume large dimensions as sometimes happens. Cancers of the mouth are nearly all of the epithelial variety. They are of very frequent occurrence on the lips and are also common on the tongue. On the lips epithelioma is almost con- fined to the male sex, and has its seat in the great majority of cases in the lower lip. This is frequently ascribed to the fact that in men the lip is more frequently exposed to irritation by smoking short pipes and in shaving. On the tongue the epithelioma usually forms at the edge, and it is often said that the irritation of tlie sharp edge of a carious tooth has been the starting-point. The epithelioma begins in a limited infiltration of the lip or tongue, but as a rule ulceration soon occurs, and the tumor presents itself as a flat or excavated ulcer with infiltrated edges. By ulceration great destruction may take place of the lips and skin around, or of the tongue. Secondary epitheliomatous formation frequently occurs in the submaxillar}' lymphatic glands, and may extend to the glands of the neck. Macroglossia is a condition in which the tongue is greatly in- creased in bulk, the enlargement being nearly always congenital. Even at birth the tongue may be too large for the mouth and project beyond the lips. Afterwards it may increase still more, and as the child grows it may displace the alveolar processes considerably. For the most part there is no hypertrophy here except of the interstitial connective tissue, but evidences of new formation of muscular tissue have been observed. As a rule, the lymph-spaces of the hypertrophied connective tissue are greatly enlarged, and there is even a formation of cavernous tissue, the spaces in which are filled with lymph. In this way we may speak of lymphangioma cavernosum as taking part in the condition. It will be observed that the condition here somewhat resembles that in elephantiasis, there being in both cases a great new formation of succulent connective tissue with wide lymph-spaces. The re- semblance is further indicated in the fact that the lips frequently hypertrophy as well. E.ANULA is a name applied to cysts which foi'm beneath the tongue. These mostly arise as retention cysts from closure of Wharton's duct (duct of the submaxillary gland) or the duct of the sublingual gland, but they may take origin in the mucous AFFECTIONS OF THE TEETH. 531 glands. Before the occurrence of the cyst there is usually some inflammation of the floor of the mouth very often connected Avith affections of the teeth. According to the observations of Reck- linghausen, referred to at p. 199, the cyst arises by dilatation of the duct, while the gland structure persists and furnishes the ma- terial by whose accumulation the cyst forms (see Fig. 81, p. 199). AFFECTIONS OP THE TEETH. In studying the diseases of the teeth, we have to remember what are their constituent and related structures. The hard part of the tooth consists of enamel, dentine, and cement. The enamel, containing very little organic matter (only about two or three per cent.), is for the most part passive, and even presents great mechanical resistance to destructive processes. In its original formation it is a superadded structure, and for this reason also it takes little part in the morbid changes which occur in the teeth. The DENTINE, consisting of tubules with a hard matrix, possesses a much larger proportion of organic matter (twenty-eight per cent.), and is much more directly involved in morbid processes. The CEMENT, which covers those parts of the tooth which are devoid of enamel, consists of true bone, and is liable to changes of a similar nature to those of bone. Turning to the soft parts, the pulp fills the cavity of the tooth and has an outline parallel to that of the tooth as a whole. The pulp is a soft, highly vascular tissue, and is concerned in the nutri- tion of the dentine. It is also richly supplied with nerves whose filaments pass in part into the dentinal tubules. The pulp is so sensitive that in popular language it is called " the nerve." In the original formation of the tooth the dentine is produced by the structure which is afterwards represented by the pulp, and through life the latter retains to a considerable extent its formative power. As we shall see afterwards, it is concerned in the formation of the secondary dentine. The tooth is fitted accurately into the alveolus by means of the cement on the one hand and the dental periosteum or periodontal membrane on the other. This membrane, lying between the cement and the bone of the jaw, forms a kind of double periosteum, and is, from its position, very liable to the action of mechanical forces, being placed between two rigid structures, one of which (the tooth) is peculiarly exposed to mechanical interference. It is continuous at the apex of the root with the pulp, and at the neck with the mucous membrane of the gums on the one hand and the periosteum of the jaw on the other. We shall see afterwards that inflammations are apt to extend from the pulp to the dental peri- osteum, and from the latter to the gums and maxillary periosteum. Caries. — This name is applied to a condition which is not quite analogous to caries of bone, except in so far as in both thei'e is 532 DISEASES OF THE ALIMENTABY CANAL. Fig. 240. destruction of the dense calcified structure. Caries of bone is related to inflammatory processes, but caries of the teeth has no such origin. It consists of a softening usually progressive, of the enamel and dentine and their subsequent disintegration. The pro- cess appears to begin very commonly in places where the enamel shows normally rather deep furrows, and is therefore thinner and more easily destroyed than elsewhere. "When the caries reaches the dentine it advances more freely, so that the enamel may to some extent be undermined. The lime salts are first absorbed, and then the organic basis is broken down. The caries advances in the direction of the dentinal tubules, as shown in Fig. 240. Various views have been held as to the nature of the process. At one time it was regarded as inflammatory, but this view may be set aside, chiefly on the ground that a process exactly similar occurs in teeth which have been drawn and reinserted, as well as in artificial teeth made of the ivory of the hippopotamus. The caries consists, in fact, of a gradual solution of the lime salts, and for this solution we must infer the existence of an acid. The secretion of the mouth is naturally alkaline, but in carious teeth an acid reaction has been detected. The acidity is often connected with derangements of the stomach, but it may have a more local origin, as when the secretion of the gums is abnormal, or perhaps when food is undergoing acid fermen- tation in contact with the teeth. It may be that before the teeth yield to an undue aciditj^ they have already an abnormally weak power of resistance, and this may be related to personal peculiarities, inherited or otherwise. At the advancing margin of the caries a widening of the dentinal tubes is visible, and in these widened tubes, as well as in the carious cavity, bacteria and leptothrix threads are to be found. By some the process has been ascribed to the action of these organisms, and especially by Klebs, but these views stand in need of con- firmation. Section of tooth with caries. There are two cavities, one on each side, and in the pulp- cavity a new formation of secondary dentine. The secondary dentine is not exactly on the same level as the cavi- ties, but at the ex- tremities of the denti- nal tubules leading from these. (After Salter.) Inflammation frequently follows on caries, and the pulp is usually involved. It is almost cer- tainly attacked if the caries causes penetration into the pulp, but even before this takes place there is frequently some infiammation. This sometimes expresses itself in a new formation of SECONDARY DENTINE insidc the tooth around the point to which the caries is advancing (see Fig. 240). In this way the carious cavity may be shut oft' from the cavity of the pulp, and so a more serious inflammation warded ofi'. Yery frequently, THE SOFT PALATE, PHAEYJSTX, AND TONSILS. 533 however, a more acute inflammation of the pulp occurs, with redness, swelling, great pain, not infrequently also with complete necrosis of the pulp, and, in consequence, of the whole tooth. The inflammation often extends to structures around the tooth. The root-membrane or dental periosteum, which covers the root portion of the tooth, is the structure most directly attacked. This membrane is, as we have seen, intimately connected towards the neck of the tooth Avith the submucous tissue of the gums, and the periosteum of the alveolar process of the jaw. Inflammations of these' structui-es, especially of the gums, very frequently ensue, resulting in the well-known gum-boil, which often goes on to sup- puration and abscess, forming the so-called parulis. The abscess usually bursts into the mouth, but it may produce extensive swell- ing of the gum, and lead even to penetration outwards, resulting in a fistulous opening in the skin. The result may be even more serious if the periosteum of the jaw becomes inflamed, resulting, it may be, in suppuration which is apt to be chronic. With the periostitis there is usuallj" new formation of bone, causing thickening of the jaw. It is to be added that these inflammations of the root-membrane and periosteum of the jaw sometimes occur apart from caries, as a result, for instance, of poisoning with phosphorus or mercury, and in scurvy. In that case the inflammation is not limited to the neighborhood of one tooth, but extends probably to a series. The cement, which, it must be remembered, is composed of bony tissue, sometimes undergoes a hypertrophy to which the name exostosis or osteoma is often given. This is scarcely a true bony tumor, but originates rather in a chronic inflammation of the cement, leading to a considerable new formation of bony tissue. In this way are formed prominent tuberous' outgrowths from the roots of the teeth, which may be localized in one part of the fang, or cover a considerable portion of it, or even the whole root por- tion of the tooth. In the latter case it is as if the root was enlarged by rough accretions on its surface. These so-called exostoses sometimes oflier serious resistance to the extraction of the teeth. Another form of tumor connected with the teeth is that which Virchow has called the odontoma. This tumor arises in connec- tion with teeth retained in the alveoli by faulty development. The tumors are composed of dentine and enamel, and are of small size and rare occurrence. B.— THE SOFT PALA.TE, PHARYNX, AND TONSILS. Introductory Observations. — In studying the diseases of these parts there are two circumstances to be taken into account very carefully : the one concerns the structure of the mucous membrane, and the other the circumstances as to its exposure to influences from without. 534 DISEASES OF THE ALIMEX'TARY CANAL. The mucous membrane here differs from that of the mouth proper chiefly in respect that in addition to the ordinary mucous glands there are numerous lymphatic follicles. The distinction between these two is not always correctly appreciated. The mucous glands are racemose glands with proper ducts, opening on the surface of the mucous membrane. The follicular glands, as they are often called in rather a confusing way, are strictly com- parable with the closed follicles of the. intestine. In the pharynx, soft palate, and root of the tongue they occur in the form of isolated rounded masses of lymphatic tissue, like the solitary follicles of the intestine. In the tonsils we have aggregations of these follicles not unlike Peyer's patches. The prominence of these follicles in the tonsils causes the mucous membrane to be thrown into folds, and so we have comparatively deep recesses, which are sometimes called crypts, and in which secretions may accumulate, especially if their depth is exaggerated by diseased conditions. The other circumstance alluded to is that from their exposed condition these parts are peculiarly prone to irritation from agents coming to them by the inspired air. The mucous membrane of the mouth generally seems peculiarly resistant to external irrita- tions, but here, where there is the transition, as it were, from the mucous membrane exposed to external influences to that protected from them these inflammatory manifestations occur with peculiar frequency. Almost all the diseases we have to treat of here are forms of inflammation, and it is usual to describe these under the general designation of Angina. INFLAMMATIONS OP THE PAUOES. Acute Catarrhal Angina. — This forms the most ordinary sore throat, and occurs either from " cold," especially at seasons of the year when sudden changes of temperature are prevalent, or as a local symptom of a general disease, such as measles, scarlet fever, smallpox. It may be said regarding scarlet fever, smallpox, and diphtheria that the throat affection in them begins with an acute catarrh, but that, especial^ in scarlet fever and diphtheria, it nearly always goes on to something more serious. In the simple catarrh there are redness and swelling of the mucous membrane with a mucous exudation which covers the surface and may have a tough consistence. Sometimes vesicles form on the mucous' membrane. Chronic catarrh very frequently follows on the acute form, especially when there have been repeated attacks. The conditions are somewhat different in different cases, and rather complicated classifications have been introduced. As in other chronic inflam- mations, there is here, for the most part, thickening of the mucous membrane, but there are different ways in which this may, to some INFLAMMATION OF THE FAUCES. 535 extent, localize itself. There may be a general hypertrophy of the superficial layers of the mucous membrane, and, as the bloodvessels remain congested, it is a rather succulent swelling. This causes what is called the relaxed throat. The appearances are most pro- nounced in the case of the uvula, which becomes elongated, some- times to a very marked extent. At other times the swelling is not so uniform, but with some general thickening there is an occasional localized prominence, causing the mucous membrane to assume a granular appearance. This form occurs mostly among clergymen, singers, actors and others whose occupation requires them to use their voices for prolonged periods with a loud tone. It is not by any means certain what the exact structure of the prominent granulations in this disease is, but it seems likely that there are really two conditions included under the name. In one of them, the mucous glands are involved and may be seen dis- charging a milky fluid. In the other, the enlargement is not connected with the mucous glands, but is usually supposed to depend on enlargement of the closed follicles, although Stoerk has recently stated that it really consists of a hypertrophy of the epi- thelium. The condition is often called follicular pharyngitis from the view that the closed follicles are mainly concerned. Ulcers may form in .connection with these swellings, and they are called follicular ulcers. Acute phlegmonous inflammation of the fauces frequently results in the formation of abscesses. It is a condition of some- what common occurrence. Here there is not merely a surface catarrh, but the mucous membrane and submucous tissue are involved in an acute inflammation of a very intense kind which usually goes on to suppuration. The disease very commonly begins on one side and frequently involves the tonsil, sometimes extending thence to the posterior wall of the pharynx. The swelling and redness are very great from hypersemia and cedema of the whole structures, and the patient msiy have ditficulty in opening the mouth. If it goes on to suppuration, the pus often collects and forms an abscess which bursts into the throat. In some cases the acute inflammation extends downwards to the base of the epiglottis, and the case becomes dangerous because of the possible supervention of cedema glottidis. It should be added that the name quinsy is applied to this disease as well as to a more local inflammation of the tonsils alone. The causes of the inflammation are frequently obscure. It seems as if some intense irritant were acting on the fauces, and the fact that severe sore throats often occur in a number of per- sons about the same time would point to the existence of a virus of some kind. The occurrence of a similar inflammation in scarlet fever is also conflrmatory of the supposition that the disease owes its origin to a virus. It sometimes happens that the inflammation, after attacking one side, passes round and involves the other, and this looks like an irritant which propagates itself. 536 DISEASES OF THE ALIMENTARY CANAL. Diphtheria. — The changes which occur in this disease have already been referred to in considering its manifestations in the air-passages. It usually begins in the fauces and has its centre there. The characteristic phenomenon here is the formation of a fibrinous exudation. In order to that there must be necrosis of the epithelium on the surface. As we have seen, there is usually in the fauces a deeper necrosis involving the mucous membrane to a greater or less depth. Besides the exudation and necrosis there are other signs of inflammation, chiefly in the pres- ence of leucocytes infiltrating the mucous membrane and passing into the exudation. It sometimes happens that the mucous membrane is not in- volved in the exudation, so that Avhen the exudation is removed there is no loss of substance. As a rule, however, there is necrosis of the mucous membrane, and this in all degrees till we come to the so-called gangrenous form. In this form, as the exudation separates, it carries with it portions of tissue, and as these only by degrees become detached from the living tissue, it looks as if exudation and dead tissue were together sloughs of the mucous membrane. These sloughs frequently look more serious than they are, but there may be considerable loss of substance, and ulcers of some depth and size may be left. The disposition of the patches of exudation is very various. Sometimes they are mainly on the tonsils, sometimes on the soft palate and uvula. Extension to the posterior nares on the one hand and to the larynx on the other is very frequent, the latter, as we have seen, being particularly common. Acute Tonsillitis is, as we have seen, occasionally a part of a general phlegmonous inflammation of the fauces. Occurring more independently it is accompanied by considerable swelling, consisting of an inflammatory infiltration of the lymphatic follicles of the tonsils. Sometimes it goes on to suppuration, but rarely does so when the tonsils alone are affected. The swelling in many cases does not fully subside, and gives rise to a more or less per- manent enlargement such as we have next to consider. Chronic Tonsillitis mainly shows itself in the form of hyper- trophy OF THE TONSILS. Certain persons, especially in jouth, are prone to repeated subacute inflammations of the tonsils, and as these recur the tonsils acquire a permanent enlargement. This consists anatomically in a true hypertrophy of the lymphatic follicles, although there is sometimes also an increase of the interstitial con- nective tissue. For this reason the tonsils are rarely much indu- rated, the soft lymphatic tissue existing so abundantly as to make the structure as a whole somewhat soft. The hypertrophy appears to be not always the result of chronic inflammation, or at least it is frequently altogether out of proportion in amount to the inflam- mation. The greatest degree of hypertrophy is met with ift children, and they are not so liable to acute tonsillitis as youths. DILATATION OF THE (ESOPHAGUS. 537 There are cases even of congenital hypertrophy of the tonsils, and there are still more frequent cases of a gradual enlargenaent with- out any apparent attacks of inflammation. In this way the tonsils may acquire very large dimensions, reaching the size of a hen's egg on some occasions. Syphilitic Disease of the Fauces. — This manifests itself in multifarious ways. A persistent catarrh having the ordinary characters of subacute simple catarrh is very common. Mucous tubercles or condylomata are tolerably frequent, especially in the pillars of the fauces and in the soft palate. In the tertiary stage, with or without the formation of gummata, there may be ulcer- ation of the mucous membrane. Not infrequently the ulceration extends very deeply and causes destruction of the uvula and palate. It ma}- extend to the epiglottis and no further. It is frequently accompanied by considerable thickening and cicatricial conti'action, so that it may lead to great deformity and sometimes to stenosis of the pharynx. Tubercular Ulcers. — These are of very rare occurrence here, although so common in the larynx. The disease is associated with phthisis pulmonalis, and is really due to an extension upwards of tubercular ulceration of the larynx. It occurs in the form of superficial ulcers, originally of a circular form. The Tumors of the Fauces are not so different from those of the mouth as to call for very special remark, and they are altogether of much' less frequent occurrence. We meet with papillary excrescences, cysts, sarcomas, and epitheliomas. C— THE OESOPHAGUS. The diseases of this part of the alimentary canal are important from a practical point of view, chiefly because of the natural narrow- ness of the tube. The mucous membrane of the oesophagus is covered by a thick layer of stratified flat epithelium, and the mucous glands are comparatively few. Dilatation of the (Esophagus. — Of this somewhat frequent condition two forms may be distinguished. Besides a local dilata- tion about to be mentioned, we have a general dilatation of the tube as a result of obstruction at any part of its course. The obstruction is mostly low down in the cesophagus and may be even at the cardiac end of the stomach ; or the stomach and cesophagus may be simultaneously dilated by ol)struction of the pyloric end of the stomach. "With the dilatation in these cases there may be con- siderable thickening of the muscular coat, although this is not always present. 538 DISEASES OF THE ALIMENTARY CANAL. Contrasted with this general dilatation is the partial dilatation or diverticulum. The mode of origin of these diverticula is sometimes obscure. There are some which seem to owe their origin to an imperfect closure of the communication between the oesophagus and the trachea during- foatal life. If this closure be delayed, then the wall of the oesophagus may remain bulged out in front and from this beginning a larger diverticulum may arise. More commonly, however, the diverticula form on the posterior wall at the lower part of the pharynx or upper part of the oesoph- agus. It is probable that for the most part these originate by a piece of hard food lodging in a fold of the mucous membrane, and being gradually pushed outwards, carrying the wall of the tube with'it. As the sac enlarges, it hangs downwards with its mouth presenting upwards, and so it is always ready to receive the food in its passage downwards. It is probable that in most of these cases there is a separation of the fibres of the muscular coat of the oesophagus or pharynx, and that the mucous membrane is pushed, as it were, through the muscular coat. It is consistent with this view that the diverticula are most tommon at the junction of pharynx and oesophagus, where the circular muscular coat is thinnest. If the sac is of any consideraole size and filled with food, it will press on the oesophagus" below its mouth, and of itself produce an obstruction. In this way the food is prevented passing down the oesophagus and goes readily into the sac. "We have, therefore, for the most part, a continually increasing enlargement of the diverticulum which may reach the dimensions of a child's head or larger. It contains the remains of the decomposing food, with more or less mucus, which is sometimes present in consider- able masses. If the diverticulum is moderate in size its wall may still contain some muscular fibre, although, from what has been already mentioned, it will appear that the muscular coat is mostly absent except just at the neck. Besides the two modes of origin already mentioned a third has been distinguished. The lymphatic glands at the root of the lung sometimes, after enlarging, undergo softening and cicatricial con- traction. If a gland, under these circumstances, has acquired adhesion to the oesophagus, it may in its contraction drag the wall of the latter outwards. In this way the oesophagus may acquire a funnel-shaped pouch which is liable to enlargement by the food being pushed against it. As it is mostly the bronchial glands that are concerned here, such diverticula are usually found near the bifurcation of the trachea, and they sometimes perforate into the trachea, forming fistulous openings. They have also been observed to perforate into neighboring cavities such as the pericardium or pleura, producing serious inflammations of these. Obstruction of the Oesophagus. — -This condition may arise as a consequence of pressure from without, by tumors, aneurisms, abscesses. But it is much more frequent from disease in the tube itself. Ulcers of various kinds, by the cicatricial contraction PERFORATING ULCERS OF THE (ESOPHAGUS. 539 incident to attempts at healing, may induce obstruction, as, for example, ulcers from swallowing strong acids, syphilitic ulcers, etc. Still more frequent are obstructions from tumors of the oesophagus, and especially cancers, which we shall have to refer to immediately. As we have already seen, obstructions of the a3sophagus frequently give rise to dilatations with hypertrophy of the muscular coat above the seat of constriction. Sometimes the dilatation becomes more partial, so that with a general dilatation there is a partial diverticulum. Fig. 241. Inflammations of the oesophagus are of comparatively little moment. The mucous membrane is formed so as to resist the action of irritants, and unless the action be peculiarly strong we have not considerable inflammation. "When strong acids or alkalies, or substances at a high temperature, are swallowed, they may cause superficial necrosis and considerable inflammation of the mucous membrane. The small- pox eruption may extend into the oesophagus, producing inflammation there. Strong acids or alkalies when swal- lowed usually produce much more serious results in the stomach than in the oesophagus, as they pass rap- idly over the surface of the latter. Acids produce whitish, yellowish, or brownish sloughs of the epithelium, sometimes penetrating to the mucous membi'ane itself. Caustic alkalies, on the other hand, dissolve the epithelium, producing a grayish gel- atinous material which lies on the surface. If they penetrate to the mucous membrane they reduce it to a soft, brownish, half-diffluent sub- stance. If recovery occurs, there are at first ulcers with more or less violent inflammation, and afterwards healing with contraction of the ulcers and possibly considerable narrowing of the tube. Smallpox pustules in the oesoph- agus are very similar to those in the mouth, and, like them, they readily lose their epithelial covering and become convei'ted into ulcers. They are accompanied by signs of inflammation of the mucous membrane generally. Perforating Ulcers of the (Esophagus. — A few cases have been observed of round ulcers in the lower part of the oesophagus similar to those which will be described as of common occurrence Perforating ulcer ill lower part of oesophagus. The ulcer penetrated the main bronchus of the left lung. 540 DISEASES OF THE ALIMENTARY CANAL. Fig. 242. in the stomach. Fig. 241 represents an ulcer of this kind which perforated into the left main bronchus, causing gangrene of the lung on account of the food passing in. There have been cases also in which the ulcer has penetrated into the aorta. Tumors of the OEsophagus. — Simple tissue tumors are rare. We meet with lipomas and fibkomas, and the author has described a case of MYOMA (Fig. 242) in which a tumor four and three-quarter inches long and two inches in thickness was attached by a comparatively narrow neck, and produced death by obstructing the tube. Polypoid tumors of a similar form are met with having a fibrous structure. Cancer of the oesophagus is by far the most important form of tumor met with.- The cancer is nearly always in the form of flat-celled epithelioma, and in its his- tological details closely conforms to cancer of the lip. The masses of epi- thelial cells infiltrate the spaces in the underlying connective tissue, and the tumor also projects somewhat into the calibre of the tube. Here also there is a great tendency to ulceration, the me- chanical action of the food in swallowing doubtless contributing to this result. The tumor begins at a limited part of the mucous membrane, but it has a special tendency to extend round the tube in the form of a ring. There has been considerable discussion as to the most common situation of the tumor, and the result of the comparison of various statistics seems to be that the most frequent seat is the lower third. Scarcely less frequent than this is the middle third, and especially the place correspondmg with the bifurcation of the treachea.. In the upper third epithelioma is comparatively infrequent. This form of tumor frequently leads to obstruction of the 03Sophagus, and it produces this result in more ways than one. On examining the cesophagus after death the seat of the tumor is often indicated externally by a narrowing of the tube, which is also more rigid here than elsewhere. The infiltration of, the walls of the cesophagus, by irritating the connective tissue, causes a chronic inflammation with the usual new-formation of connective tissue, which contracts and narrows the tube. Besides this, the mere rigidity of the tube preventing its dilatation when the morsel is being swallowed, may produce during life a feeling of obstruction Polypoid myoma of cesophagus in section, and semi-diagram- matic. Tine tumor was attached by a band-lilie pedicle u. It caused considerable distention of the oesophagus, and obstructed the tube. b cardiac orifice of stomach. Half the natural size. THE STOMACH — INTEODUCTOEY. 541 at the point concerned. The projection of the tumor into the calibre is another element, which tells especially in the earlier periods. But as ulceration occurs, this projection of the tumor usually becomes inconsiderable, and there may even be a temporary relief to the stricture by partial destruction of the tumor. The ulceration itself, however, by inducing still further cicatricial con- traction, may ultimately confirm the obstruction. The tumor sometimes extends from the oesophagus to neigh- boring lymphatic glands, or to surrounding structures, and so we may have the trachea, bronchi, or lungs involved in it. Some- times it extends to the diaphragm, pericardium, vertebrae, etc. D.— THE STOMACH. Introductory. — In considering the diseases of the stomach, it is necessary to bear in mind certkin points in regard to its structure and functions. The innumerable glands which exist in the mucous membrane are regularly engaged in the formation of the gastric juice for the purposes of digestion. The diseases of the stomach very readily interfere with the function of these glands, so that the secretion of gastric juice is insufficient in quantity or deteriorated in quality. In that case the food is apt to lie in the stomach undigested, and it very commonly undergoes various forms of decomposition. The products of decomposition acting on the mucous membrane still further interfere with the process of secretion, and by their irritative action keep up or induce a con- dition of catarrh of the stomach. Gases also develop in the process of decomposition, and these, by distending the organ, interfere with its proper peristaltic movements, and so hinder the passage of the food through the pylorus. But it is not merely local diseases, such as inflammations and tumors, which interfere with the secretion of the gastric juice. Changes characterized by cloudy swelling and fatty degeneration are met with in the glandular epithelium in numerous infective diseases, smallpox, typhus, septicaemia, as also in poisoning with phosphorus, etc. In these cases the secretion of the gastric juice may be almost at a standstill, and if food be introduced it is apt to lie in the stomach; by its mere presence, and by the action of the products of decomposition, it may produce still further struc- tural changes. ■ The forms of decomposition which the food undergoes when it lies undigested in the stomach are various, but the chief are those characterized by the development of acetic, lactic, and butyric acids. The agents in these changes are micro-organisms which are introduced in abundance Avith the food and propagate in the stomach, unless their multiplication is hindered by the action of the gastric juice. In the contents of the stomach, when at any time they are discharged during life, swarms of bacteria are found, 542 DISEASES OF THE ALIMENTARY CAKAL. and in addition there are nearly always proliferating spores of fungi and sometimes large numbers of sarcinse. It has been mentioned that the products of decomposition irritate the mucous membi-ane, but in addition to that the organisms have been found in some cases to enter the glands and mucous mem- brane. In cases observed the action of such organisms has pro- duced little pustules in the mucous membrane, or even larger prominences with necrosis and ulceration. It may be inferred that it is organisms of a special kind or in a peculiar state of activity which thus penetrate into the mucous membrane. Stagnation of the food in the stomach and its decomposition will occur, as we have already mentioned, when anything interferes with proper digestion. But it will opcur still more when by stricture of the pylorus there is a mechanical obstacle to the pass- age from the stomach. In such cases the gastric juice may be secreted nearly in the normal way, or it may not, and so according to circumstances there will be greater or less decomposition of the food. Besides the mere local eflects induced by the products of decom- position, it is to be remembered that the mucous membrane of the stomach is actively engaged in absorption, and that these products ma}' to some extent be taken into the blood. It is probable that much of the headache and other nervous symptoms occurring in dyspepsia is due to the existence in the blood of small quantities of these poisonous agents and their action on the nervous system. Some of these symptoms may be reflex, but to a certain extent they are more probably direct. When the food remains in the stomach and accumulates there, it is usually got rid of after a time by vomiting. This action is produced by irritation of a centre in the medulla oblongata, and the muscles emploj'ed are mainly those used in respiration, but in different combinations. The centre may be irritated directly, as by introducing apomorphia or tartar emetic into the blood, or by disease of the brain itself But in the case we are considering it is irritated by reflex stimulation, the stimulation taking origin ^Tn centripetal fibres in the stomach itself. The occurrence -of vomit- ing is dependent on the nature and amount of the irritation ap- plied, and on the sensitiveness of the centre in the individual. Post-mortem Changes. — After death any remains of food lying in the stomach are apt to decompose rapidly, especially as the gastric juice in most cases is not secreted in the normal way up to the period of death, and so the decomposition is not interfered with. The decomposing juices therefore act readily on the mucous membrane, and the decomposition may even extend to the latter. The principal changes produced are alterations in color, result- ing li'om chemical changes in the coloring matter of the blood. The coloring matter may become difli'used out of the bloodvessels and stain the mucous membrane of a generally red hue, the color being specially pronounced in the neighborhood of the lai'ger DILATATION AND HYPERTKOPHY OF THE STOMACH. 543 vessels. There is often a greenish color developed by the decom- position of the blood. Lastly, the color may be almost black or slaty, but in many cases this deep color is not altogether post- mortem, depending rather on a true pigmentation from chronic catarrh of the mucous membrane. Softening of the stomach is also a post-mortem change. It is really a digestion of the coats of the stomach by the. gastric jxiice. As a rule, in persons near death the gastric juice is not secreted 'normally, but if the person die somewhat suddenly then there may be a considerable amount of active gastric juice in the stomach at the time of death. When the mucous membrane of the stomach dies, the gastric juice in such cases begins to digest it, and so a softening occurs which may extend beyond the mucous membrane. As already hinted, this condition occurs mostly in persons who die suddenly, especially if the body is kept in a warm place, and it is more frequent in children than in adults. In the slightest degree the mucous membrane alone is softened, and it can be removed from the surface of the muscular coat with the finger as a soft paste. Penetrating deeper, the muscular coat and even the serous coat may be half liquefied, so that on handling the stomach it may be perforated. The stomach may even rupture in the body, and the contents pass outwards producing softening in neighboring parts. In some cases the diaphragm has been softened in this way, and the stomach contents have passed partly into the pleural cavity. These changes, both the ordinary alterations from decomposition and the softening of the coats by digestion, occur in those parts of the stomach where the contents have been lying after death. This is generally the neighborhood of the fundus. As the contents are usually fluid, it is often seen that the changes stop short at a definite level and the unaltered mucous membrane rapidly emerges from the altered part. The pyloric portion of the stomach, as it usually lies highest, is least frequently afl'ected, and this is im- portant, as that part of the stomach is the most frequent seat of disease. It will be understood that many of the pathological changes of the stomach will be obscured by the occurrence of these post- mortem changes. DILATATION AND HYPEETEOPHY OP THE ST03IACH. These conditions mostly result from obstruction to the passage of food through the pylorus from contraction of that orifice. It is also stated that sometimes a simple weakness of the muscular coat allows of passive distention. Obstruction of the pylorus causing an accumulation of the stomach contents leads in the first instance to a simple distention of the organ. The distention tells chiefly on the parts which are free to swell out. The lesser curva- ture is fixed by its attachments, and it usually retains nearly its 544 DISEASES OF THE ALIMENTARY CANAL normal position except that its middle part is somewhat dragged downwards (see Fig. 243). The greater curvature, on the other hand, is carried downwards, and the stomach may virtually fill the entire abdomen, reaching as far as the symphysis pubis in some Fig. 243. Dilatation of the stomach, shown diagrammatioally. The stomach is shaded, a being cardiac, and h pyloric orifice. The greater curvature is much depressed, "while the lesser curvature fixed at its two extremities forms a sharp curve, in the bend of which are visible the first loop of the jejunum (e), and the region of the pancreas {d); ff, transverse colon depressed ; in the midst of it the position of the umbilicus is indicated. (After Penzoldt.) eases. Sometimes the pylorus is depressed and the duodenum correspondingly displaced. It may be anticipated that when there is obstruction of the pylorus there will be an effort on the part of the muscular coat to overcome it, just as in the hypertrophy of the heart from obstruc- tion of the aortic orifice, or the similar hypertrophy of the urinary bladder. But the muscular coat of the stomach has a somewhat different function to that of the heart or bladder. In the latter there is a simultaneous contraction of the entire muscle with a view to the emptying of the viscus. In the stomach, however, the contraction is vermicular, and its object is as much to move the contents about inside the stomach as to empty them into the duodenum. In the actual propulsion of the contents into the duodenum it is the pyloric portion of the stomach that is engaged, and here also the material is carried forward by a vermicular move- ment. Hence the hypertrophy of the muscular coat in obstruction of the pylorus does not occur uniformly in the stomach, but INFLAMMATIONS OF THE STOMACH GASTRITIS. 545 localizes itself in the pyloric portion, sometimes even with a special thickening just at the orifice, forming a tight sphincter. In these cases, when the wall of the stomach is divided the progressive thickening of the rigid muscular coat can often be distinguished as the pylorus is approached. Along with hypertrophy of the muscle there is very often thickening of the connective tissue in the mucous membrane and submucous tissue, as well as of that between the muscular bundles. INFLAMMATIONS OF THE STOMACH.— GASTRITIS. Acute inflammations may be produced by the action of irritant poisons which have been swallowed, the inflammation here being accompanied by sloughing. Acute spontaneous inflammation is rare except in the milder forms which constitute catarrh, and we have very rarely, in the stomach, conditions comparable with the phlegmonous angina of the fauces, or the dysenteric inflammation of the intestine. Such phlegmonous inflammations are met with occasionally in severe infective diseases, and particularly in puer- peral fever. There is^reat swelling and redness of the mucous merabrane, terminating in a diffuse purulent infiltration of the wall of the stomach. Sometimes abscesses have been formed in the ^^'all of the stomach which have burst into its cavity. Catarrh of the Stomach, on the other hand, is a condition of YBvj frequent occurrence, and is met with in the acute and chronic . forms. Acute Catarrh. — This is induced for the most part by the direct action of irritants on the mucous membrane, mainly by the use of irritating foods or drinks. "We have already seen that, when food remains in the stomach undigested, it undergoes de- composition, and the irritating products may induce an acute catarrh. The mere prolonged stay of food in the stomach prob- ably induces it, as when by exposure to cold the secretion of the gastric juice and the peristaltic action necessary to the process of digestion are interfered with. It is seldom that the stomach can be examined after death in this condition, but from observations of Beaumont on his patient with a gastric fistula, as well as from experiments on animals, the appearances of the mucous membrane have been tolerably well made out. There is intense redness with swelling of the mucous membrane, which is covered by a layer of mucus or muco-pus, sometimes slightly mixed with blood. The appearances are most marked towards the pylorus, and sometimes confined to that region. IJnder the microscope the bloodvessels in the mucous mem- brane, and especially in the submucous tissue, are found enor- mously distended, and the epithelial cells, both those of the surface and of the glands, enlarged and granular. 35 546 DISEASES OF THE ALIMENTARY CANAL. Chronic Catarrh. — This often remains after one or more attacks of the acute form. It is also present in cases of passive hypersemia of the stomach, which so frequently occurs in consequence of dis- ease of the heart and liver. Cancer of the stomach is also accom- panied by chronic catarrh in most cases. If the catarrh is prolonged, there usually occurs a considerable new-formation of connective tissue, as in other chronic inflamma- tions. There is thus a thickening which atfects mucosa, sub- mucosa, and muscular coat, and causes the surface of the mucous membrane to assume an irregularly folded or wartj' appearance, which has given rise to the designation etat mamelonne. The mucous m.embrane also presents, in many cases, dark spots or a general deep color from the presence of pigment granules in the tissue. The pigment is deiived from the blood, and indicates the occurrence of hemorrhages, probably by diapedesis. The increase of the connective tissue produces atrophy of the glands, which are also considerably distorted. It sometimes happens that the increase of connective tissue is specially great, and the wall of the stomach may be converted into a thick, hard, resistant structure. As all these processes occur mainly in the pyloric portion of the stomach, considerable narrow- ing of the orifice may result. The rigidity of th« wall and the narrowing of the orifice induce more forcible muscular contrac- tions, and the muscular coat therefore hyperti'ophies. In the interstitial tissue of the muscular coat there is also thickening, and the fleshy muscular bundles are separated by trabeculae of connective tissue. The resulting appearance is often very charac- teristic, the hypertrophied connective tissue dividing the hyper- trophied muscular bundles into divisions, which on section are somewhat like the pieces of a fan. This thickened and indurated condition may closely resemble scirrhus of the stomach, especially as a similar appearance is presented by the muscular coat in that disease. Occasionally mucous polypi develop in connection with chronic catarrh, and these may ctevelop into mucous cysts. THE SIMPLE PERFORATING ULCER. This peculiar form of ulcer is met with only in the stomach, first part of the duodenum, and lower part of oesophagus. It is also called sometimes the round and the chronic ulcer. It is clear from the localities in which it occurs that its peculiarities are due to the action of the gastric juice, but the more detailed con- sideration of its mode of origin will be better taken up after the appearances of the ulcer have been described. The ulcer is usually round or oval in shape, and presents the appearance as if a conical piece of the wall of the stomach had been punched out from within, its edges being pertisctly defined without any considerable thickening of the neighboring mucous THE SIMPLE PERFOEATING ULCEE. 547 membrane, and the floor of the ulcer perfectly clean (see Fig. 242, in which an ulcer of the cesophagus having all the characters of that of the stomach is represented). The superficial extent and depth of the ulcer vary considerably. The commonest size is about that of a shilling, but this may be exceeded considerably, and Cruveilhier has described an ulcer which was 6|- inches long and SJ inches broad. In the smaller ulcers the floor is formed of the coats of the stomach, probably with some new-formed con- nective tissue. In the larger and deeper ones the tissue of neigh- boring organs may be exposed, such as the pancreas or liver. The floor of the ulcer does not present any of the usual appear- ances of a granulating wound, but is clean and smooth, the actual tissue of the part being exposed, perhaps with some induration from new formation of connective tissue. The situation of the ulcer is mostly in the neighborhood of the lesser curvature, and nearer the pyloric than the cardiac orifice. It is more frequent on the posterior than the anterior wall. It is not uncomuion to find more than one ulcer present in the same case. Though the ulcer is much more common iu the stomach, yet the duodenal situation has been observed in a considerable number of cases, the cesophagus being, however, exceedingly rare. The ulcer in these situations has exactly the same characters as that in the stomach. The ulcer presents a tendency to penetrate more and more deeply, from which circumstance it is named the perfoeating ulcer. It does not appear to extend laterally to any considerable degree ; it is probable that at the ver^' first the ulcer assumes its full superficial dimensions. Eating into the wall of the stomach, it may penetrate through the entire coats, and sundry accidents are liable to ensue. One of the commonest of these accidents is hemorrhage. The ulcer penetrates one or more vessels at its base. The vessels may be small and the hemorrhage not very considerable, but sometimes a considerable artery is laid open, and a serious, even a fatal, hemorrhage results. From the commoner situations of the ulcers the arteries most frequently penetrated are these— the coronary artery or one of its branches, the gastro-epiploic, the pancreatic, and the splenic. Sometimes the open mouth of the vessel can be seen after death in the floor of the ulcer. Perforation is another result of the penetration of the ulcer, but a much less frequent one than hemorrhage. For the most part, by the time the ulcer has eaten through the wall of the stomach, the latter has already acquired adhesion to some neigh- boring structure, and so actual rupture of the stomach and escape of its contents into the peritoneal cavity is not common. The adhesion may be to the liver or pancreas, or, more rarely, to the spleen, diaphragm, colon, abdominal wall. By the extension of the ulcer, these structures may be eaten into and their tissue exposed. The tissue when first exposed has its normal appear- ance, but it usually becomes condensed and cicatricial. Some- 548 DISEASES OF THE ALIMENTAEY CANAL. times the irritation of the gastric juice produces suppuration and the formation of abscess, especially in the case of penetration into the liver. But if adhesion does not occur, then the ulcer is likely to cause rupture of the stomach. This will happen most readily ■where the wall of the stomach is most liable to shift about during the regular peristaltic movements, and also where there is no solid viscus to which it may readily adhere. Both these conditions are fulfilled in the case of ulcers of the anterior wall, and so it hap- pens that rupture most frequently occurs in this situation. The ulcers which lead to perforation are frequently very small, and the aperture in the serous coat may be as large as the ulcer itself. The result of the perforation is acute and fatal peritonitis. Healing of the perforating ulcer is by no means an unusual occurrence. In the experiments to be referred to presently, in which ulcers •were produced artificially in animals, they healed very readily. In man, also, they are frequently recovered from, and we otten meet with cicatrices in the stomach. They may indeed heal without leaving a very obvious cicatrix at all. The author met with a case in which three weeks after a very severe hemorrhage, presumably from an ulcer of the stomach, only an obscure cicatrix could be found. "We have now to consider the mode of oeigin of these ulcers, and this is a matter of some difficulty. It is obvious from the shape and appearance of the ulcer that it has arisen by the necrosis and subsequent digestion of a piece of the wall of the stomach. The question arises as to the cause of the necrosis. The funnel- shaped outline of the ulcer suggested to Virchow that the necrosis occurred by obstruction of or interference with an arterial branch, and he observed as confirmatory of this that the ulcers most fre- quently had their seat at the point of entrance of arterial branches into the wall of the stomach. The experiments of Panum and Cohnheim confirm this view in so far as they show that ulcers may be produced by embolism of the arteries of the stomach. In Cohnheim's experiments, if the animals were killed a day or two after embolism had been pro- duced there were found large ulcers with abrupt edges and perfectly clean floors. The difficulty of the case is, however, that the per- forating ulcer is not met with specially in cases of embolism or thrombosis of the arteries of the stomach, but in the immense majority of instances in cases where no such disturbance of the circulation exists. It has been suggested again that a venous hyperemia, by causing stagnation and even hemorrhage (see after- wards) in defined areas of the mucous membrane, may produce such weakening of the tissue as to induce necrosis and digestion of it. In most cases of gastric ulcer there is serious and usually prolonged dyspepsia, and the persons are frequently anjemic. This seems to indicate that the condition of the gastric juice has an important relation to the gastric ulcer. It is also important in this HEMORRHAGE FROM THE STOMACH. 549 connection that, Avhile ordinary ulcers of the stomach such as are produced by wounds or the action of caustics, or by such experi- ments as those ah'eady referred to, heal readily, this form of ulcer is peculiarly chronic and shows a tendency rather to extend deeply than to heal. Some abnormal condition of the gastric juice by virtue of which it is peculiarly irritating to the mucous membrane seems to be the essential factor, while a weakened condition of the mucous membrane is also of consequence. In most cases the gas- tric juice is abnormally acid, and it has been thought that by neutralizing the natural alkalinity of the tissues it may lead to their necrosis. On the whole it seems probable that an acrid gastric juice, taking advantage of any accidental stagnation in a defined area of the mucous membrane, may lead to its necrosis and the formation of the ulcer. It has been already stated that while ordinary ulcers heal readily this form is peculiarly persistent. But if the condition of the gastric juice be improved, and especially if its excessive acidity be corrected while solid food is prevented acting on the surface of the ulcer, the ulcer often heals i-eadily, leaving a cicatrix which is sometimes very obscure, but may be more distinct and with some puckering. The frequency of ulcer of the stomach may be judged fijom the fact that according to the results of post-mortem examinations it is said that there are ulcers or cicatrices in about one in twenty of the cases examined after death. HE3I0KRHAGE FEOil THE STOMACH. Besides the hemorrhage which occasionally supervenes in the case of the perforating ulcer, and that which is occasionally a feature in cancer of the stomach, we have certain other forms which call for notice here. The vessels are apt to rupture when the pressure of the blood in them is considerably raised above the normal. This will occur especially with disturbances of the vascular system involving hyperemia of the portal system. In diseases of the heart leading to general venous engorgement, we have passive congestion of the liver reflected to the portal vein. In this case there are signs of general venous engorgement probably including dropsy of the limbs, etc. But disease of the liver itself, especially cirrhosis and cancer, may cause obstruction to the portal circulation. In these cases there is a general engorgement of the portal vessels, and hemorrhage from the stomach frequently occurs. The blood mostly escapes from the superficial vessels of the mucous membrane, which are least supported, and it passes into the cavity of the stomach. In some cases it is from a large number of small superficial vessels, and the exact source is not 550 DISEASES OF THE ALIMENTARY CANAL. apparent. At other times the blood passes to some extent into the superficial layers of the mucous membrane, infiltrating it. The mucous membrane infiltrated with blood is acted on by the gastric juice and digested by it, so that small flat superficial ulcei's are formed, the so-called hemorrhagic erosions. These are generally present in considerable numbers, chiefiy in the pyloric region. In the erosions there may be still some remains of blackened blood, and alongside them there are little areas of mucous membrane infiltrated with blood. In these cases also the mucous membrane is often generally red from the passive hyperasmia, and possibly thickened by catarrh. The blood is generally mixed with the contents of the stomach, and blackened by the gastric juice. If the hemorrhage be very severe, as from an ulcer perforating a considerable artery, the blood may be vomited nearly in the fresh state, but usually it is tarry or like cofiee-grounds. The altered blood may also pass into the duodenum and onwards. TUMOES OP THE STOMACH. Cancer. — This is the only form of tumor which is of much prac- tical inportance, and it is of exceedingly frequent occurrence. From the statistics of a considerable number of observers it ap- pears that cancer occurs more frequently in the stomach than in any other situation in the body, the uterus being the next most frequent site. The great frequency of cancer in the stomach is probably re- lated to the fact that the epithelial structures of this organ are more exposed to various irritations than those of any other part -of the body. ISTot only are there varieties of irritating foods, but the foods are liable, as we have seen, to decomposition, the products of which produce irritation. In cases of cancer there is very com- monly a history of prolonged dyspepsia, perhaps from youth. In this regard the simple ulcer may be again referred to. There have been cases observed in which cancer seemed to originate in the simple ulcer; but the simple ulcer is a disease mostly of youth, whereas cancer is a disease of middle life, the average age being fifty years. It is almost as if similar causes produced the simple ulcer in youth, and cancer in middle life. In its structure cancer of the stomach is like cancer elsewhere. There are epithelial masses which tend to insinuate themselves among the neighboring tissue elements, and there is a connective- tissue stroma. The epithelial elements also originate in the ex- isting epithelium, chiefly that of the glands. But in the mode of growth of the epithelium and its relation to the stroma there are considerable difterences presented, and although not rigidly to be distinguished from each other it is possible to divide the cases into four forms. CATSrCBE OF THE STOMACH. 551 In EPITHELIAL CANCER there is a tolerably definite gland-like new-formation, as we have in other cases of cylinder-celled epithe- lioma. There are ducts and acini lined with cylindrical epithelium, but very often this regular arrangement is lost in great part, and, except in the more recently formed part, we have more irregular masses. The glandular structures are limited by a distinct stroma, which is Avell formed. As in all cancers of the stomach, the new formation of epithelium begins in the glands, and at first the tumor grows in the mucous membrane. But the growth extends into the submucous tissue, and insinuates itself among the other coats of the stomach, passing into the muscular coat, and even outside it into the serous coat. From the glandular character of the tissue in this tumor it is sometimes called adenoma. The tumor is a slowly growing one, and it generally involves a considerable portion of the stomach before the death of the patient. It usually begins in the pyloric region, frequently forming a ring around the stomach, but it extends inwards from this, it may be for some distance. The surface is nearly always ulcerated, and may be considerably excavated. There are sometimes papillse on the surface of the tumor, especially at the marginal parts, which give the surface a warty appearance. The advancing tumor infil- trates and thickens the mucous membrane and the subjacent coats, and so while the greater part of the tumor may be rough and warty and somewhat excavated, the edges are usually prominent, and sometimes rather abrupt. The epithelioma of the stomach is not a very frequent form of tumor, and it does not so readily extend beyond the neighboring lymphatic glands to the liver as the next form. Medullary or Soft Cancer of the stomach is probably the most frequent of all forms of tumor. In it the epithelial growth does not arrange itself in proper glandular structures, but there are large masses of comparatively loose epithelium in a sparse and deheate stroma. Hence the tissue is very soft. The epithelial masses tend to infiltrate the subjacent structures as well as to ex- tend laterally. The tumor is usually seated near the pylorus, forming, in some cases, a ring or a defined circular tumor. The tissue being soft it is specially liable to bleed and to ulcerate. The latter condition is so frequent and characteristic that the tumor often presents itself as a round, shaggy ulcer with prominent edges. Doubtless the gastric juice and the food acting on the surface of the tumor break down its tissue and lead to the ulceration. At the margins the cancer is infiltrating the mucous membrane, and so the edges are raised and somewhat abrupt. This form of tumor is exceedingly malignant, the soft and loose cancerous elements readily finding their way into the lymphatic channels. Hence cancerous formations in the lymphatic glands around the stomach and in the other glands of the abdomen are very frequent. The liver also is very often the seat of numerous 552 DISEASES OF THE ALIMENTAEY CANAL. and large cancerous tumors, and a large proportion of the cases whicli clinically have the characters of cancer of the liver are primarily cases of this disease. The enormous secondary growths in the liver may contrast very mai'kedly with the insignificant primary lesion, sometimes little more than a comparatively small round ulcer with irregular surface and prominent margins. The tendency to hleed which this tumor presents is to be borne in mind. The bleeding may he slight but frequent, and the blood carried off into the intestines. Or it may be more considerable, and even fatal. SciRRHUS is a somewhat frequent form of cancer of the stomach. Here, the new formation of epithelial cells is not very rapid or vigorous, and it is accompanied by an excessive formation of con- nective tissue in the form of stroma. Originating in the glandular epithelium, long processes composed of rows of cells, often with few abreast, are produced, and they grow not only into the mucous membrane, but also into the muscular coat separating its trabeculas, and even into the peritoneal coat. These processes seem to be peculiarly irritating, as they give rise to the production of dense connective tissue which is nmch more manifest than the proper epithelial elements. These elements may, in fact, degenerate, and leave little besides condensed hard connective tissue. The cancer mostly begins in the pyloric region, but extends inwards till, in some cases, it has involved the entire wall of the stomach, except the fundus. The wall of the stomach is con- verted into a stiff hard mass which may be, in some places, an inch in thickness. This dense structure has replaced the mucous mem- brane, and, to a certain extent, the other coats which, however, are usuallj' separately distinguishable. The muscular coat is much hypertrophied by the new formation both of muscle and of hard connective tissue, and a section of it presents the peculiar fan-like appearance already mentioned. The surface of the affected por- tion of the stomach is irregular, with rounded prominences, and there are sometimes ulcers present, but there is not a general ulceration as in the case of the epithelial and medullary forms. The stomach is often greatly contracted in this disease. The edges of the cancerous portion are not well defined, but shade off' gradually into the normal mucous membrane. Extension of the cancer to the liver does not readily occur, although neighboring lymphatic glands may be involved. Colloid Cancer is not a frequent form as compared with the medullary, but is met with in a considerable number of cases. The other forms and especially the epithelioma, occasionally undergo a partial colloid degeneration. In the colloid form as in the others the epithelial elements take origin in the glandular cells, and after infiltrating the mucous membrane these epithelial masses insinuate themselves among the muscular trabeculse (Fig. 102, p. 220), and even into the serous coat. The stroma consists of a CANCER OF THE STOMACH. 553 somewhat abundant well-developed network of connective tissue. The peculiarity of this form is that the cells have a special tendency to undergo colloid metamorphosis. They seem from their first formation to present a regular intention in this direction, and even in the more recent parts there is often already a considerable advance in the degeneration. The outlines of the cells disappear as the protoplasm becomes transformed into colloid material, and as the nuclei resist the degeneration longer, we sometimes see the jjcculiar appearance of oval nuclei as if floating in a clear trans- parent material. Finally, the whole epithelial elements are converted into colloid material, and the structure presented is a beautiful reticulated network with spaces filled with a transparent colorless jelly (Fig. 101, p. 220). As the colloid material occupies more space than the original cells, the spaces of the alveoli are, as it were, tightly packed Avith the jelly, and the fibres of the stroma rendered tense and rigid. Hence, it happens that although the structure is composed mainly of a soft jell}', yet it is to the feeling hard and rigid, just as a tensely filled bladder may be. The tumor, like other cancers, usually begins towards the pyloi'is, but it extends gradually till it comes to involve a large area, sometimes even as much as three-fourths of the entire extent of the viscus. The wall of the stomach is converted into a trans- parent glancing tissue, and in the more advanced parts it is impossible any longer to distinguish the difierent coats, all being homogeneously replaced by the cancerous tissue. The wall of the stomach is considerably thickened, and the internal surface may present an irregular aspect with prominences; but there is little tendency to ulceration. As the thickened wall is tense and hard, the stomach when cut into does not generally collapse but keeps its shape. There is no tendency to contraction of the stomach as in scirrhus, but, on the contrary, the organ may be considerably enlarged. This form has a very marked tendency to extend continuously both along the stomach, and also through the stomach to the peritoneum. Hence it produces secondary tumors in the perito- neum itself much more readily than in the lymphatic glands and liver. It will appear from what has been mentioned above that cancers of the stomach frequently lead to the formation of secondary tumors elsewhere. In this respect the cancers of the intestine resemble those of the stomach, and as the modes of extension present certain points of interest and practical importance, a special section will afterwards be devoted to this subject in general. The remaining tumors of the stomach are of trivial consequence. "We have already seen that mucous polypi and cysts occur in chronic catarrh. Lipomas and myomas have been met with, as also FiBROMAS and sarcomas, but they are very rare. 554 DISEASES OF THE ALIMENTARY CANAL. E.— THE INTESTINES. Introductory. — The diseases of the intestines resemble in many respects those of the stomach, but there are important diiferences. In structure, the intestine differs from the stomach in several respects. We no longer have the specific glands peculiar to the stomach, but, on the other hand, the intestine presents numerous closed lymphatic follicles in its mucous membrane, and these are only present to a very slight extent in the stomach. These Ij^mphatic follicles are solitary or collected into groups, in the latter case forming the well-knovi'n Peyer's patches. Of considerable importance in regard to the diseases of the intestine are the time which the intestinal contents stay in the different parts of the canal, and the changes they undergo there. After leaving the stomach, the food appears to pass rapidly through the upper part of the small intestine, occupying on an average from two and a half to three hours in doing so, and it is at the same time rendered alkaline and partially protected from further decomposi- tion by the pancreatic ffuid and the bile. The movement of the intestinal contents is effected by the peri- staltic contraction of the bowel, and the rapid passage of the con- tents through the small intestine indicates that here the peristalsis is peculiarly active, whereas, in the large intestine, it is slow. When the feces reach the large intestine they are still fluid, and the chief function of the colon seems to be to complete the absorp- tion of the fluid, and allow the feces to become thicker. But if the peristaltic action of the large intestine be increased, then there will be no time for the feces to become thick, and fluid evacuations will be the result. This will be still more the case should the movement of the small intestine be increased, and the contents carried even more quickly than usual through them. It will be seen that diarrhoea results from increased peristaltic movement, and that the evacuations Avill be more fluid the higher up the increased movement begins. It is well known that certain medicinal agents produce fluid motions, and these seem all to act by increasing the peristalsis, their relative vigor depending greatly on the part of the intestine at which they begin to produce their effects. Irritating articles of food produce a like increase of the peristalsis and diarrhoea, and so may ulcers and inflammations of the intestine itself. In the stools of diarrhoea we may expect to find chemical con- stituents which normally are present in higher parts of the intes- tine, but absorbed before reaching the rectum. If the diarrhoea arises from increased peristalsis of the colon, then we shall find material which is normal in the ctecum, such as undecomposed bile, leucin, chloride of sodium, peptones, and sugar, some of which are present in appreciable quantity in normal feces. But if the diarrhoea has involved the small intestine, then we shall MALFORMATIONS OF THE INTESTINE. 555 find these constituents much more abundantly, and also remains of undigested food. We have already seen in the case of the stomach that many of its diseases are connected with the fact that the food stagnates and decomposes in that viscus. It will be seen from what has gone before that the intestinal contents stagnate chiefly in the large intestine, and next to that in the lower part of the small intestine. It is probably due to this that we find the jejunum peculiarly free from all forms of disease ; in this respect it contrasts with the lower part of the small intestine, the ileum, but still more with the large intestine. Hence it is that the diseases of the large intestine resemble those of the stomach much more than those of the small intestine do. This is especially true in regard to simple inflammations, which very often concentrate themselves in those parts where the intestinal contents most readily stagnate, namely, the CEecum and the rectum. It is true also of cancer, which is very rare in the small intestine but common in the large, especially in the csecum and rectum. It is to be remembered, further, that the intestine is a compara- tively narrow tube, and is subject to obstruction in various ways. Post-mortem Changes. — These are not so important as those of the stomach. After death the blood is apt to gravitate towards the more dependent parts of the wall of the intestine, and the coloring matter being dissolved out and staining the mucous membrane, it may give rise to a deceptive appearance of inflam- mation. Similarly the intestine may be stained with the biliary coloring matter in the neighborhood of the gall-bladder. MALFORMATIONS OF THE INTESTINE. Congenital malformations of the intestine are of considerable frequency. The most important are those in which, from a fault of development, a part of the intestine is wanting. The colon or the rectum may be entirely absent at birth, being represented by a solid cord ; or the rectum may be partially occluded, in some cases in its middle part, in others at its lower extremity. All these cases present the characters of imperforate anus, but of course in view of possible surgical interference their gravity varies, ths most hopeful being those m which only the extreme lower part of the rectum is defective, and the gut is separated from the anus only by a membrane. There occur also narrowness and defect of the small intestine, especially in the duodenum and lower end of the ileum. The whole intestine is sometimes deficient in length, having something like the form of the letter S instead of the usual convolutions. In such cases the absorption and digestion of food must be defective, but the persons may live on to old age. 556 DISEASES OF THE ALIMENTARY CANAL. The commonest malformation is Meckel's diverticulum. This consists in a finger-lil-ce projection from the intestine. It occurs in the ileum, about three or four feet above the ileo-caecal valve in the adult, and about a foot above it in the new-born; it projects from the free convex border of the gut. It is from one to six inches long, possessing the same structure as the intestine, and communicates with the latter : it is narrower in its calibre, being of a diameter rather more than that of the finger. The diver- ticulum arises by the imperfect closure of the omphalo-mesenteric duct, and sometimes it is united to the umbilicus by a cord. Very rarely the diverticulum is continued to the umbilicus, and opens there by a fistula at the surface. HERNIA OR RUPTURE. True hernia consists in a protrusion of the intestine, omentum, or other abdominal organ into a sac formed by a prolongation of the peritoneum. The sac may project externally, or it may be contained within the abdomen, and so we may distinguish ex- ternal and INTERNAL hernias. The hernias, especially the ex- ternal ones, are of so much importance in a surgical point of view that full descriptions are given in the surgical text-books, and need not be repeated here, except in outline. For the most part the sac is an entirely abnormal projection of the peritoneum, and seems to be protruded before the contents. An exception to this occurs in the case of congenital inguinal hernia, in which the sac is formed by the persistence of a fcetal condition. There is a partial exception also in the case of most internal hernias, where the sac usually arises by the exaggeration of an existing normal pouch. In the PRODUCTION of hernias, we have to account for the ab- normal protrusion of the viscera. This is usually due to the abdominal contents being subjected to undue pressure. In severe muscular efforts, such as are involved in lifting heavy weights, the glottis is closed, and the muscles of expiration fix the chest and abdomen, the contents of the abdomen being subjected to severe pressure by the contraction of the muscles of the abdominal wall. If there is any part of the wall which is unduly weak a bulging outwards may occur here, and so give the starting-point for the hernial protrusion. In this connection the greater frequency of hernia on the right side may be noted. In violent exertions the right arm is usually more used than the left, and as the chest is bent over to the left side to counterbalance the strain on the right, the lower surface of the diaphragm faces more to the right and presses the viscera towards that side. It is clear that straining at stool or otherwise will also increase the pressure on the abdominal contents, and any excess will predispose to hernia. It has been said that the protrusion takes place where there is any weakness of the abdominal wall, and it is well known that the HERNIA OE RUPTURE. 557 external hernias occur at specially unsupported parts of the wall, while the internal ones have usually a pouch ready made as a starting-point. The ahdominal wall Irom its anatomical conforma- tion is weak at ceitain points in every person, but there may be congenitally a special weakness, which in some cases seems to be hereditary. Or the weakness may be induced by stretching of the abdominal parietes by increase in their contents (ascites, tumors, pregnancy, etc.), or more directly by injury to a particular part. In protruding, the viscera nearly always push the peritoneum before them, and the proper sac is formed by the peritoneum, which shows a remarkable power of stretching. But there are cases of protrusion in which the aperture has been produced by actual rupture of the wall, and in these cases the hernia may be devoid of a proper sac. These cases, however, of what may be called FALSE hernia, are exceedingly rare, as an injury, although tearing the muscular wall and other tissues, will very often leave the elastic peritoneum uninjured and capable of protrusion. The hernial sac acquires for the most part adhesion to the structures among which it is protruded, and it does so by a chronic inflammation. It very often happens also that the contents of the sac become adherent to its internal surface by inflammation, and in that case the hernia is irreducible. It is not necessary to enter fully into the individual forms of hernia, and of the external ones little more than an enumeration will suffice. The external hernias are, (1) Inguinal hernia in the congenital and acquired forms, or, as otherwise divided, direct and oblique. (2) Femoral hernia. These two are by far the commonest foi'ms. Of comparatively rare occurrence are, (3) Hernia of the sciatic notch; (4) Perineal hernia, protruded between the fibres of the levator ani; (5) Vaginal hernia; (6) Hernia of the foramen ovale; (7) Umbilical hernia which is congenital or acquired, in the former case arising b^' protrusion into the dilated umbilical cord; (8) Ab- dominal hernia occurring in various parts of the abdomen, chiefly towards the edges of muscles, and arising by tearing of tendons or muscular fibres, hence, frequently, traumatic. Its commonest situation is near the linea alba. Internal hernia comes less frequently into sight, and the possi- bility of its existence is apt to be forgotten. (1) Diaphragmatic hernia is perhaps the commonest. There is a congenital form in which a sac is protruded through one of the normal apertures, or through a part of the diaphragm which by reason of defective development has given way. The protrusion is into the chest, and the sac may contain intestine, spleen, liver, stomach. There is also an acquired form, due nearly always to some injury to the diaphragm, and the hernia is frequently devoid of a proper peritoneal sac. From a case recorded by Dr. Adams, 558 DISEASES OF THE ALIMENTARY CANAL. it appears that a tumor growing against the diaphragm (in his case from the capsule of the spleen) may so weaken it as to lead to her- nial protrusion. In diaphragmatic hernias from rupture, a large portion of the abdominal viscera may be protruded. (2) Retroperitoneal hernia includes cases in which the intes- tine passes into a preexisting pouch in the peritoneum, greatly enlarging and filling it. The hernial sac hence lies behind the peritoneum of which it is an oft'set. There are three pouches in the peritoneum which are capable of giving rise to such hernias. The JEJUNo-DUODENAL pouch is the most important. It exists just where the jejunum arises from the duodenum, and lies be- tween the last part of the duodenum, which bounds it on the right, and the aorta, which bounds it on the left. The pouch was present, according to Waldeyer, in about 70 per cent, of the bodies which he has examined, and is generally large enough to admit the terminal phalanx of the thumb. It is best seen when the jejunum and small intestine generally are raised and carried to the right, so that the origin of the mesentery may be exposed. The little pouch, if present, is then seen lying in the posterior wall of the abdomen with sharp sickle-like margins. ' Sometimes a fold of the jejunum passes into this pouch, constituting a hernia. The pouch may be greatty enlarged by the protrusion of further portions of the in- testine into it, and cases have been recorded in which the entire intestine has passed into the greatly distended sac. Another pouch of the peritoneum is the suB-CiECAL, which has its seat between the folds of the meso-colon ascendens. Into this pouch the intestine is very rarely protruded, and the pouch itself only occurred in about 30 per cent, of the bodies examined by Waldeyer. The FOSSA INTERSIGMOIDEA is a pouch in the mesentery, lying between the two folds near the beginning of the sigmoid flexure. The aperture is in the under layer. This is the commonest of these pouches, occurring in about 80 per cent, of the bodies, but from its position it does not appear ever to become the seat of hernia. The CONTENTS OP HERNIAS are usually the intestine, and, for the most part, the more movable small intestine. Sometimes also the great omentum is carried into the sac. The large intestine pos- sesses for the most part no free mesentery, being only partially covered with peritoneum, so that it is hardly possible for it to pass into a sac unless it be dragged down with considerable force. The method of descent of the large intestine merits a more special notice. The process may in some respects be compared to the descent of the testis in the fcetus. Before its descent the testis is only partially covered with peritoneum, being free of it at its posterior aspect. As it descends it remains with only a partial peritoneal covering, and even in the tunica vaginalis, after the sac has separated from the general peritoneum, the testis lies behind with its posterior aspect free of peritoneum. And. so in a hernial sac, the caecum may be carried down, but in its new position it HERNIA OE BUPTUBE. 559 remains only partially covered with peritoneum, and really forms as it were a part of the wall of the sac. This will only occur in very large hernias as a rule, but when it does occur the piece of intestine will be irreducible. A still more peculiar condition sometimes occurs. The intestine may be protruded mainly at the part where it is uncovered by peri- toneum, and instead of pushing a-peritoneal sac before it, it may as it were drag it after. As the gut is protruded it may even get more and more stripped of peritoneum, so that the hernia may be much more extensive than the sac. This, however, is an exceed- ingly exceptional occurrence, and it is more common to lind that as an ordinary hernia advances it drags the colon into it, so that besides free loops of small intestine there may be, fixed in the wall and only partly covered by peritoneum, a piece of the CEecum, or the sigmoid flexure, or even the fundus of the bladder. In a similar fashion to that just described, the ovary may be protruded. A large majority of cases of ovarian hernia are con- genital, and they appear to arise by a fault of development by which the ovary descends as the testis does normally. The ovary passes through the inguinal ring and takes a sac with it, but just like the testis it is itself attached to the wall. The sac remains open like the tunica vaginalis in a congenital inguinal hernia. The ovary in that case will be irreducible, unless, as sometimes happens, the broad ligament is so long as to allow the ovary to pass back through the neck. In this case, however, the ovary will still have its fixed attachment in the sac. Apart from this con- genital inguinal form, ovarian hernias may be acquired, and these may be either inguinal or femoral. The strangulation of hernias is of great importance. By this expression is meant the condition in which the neck of the sac is so tightly impacted that not only is the return of the contents pre- vented, but even the bloodvessels are obstructed by the pressure of the ring. This mostly occurs when, on account of some pecu- liarity in the situation of the intestine as it issues from the sac, there is, to begin with, a partial obstruction. If the intestine at its entrance into the sac be free, while at its exit it makes a sudden bend so as to cause a partial obstruction, then the feces will pass readily in, but will accumulate inside as they do not find free exit. The mere loading with feces may cause irreducibility, and if the feces decompose the development of gas may still further increase the bulk of the contents. In this way the sac will become too full, and as the neck is narrow there will be special constriction here. Again, the intestine already in the sac by its peristaltic movement may drag more and more of the gut after it, till stopped by the intestine becoming too tight for the neck. In any case the neck of the sac constricts the portion of intestine concerned, and the most direct efifect is obstruction of its veins. This itself, by producing hypersemia, and, it may be, oedema of the 560 DISEASES OF THE ALIMENTARY CANAL. mucous membrane, leads to swelling and further constriction. The whole protruded piece becomes of a dark color from venous engorgement and hemorrhage. Finally the pressure may be enough to close even the arteries. The venous obstruction alone seems sufficient, if complete, to cause necrosis of the intestine, and so gangrene is an occasional result. If the arteries are also obstructed there is still greater probability of the occurrence of gangrene. But sometimes the obstruction is relieved before gangrene has occurred, and yet in some of these cases a sevei'e inflammation results after the intestine has been returned to the abdomen, leading on, it may be, ultimately to gangrene of the affected piece of gut. The probable explanation of this is that during the incar- ceration the arteries have been obstructed, and during this period the bloodvessels have been so damaged that on the restoration of the ch'culation they are no longer able to recover. It has been shown by experiment (in the ear of the rabbit) that if, by liga- turing the main arteries, the vessels of the part are deprived of blood for a time, and then the circulation restored by loosening the ligature, the result is, active hypersemia, acute inflammation, or the hemorrhagic infarction, according to the time during which the ligature has acted. So in the case before us, the release of the constriction, by allowing of the reestablishment of the circulation in vessels seriously compromised, may lead to inflammation or gangrene. TWISTING OP THE INTESTINE. EiG. 244. This is a condition probably of frequent occurrence, but one which is perhaps too little borne in mind as a cause of obstruction. It occurs in the great majority of cases at the sigmoid flexure of the colon, and the reason of this will appear from the anatomical re- lations of that part of the gut. The ascend- ing colon above the flexure, and the rectum below it, have virtually no mesentery, being fixed to the abdominal wall. The flexure therefore is flxed at its two extremities and these are near one another, while the loop forming the flexure is movable. It is as if the loop were attached by its two ends to a flxed point, and it is easy to understand how it should sometimes twist round this as an axis. The twist is, as it were, in two half turns (see Fig. 244), and it is usually the upper limb of the loop which turns round the lower at its neck. It is clear that the twisting will cause some obstruction of the intestine, but this will not usually be complete. The lower limb is narrowed at its neck by being grasped by the upper limb twisted round it, while Twisting of tlie sigmoid flexure. The upper limb has a much sharper turn than the lower, so that a flexible tube could be passed up from the rectum. INTUSSUSCEPTION OE INVAGINATION. 561 the upper limb is narrowed by the sudden curve which it makes. Feces still pass into the flexure, however, and they may ac- cumulate in enormous quantity. This partial obstruction Avith accumulation of feces may persist for months and lead to extreme dilatation of the flexure, so that it may fill the abdomen and reach up to the diaphragm. As the upper limb is twisted over the lower and the latter is straight, a tube may be passed from the anus up into the enormously dilated flexure. The walls of the intestine in these prolonged cases may be greatly thickened, especially the muscular coat. In some cases twisting may exist without any obstruction of consequence. While twisting is most common in the sigmoid flexure, it is liable to occur also when other parts of the intestine assume similar relations, that is to say, when a free loop of small intestine becomes fixed at its extremities, and these extremities are near each other. This will happen most frequently when one extremity is already fixed, as is the case at the upper and lower ends of the small intestine, where, on the one hand, the duodenum, and on the other, the colon, is fixed to the abdominal wall and holds the intestine down. If, by inflammation or otherwise, an abnormal adhesion is acquired, so that the gut is fixed at a point near the situation of the natural fixation, then twisting is apt to occur, and probably more readily here than in the sigmoid fiexure, as the small intestine is naturally more mobile. INTUSSUSCEPTION OE INVAGINATION. In this condition a portion of the intestine passes into a succeed- ing portion. In order that one piece may slip inside the other, the one must present active peristaltic contractions, while the other is relaxed. The portion narrowed by the violent peristalsis passes inside of the relaxed part. These conditions are most frequently found at the junction of the small and large intestines. The large intestine is naturally wide, and its peristaltic movements sluggish. If then the ileum at its last part presents peculiarly violent peristaltic contractions it may pass into the large intestine. This may explain the fact that the most frequent seat of invagination is in this situation. The invagination, however, is not usually a simple inversion of the ileum into the colon; in most cases the ileo-csecal valve is carried before the advancing ileum and forms the apex of the in- truded piece. This inaplies that the caecum itself is carried inwards and inverted, and the orifice of .the vermiform appendage is some- times to be found near the apex of the invagination. The in- vagination is not infrequently very extreme, so that in children (in whom it most commonly occurs) the invaginated part may be carried right on to the rectum, so that the apex may be felt per anum. Besides this form we also meet with invagination of the large 36 562 DISEASES OF THE ALIMENTARY CANAL. intestine itself, one part into a succeeding. It occui's but rarely in the small intestine. It has been stated above that invagination is peculiarly frequent in children, especially that form in which the large intestine is in- volved, and this is probably due to the much greater mobility of the colon in children than in adults. In the bodies of children also we frequently meet with a form of invagination which has produced no symptoms during life, and has really occurred just at the time of death. It is usually present in the small intestine, where a small inversion of one part into a succeeding one is found. The invagination is easily reduced by slight dragging, and there are none of the secondary changes visible, such as are to be men- tioned immediately as following invagination. Just at death, or immediately after it (as may be frequently seen in animals), the intestine commonly shows violent peristaltic movements, but these are irregular, and it readily happens that a much contracted part passes inside a relaxed portion. This form of invagination is, therefore, either post-mortem or occurs just at the agony. When a piece of intestine is invaginated, there are three tubes, the outside one in its natural position, forming the sheath, the internal one, which, although abnormal in position, runs in the usual direction, anct the middle one joining the other two, and with its mucous surface directed outwards. It sometimes happens that a second invagination occurs, and then there are five tubes, or a third, in which case there are seven. The mesentery is carried in with the intestine, and by dragging on it at one side, it may give the gut a somewhat oblique direction. The packing of intestine into the interior of succeeding portions causes considerable interference with the circulation, and this is increased by the mesentery being partly included and its vessels pressed on. In this way there usually occurs an acute inflamma- tion, with swelling and hemorrhage of the mucous membrane, and fibrinous exudation on the peritoneal surface. The inflammation may lead on to a general peritonitis Avith fatal issue. Again, the obstruction of the vessels may be such as, with the added inflam- mation, to lead to gangrene of the gut, and this by the slough separating and causing perforation may produce a fatal peritonitis. On the other hand, permanent adhesion may occur between the sheath and the upper end of the included part at the proximal extremity of the invagination, and, the inner and middle tubes becoming gangrenous, they may come away in whole or in part, as a slough, and the continuity of the intestine be restored with the loss of a piece. It is not usual for complete gaiigrene of the included tubes to occur, but what remains becomes adherent to the sheath, and, by contraction, gradually accommodates itself, and so the calibre is fully restored. SIMPLE INFLAMMATIONS OF THE INTESTINE. 563 PROLAPSE OP THE INTESTINE. This condition connects itself naturally with invagination. It is the protrusion of the intestine outside the body through the anus or through an artificial anus. The commonest form is the ordinary PEOLAPSUS ANI. This only occurs when the sphincter is greatly relaxed by catarrh or by violent pressing at stool, but when it has frequently happened the sphincter atrophies and the prolapse occurs very readily. There are, strictly speaking, two forms of prolapsus ani. In the one little more than the mucous membrane is protruded, and it is seen to be continuous with the skin at the anus. In the other form there is really an invagination as well as a protrusion. The lower part of the rectum is so fixed that the whole wall cannot be protruded, but only its mucous membrane as in the form just con- sidered. But the upper more movable part may be invaginated into the lower part and then protruded. This mostly occurs as a consequence of violent peristaltic contraction of the rectum in cases of severe diarrhoea with tenesmus. In both forms the exposed mucous membrane becomes inflamed and liable to bleeding. The inflammation sometimes causes through time adhesion and fixation of the bowel in its abnormal position. SIMPLE INFLAMMATIONS OP THE INTESTINE. "\Ve have already seen that the mucous membrane is frequently irritated by the contents being of an obnoxious nature by reason of decomposition or otherwise. In addition to that, inflammation may be produced by the action of specific morbid poisons, chiefly those of dysentery, typhoid fever, and cholera. "VVe have there- fore in the first place to consider the simple inflammations and afterwards these others. The term enteritis is often used to designate inflammations of the intestine of all kinds. Phlegmonous inflammations of the intestine sometimes occur as the result of peculiarly irritating contents. We shall see that in dysentery we have an inflammation of this kind, but there are what may be called dysenteric inflammations without the special dysenteric poison, the anatomical changes being virtually the same, although as a rule much less intense. Catarrh of the Intestine. — As already indicated, this occurs chiefly in connection with the presence of irritating contents, but exposure to cold may also lead to it. Perhaps this latter cause produces its eftects by means of the former. That is to say, the exposure of the surface to cold may interfere with digestion and absorption, and so leave the contents to decompose and become irritating. The influence of the intestinal contents in producing catarrhs is 564 DISEASES OF THE ALIMENTARY CANAL. shown by the localities at which inflammations are most common. The large intestine is much more frequently aftected than the small, and in the large intestine the caecum, with the vermiform, appen- dage, is the most frequent seat, and next to that the rectum, appar- ently because the contents stagnate especially in these parts rather than in the much more movable transverse colon. The catarrh is characterized by hyperemia and swelling of the mucous membrane, with exudation of serous fluid and leucocytes. There is also increased secretion of mucus, which in the case of the colon may be very excessive. The exudation is usually mucous in character, but in the more acute inflammation it may assume more or less of a purulent character. If this be the case, the mucous membrane is liable to be infiltrated with inflammatory cells, and after a time to undergo ulceration. This occurs with peculiar frequency in the caecum, and next to it in the rectum. Catarrhal ulcers are usually of considerable area and compara- tively superficial. ^Neighboring ulcers may coalesce so as to produce extensive, variously shaped losses of substance, in the midst of which the remaining mucous membrane appears as raised patches with irregular outline. Sometimes the floor of the ulcer is so smooth, and the remaining mucous membrane so irregular from inflammatory infiltration, that it looks as if the ulcer were the normal mucous membrane and the patches of persisting mucous membrane adventitious. In the course of catarrhs, ulcers also arise from the closed follicles. There are indeed some catarrhs in which the latter are mainly atfected, appearing as rounded prominences and flat eleva- tions, corresponding to the solitary follicles and Peyer's patches. This form is called follicular catarrh, or follicular enteritis. But without the inflammation preponderating in the follicles thej' are often enlarged, and may be so infiltrated with inflammatory products as to form virtually small abscesses resulting in crater- shaped ulcers which may afterwards enlarge. In this way arise the so-called follicular ulcers. The ulcers of ordinary catarrh are superflcial, and unless exposed to continued irritation, as by the prolonged presence of hard feces, they do not tend to perforation, and readily heal when the cause of catarrh is removed. If the catarrh be moderate — not so intense as to lead to ulceration — then, if long continued, it will give rise to hypertrophy of the mucous membrane such as we find so frequently' in the case of the stomach. Here also there may be mucous polypi and cysts as in the stomach. They are most frequent in the large intestine, and if seated in the rectum they may project through the anus. Localized Inflammations. — It has already been indicated that certain localities are more liable to inflammation than others, and as the inflammations of certain of these regions present special points of importance they have received special names, and require more particular attention. SIMPLE INFLAMMATIONS OF THE i;STESTINE. 565 Duodenitis is usually an extension of a catarrh of the stomach, and it would not warrant any special reference except from the fact that the common bile-duct often takes part in the catarrh, and we have obstruction and icterus sometimes resulting from this simple cause. Typhlitis and Perityphlitis designate conditions which require very special notice. These two terms mean respectively inflam- mation in and around the csecum, but they are frequently used so as to include inflammations in connection with the vermiform appendage, and, in fact, Ziegler seems to limit the designations to these latter inflammations. In some cases the csecum is very seriously inflamed and ulcer- ated, especially when large masses of hard feces lodge in it. Under these circumstances the ulcers may increase in depth, and extend, in the posterior part of the wall where the gut is not covered by peritoneum, through the entire thickness of the intes- tine so as to penetrate into the retroperitoneal connective tissue. The result is acute inflammation in this region, often going on to the formation of abscess. It will be inferred that this condition is that designated perityphlitis. The VERMIFORM APPENDAGE much more frequently gives rise to acute inflammations around the csecum than the csecum itself does, so that, although the term typhlitis is not applicable, yet perity- phlitis is. It may here be mentioned in the first place that the appendage sometimes undergoes peculiar transformations on account of the closure of its orifice, with or even without inflammation of its mucous membrane. If, as a result of inflammation or otherwise, the orifice be closed, the secretion, along with the catarrhal exudation, accumulates in the appendage and distends it, so as to convert it into a large retention cyst (Pig. 245). The contents usually become serous, so as to constitute a dropsj' of the vermi- form appendage, but they may continue mucous in character and form a thickish jelly. The dilated appendage may acquire con- siderable dimensions, as in the case from which the accompanying figure is taken. But of more importance are the inflammations due to the presence of foreign bodies in the appendage. Any hard substance lying in the csecum may, if small enough, pass into the vermiform appendage. In this way apple, grape, cherry, or orange seeds are said to get into it. But much more frequently pieces of hardened feces are met with, and as these dry and frequently assume the shape and appearance of cherry or orange stones, they are fre- quently mistaken for them. This occurs all the more because the inspissated feces are often coated with phosphates which form a kind of rind. The presence of the foreign body causes inflammation of the mucous membrane, and this, from the continued pressure and con- fined space, readily results in ulceration. The ulcers frequently 566 DISEASES OF THE ALIMENTARY CANAL. penetrate through the appendage and lead to peritonitis. As a general rule the appendage has acquired adhesions before actual perforation occurs, and so the peritonitis is limited by the adhe- sions. But the inflammation is apt to recur, and not infrequently Fig. 2i5. Cyst of Termiform appendage. The appendage is converted into a bulky cyst whicli was filled with gelatinous material. results in the formation of recurring abscesses. The bursting of one of these into the cavity of the peritoneum often leads to fatal pei'itonitis. From the accounts in the newspapers, the death of M. Gambetta seems to have been due to this cause. From the relation of the parts it will be seen that a perityphlitis arising from the csecum will usually be in the subperitoneal tissue, whereas that from the vermiform appendage will be in the perito- neum, as the appendage is' completely surrounded by peritoneum and has a mesenterj'. It follows that the latter is much the more dangerous as it is also the more frequent form. It is, indeed, much more frequently a cause of death than is usually supposed. Proctitis and Periproctitis are inflammations in the rectum and around it, of an equivalent character to those in and around the CEecum. If the ulceration leads to perforation and the forma- tion of abscess, then the disease may have a very chronic course with fistulse discharging into the rectum. Sometimes these burst externally, or into the vagina, and they may retain their communi- DYSENTEEY. 567 cation with the rectum, so forming false passages for the feces and flatus, or the internal aperture may close, leaving merely an ex- ternal fistula. SPECIFIC IKFLA:MMATIO]SrS OP THE INTESTINE. Dysentery. — This inflammation is determined by the action of a specific morbid poison. As already indicated, similar lesions sometimes occur in connection with other diseases, such as typhoid fever, cholera, acute rheumatism, but in these also, although the virus is not the same, we may presume that a violent irritant is present. It is difiicult to say whether the poison acts on the mucous membrane by being present in the intestinal contents, or because it is carried by the blood. At any rate, the locality of the disease is evidently determined by the stagnation of the intestinal contents. It is always most marked in the large intestine, and especially in the flexures, these being the parts where the feces tarry longest. It usually decreases in intensity, from- the rectum upwards, but not uniformly, there being more affected and less affected parts, the former corresponding usually with the flexures. In severe cases the whole colon is afl'ected, and sometimes even the lower part of the ileum. The disease manifests itself as an acute inflammation, which, in the milder cases, may present the characters of a severe catarrh, but is apt to go on to phlegmonous inflammation with sloughing of the mucous membrane. In the earlier stages the mucous mem- brane is swollen by serous exudation, soft and juicy, and it is thrown into folds on the summits of which it is peculiarly hy- persemic. The surface is covered by a mucous or grumous ma- terial, consisting of shed epithelium with mucus and inflammatory exudation. The mucous membrane and submucous tissue are in- filtrated with serous fluid and leucocytes in great abundance. In higher degrees the mucous membrane is still more thickened and thrown into still more prominent folds. There is also con- siderable hemorrhage in its substance occasionally. The summits of the folds being specially exposed to mechanical irritation, very commonly undergo necrosis, and the sloughs are generally dis- tinguishable by the brown color which they assume from becoming stained with the bile pigment. The necrosis involves the mucous membrane to varying depths, sometimes very superficially, some- times through its whole thickness, and, if the slough surrounds the gut, we may have a ring of necrosed tissue ultimately dis- charged by the anus. Of course, these sloughs leave ulcers behind, whose walls present great infiltration of leucocytes. But ulcers form also by processes similar to those in catarrh, namely, by inflammatory inflltration and molecular destruction of the mucous membrane, and by sup- puration of the closed follicles. The contents of the intestine are in severe cases formed of dark 563 DISEASES OP THE ALIMENTARY CANAL. decomposing material, mixed with blood. The mesenteric glands are always secondarily affected, being enlarged and hypersemic. If the patient survives the acute attack, the disease very_ com- monly passes into ciikonic dysentery. The ulcers formed in the various ways described above show little tendency to heal, but remain as open, discharging sores. Sometimes they penetrate more deeply, and lead to abscesses in the surrounding tissue, especially of the rectum (periproctitis). The remaining mucous membrane is swollen and in a state of catarrh. The whole intestinal wall is thickened, except where the ulcers exist, and it is irregularly drawn in and adherent to the surrounding parts. In some cases a tendency to healing manifests itself If the attack has been slight and the ulceration only superficial, there may be a complete restoration of the mucous membrane, with insignificant cicatrices. But for the most part the ulceration has been considerable, and the cicatrices are of considerable superficial extent, perhaps surrounding the gut. When such cicatrices, in the usual fashion, contract, they cause narrowing of the intestine, which, in some cases, is very considerable. Alternating with the narrowing, there is very commonlj' dilatation of the more healthy parts, so that a very remarkable pouching of the colon may result, the narrowed parts being probably adherent to the tissues around. The obstruction produced in this way is all the greater because the contraction often throws the remaining mucous membrane into folds which may act as valves to the constricted part. Cholera. — This disease, which occurs in an epidemic form, de- pends on the action of a specific virus. In addition to the epidemic disease known as Asiatic cholera, there is a condition known as British cholera, in which the poison does not appear to be a specific one, but in which the anatomical changes are identical with those in the epidemic form. From an individual case, there- fore, it would be impossible to say which form is present; this must be judged from circumstances, bearing in mind especially that the Asiatic form is preeminently epidemic, and spreads by the extension of a specific virulent poison. The exact form of the virus is unknown, although there is room to believe that it is a micro-organism. In both forms it is clear that a very violent irritation of the mucous membrane of the intestine is produced. During life, the disease is characterized by the discharge of extremely fluid stools, which, from the intermixture of finely divided material, give the characteristic rice-water appearance. Sometimes a patient dies without the bowels having been moved, but in that case they are found distended with the rice-water discharge. It is obvious that there is here an enormous transudation from the vessels of the intestine. The chemical character of the dis- charge, however, seems to indicate that it is not a mere inflamma- tory exudation from the vessels, but rather a secretion of the glands. Its specific gravity is low, 1006 to 1013. There is very TYPHOID FEVER. 569 little albumen present, and the discharge contains a ferment which has the power of converting starch into sugar. It is commonly stated that the flakes which give their character to the rice-water evacuations are composed of desquamated epi- thelium. Investigations have shown, however, that this is not the case ; they are little masses of mucus containing leucocytes. After death the epithelium may be found loose in the intestine, but this appears to he from post-mortem maceration, for, if examined suf- ficiently early, the epithelium is found present and apparently normal. The most marked post-mortem appearance in the intestine is a remarkable rosy injection of the vessels of all its coats, so that a red appearance is visible even in the serous coat whenever the body is opened. The mucous membrane is swollen and the closed follicles prominent. Occasionally there is a decidedly inflam- matory condition present, which may be even of a dysenteric character. The condition of other parts of the body is directly referrible to the enormous withdrawal of water from the blood. The blood itself is thick, dark, and imperfectly coagulated. The skin, serous membranes, and all the soft tissues are shrunken, and dry, and parchment-like. The membranes of the brain are frequently in- jected. The kidneys present the characters of a slight parenchy- matous inflammation. Typhoid Fever. — This disease is also due to the action of a specific poison. In the afi[ected parts of the intestine, bacilli have JTiG. 246. Bacillus from mesenteric gland in a case of typhoid fever. The rods are shown. The large bodies beside them are blood-corpuscles, the paler ones the red, the darker ones the white. Preparation stained with metbyl-violet. X 1800. been found, and exactly similar bacilli have been found in the mesenteric glands (see Fig. 246) and in the spleen. It may be in- ferred that the virus is present in the blood, and from this produces the general symptoms of the disease, while locally it produces the 570 DISEASES OF THE ALIMENTARY CANAL. changes to be presently described. It is very probable that it finds entrance by the intestine and produces irritation of the follicles and mesenteric glands in its passage. The affection "in the intestine consists of an inflammatory swell- ing of the closed follicles and of the mucous meinbrane in their neighborhood, the inflammation often going on to necrosis and sloughing. The disease has usually its point of greatest intensity at the lower extremity of the ileum, and it is often possible to see various stages of the process in proceeding from above downwards through the small intestine till it culminates close to the ileo-ceecal valve. In the normal state, especially in the adult, the Pej^er's patches and the solitary follicles are very slightly prominent. The patch Fig. 247. Portion of a Peyer*s patch in an early period of typhoid fever; o, mucous membrane which becomes raised when the swollen patch is reached; h, internal layer, and c, external layer of muscular coat; d, swollen patch composed of round cells with dilated bloodvessels. At the right of the section the round cells are invading the submucous tissue and approaching the muscular coat. X 16. viewed from the surface shows a congeries of shallow depressions separated by slightly elevated ridges, which run in from the general mucous membrane, and form a kind of network. It is in the depressions that the follicles are placed. In typhoid fever there is at first a general swelling of the patch ; it is an inflammatory swelling accompanied by abundant infiltration of leucocytes which occupy both the closed follicles and the mucous membrane. The patch is obviously raised and its margins somewhat abrupt (Fig. 248, a). Viewed from the surface there is at this early stage simply an exaggeration of the normal appearance. The ridges of mucous membrane are swollen so that the depressions are more TYPHOID FBVEE. 571 Fig. 248. -hidden, and an appearance is produced which has heen compared to that of the convolutions of the brain in miniature. The swollen patch has a pinkish or whitish color. At the same time the solitary follicles show themselves as elevations at intervals. As time goes on the whole tissue gets more and more infiltrated with leucocytes (Fig. 247), and the raised patch gets more solid and its surface more homogeneous. The invasion of round cells extends to the submucous and muscular coats, even to the serous, and passes to some extent beyond the patch. A similar condition occurs in the solitary follicles ; they also present a marked increase in size, and are less defined, by reason of the infiltration around them. On this condition follows necrosis (Fig. 248, b). The infiltrated and altered patch or solitary follicle forms a slough, of larger or smaller size. This slough remains ad- herent for a time, and like all sloughs in the intestine it becomes brown or yellow from the biliary coloring n:iatter, which stains dead tissue, while the living structures are able to resist it. Generally there is a single slough on a Pey er's jjatch, not involving the whole patch, but of con- siderable superficial extent (see figure). Sometimes there are several sloughs cor- responding to some of the closed follicles of which the patch is made up. After a time the slough separates and an ulcer is left with infiltrated base and margins (Fig. 248, c). The ulcers are confined to the patches and solitary fol- licles, so that they repeat their shape and locality. The walls are succulent and vascular, and considerable hemorrhage may occur from them. The ulceration may extend more deeply than the mucous membrane, involving a necrosis of the muscular and even of the serous coat, so that per- foration may result. Perforation may occur in one of two ways. In the first place an ulcer may extend in depth till it penetrates through the muscular and serous coats. In this case the process is somewhat gradual, and there is generally a sufficiently acute inflammation of the peritoneum to cause adhesion and prevent the intestinal contents passing into the abdominal cavity. In the second place, perforation sometimes occurs in a manner com- parable to the perforation of the pleura in phthisis pulmonalis which leads to pneumothorax. The serous coat is undermined by the ulcer, and as its nutrition is cut ofi^ it undergoes necrosis. In such cases the brown slough may be visible on viewing the in- testine externally. A partial separation of the slough may allow perforation, and as this form is more acute and not so likely to be accompanied by considerable adhesions, the contents of the in- Diagrammatic representation of Payer's patches in typhoid fever, a, early stage with swell- ing of the patch; b, later stage with sloughing ; e, ulcer with in- filtrated walls. (THIERPELDEn.) 572 DISEASES OF THE ALIMENTARY CANAL. testine are more apt to escape into the peritoneal cavity and pro- duce fatal peritonitis. When recovery takes place from the fever, the process in the intestine retrogrades. According to the stage reached will be the exact process of resolution. If, in any part, ulceration has not yet occurred, then there is a gradual diminution of the patch and a return to the normal. If ulceration exists, the ulcer fills up and cicatrizes. The cicatrix, however, remains long, often with a slaty color, but not usually with much puckering. In the LYMPHATIC GLANDS of the mesentery processes occur which are quite parallel to those in the follicles of the intestine. The glands enlarge, and present on section a red injected appearance and soft consistence. There may be necrosis here aLo, giving rise to an opaque grayish condition in the midst of the gland. When recovery takes place the glands return to the normal, and the sloughs are usually absorbed, although they may become caseous and subsequently calcareous. It is to be remembered also that the spleen is enlarged, and there is here more than in typhus fever a swelling of the Malpighian follicles, which are Ij'mphatic in structure, and so the spleen is firmer and paler on section. TUBERCULOSIS GP THE INTESTINE. In the great majority of cases this condition is secondary to pulmonary phthisis, and it occurs in about three-fourths of the cases of that disease examined after death. It may be doubted whether it ever occurs as a primary disease. "We have already seen that tubercular ulceration is very common in the mucous membrane of the bronchial tubes in connection with pulmonary cavities, and that it is also frequent in the tracheal and laryngeal mucous membranes. The tubercular lesions are doubtless due to the direct action of the virus carried from the lungs. The tuber- cular disease in the intestine is to be accounted for by the sputa being partly swallowed, and the virus applying itself to the in- testine directly. The virus here attacks the same structures as in typhoid fever, namely the closed follicles and Peyer's patches, and at first it pro- duces a change of a somewhat similar kind. There is an enlarge- ment of the closed follicles by reason of a great new-formation of cells which infiltrate the neighboring mucous membrane as well as the follicles. This primary enlargement is, however, much less uniform than in typhoid fever. On the whole, it is greatest towards the lower part of the ileum, but it presents great irregu- larities. Even on the Peyer's patch it generally affects a tew closed follicles, and not the whole, so that there are rounded prominences dotted over the patch. Moreover, it is not simply an inflammatory infiltration which occurs ; there are tubercles present of characteristic structure. TUBERCULOSIS OF THE INTESTINE. 573 The enlarged follicles undergo caseous necrosis, so that very soon they are seen to have an opaque yellow kernel, while the epithelium still covers them. In the next place softening occurs, and the caseous mass is discharged, leaving an ulcer. The ulcer is crater-shaped with overhanging edges, which are infiltrated with leucocytes and contain miliary tubercles (see Figs. 249 and 250). There may be at first several such ulcers on a Peyer's patch, and EiG. 249. Tubercular ulcer of the intestine. Naked-eye nppearance. The swollen overhanging edges are indicated. other solitary ones in other parts. They extend by fresh infiltration of the neighborhood and fresh necrosis, while at the same time miliary tubercles are visible in the midst of the inflammatory in- filtration. The infiltration very commonly involves the muscular coat, and even the serous (see Fig. 250), but the ulcer rarely extends in depth beyond the mucous and submucous coats. On the other hand tubercles are often to be seen almost free of inflam- matory infiltration at a distance from the ulcers in the midst of the muscular coat, or even outside it and in the peritoneum. The ulcer extends much more laterally than deeply, involving ever increasing portions of the mucous membrane. In its extension it does not in the least respect the boundaries of the Peyer's patches or solitary follicles, but extends beyond them, generally advancing more across the gut than longitudinally. In this way ulcers are, not infrequently, much elongated in a direction transverse to the intestine, and may even form a ring around it. As they begin largely in the Peyer's patches, the ulcers have usually their centres at the part of the gut opposite the mesenteric attachment, the patches having their seats along this free portion. The position of the ulcers is often indicated before opening the intestine by the appearance of the peritoneal surface. If the ulcer be of any considerable size there is some inflammation of the peritoneum, evinced by redness and, very often, elongated pro- 574 DISEASES OF THE ALIMENTARY CANAL. jections of vascular connective tissue. But above all we can generally see in tlie peritoneum groups of little white nodules, which are tubercles in or under the serous coat. The existence of these tubercles is sonaetimes even useful in determining whether an ulcer is a tubercular one or not. It is very rare indeed that the "Fio. 250. Section of a small tubercular ulcer. In the middle there is a crater-shaped ulcer (a) with overhanging edges. The mucous membrane around is infiltrated with round cells in the midst of which a few tubercles are indicated. Beneath the ulcer the muscular coat is in- filtrated. At d there is a small sub-serous tubercle. X 16. ulcer penetrates through the peritoneal coat, and if it does, it is usually protected by adhesion to neighboring loops of intestine. As a general rule the tubercular ulceration is most marked in the ileum, but not infrequently the colon is attacked, and there may be ulcers of very large size there. The process is for the most part a chronic one, and the ulcers advance slowlj'. Sometimes, however, and usually in connection with acute phthisis, there is a rapid swelling of the follicles, and ulceration occurs by softening without preliminary caseous necrosis. In these cases perforation is much more liable to occur. TUMOES OF THE INTESTINE. Cancer. — This is by far the most frequent and important form of tumor. Cancers are almost confined to the large intestine; we have already connected this with the fact that this portion is most exposed to the irritation of the stagnant feces. This is the more evident as the most frequent localities are the rectum, the flexures. TUMOES OF THE INTESTINE — CANCEES. 575 and the caecum. At the same time, cancers are not unknown in the small intestine. The commonest form of cancer is a very chronic epithelioma with gland-like masses of cylinder cells (Fig. 251). The tumor is very frequently ring-shaped, and, as ulceration readily occurs, there may be little more than an ulcer with infiltrated edges. Even the infiltration of the edges may be very slight, and it may Fig. 251. /M y>Mi4^j. ■■ \ / Cylinder-celled epithelioma of rectum. There are gland-like spaces containing epithelium, which at the periphery is characteristically cylindrical. be difiicult to be sure that the disease is cancerous. The ulceration is accompanied by new formation of connective tissue in all the coats of the intestine, and, while adhesion occurs to parts around, there is great contraction of the intestine. In this way strictures arise, and the occlusion of the calibre may be increased by the mucous membrane at the edges of the ulcer being thrown into folds. In fact, if we except hernias, this is probably the most frequent cause of intestinal obstruction. It has been already noted that the proper cancerous structure is often to a large extent destroyed by ulceration, but at the edges we may distinguish masses of epithelial cells Avith a glandular arrangement. In the adhesions around the affected part of the intestine enlarged glands may be found with cancerous tissue. iSText to the epithelial, the most common is colloid cancer. This forms a much more prominent tumor, which may involve a considerable length of the gut, and incorporate the entire coats. This form may produce obstruction by its mere bulk, although it also is liable to ulceration, and the consequent contraction of the gut, added to the bulk of the tumor, frequently effects obstruction. It does not so readily affect the lymphatic glands, but more usually extends through the wall into the peritoneum. 576 DISEASES OF THE ALIMENTARY CANAL. Soft cancek is much less common Iiere than in the stomach, and it resembles the same form of tumor there. It extends to the lymphatic glands and frequently also to the liver. The remaining tumors of the intestine are of little importance. FiBROMAS, LIPOMAS, MYOMAS, and SARCOMAS occur, and they are all apt to pass into the interior of the intestine and assume the foi-m of SUBMUCOUS POLYPI. It is Said that these polypi, by being dragged on in the peristaltic movements ol the intestine, may produce^ in- vagination. Mucous POLYPI are also to be mentioned as occurring, especially in the rectum in catarrh. OBSTRUCTION TO THE CALIBRE OP THE INTESTINE. This condition has been incidentally mentioned as occasioned by several of the lesions already described. It may be well here to sum up the various forms of intestinal obstruction and to describe the etfects produced vi^hen the calibre of the intestine is interrupted. Next to hernia, the most frequent cause of obstruction is the contraction of cicatrices resulting from ulceration, and in the great majority of cases the ulcers are malignant, that is to say, they arise by the breaking down of cancers. It is to be remem- bered that, in contractions of the calibre such as these, the direct cause of the final obstruction may be the folding of the mucous membrane above the stricture, this acting like a valve to the narrowed part. Tumors also obstruct sometimes by their bulk. Similarly, gall-stones, masses of feces, collections of round worms may occlude the calibre. Invagination is the commonest cause in children. There is also twisting or torsion. Lastly, we have obstruction by incarceration, the intestine passing into a position where a loop is caught at the neck and strangled. Hernias form the commonest examples of this kind, but there are a number of cases in which the intestine slips under a bridge or ligament and gets, as it were, pinioned and compressed. This last cause of obstruction occurs so obviously to the mind- that its frequency is apt to be thought much greater than it is. In reality it forms a small proportion of the entire cases. The ab- normal band may be formed by the adhesion of structures to various parts of the abdomen so as to form bridges. Thus the vermiform appendage may adhere by its tip and form a bridge; or a Meckel's diverticulum may similarly adhere; or the omentum may be tied down in such a way as to form a narrow bridle. But sometimes the band is itself distinctly of new formation; there has been a local peritonitis, and two opposing surfaces have be- come adherent in the usual way of inflammatory adhesion, by vas- cular connective tissue; by the movements of the intestine the connective tissue has been dragged upon and elongated till it forms a band or ligament, which may afterwards tie down a loop of in- testine. OBSTEUCTION TO THE CALIBRE OF THE INTESTINE. 577 A very unusual form of incarceration is that in which there is an APERTURE IN THE MESENTERY through which the intestine passes. This may be produced by a tear in the mesentery. But in a case observed by the author, there was a large round gap about 5 inches in diameter with rounded edges, and obviously of long standing, perhaps congenital. The greater part of the small in- testine had become impacted in a complicated fashion into the aperture, and obstruction had finally resulted. "When obstruction occurs the intestinal contetits accumulate in the parts of the intestine above. The boAvel may be greatly dis- tended and its muscular tissue paralyzed by the internal pressure; the stagnating feces decompose, and the contents of the small in- testine ' may acquire the characters of those of the large. This decomposition of the intestinal contents leads to several important results. In the first place there may be great formation of gas which still further distends and may produce the condition of ex- aggerated inflation called meteorism. Then a return of the feces in the reverse direction may occur, and if the decomposition is sufiiciently advanced there may be a vomiting of matter having the characters of feces. This alarming phenomenon of stercora- CEOUS VOMITING Is Sometimes referred to the reverse current ex- tending from the colon. We can hardly suppose, however, that the feces are able to pass the ileo-csecal valve, and for the most part the vomited matters are really the stagnant contents of the small intestine which have undergone the fecal decomposition. Of course there is a reverse current, else the intestinal contents would not reach the stomach. But this does not necessarily imply a vermicular movement in the reverse direction. If the intestine is distended, and is interrupted at a particular point, then the vermicular movement in the usual direction will carry the external layer of contents downwards to the point of obstruction. But in order to accommodate this fresh arrival there must be a return current upwards in the centre of the tube. There is a similar condition to what exists normally in the stomach where the con- tents are carried to the pylorus, and meeting the obstructing sphincter return for the most part down the centre of the cavity towards the fundus. Again, the products of decomposition maj' be absorbed to an abnormal extent and appear in the urine. There are two sub- stances resulting from the decomposition of albuminous substances which are normally present to a limited extent in the urine, namely, indican and carbolic acid. In cases of obstruction these substances, or one of them, are increased in quantity sometimes to a very striking extent. This increase does not occur unless the stagnation extends to the small intestine where the albuminoids are present. It does not occur therefore in ordinary constipation which affects the large intestine alone, apparently because the al- buminoids are absorbed before they reach the large intestine. 37 DISEASES OF THE LIVER, PAN"OREAS, AND PEEITONETM. A.— THE LIVEE. Inteoductory. — The liver is the largest gland in the body, its weight being on an average from 48 to 58 ounces in the adult male and 40 to 50 ounces in the female. From this alone it may be inferred that its diseases are of great importance. When we come to consider the functions of the liver we are met with serious difficulties from the pathological point of view. Diseases may largely destroy or render inactive the proper paren- chyma without seriously interfering with the general health of the patient unless, by interfering with the bloodvessels in the liver, they produce secondary eflects in the portal circulation. Even the suspension of the biliary secretion may be without serious effect on the nutrition of the body. In considering the subject of diabetes mellitus (p. 74) the glycogenic function of the liver has been sufficiently referrea to, and it only remains to be said here that, practically, nothing is known of the influence on this function of lesions which destroy the liver tissue. The influence may be very great and important, but no facts are known in regard to it. It is not to be inferred, however, that the liver is unimportant to the organism, but merely that the organism seems to have a remarkable power of compensation when its tissue is diseased. In considering the diseases of the liver the arrangements of the circulation must be borne in mind. It is well known that most of the blood comes to the liver by the portal vein, and the proper hepatic tissue is arranged in relation to the ultimate ramifications of that vessel. The interlobular veins forrd these ultimate ramifi- cations, and these are in immediate connection with the hepatic lobules. The hepatic lobule is a group of hepatic cells with blood- vessels, having in man a polygonal or somewhat globular shape ; it measures about the twentieth of an inch in diameter. The interlobular vein lying outside the lobule sends multitudinous capillaries into it, and these seeking the centre of the lobule open into the central or intralobular vein which is the radicle of the hepatic vein. Blood is also brought to the liver by the hepatic artery which supplies the connective tissue and walls of the blood- vessels chiefiy. Its capillaries terminate in veins which open into the interlobular veins (according to Cohnheim and Litten), so that MALFORMATIONS AND DEFORMITIES OF THE LIVER. 579 this blood also finds its way into the hepatic capillaries and on into the hepatic vein. The connective tissue of the liver is often described as if it formed a special covering to the portal vein, being called G-lisson's capsule. It really forms a supporting stroma which holds the portal vein, the hepatic artery, and the hepatic duct, which all lie side by side. The lymphatic channels are also contained in it. In some animals the connective tissue surrounds each lobule and defines it distinctly from its neighbor, but in man it stops short at the interlobular vein, and except where this vein is, the lobules at their margins merge into each other, and their capillaries are in common. Examination of Fig. 254, in which the lobules are demarcated by fatty infiltration, will show how they run into one another at their peripheries. Although no proper fibrillated con- nective tissue is present inside the lobules, yet a fine recticulum accompanies and supports the capillaries. The lobules are large enough to be visible to the naked eye, yet unless there is some abnormal condition present, they are not indi- vidually distinguishable. On the other hand, it is they which give the liver when torn that granular appearance with which we are familiar. It is important to remember that the circulation in the portal vein, and especially in the capillaries of the liver must be unusually slow. The blood before it reaches the liver has passed through one set of capillaries, and here it passes through a second set; it has, therefore, lost very largely the force derived from the contrac- tion of the heart. It is probably for this reason that the liver is so very frequently the seat of secondary diseases, such as tubercu- losis, abscesses, cancers, etc. We may suppose that as the blood moves so slowly there will be time for any infective material to settle down and produce its special effects. We know that when vermilion is injected into the blood it is found largely in the capillaries of the liver. Similarly the abnormal pigment present in the blood in melanasmia is found largely in these capillaries. MALFOEMATIONS AND DEFORMITIES OE THE LIVER. Congenital malformations of the liver are not common. There are cases of absence of the liver, and of defect of one of the lobes, or irregularity in the lobes. What may be called supernumerary livers have also been found in the form of isolated pieces of liver tissue in the suspensory ligament. Of more importance is con- genital absence of the gall-bladder, along with which there is usually a dilatation of the bile-ducts. The liver is sometimes transposed along with a general trans- position of the viscera. In a case recorded by Fraser, there was not only a transposition, but an occasional dislocation of the liver, which came down into the left inguinal region. An ACQUIRED DEFORMITY is Very frequently met with in females, 580 DISEASES OF LIVEE, PANCREAS, AND PERITONEUM. and is to be associated with the method in which the clothes are worn. This deformity is usually stated to he due to ti^ht lacing, but, although doubtless greatly aggravated by this, it is also in- duced by the ordinary methods of suspending the garments used by females. These are held up by being drawn tight at the waist above the crest of the ilium, the projection of this bone preventing them slipping down. By this tight band, often of considerable breadth, the abdominal organs are compressed and the lower ribs are held down and pressed inwards. This is greatly aggravated by the wearing of stays, even although they be not tightly laced, as by them the lower ribs are kept compressed inwards. The effect on the liver is that it is greatly flattened, while a transverse shallow depression forms along the upper surface, atfecting chiefly the right lobe. In this groove the capsule is thickened, and there is obviously considerable loss of liver tissue. Sometimes the atrophy along this groove is such that the liver is, as it were, divided by it, and the two portions can be folded together. "With the flattening there is great displacement of the liver, whose lower edge may extend as far down as the umbilicus. More or less of this deformity is to be found in nearly all female bodies, and is even found in the bodies of men who have been in the habit of wearing tight belts round their waist. Sometimes the upper surface of the right lobe of the liver pre- sents elongated depressions passing from behind forwards, which are really folds of the liver, and are produced chiefly when there is some obstruction to expiration. In that case the diaphragm is depressed by the dilated lung, and at the same time the lower ribs are drawn down in violent expiratory movements by the abdominal muscles, and pressed against the liver, which is supported below by the contraction of the abdominal muscles. The liver is very liable to changes of position. Tumors or fluid in the abdomen carry it upwards. Depressions of the diaphragm press it downwards. The suspensory ligament may be elongated so that the organ is unduly movable, and may undergo displace- ment downwards. PASSIVE HYPEREMIA OF THE LIVEE. The names nutmeg liver and red atrophy are sometimes given in cases of prolonged passive hypersemia, these names indicating- certain appearances presented by the tissue, and to be referred to afterwards. Passive hypersemia occurs when any obstruction exists in the circulation of such a nature as to interfere with the return of blood from the inferior vena cava to the right side of the heart. The commonest cause is valvular disease of the heart, especially mitral disease, but it also results from obstruction to the pulmonary circulation as in bronchitis and emphysema, etc. In these cases there is a general engorgement of the systemic venous circulation. PASSIVE HYPERJiMIA — NUTMEG LIVER. 581 with increase of blood-pressure in the veins. "We have already seen that in the capillaries of the liver, and consequently in the hepatic veins, the normal circulation is unusually slow, and the blood-pressure low. Any increase in the blood-pressure in the general venous circulation will, consequently, tell particularly on the vessels of the liver, and we may even suppose that the blood passing up the inferior cava may in such cases regurgitate into the hepatic vein. The result of this is a very great distention of the hepatic vein and its radicles — the central or intralobular veins. The distention extends to the capillaries, which, as in Fig. 252, are sometimes Fig. 252. Passive hyperaemia of the liver. One lobule and parts of other two are shovpn. In the central parts of the lobules there is almost nothing but dilated capillaries containing blood- corpuscles only J a few atrophied and pigmented hepatic cells being visible. At the peripheral parts of the lobules the hepatic cells are seen, many of them pigmented. X 90. found enormously dilated. The dilated capillaries by pressure cause ATROPHY OP THE HEPATIC CELLS, and it often happens that the central parts of the lobules are entirely occupied by enormously dilated capillaries, while the hepatic cells are hardly visible (see figure). The remains of the hepatic cells frequently contain brown pigment-granules. The atrophy of the hepatic cells in these regions may be complete, only a few pigment-masses representing them. Sometimes, in addition to these changes, there is hypertrophy 582 DISEASES OF LIVEB, PANCREAS, AND PERITONEUM. of the connective tissue surrounding the lohules, but this is usually inconsiderable, and it is a mistaken view that a cirrhosis of the liver arises out of passive hyperemia. The naked-eye appearances may be directly connected with these minute changes. At first there is a general enlargement of the organ, which, on section, appears unduly red. On closer examination it is seen that there are minute areas of a deep-red color corresponding with the central parts of the lobules, and these are surrounded by zones of a gray or yellowish color. The result is that the lobules are, as it were, mapped out by these con- trasting colors, and are for the most part individually visible to the naked eye. Sometimes several adjacent lobules are almost completely occupied by dilated vessels, and there is a narrower ring of normal tissue around each, so that the part of the liver as a whole has an almost cavernous structure, and presents a deeper red color on section. It is these variations in color and figuring which give the cut surface the appearance of the section of a nutmeg. In parts where there has been great loss of the proper tissue, the liver may appear to the naked eye after death partially atrophied. During life the dilated veins and capillaries are dis- tended vnth blood, but after death, the blood-pressure being removed, these may, to some extent, collapse. In this way the surface has sometimes an irregular appearance, which may be mistaken for that of cirrhosis, but it will be noticed that the depressed or atrophied parts have a deep-red color. THEOMBOSIS AND EMBOLISM IN THE LIVEE. Thrombosis of the portal vein is of somewhat frequent occur- rence, especially as a result of cirrhosis. It also occurs sometimes by propagation of a thrombosis frOm the radicles of the vein, or by embolism from them. The embolus may be a septic one, and there will be a phlebitis with the thrombosis. The coagulum in the vein, if not of a septic character, leads to a chronic inflamma- tion Avith adhesion in its neighborhood. The consequences to the liver itself, even of complete closure of the portal vein, are not so important as might be looked for. It is stated by some that it may lead to cirrhosis of the liver, but there is no proper founda- tion for this statement, and cirrhosis is much more frequently the cause than the result of thrombosis. It has also been asserted that diabetes mellitus may occur as a result of thrombosis of the portal vein. The consequences outside the liver are much more important. There is dilatation of the radicles of the portal vein in the abdominal viscera, with ascites, which is generally very extreme. The results in this regard are essentially similar to those which occur in cirrhosis, and are referred to more particu- larly below under that heading. Thrombosis and embolism of the hepatic artery are not of RETEOGBADE CHANGES IN THE LIVER. 583 consequence unless the plug be of a septic nature. The hepatic artery is not an end-artery, and, if some of its branches be ob- structed, the anastomosing communications restore the circulation. If the main branch of the artery be obstructed, then we may have necrosis of the liver, but such an obstruction is scarcely liable to occur in man, and its effects have only been studied in experi- ments in animals. HYPERTROPHY OP THE LIVER. "When considerable portions of the liver are destroyed, there is liable to be a oompensatort hypertrophy of remaining parts. The loss of liver substance may be congenital, as in a case observed by the author in which, probably from some injury early in foetal life, the right kidney and the greater part of the right lobe of the liver were wanting. In that case the left lobe was greatly increased in size, and the liver as a whole was of the normal weight. There may be a similar compensatory hypertrophy from destruction of liver tissue in after-life. The destruction may be by pressure of hydatid cysts, syphilitic gummata, and cicatrices, or even by cir- rhosis. The region of the atrophy will determine that of the hy- pertrophy, but sometimes the left lobe or the lobus Spigelii under- goes great enlargement. Hypertrophy of the liver has been described as occurring in DIABETES. Undoubtedly the liver is frequently enlarged in this disease. Some of the enlargement is due to hypersemia, and some to swelling of the hepatic cells. This latter is probably a true hy- pertrophy of the liver tissue. RETROGRADE CHANGES IN THE LIVER. Atrophy of the Liver. — We have already referred to the atrophy which occurs in passive hypersemia. In the preceding section also we have seen that pressure, as by a hydatid cyst, pro- duces atrophy. In old persons we meet with a senile atrophy, the organ as a whole being reduced in size, and more deeply colored than normal. Parenchymatous iNFiLTRATiON.of the liver occurs, as we have previously seen, in connection with many acute diseases. It is this which causes the enlargement of the liver in the acute fevers, pneumonia, erysipelas, etc. The hepatic cells are highly granular, and if the albuminous granules be destroyed by liquor potassse it will be seen that there are numerous fine fat-granules, the cloudy swelling passing into fatty degeneration. Fatty Degeneration is not common except as a further stage of the condition just mentioned, and as occurring in acute yellow atrophy to be presently described. 584 DISEASES OF LIVEB, PANCREAS, AND PERITONEUM. Fatty Infiltration was referred to in a former part of this work, and its pathology considered (see p. 123). In this place we have to consider the locality of the fat and the changes it effects. In the normal liver there is very little free fat in the hepatic cells. In fatty infiltration fat is brought in quantity by the portal vessels and deposited in the hepatic cells. It is first deposited in those nearest the terminals of the portal vein, that is to say, in the peripheral parts of the lobules (see Fig. 253), so that at first each Fig. 253. Fatty infiltrations of the liver, osmic acid preparation as seen with a very low power. The peripheral parts of. the lebules are demarcated by the fatty infiltration. X ^6. lobule has a peripheral zone of fatty infiltration. This is still more strikingly seen when a microscopic section is treated with osmic acid. The fatty peripheral parts become of a blackish color, and the section assumes a very striking figured appearance, as shown in the figure. As the condition advances, more and more of the lobule is affected, and the infiltration may overtake its whole ex- tent. Even in extreme cases, however, it usually preponderates at the peripheral parts. The fat is present in larger and smaller drops inside the hepatic cells, but the tendency is for the drops to assume a considerable size (as in Fig. 254). The protoplasm of the cells is pushed aside by the fat, but probably its function is not greatly interfered with. The fatty liver presents usually distinct appearances to the naked eye. According to the extent of the infiltration is the organ in- creased in weight, but in extreme cases it may be double the normal. The enlargement is general, the thickness especially AMYLOID DEGENERATION OF THE LIVER. 585 being mucli increased. The consistence is unduly soft, and the color more or less opaque yellow. If the infiltration be not ex- treme, so that the whole lobule is not infiltrated, then with the naked eye we can see on the cut surface the indications of its presence. The lobules are, in fact, mapped out in the most char- acteristic figured manner, so that, on looking closely, we can dis- tinguish each with perfect accuracy. The appearance presents a Fatty infiltration of liver. The cells are isolated, and they contain larger and smaller drops of oil. X 350. considerable resemblance to that of the nutmeg liver, where also the lobules are mapped out ; but in the fatty liver it is by unduly pale tissue at the peripheral parts of the lobules, which contrasts with the normal central parts; while in the other case it is the normal which is at the periphery, and it contrasts with the red central parts, and the whole cut surface is unduly red. Amyloid degeneration of the liver has already been considered in its general aspects (see p. 132). The degeneration appears first in the arteries and capillaries, the appearance in the latter being as if, at intervals, the wall were swollen with a translucent material. In these earlier stages there is no difficulty in making out that inside the lobules it is the capillaries which are affected. The general arrangement of the capillaries is beautifully shown by the rose-pink color of the amyloid ones in a section stained with methyl-violet, the appearance being almost that of an injected specimen. Even in the earlier pei'iods considerable atrophy of the hepatic cells can be observed as a result of pressure from the swollen capillaries, and the atrophic cells frequently contain fat. In advanced stages, however, the cells are very greatly destroyed, so that the liver tissue is replaced by amyloid substance. It is remarkable that with this great loss of the secreting sub- stance there is actual increase in size and weight of the liver. It is not uncommon to find the liver weighing two or three times the normal. The increase in size is not proportionate to that in weight, as the amyloid substance is of greater density than the liver tissue. The edges of the organ are rounded and its consist- ence elastic and resistant. The surface, and especially the cut surface, presents a peculiar translucent waxy appearance, which in advanced stages is highly characteristic. 686 DISEASES OF LIVEE, PANCREAS, AND PEEITONEUM. "We have already seen that amyloid degeneration of the liver is part of a general condition, and that it is associated with a similar condition in other organs, especially the spleen, kidneys, and in- testine. We also know that the amyloid disease is very often the result of a chronic tuberculosis, and it not infrequently happens that miliary tubercles are to be found in the amyloid liver. ACUTE YELLOW ATEOPHY. This is a disease whose exact pathology is somewhat obscure. It is characterized by a rapid destruction of the hepatic cells, but the exact cause of this destruction is doubtful. It is obviously due to the action of a morbid poison circulating in the blood, because changes of a somewhat similar nature are met with in the epithe- lium of the kidneys, and in the muscular jGLbre of the heart, and elsewhere. This view also receives some confirmation from the fact that in acute poisoning with phosphorus changes occur in the liver and other organs very like those in the disease under con- sideration. In this regard also it is interesting to observe that two writers, Waldeyer and Zander, have described colonies of bacteria as existing in the liver in cases of this disease. When the liver is examined after death it is generally found smaller than normal, and its tissue is soft and flabby. In some Pia. 255. From liver in acute yellow atrophy. The hepatic cells form irregular clumps. There are numerous pigment-crystals of similar shape to the crystals of hsematoidiu (Figs. 5 and 11), and of a similar deep-red color, but smaller. X 350. cases it is of the normal size, and it is stated that in the earlier stages it is even enlarged, although the disease is not fatal during these periods. The capsule is often wrinkled from the atrophy of the substance of the organ, and the organ flattens out by its own INFLAMMATIONS OF THE LIVER. 587 weight, its thickness being greatly diminished. The diminution in size sometimes affects the left lobe especially. On cutting into the organ the section shows usually different shades of color. The predominating tint is yellow, varying from the color of gamboge to a dark yellowish-brown. Mixed with this, however, there is a red color forming the red substance of Zenker. Where the color is yelloAv the tissue is softest, but the red parts are the most atrophied, the red substance arising by the absorption of the degenerated hepatic cells. On examining the yellow tissue under the microscope, it will hardly be recognizable as that of the liver (see Fig. 255). There are no proper hepatic cells, but instead, larger and smaller fat- drops, with granular debris, and here and there rhombic crystals of a reddish-brown color (see figure). Sometimes leucine is found in opaque clumps, white in color and generally stratified. Acicular crystals of tyrosine are also found. The crystals of pigment, which resemble those found in old blood-clots in the brain, may be really formed from the biliary coloring matter. The red substance does not present the abundant fatty debris; that has been cleared away, and there is now a fibrous material visible, merely sprinkled with fat-granules. In some cases glan- dular-looking processes have been observed, and have been taken to indicate an attempt at regeneration of the lost hepatic substance, beginning in the capillary network of the hepatic diicts. INFLAMMATIONS 0¥ THE LIVER. 1. Purulent Hepatitis. — Abscess op the liver occurs in two forms, the tropical and the pysemic or metastatic abscess. (a) The tropical abscess is not met with in this country, except in persons who have been in hot climates, especially in India. Much doubt exists as to the cause of the inflammation which gives rise to the abscess. In a large proportion of cases it is associated with dysentery, and it is believed by many that the abscess in the liver arises by material being carried from the ulcerated intestine to the liver. This material presumably contains minute organisms, and the abscesses would be septic. This view, however, is not beyond question, and post-mortem examination shows that the tropical abscess is by no means uniformly associated with dysen- tery. While, therefore, we may admit that bacteria probably have to do with the causation of the tropical abscess, yet it is not unlikely that certain states of the liver predispose to their develop- ment, and that they may find entrance to the body by other paths than the intestine. The abscess is mostly solitary, and it may grow to large dimen- sions, causing great enlargement of the liver. Having approached the surface, it sometimes causes a marked projection from the liver. The capsule, being undermined, may undergo necrosis, and the abscess rupture by the separation of the slough. In this 588 DISEASES OF LIVER, PANCEEAS, AND PERITONEUM. case, the abscess may rupture into the peritoneum and cause fatal peritonitis. Or the capsule may adhere to the abdominal wall, and the abscess by and by find its way to the surface of the body, there to discharge. It also occasionally bursts in other directions, as through the diaphragm into the pleural cavity, or even the lung; into the colon or other part of the intestine; or into the gall-bladder from which the pus is carried into the duodenum. In these various ways the pus may be disposed, of and perhaps re- covery occur, but more probably a wasting discharge from the cavity of the abscess remains. In other cases the abscess does not enlarge, but rather dries in. A thick connective-tissue capsule forms around it like the wall of a cyst, and the pus thickens to a cheesy consistence. Afterwards the contents may become calcareous and the disease virtually ob- solete. (6) PYiEMio ABSCESSES are much more definitely understood in their causation and mode of formation. They are ^mdoubtedly produced by bacteria being cai'ried by the blood to the liver and propagating themselves there. Sometimes the abscesses in the liver are secondary to those in the lungs, the organisms being carried on by the blood after having developed there. But there are cases where abscesses occur in the liver alone, and these also arise in connection with putrid external wounds. So long as it was supposed that, in order to the formation of such abscesses, an obstruction of an artery with an embolus was necessary, the occurrence of such abscesses in the liver was obscure. We know, however, that micro-organisms may be conveyed by the bloodvessels, and, after passing the pulmonary capillaries, be carried to the liver by the hepatic ai'tery, or even, after traversing the intestinal capillaries, by the portal vein. We have already seen that the circulation in the capillaries of the liver is peculiarly slow, and it is probably for this reason that the bacteria so readily lodge there and propagate. Abscesses may also be induced in cases where there is stagna- tion of bile, and where decomposition occurs in the bile, extend- ing upwards from the intestine. Such abscesses will be referred to afterwards. The bacteria multiply and form zoogloea in the capillaries and interlobular veins, passing into the central veins. "Wherever the colonies of bacteria extend, the liver tissue undergoes necrosis, the cells lose their nuclei, and become individually indistinguishable. We have already seen that this arises, not from the direct action of the bacteria, but by the chemical products which are given off". These irritating stuflis also produce inflammation around, and there is here, as elsewhere under similar circumstances, an acute sup- purative inflammation. The round cells accumulate around the necrosed portion, and gradually infiltrate it and break it down, so that an abscess forms. The abscess may be primarily a small or a large one according as the capillaries over a smaller or larger area are invaded, but INFLAMMATIONS OF THE LIVER. 589 several abscesses may ultimately coalesce, and so we have them sometimes of very considerable dimensions. The abscesses in this form are always multiple. In accordance with what has been stated the actual abscess is preceded by a gray or yellowish discoloration indicating the existence of necrosis of the tissue. There will be probably a group of such areas corre- sponding to necrosed hepatic lobules. Ultimately these break down and form a common abscess. 2. Chronic Interstitial Hepatitis or Cirrhosis. — This is, for practical purposes, the most important affection of the liver, at least in this country. We have to do here with a chronic inflam- mation of the interstitial connective tissue of the organ. As in the case of other inflammations, we have to consider here the nature of the irritant which induces the inflammation. Leaving aside in the mean time the case of syphilis, which will be taken up afterwards, it may be said that, as the disease occurs for the most part homogeneously throughout this organ, the irritant is contained in the blood circulating in the liver. The name " gin-drinker's liver," frequently applied to this disease, involves the view that alcohol is commonly the irritant. Alcohol taken frequently in the form of undiluted spirits is believed to cause the disease, while beer and wine do not. This is probably in most cases the cause, but the disease may originate from other kinds of irritation whose nature is obscui'e. This is evident from the fact that it has been met with in young children, and the author has recorded a case in which a typical cirrhosis with the usual secondary phenomena occurred in a cat. The fact that it was a butcher's cat may indi- cate that it indulged in excess of eating rather, than of drinking. It has been asserted of recent years that obstruction of the bile- ducts is a cause of cirrhosis, and a special form of " biliary cirrhosis " has been distinguished. The frequent occurrence of obstruction by gall-stones and otherwise without any of the ap- pearances of cirrhosis, however, rather contradicts this view. It is also stated that tuberculosis may induce cirrhosis, and there are some facts which seem to support this view. In cirrhosis we have chronic inflammation of the connective tissue of the liver, resulting in new formation of a similar tissue, which, like such inflammatory new-formation, has a special tendency to shrink. It will be proper to consider the distribution of this new formation and its effects on the hepatic tissue on the one hand and the bloodvessels and ducts on the other. The interstitial connective tissue of the liver follows, as we have seen, the portal vessels, forming a frame-work in which are sup- ported the portal vein and its branches, the hepatic artery and hepatix; duct. The new formation occurs in the great majority of cases only in these regions, that is to say, outside the lobules. Cases have been described, however, in which the new formation has extended into the interior of the lobules (so-called intercellular 590 DISEASES OF LIVER, PANCREAS, AND PERITONEUM:. cirrhosis), but this is exceedingly rare ; it is stated to occur_ in cases of syphilis of the new-born. As a rule the new formation occurs in such a way as to surround groups of lobules, so that as the disease progresses the liver is subdivided into larger and smaller areas, each representing a set of lobules surrounded by new-formed connective tissue (so-called multilobular cirrhosis). In other cases the new formation, although not extending into the interior of the lobules, is homogeneous in its distribution, occurring wherever there is fibrillated connective tissue, and so present at the peripheries of all the lobules (so-called unilobular cirrhosis). In the earlier stages the affected connective tissue is abundantly cellular, like granulation tissue, and the process of new formation is evidently similar in its details to that in other chronic inflam- mations (see Fig. 256). Along with these changes, however, there are appearances, which have received various interpretations. In Pig. 256. Cirrhosis of liver in early stage. The connective tissue is occupied by numerous round- cells which are involving the peripheral parts of the lobules, the hepatic cells being here frequently isolated in the midst of the round-cells. X 75. many cases there are elongated gland-like processes in the midst of the tissue which look like new-formed ducts. Some suppose them to be ducts in process of formation from the existing bile- ducts. Certain French observers regard this condition as a special feature of " biliary cirrhosis," and take the changes in the ducts as well as the other changes to be the result of obstruction. Hamilton has stated that these duct-like processes are really com- posed of hepatic cells which are in process of forming connective INFLAMMATIONS OF THE LIVER. 591 tissue. The, most probable explanation is that they are really capillary ducts which have undergone enlargement, and so have become prominent. The normal capillary ducts are seated inside the lobules between the rows of hepatic cells. "We shall see after- wards that the hepatic cells undergo great destruction in cirrhosis, but the capillary ducts may survive, and their epithelium may enlarge so as to give them the appearance of new-formed ducts. This appearance is only observed when the disease is in active progress, and the connective tissue shows a cellular character. If' there were nothing more than the new formation of con- nective tissue hitherto mentioned, then the liver would be enlarged in this disease. In the earlier stages there is such enlargement, but the existence of the disease is not generally distinguished in these stages. On the other hand, Charcot and others have de- scribed a special form of hypertrophic cirrhosis in which vsry great enlargement of the organs occurs. In this condition the distribution of the new formation is unilobular, and the appear- ance of new formation in the ducts referred to above is manifest. It will be seen that the names biliary, unilobular, and hypertrophic cirrhosis are used to designate a condition whose pathological bearings can hardly be said to be fully established. As a general rule, the new-formed tissue undergoes develop- ment into dense connective tissue which has a tendency to shrink. By its shrinking it causes atrophy of the proper hepatic tissue. As the cirrhosis is usually multilobular, the contracting tissue isolates groups of lobules of larger or smaller size, and these, consisting of soft tissue, stand out somewhat when the liver is divided, or present themselves prominently at the surface. There are thus areas of remaining hepatic tissue which are being grad- ually encroached on by the connective tissue. The atrophy of the hepatic tissue takes place by the supply of blood being cut off. By the contraction of the new-formed tissue the portal vessels are narrowed, and there is in addition, according to Ziegler, thicken- ing of the internal coat of the portal vein, an endophlebitis oblit- erans, similar to the endarteritis obliterans which exists in cirrhosis of the kidney. This will increase the obstruction of the portal vessels. The hepatic artery is not much affected by the contract- ing tissue, and it is generally possible to inject it with considerable success. As it is the portal vessels which supply the proper hepatic capillaries, the hepatic cells will by these processes be deprived of their nutrition, while, as the hepatic artery supplies the connective tissue, the latter will be well nourished. The consequence of this is great destruction of the hepatic cells. To a large extent this takes place by fatty degeneration, and one can often see, in the midst of connective tissue, islands of remain- ing hepatic tissue consisting of little more than collections of oil- drops (see Fig. 257). The hepatic tissue is also commonly stained with bile-pigment of a yellow or brown color, and this we may associate with obstruction of the bile-ducts by the contracting connective tissue. For the most part the pigment is biliary, but 592 DISEASES OF LIVER, PANCEEAS, AND PERITONEUM. it is also to some extent blood-pigment arising from the obstruction to the circulation. The connective tissue is also commonly stained, and to the naked eye the cut surface has a yellow color, sometimes with here and there quite an orange tint. The name of the dis- ease, cirrhosis, was originally applied from the color of the altered organ. The gall-ducts are for the most part structurally unaltered. They are partially obstructed by the new-formed tissue, and, on account Fia. 257. Cirrhosis of liver in an advanced stage, shown with u very low power. There are great areas of iibrous connective tissue, in the midst of which are islands of hepatic tissue havino' an opaq^ue appearance from the presence of fat in the cells. X 20. of reabsorption of the bile, there may be staining of the tissues and icterus. In some cases, as we have seen, and especially in hypertrophic cirrhosis, there is the appearance of new-formed bile- ducts, already referred to. The result of all these changes is not only atrophy, but distortion of the liver. The connective tissue contracts, and, as it is irregu- larly distributed, the contraction is irregular. The surface of the organ presents larger or smaller projections consisting of the less atFected hepatic tissue between the cicatricial depressions. These projections may be comparatively large, forming the hob-nail appearance of the surface, or they may be smaller, giving a generally granular appearance. They are usually yellow or brown and opaque, being fatty and stained with pigment. Sometimes there is special shrinking of the left lobe, and generally there is INFLAMMATIONS OF THE LIVER. 593 dragging in of the edges, so that the liver assumes more of a compacted form, being perhaps even thicker than usual, but re- duced in superficies. It is dense to the feeling, and more tough to cut than normal. On the cut surface it may be possible with the naked eye to make out the gray connective tissue, with islands of opaque or pigmented hepatic tissue in it. In hypertrophic cirrhosis the liver is not only enlarged, but smooth on the surface. Sometimes it is adherent to surrounding parts, and there may even be a fibrinous exudation on the surface. On section, also, the cut surface is much more homogeneous both in color and otherwise. Outside the liver the principal changes depend on obstruction of the portal circulation, which, it is obvious, must be very great. There is a chronic passive hypersemia in all the radicles of this vein, in the peritoneum, in the mucous membrane of the stomach and intestine, in the spleen, and so on. The most frequent conse- quence is ascites, but we also meet with hemorrhages from the mucous membrane, especially of the stomach and large intestine, as well as catarrh of these. The spleen is also enlarged. The obstruction of the portal vein often leads to widening of the venous channels which form communications between the portal radicles and the systemic veins. In this way we may have great dilatation of the internal hemorrhoidal veins (leading to piles) and of the hypogastric. The cutaneous branches of the latter often stand out prominently on the abdominal wall. The hemorrhoidal veins also communicate with the vesical, and these latter may undergo dilatation. There may also be widening of communications with the veins of the diaphragm and oesophagus, which have sometimes been found highly varicose. Another channel occasionally met with is a small vein which runs from the portal vein to the umbilicus. In some cases this is so much en- larged as to approach the size of the portal vein itself. The patient generally dies from the disorders due to the con- tinuous passive hypersemia — the persistent catarrh of the alimen- tary canal, perhaps with hemorrhages, the ascites, etc. There is great emaciation, and sometimes icterus. It is not clear that the mere loss of the function of the liver bears an important part in the fatal result. 3. Perihepatitis. — This condition is an inflammation of the capsule of the liver, and it is always secondary to some other lesion. A chronic pleurisy of the right side often extends through the diaphragm, and causes inflammation of the subjacent perito- neum, including the under surface of diaphragm and upper sur- face of liver, so that firm adhesion is the result. This is often the case in phthisis pulmonalis. A general chronic or acute peri- tonitis usually involves the capsule of the liver as well as other parts of the peritoneum. Sometimes cirrhosis or syphilitic disease of the liver extends to the capsule. 594 DISEASES OF LIVER, PANCREAS, AND PERITONEUM. The inflammation is in most cases chronic, and results in a thickening of the capsule. Sometimes there are shaggy papilliform projections from the capsule, which have been compared to the Pacchionian bodies of the dura mater. There is frequently also adhesion to the parts around, especially to the diaphragm. The thickened capsule undergoes contraction like the new-formed connective tissue in other inflammations, and the result frequently is considerable deformity of the liver. This is most marked when there is a general inflammation of the capsule as in cases of chronic peritonitis. The capsule contracting all round the liver doubles in its sharp anterior edge, and causes the organ to assume an ap- proach to the globular shape. The contraction causes also atrophy of the liver tissue, and seriously interferes with the circulation in the organ. This deformity of the organ may be compared with that of the lung which occurs in consequence of the contraction of the pleura in chronic pleurisy, especially with empyema. SYPHILITIC DISEASE OF THE LIVEE. Syphilis manifests itself for the most part as an indurative in- terstitial inflammation, with or without the formation of gummata. There may be a cii-rhosis indistinguishable from the ordinary forms of this disease, and only judged to be syphilitic from other circum- stances. Sometimes in the midst of the general new-formation of connective tissue there are numerous small gummata, distinguished especially by their caseous condition. For the most part, however, the disease is localized. To the naked eye the liver is seen to present one or several cicatrices which often make deep indentations in its surface. These cica- trices are most frequent in the neighborhood of the suspensory ligament. On cutting into the middle of the cicatrix a gumma- tous tumor is usually divided with its caseous central part. The periphery of the gumma is not distinctly demarcated from the surrounding connective tissue which extends outwards into the hepatic tissue. Other gummata may be found more deeply in the liver tissue, and these also are surrounded by cicatricial tissue. The cicati'ix is composed of flbrous tissue, and the gumma itself frequently presents irregular strands of connective tissue, but giving place to round-cell tissue. The central caseous portion contains merely granular debris (see Fig. 258). Sometimes at the periphery of the gumma there is great dilatation of bloodvessels, giving almost a cavernous appearance. When there are a considerable number of gummata, the cirrhosis may be nearly continuous, but with special cicatricial contraction at intervals corresponding to the gummata. The liver in this way may assume a very striking appearance, as if subdivided into manifold small lobes. Be the cicatrices large or small in number the lobed and subdivided condition is characteristic of the syphilitic liver. TUBERCULOSIS OF THE LIVER. 5-95 The liver is sometimes found affected in infants who are the subjects of CONGENITAL SYPHILIS. It may be a general induration forming a cirrhosis, usually of the hypertrophic form, with perhaps numerous small gummata ; or the induration may be more localized , but never with that cicatricial condition which we find in acquired Fig. 258. Grumma of liver, a, normal hepatic lobules ; h, recent tissue of gumma with dilated blood- vessels j e, caseous part of gumma j d, d, d, connective tissue outside gumma extending into the hepatic tissue. X 16- syphilis. The connective-tissue formation in this case does not confine itself to the neighborhood of the portal vessels, but extends into the lobules, so that between the cells and around the capillaries there is connective tissue. TUBERCULOSIS OF THE LIVEE. In ACUTE MILIARY TUBERCULOSIS the livcr is almost without excep^ tion the seat of myriads of minute tubercles which are usually 596 DISEASES OF LIVEE, PANCREAS, AND PERITONEUM. invisible to the naked eye. In phthisis pulmonalis examination very often shows the presence of tubercles in the liver, but much more sparsely distributed, and often associated with fatty infiltration. The tubercles are situated in the connective tissue, and are there- fore outside the lobules. They present (Fig. 259) the usual con- Fro. 259. Tubercle of liver from a case of acute miliary tuberculosis. The tubercle is of a rounded form, and presents chiefly round cells with three giant-cella in the midst of these. X ^5- stituents ; round cells with large giant-cells in their more central parts. Very often the central parts are already caseous, or in more acute cases they may be affected by a more ordinary fatty degener- ation with distinct refracting oil-drops. Along with the eruption of tubercles there is some interstitial inflammation affecting the connective tissue, and evidenced by the presence of round cells, but in acute miliary tuberculosis this is not usually considerable. Besides this form of tuberculosis we sometimes meet with a con- dition in which numerous larger caseous tubercles are present, and are associated with a much greater indurative inflammation. The nodules are distinctly visible to the naked eye and sometimes are as large as peas. The larger ones may soften in the central parts and so small cavities may result. Cases have also been described in which large solitary caseous tubercles have occurred, like the scrofulous tubercles of the brain, but all these forms are exceed- ingly rare. TUMOKS OF THE LIVER. Primary tumors of the liver are not very common, but secondary forms, especially cancers, are frequent. Cavernous Angioma of the liver is the commonest form of primary tumor. Its structure has already been described (see p. TUMORS OF THE LIVER. 597 194). It develops apparently by dilatation of the existing capil- laries and atrophy of the intervening hepatic cells. Subsequently the walls of the capillaries become thickened by new-formation of connective tissue and converted into the trabecu'lse of the cavernous tumor (Fig. 260). Hence it is that the tumor replaces a certain Fig. 260. ,'V|;/i^^y^2;5e Angioma of liver. X 90. portion of hepatic tissue. "When seated immediately under the capsule the tumors are visible as red blotches, and on section they have a red color and collapsed appearance, and usually it is only after the blood is washed out that the white trabecu'lse become visible. The tumors present great varieties of size and may be as large as the fist. A case has been described by Ziegler of multiple Fibhonburoma in the liver on the fibres of the sympathetic, there being similar tumors on the various nerves of the body except the olfactory and optic. Concerning Adenoma of the liver there is considerable variety in statement and opinion, mainly because on the one hand this form of tumor is rare, and on the other there are tumors concerning which it is difficult to say whether they should be called cancers or adenomas. There is one form of adenoma about which there is not much doubt; it is that already mentioned in the general section. It is sometimes designated nodular hyperplasia, and occurs as solitary or multiple tumors which, while perfectly defined, have the same structure as the proper hepatic tissue, the cells being usually larger and some having double nuclei. If single, they may reach the size of a cherry or larger; if multiple, they are smaller. The larger ones are sometimes surrounded by a connective-tissue capsule. These tumors are of no practical consequence and are met with accidentally. They are not uncommon in the liver of the dog. Another form some'times called tubular adenoma is described, in which, while the individual cells are like those of the liver, they are arranged not in groaps like the acini of the liver, but rather in gland-like masses, which have been compared to the convoluted 598 DISEASES OF LIVER, PANCEEAS, AND PERITONEUM. tubules of the kidney. It is clear from the epithelial character of these glandular masses that the structure approximates to that of cancer, and indeed some of these cases can hardly be distinguished from cases of cancer. The adenoma may grow to a considerable size, while secondary tumors develop in the hepatic tissue around. This latter fact again suggests cancer, and an observation by Pro- fessor Greenfield in which tumors formed by metastasis in the lungs is still more suggestive. According to some the glandular processes grow from the liver cells, while others hold that they sprout out from the bile-ducts. Primary Cancer of the liver is of rare occurrence, and yet several varieties are described. The cancer may be in the form ol several small tumors, or a large growth infiltrating a considerable portion of the liver. The structure resembles that of tubular glands but less regularly formed than in the case of the adenoma, and more interpenetrating among the proper hepatic tissue. Another form has been described in which the cancer originates in the bile-ducts, and the cancerous processes have at first their seat in the connective tissue accompanying the portal vessels, etc. There are in this form numerous tumors which follow the portal distribution. They may cause obstruction of the ducts and the formation of cysts with bile-stained contents. Secondary Cancer is exceedingly frequent in connection with primary cancer of the stomach, pancreas, and large intestine, but it occurs also in cancers of the uterus, the oesophagus, and mamma. In the case of these last-mentioned localities the metastasis is pro- duced by the way of the hepatic artery, while in the other case" it is by the portal vein. We shall afterwards discuss in a separate section the subject of the secondary extension of cancers of the abdomen. In the great majority of cases the primary seat of the cancer is the stomach, and next to that it is the large intestine, and the secondary tumors arise by pieces of active cancerous tissue being carried to the liver by the portal vein. We shall see afterwards that there is reason to believe that, in some cases at least, the cancerous material does not come directly from the primary tumor. As the cancer is sown in every part of the liver, the con- sequence is the development of numerous tumors which may be found in all stages of growth. It is usual to find a large number of isolated tumors of circular form and pale color (see Fig. 261). They are seated in the liver- tissue, but those near the surface produce rounded elevations of it which can often be felt through the abdominal parietes during life. Even to the naked eye the tumors show evidences of fatty degener- ation in the appearance of opaque yellow coloration. The absorp- tion of the degenerated cells is also indicated by the partial con- traction of the larger tumors in their central parts, producing in the superficial ones a dimpling or umbilication of the rounded TUMORS OF THE LIVEE. 599 projections. The liver, as a whole, is sometimes enormously enlarged, weighing not infrequently as much as ten or twelve pounds. In some cases the new-formation is not so much in the form of individual tumors as a general cancerous infiltration, as if almost Fig. 261. / > ■ tU V ■^ u Pieces of liver with secondary cancerous tumors in it. A larger one, a, is viewed from the surface. Another large one, 6, in section. There are several smaller tumors, c, c. d, a vein in section. (Virchow.) throughout the liver a simultaneous development had occurred, and the cancerous tissue had grown vigorously, displacing the proper hepatic tissue. In structure the tumors follow the primary ones. For the most part it is soft cancers of the stomach that form the original tumors, and we have a well-formed stroma with irregular masses of epithe- lial cells. But sometimes the primary tumor is an epithelioma, and in that case the tumors in the liver are usually fewer in number, firmer and more distinctly defined. "When the primary tumor is in such a position that the cancer reaches the liver by the hepatic artery, the tumors are usually smaller in size and the liver not so much enlarged. This was at least very strikingly true in a case seen by the author where the primary tumor was in the mamma. The cancerous material, as it is brought by the bloodvessels, develops inside them, and particularly in the portal vessels. It seems also that the tumor to a large extent develops by growing inside the capillaries, although also in the spaces in the connective tissue. The consequence of this great new-formation in the vessels is atrophy of the hepatic cells. These are often to be seen at the peripheral parts of the tumors arranged in concentric layers as the pressure is exercised, and they undergo atrophy. It is asserted by 600 DISEASES OF LIVEK, PAJS'CBEAS, AND PERITONEUM. several authors that the cancerous tissue sometimes develops di- rectly from the tissue of the liver, arising largely by a transforma- tion of the latter. This is supposed to be effected by the influence of some infective material brought from the primary tumor, v^'hich induces the hepatic tissue to undergo this peculiar change. This view, however, stands in need of confirmation. The hepatic cells are often deeply stained with bile, and it is clinically of importance that the whole white structures of the body are usually jaundiced. This implies that the ducts are ob- structed, and the biliary coloring matter absorbed into the circu- lation. The numerous developing tumors press on the bile-ducts and obstruct them, and this occurs all the more as the growths arise by embolism of the portal vessels, and are, in the first place, related to them. As the ducts are in the immediate neighborhood of these vessels, they are liable to be pressed on very soon. The hepatic cells are frequently of a greenish color, and the biliary pigment is sometimes extensively deposited in them as brown granules. The portal vessels suffer obstruction, not only by the pressure of the tumors, but as being the seat of their primary growth, and hence we meet with ascites as a common result. Sarcoma is of occasional occuri'ence in the liver in the spindle- celled and pigmented forms. Some cases of melano-sarcoma have been described as primary tumors, but secondary tumors following melanotic sarcomas of the eye are more common. The liver maj' be largely occupied by these black tumors, and greatly enlarged. Here also the growth appears to occur in the bloodvessels and results in destruction of the hepatic tissue proper. PARASITES OP THE LIVEE. These have already been somewhat fully described. The most important constitute the hydatids of the liver arising from the taenia echinococcus. When the liver is examined after death there is found a sac or sacs of very various size, up to that of a man's head. The larger ones produce necessarily great enlargement of the liver as* a whole, and atrophy of the hepatic tissue around them. They present first a connective-tissue capsule, inside which the proper wall of the cyst appears. As the vesicles are some- times much broken down, and it may even be diflicult to find booklets, it is important to remember that the proper cuticula of the cyst is lamellated (Fig. 146, p. 273). Sometimes the contents of the cyst, after the death of the parasite, form a fatty athero- matous or mortary material, in the midst of which pieces of this chitinous membrane may be found with its characteristic lamella- tion. The multilocular and exogenous forms of hydatids are to be remembered, the former resembling colloid cancer in its general THE BILE-DUCTS AND GALL-BLADDER. 601 appearance. Flukes do not frequently occur in the human liver, yet they have been observed (see p. 261). B.— THE BILE-DUCTS AND GALL-BLADDER. Gall-stones. — As gall-stones not infrequently form the primary cause of further disease of the bile-ducts, we may begin our de- scription with them. They are of very frequent occurrence, espe- cially in people past middle life, and they are often found in the gall-bladder after death without their existence having been sus- pected during life. The cause of their formation is very obscure. They are formed in the gall-bladder by the deposition of the constituents of the bile, chiefly cholestearine, and next to that bile-pigments, but also lime and magnesia salts in varying proportions. Probably stagnation of the bile in the gall-bladder at least predisposes to their forma- tion, and this is rendered the more probable from their more frequent occurrence in old people where the actions are sluggish. In the centre of gall-stones there is frequently a nucleus composed of remains of epithelium or mucus. Gall-stones occur singly or in numbers. The single gall-stones are commonly composed almost purely of cholestearine, of which there may be over ninety-eight per cent. They are oval in shape, somewhat nodulated on the surface, and have a glistening appear- ance, altogether not unlike that of a sugar-plum. When divided or broken they present a characteristic radiating appearance from the centre, and also sometimes a concentric stratification. The broken surface has the same glistening appearance as the outer surface, and distinct scales can be separated. The stone is very light in weight, floats in water, and has a soft almost soapy feeling. Multiple Gall-stones are more frequent, and although some- times nearly pure, they are more frequently composed of choles- tearine mixed with bile-pigment and lime salts. There may be two or three, but they may be present in large numbers, fifty, a hundred, or several hundreds. If few they may be comparatively large, but if numerous they are small, the bladder sometimes having the appearance of a bag filled with peas. The multiple stones are always facetted, taking their shape according as there is room, and fitting into each other. In appearance they have been compared to the macerated carpal bones, having somewhat similar facets, and often presenting a similar grayish color, although some- times yellow, brown, or even black. They are very light in weight, and on section present little of the glistening appearance or radi- ating arrangements of the single ones, being rather stratified, more deeply pigmented strata alternating with less. Gall-stones are sometimes met with which are composed almost entirely of bile-pigment. They are small and nearly black, and occur in considerable numbers at a time. They are very rare. 602 DISEASES OF LIVER, PANCEEAS, AND PEEITONEUM. Sometimes there are stones composed mainly of lime salts, espe- cially the carbonate, but these also are very rare. The calculi may remain long in the gall-bladder, which may be found full of them, and with no bile in'it. Its mucous membrane may be inflamed, and the calculi surrounded by an abundant mucous secretion. On the other hand a gall-stone often passes into the cystic duct, where it may remain for a time and obstruct it. After a time it often passes on into the ductus choledochus. The last part of this duct is narrow, and, if the stone is of any considerable size, it usually sticks here, at least for a time. By dilating the duct it may get into the duodenum, but very commonly it does not find its way through without ulceration, and sometimes it ulcerates into the peritoneum, producing inflammation of this serous membrane. Lying at the mouth of the ductus communis it obstructs the out- flow of bile and produces the results to be presently described. When it gets into the duodenum it usually passes off with the feces, but if large, it may produce obstruction of the intestine at some point. This is of rare occurrence, and only in the case of large stones, chiefly of the solitary kind. Obstruction of the Bile-ducts and its Results. — Obstruction occurs from various causes, of which the commonest is that just considered, namely, gall-stones. Inflammation of the duets sometimes produces obstruction, the inflammation being nearly always secondary. It occurs most frequently at the terminal por- tion of the ductus communis from prolongation of catarrh from the stomach and duodenum. As the duct here is narrow a' trivial inflammatory swelling may produce an obstruction, which the bile, possessing a low pressure, is unable to overcome. Then gall- stones themselves may produce inflammation, leading to a more or less prolonged closure of the ducts. We shall see afterwards that inflammation is not infrequently a consequence of obstruction, and these two should not be confounded. Tumors and inflamma- tions AROUND the duet may cause obstruction. This is not infre- quently the case with cancers where the head of the pancreas or the lymphatic glands in the portal region of the liver are engaged. We have already seen that an obstruction of the hepatic ducts in the substance of the liver occurs in cancer of the liver, in cirrhosis, etc. The RESULTS OF OBSTRUCTION Vary according to the site of the obstruction. If the CYSTIC DUCT ALONE be obstructed, then the consequence is that no bile can get into the gall-bladder. In that case the bladder may shrink, and any mucus in it dry in and perhaps afterwards become chalky. In many cases, however, there is an abundant secretion of mucus, and the bladder gets filled with it. The mucus often after a time gives way to a more fluid secretion, and the bladder may be converted into a thin-walled cyst, which may be as large as the fist, with clear fluid contents. When the gall- bladder is thus cut off and no longer available as a store for the THE BILE-DUCTS AND GALL-BL ADDER . 603 bile, there sometimes occurs a dilatation of the larger bile-ducts, so that the bile may lie here instead of in the gall-bladder, and pass into the duodenum during digestion. This constitutes an imperfect compensation for the loss of the gall-bladder. In the case of obstkuction of tub ductus choledochus, there is of course stagnation both in the gall-bladder and in the whole system of bile-ducts. The stagnation tells first on the gall-bladder, which dilates readily and stores up the bile. There may even be rupture of the gall-bladder from excessive dilatation. If the ob- stniction be prolonged, great dilatation occurs throughout the whole system, and serious changes frequently result in the liver itself. Next to the gall-bladder, the ductus choledochus and the larger bile-ducts, which are not supported by the firm liver tissue, are most liable to dilate. This dilatation may be very extreme, these ducts becoming sometimes as great in external size as the thumb, and sometimes even going on to rupture. In the liver itself the dilatation is not generally so great, at least at first, but if prolonged it may lead to serious dilatation after- wards. The first result on the proper hepatic tissue is staining of it with the bile-pigment. The hepatic cells assume a deep yellow color, most marked at the peripheral parts of the lobules, being the parts nearest the bile-ducts. In these the bile-pigment is often deposited in the granular form, as green or brown masses. The pigment, which is at first brown, may, after the tissue has been in alcohol or other fluid, become green. These conditions indicate the reabsorption of the bile, and this is also manifested in the staining of all the tissues of the body, forming a general jaundice. The absorbed biliary coloring matter is often deposited in the uriniferous tubules of the kidney, presumably in the process of excretion. Sometimes considerable atrophy of the proper tissue of the liver occurs, and we hav,e the smaller bile-ducts dilated and forming numerous cavities or cysts througout the liver. This probably does not occur without inflammation of the ducts, and may be accompanied by ulceration, so that the cysts are cavities like those occurring in the lung from dilatation of bronchi; they contain inflammatory products as well as bile. There is sometimes even a more definite acute inflammation of the bile-ducts apparently from decomposition of the bile, and this may lead to what may be called biliaky abscesses, which contain a mixture of pus and bile. These abscesses may contain gall- stones deposited by the stagnant bile, and the irritation set up by these may have been concerned in causing the inflammation. According to Charcot and others, as previously mentioned, the stagnation sometimes leads to inflammation of the connective tissue of the liver, producing cirrhosis of the hypertrophic kind. Tumors op the Bile-ducts and Gall-bladder. — Of these the most important are the cancers. We sometimes meet with pri- 604 DISEASES OF LIVEK, PANCREAS, AND PERITONEUM. mary cancer of the gall-bladder resem'bling in structure cancer of the stomach and intestine. By extension it may largely involve the liver tissue. We have already seen that some of the cancers of the liver probably take origin in the finer bile-ducts in its substance. C— THE PANCREAS. In some aspects the diseases of the pancreas are not of very great practical importance. Although the secretion of the gland is known to have important functions in the digestion of food, the starches, albuminates, and fats being all affected by it, yet lesions of the gland which destroy its functions seem to be compensated by the other secretions of the alimentary canal. On the other hand, the diseases of this organ, and especially cancers, may affect neighboring structures, and cause serious disturbances around. The pancreas has the structure of a salivary gland, consisting of glandular acini whose ducts communicate with a main duct lying in the centre of the gland (Wirsung's duct) and opening into the duodenum in common with the ductus choledochus. The pancreas is occasionally the seat of hemorrhages into its substance. These may be the result of injuries to the abdominal wall or the consequence of passive hypersemia in diseases of the heart, lungs, or liver. Some cases of sudden death have been recorded by Zenker, Hooper, and Klebs, in which the most obvious lesion was hemorrhage into the substance of this gland. It is supposed that the lesion caused pressure on the neighboring coeliac plexus and semilunar ganglion and a consequent reflex paralysis of the heart, just as paralysis of the heart is producible by blows on the abdomen (Groltz's experiment). Inflammations of the pancreas are of various kinds. We have suppurative pancreatitis like suppurative parotitis, resulting in abscesses; also indurative interstitial inflammation with loss of gland tissue, this condition being sometimes of syphilitic origin. Atrophy of the pancreas is observed often as a part of general emaciation, but it has been found in a good many cases of diabetes mellitus. It can hardly be held that the destruction of the function of the pancreas is the cause of the diabetes, and the probability is that, as Klebs suggests, the primary condition is disease of the coeliac plexus causing vaso-motor paralysis (see p. 78). Fatty Infiltration of the pancreas is one of the commonest lesions of this gland. There is normally some adipose tissue in the midst of the gland, and this sometimes undergoes considerable increase, the proper glandular substance becoming atrophied, and adipose tissue taking its place, the shape and general appearance of the gland being preserved. The condition may be part of a general obesity, or it may occur in old age, and, in this latter case, THE PANCEEAS. 605 it may be presumed that atrophy of the glandular tissue is the first condition, the adipose tissue developing afterwards, as in fatty infiltration of voluntary muscle. The glandular structure sometimes undergoes cloudy swelling in common with that of the liver and other organs in the acute fevers. Fatty degeneration is also met with. Tuberculosis is not common in the pancreas, but we meet with caseous masses having the characters of a local tuberculosis. More frequently the pancreas is involved secondarily in a tubercu- losis arising in neighboring lymphatic glands. Of the tumors of the pancreas, cancer is by far the most im- portant. It occurs most frequently in the head, rarely in the body or tail. It is mostly a dense tumor of fibrous appearance (scirrhus), but cases of soft and of colloid cancer have been seen. The cancer often produces obstruction of Wirsung's duct, or produces still more serious results by obstructing the ductus choledochus. It may even by its retraction cause a partial obstruction of the duodenum. There may arise in this way considerable disturbances from the continuous extension of the tumor. "We may also have secondary tumors in lymphatic glands, liver, or peritoneum. It is to be added that cancer of the stomach or duodenum may extend to the pancreas, and that the gland may be the seat of metastatic tumors when the disease becomes generalized. The Pancreatic Duct ("Wirsung's) is liable to certain changes. Concretions occur in it, comparable to those of the salivary glands. They are mostly round or oval, and white or grayish-white. In size they have been met with as large as a hazel-nut or larger, but they are usually small like grains of sand. They are composed chiefly of carbonate and phosphate of lime. They very often arise in dilated ducts, but if large may cause dilatation by obstructing the duct. Obstruction and dilatation of "Wirsung's canal may arise, as we have seen, from calculi, cancers of the head of the pancreas, or from tumors in the neighborhood. Dilatation also occurs second- arily to atrophy of the gland. The dilated duct forms a sei-ies of pouches, or else there is a more definitely localized dilatation so that actual cysts are formed. This latter will occur when the orifice is completely obstructed; the cysts may reach the size of the fist or that of a child's head, and these are sometimes desig- nated RANULA panorbatica. The contents of the dilated duct may be simply the fluid secretion, but sometimes there is thickening of the contents and even hemorrhage. In this way we may have coagula causing the cj'sts to look like aneurisms, all the more as the lining of the cyst may become the seat of calcareous plates like the internal coat of an artery in aneurism. 606 DISEASES QF LIVER, PANCREAS, AND PERITONEUM. D.— THE PEEITONEUM. Introductory. — The peritoneum which is stretched over so many different organs, and has so many recesses and pouches, is very liable to be affected by diseases having their source outside itself. It is necessary here to make some reference to the general rela- tions of the peritoneal sac. It is a large lymph-sac and fluid is continuously circulating through it. The surface of the membrane is covered with endothelium, and there are innumerable apertures or stomata by which it communicates with lymphatic vessels beneath. It is proved by experiment that finely divided solid material introduced into the peritoneal cavity is very readily ab- sorbed and carried into the lymphatics. The transudation fluid which normally passes out of the bloodvessels is doubtless absorbed by the stomata throughout the peritoneum, but there are two localities in which its absorption presents points of peculiar interest. From certain facts to be afterwards referred to in connection with tuberculosis and cancer of the peritoneum, it may be inferred that the great omentum is specially concerned in the process of absorption. This double layer of peritoneum lying free in the cavity may be regarded as A drain by means of which the fluid is drawn off. The relation of the diaphragm to the process of absorption is also important, and has already been referred to in considering the subject of acute pleurisy. The lymphatics of the diaphi'agm com- municate on the one hand with the peritoneal sac and on the other with the pleura, so that fluid and flnely divided solids may be carried through from one to the other. It is probable that the general course of the current is from peritoneum to pleura, although it may be reversed. It is very important to bear in mind this great power of absorp- tion possessed by the peritoneum, especially in relation to septic processes. The products of septic decomposition as well as the organisms which produce these changes may be absorbed, and that sometimes in such quantity as to produce fatal results before they have had time to induce any considerable local effects. Hence it is that septic processes in the peritoneum are so serious and lead so commonly to septicaemia. The fluid in the peritoneal sac is not at rest, but circulates, and the movements of the intestines doubtless have to do with its trans- portation from place to place. This fact is also of great impor- tance, because we shall find that when any pathogenetic agent is introduced into the peritoneal cavity it is generally carried to every part of the sac and produces its effects in every region. Abundant examples of this are afforded by tuberculosis of the peritoneum, inflammations, and so on. THE PEEITONEUM. 607 DISORDEES OF THE CIKCULATION IN THE PEEITONEUM. Active HYPERiEMiA of the peritoneum is not a condition of much practical importance. It is produced when from any cause a general relaxation of the arteries in the sac occurs. Leaving inflammation out of account, this will hardly occur except as a result of sudden removal of extra pressure from these vessels. If a large ovarian tumor be removed from the abdomen, or ascitic fluid drawn off', the arteries, which have previously accommodated themselves to the undue pressure on their walls', will relax, and a hypertemia result. The hypersemia may result in the occurrence of a peculiar form of chronic hemorrhagic peritonitis, compar- able with hemorrhagic pachymeningitis (see p. 442), the eff'used blood bein^ here also sometimes a prominent feature (hematoma OF THE peritoneum). As iu the other case it may be a question whether there is an inflammation preliminary to the hemorrhage, or whether the hypersemia induces bleeding, the succeeding organ- ization of the clot leading to the formation of a membranous layer on its surface. Where ascitic fluid has been drawn off" many times, there may be several layers of soft membrane on the surface of the peritoneum, the innermost being the most delicate and the newest. Passive Hyperemia occurs as a result of obstruction to the portal circulation either alone or as a part of a general venous hypersemia. It is chiefly important in relation to ascites, of which it is the most frequent cause. Ascites. — This name is given to dropsy of the peritoneal cavity, and it occurs as the result either of excessive transudation of fluid from the bloodvessels, or diminished absorption by the lymphatics. It is sometimes merely a part of a general cedema, occurring in diseases of the heart and lungs, in Bright's disease, and in anaemic states. But it is peculiarly prone to occur when the portal circu- lation is specially obstructed. This may happen by the portal vein being the seat of thrombosis, or pressed on from without, but more frequently it is by some lesion in the liver itself, such as cir- rhosis or cancer, which obstructs the portal vessels, as it were, in detail. In these cases the ascites is from increased transudation, and it is much less common to have it occurring from interference with absorption. This may have something to do with it, however, in cases of cancer of the peritoneum, where the numerous cancerous tumors originate from material carried into the lymphatic channels and growing there. These tumors will necessarily obstruct the lymphatics to a large extent in detail, although they may also produce by their irritation a hypersemia of the peritoneal vessels. In a similar way the dropsy of tuberculosis of the peritoneum, although mainly inflammatory, may to some extent be referred to obstruction of the paths of absorption. Ascites is of occasional occurrence in connection with obstruc- 608 DISEASES OF LIVEE, PANCREAS, AND PERITONEUM. TiON OF THE THORACIC DUCT by tumors, aneurisms, thrombosis, etc., interfering with the duct or with the vein into which the duct opens. If the obstruction be complete, there is great distention of the duct and its radicles below the seat of obstruction. Occasion- ally an actual rupture occurs, and the chylous fluid passes into the pleural or the peritoneal cavity. The fluid is in this case a whitish milky material, and we have the conditions named respectively, chylous hydrothorax and chylous ascites. The fluid contains abundant leucocytes in which are fat-granules. The fluid in ascites is contained in the general sac of the peri- toneum, but where adhesions have previously existed it may be confined to particular parts, and sacculated. Sometimes also, in children, there is a dropsy between the folds of the omentum. The character of the fluid in ascites is that of ordinary transuda- tions, a clear, slightly yellow, limpid fluid of low specific gravity. After it has stood for a time it often deposits a very gelatinous coagulum of fibrine. In some cases the fluid is slightly milky (chylous ascites). In prolonged ascites the peritoneum is apt to get somewhat thickened, especially when puncture has been frequently per- formed. The great omentum is not infrequently gathered up so as to be thicker and shorter than usual, and in that case it will act less efficiently as a drain. INFLAMMATIONS OP THE PERITONEUM.— PERITONITIS. Inflammation of the peritoneum is very seldom spontaneous in its origin. It seems remarkable that, compared with the pleura or pericardium, this membrane is so seldom the seat of independent inflammation as a result, for instance, of the irritation of the blood in acute rheumatism, or of the more vague causes of irritation designated as cold. The peritoneum is, however, peculiarly liable to inflammation of a secondary character, the irritant proceeding either from without, as in wounds of the abdomen, or from one of the organs lying beneath the membrane. Mere exposure to the air or the entrance of air into the ab- dominal cavity does not induce peritonitis, and even a somewhat prolonged cooling of the membrane, as during an operation, does not seem to lead to inflammation. Most of the INFLAMMATIONS of the peritoneum are septic, that is to say, they are due to the presence and propagation of bacteria, usually in the form of micrococci, and the irritating chemical pro- ducts which result. Those who are familiar with the manner in which bacteria propagate in suitable fluids will not be astonished that a limited inoculation of septic material produces a very rapid propagation in the peritoneum. The conditions are here pecu- liarly favorable to this. The movements of the intestine and the INFLAMMATIONS OF PERITONEUM — PERITONITIS. 609 normal circulation of the peritoneal fluid carry the septic particles hither and thither, so that they are sown over an extensive surface, and supplied with nutritive material. The warmth of the cavity also favors their propagation. So it happens that in comparatively few hours we may have an intense inflammation, or we may have, as already stated, such an absorption as to cause death by septi- caemia before considerable inflammation can develop. The septic inoculation may take place by a wound in the ab- domen, made by accident or by an operation. More frequently the source is an underlying organ, as the stomach, or intestine, or the uterus after deliver3^ In regard to the last-mentioned source, acute peritonitis is often a special feature in puerperal fever, and as this disease occurs in epidemics and is highly contagious, we must infer that there is something specific in the organism which causes it. The septic inflammations partake of the character of similar inflammations in the pericardium and pleura. They are pre- eminently acute, and tend rapidly towards suppuration. At first there is hypersemia and a serous and fibrinous exudation. The exuded fibrine is visible on free surfaces as a soft yellow layer, and is often present in the fluid as yellow flakes. It glues together surfaces which are in contact, such as the loops of the intestine, but the adhesions are not firm; they can be readily separated, and the gluing material is seen to have a soft gelatinous character. As the inflammation goes on, the fibrinous exudation, which from the first contains very numerous leucocytes and is correspondingly soft, becomes still more infiltrated with these, and assumes the characters of pus. Pus may be found in some parts, while in others there is still the soft fibrinous exudation. Thus pus may be found in the neighborhood of the original source of the inflam- mation, as around the vermiform appendage, the inflammation being here more intense or of longer standing. The pus, and even any free fibrine that may exist, commonly gravitate to dependent parts, and we may find a collection of yellow pus in the pelvis, and especially in Douglas's pouch. The peritoneum presents in its finer details changes similar to those in septic pleurisy and pericarditis. The endothelial cells are separated, and the connective tissue opened out by serous fluid and leucocytes. The underlying tissues are also altered, especially the wall of the intestine. The subserous, muscular, and mucous coats are often oedematous and thickened. There is not infre- quently considerable tympanitic distention of the intestine from paralysis of its muscular coat. This meteorism is sometimes a peculiarly distressing feature in puerperal fever. It will be inferred that septic peritonitis, if general, is almost necessarily fatal. Sometimes it is localized by adhesions, and even after the occurrence of suppuration may subside and give place to. chronic inflammation. 610 DISEASES OF LIVEB, PANCREAS, AND PERITONEUM. Chronic peritonitis, whether developing out of the acute form or occurring in connection with disease in an underlying organ, is characterized by new formation of connective tissue, frequently with adhesion of opposing surfaces. The details of this process are similar to those in chronic pleurisy, etc. ; it remains here to specify some of the more common occasions of the aftection. A diffuse chronic peritonitis sometimes develops in the course of Bright's disease. There is also commonly, in cases of secondary cancer of the peritoneum, a general chronic peritonitis. Local thickenings of the capsule of the liver and spleen are of frequent occurrence in connection with diseases in these organs or their neighborhood. Sometimes the connective tissue is hard, almost like cartilage. Very commonly there is adhesion to the parts around, especially to the diaphragm. On the other hand, the diaphragm may be adherent by reason of the extension of an inflammation from the jjleura, the irritant having passed down- wards in a direction contrary to that of the usual circulation. The peritoneum around the female generative organs is liable to very frequent local chronic inflammations (perimetritis), re- sulting in complex adhesions and mattings of the pelvic organs. The contraction of the new-formed connective tissue may cause considerable distortion of these organs. TUBERCULOSIS OP THE PERITONEUM. Tubercular Peritonitis. — This disease is usually a primary and independent one, due to the existence of the tubercular virus in the peritoneal cavity. It may seem at first sight remarkable that tubercular ulcers of the intestine hardly ever give rise to a general tuberculosis of the peritoneum. We have seen that in connection with these ulcers tubercles are formed in the muscular coat and very commonly beneath or in the peritoneum, and it might seem probable that the virus would get readily into the peritoneal cavity. But it is to be remembered that the lymph circulation is from the surface of the peritoneal cavity into the substance of the mem- brane, and that the normal currents will not carry the virus into the sac. Whether this be the true explanation or not, it is rare for tubercular ulcers to produce tuberculosis. In tubercular peritonitis the virus gets into the sac, and is car- ried hither and thither throughout it by the regular circulation. The consequence is the formation of innumerable tubercular nodules and an inflammation of the peritoneum. It is not clear, however, in most cases, how the virus gets into the peritoneum. In a few cases the tuberculosis of the peritoneum has obviously had its origin in a local tuberculosis of the testis and vas deferens, and has begun in the inguinal region where the vas deferens approaches the peritoneum. But in the majority of cases no such source of infection can be found, and although commonly the person is in a state of ill health before the tuberculosis begins to TUBEKCULOSIS OF THE PERITONEUM. 611 manifest itself, and may have scrofulous tubercular manifestations elsewhere, yet the disease may supervene in persons apparently healthy and robust. We can only say that the formation of tubercles in every part of the peritoneum, and the fact that by reason of the communications through the diaphragm they also spring up in the pleura, are sufficient evidences of the existence of an infective material in the peritoneal cavity. When a case of tubercular peritonitis is examined postmortem, we find evidences of chronic inflammation in the form of thicken- ing of the peritoneum and multiplied vascular adhesions in every part. The loops of the intestine are adherent to each other, and the superficial ones to the anterior wall of the abdomen, the omentum is adherent to the intestine, the liver to the diaphragm, and so on. In the midst of these adhesions are numerous yellow masses of very various sizes, some as large as split-peas, and usually flat. These caseous masses are composed of groups of tubercles which have very much the character of those found in tubercular pericarditis. The caseous tubercles have developed in the usual way out of gray miliary tubercles, and examination will usually show examples in the various intermediate stages. The condition of the omentum is worthy of special mention. It is drawn together and thickened, and closely adherent to the intestine and wall of the abdomen, while in its substance numerous tubercular masses are to be found. All these conditions indicate a chronic inflammation, accom- panied as usual by the new formation of vascular connective tissue with consequent adhesion. The yellow caseous masses are col- lections of tubercles mostly obsolete, just as the caseous tubercles of the brain are ; and here, as there, we may find recent tubercles at the margins of the caseous masses. "While this is the iisual condition found after death there is reason to believe that the inflammation in the earlier stages is more acute. There is often at first considerable accumulation of serous exudation in the abdomen. This is by and by for the most part absorbed, giving place to adhesive inflammation, but often there is serous fluid among the adhesions, and during life the hand on the abdomen may sometimes enable one to detect the move- ment of fluid from space to space among the adhesions. The dis- ease may be recovered from in these earlier stages, the virus being apparently overcome by the reinvigorated forces of the body. On the other hand the inflammation produced is sometimes more acute than usual, and in rare cases may be fibrinous and suppurative. It has already been mentioned that tubercular pleurisy often develops in association with tubercular peritonitis. There is in the pleura for the most part a serous exudation, and as the eruption is usually recent the tubercles are in the form of small white or gray nodules. They are commonly grouped mainly in the lower part of the pleural cavity, in this way indicating the source of the infective material. 612 DISEASES OP LIVEE, PANCREAS, AND PERITONEUM. Tuberculosis of the peritoneum is sometimes met with in acute MILIARY TUBERCULOSIS, but it is not frequent, and the appearances are altogether different from those of tubercular peritonitis. In the case of general tuberculosis the virus is in the blood, and the tubercles develop in connection with the bloodvessels and not specially on the surface. Besides, the disease proves fatal so soon that there is not time for the occurrence of adhesive inflammation or the development of groups of tubercles. The tubercles are very small gray nodules hardly visible to the naked eye and specially abundant in the upper part of the abdomen and omentum. TUMOES OP THE PEEITONEUM. These are rarely primary. Several cases of retroperitoneal SARCOMA have been described in which a tumor of very large size has formed and distended the abdominal cavity. Sometimes we meet with bulky gelatinous tumors in the abdo- men, and the recognition of the exact nature of some of them is matter of considerable difficulty. Colloid cancer of the stomach and intestine not infrequently, as we shall see afterwards, passes on till it reaches the peritoneum, and may result in the formation of bulky gelatinous masses there. But, besides that, there are primary tumors of the peritoneum which belong to the class of cylindroma or plexiporm angiosarcoma. In these cases there is a new formation of bloodvessels in whose adventitia is produced a peculiar gelatinous tissue. These tumors may attain a large size, weighing as much as forty pounds. Secondary cancer of the peritoneum will be considered in the next section more fully and need not be taken up here. Lympho-sarcoma is not such a common tumor here as in the mediastinum, but it sometimes originates in the lymphatic glands of the mesentery and involves all the neighboring structures. We may thus have bulky tumors occupying the place of a portion of the mesentery and intestine, and repeating roughly the anatomical relations of these. THE SECONDARY EXTENSION OE CANCERS OP THE ABDOMINAL ORGANS. We have seen in the study of the diseases of the stomach and intestine that the cancers of these organs very often lead to secondary tumors in the liver and peritoneum, and it may be well to consider here more systematically what paths the infective material follows in passing from the primary tumor to the seat of the secondary growths. The Secondary Growths in the Liver, in the case of cancers of the organs mentioned, form in connection with the portal vessels. SECONDARY EXTENSION OF CANCERS. 613 and there is no doubt that the material is brought to the liver through the portal vein from its radicles. But the question remains, how does the cancerous material find its way into the radicles of the portal vein ? We know that, as a rule, in external cancers the secondary tumors occur uniformly in the lymphatic glands, and it is only after these have been long involved that the cancerous material reaches the blood. We have to inquire whether the alimentary canal is in this regard placed in any different posi- tion to external organs or whether anj^ other explanation may be practicable. For one thing, we find in almost all cases of cancer of the stomach the lymphatic glands near it involved. They are the seat of cancerous growth, although perhaps not very large. This raises the question whether, after all, the real course of events in the abdomen is not, first, metastasis to the lymphatic glands and then from the glands into the radicles of the portal vein. In that case the formation of tumors in the liver would be an occurrence com- parable to the generalization of external cancers, where the blood becomes the vehicle of infection and tumors spring up all over the body, the material being carried by the systemic arteries. The tumors in the lymphatic glands would thus be the secondary and those in the liver really tertiary. Supposing this view to be correct, then it follows that if a cancer of the stomach or intestine causes secondary growths in lymphatic glands whose veins are not radicles of the portal, the tumors of the tertiary order would not be in the liver but in the lungs, or beyond the lungs, in organs fed by the sj'stemic arteries. The author met with a case of cancer of the stomach in which, instead of the glands immediately outside its wall, as is usually the case, the prevertebral glands were enlarged and cancerous. One of these was adherent to the wall of the inferior vena cava, and on opening this vein a little white thrombus was seen peeping out of a small branch which emerged from the enlarged gland into the vein. Thei'e were cancerous thrombi in other veins within these glands, and on microscopic examination it was found that the cancerous tissue in the glands had largely broken up the veins, and epithelial cells were found in them along with the blood. In this case there were innumerable cancerous embolisms in the lungs. Fig. 235, p. 517, shows a section of the lung with two arteries completely occluded with solid material, and with a high power cancer cells could be seen in these vessels. As shown in the figure, and the one following it, there were outside the arteries well-formed epithelial processes apparently inside the lymphatic spaces. This case would seem to indicate that cancers in lymphatic glands may, by breaking up the gland, penetrate into the venous radicles in the gland, and so pass into the genei-al circulation. It seems a legitimate inference from this exceptional case that when the liver becomes involved in cancer of the alimentary canal, it 614 DISEASES OF LIVER, PANCREAS, AND PERITONEUM. does so by the portal blood becoming infected through the lym- phatic glands. There remains one possible difficulty in the way of accepting this vie\^^ In external cancers it is exceptional for the general circulation to become infected. The disease generally ends by in- fecting the lymphatic glands, whereas in cancers of the abdominal organs the liver is affected in a large proportion of the cases. But this difficulty also is hardly insurmountable. A person with a cancer of the mamma, let us say, very commonly dies from the ulceration of the primary or secondary growth, or of both. The lymphatic glands of the axilla being situated externally, are liable to ulceration, and the patient usually dies before the infection has reached the general circulation. In the case of abdominal cancers, however, the organs themselves, and especially the lymphatic glands, are protected by their position, and the cancers are not so apt to interfere with the general health as external cancers are. If the history of even an extensively ulcerating cancer of the stomach be compared with that of a cancer of the mamma, the difference will be very apparent. If the cancer of the stomach does not produce vomiting or stricture of the pylorus, there may be for a long period very little disturbance of the general health, and little more than symptoms of dyspepsia. It seems probable, from the history of some cases, that a cancer of the stomach may go on for many years without causing death. The abdominal lymphatic glands are still more protected. They practically never ulcerate, and in relation to direct injury to health cancer in them is of little account. It seems probable, then, that in cases where the liver is affected the disease is of much longer duration in its primary seat than is often suspected. Cases of multiple cancer of the liver are often examined after death, in which no suspicion has existed during life of the existence of a primary tumor in the stomach, and this tumor may possibly have been going on for a period whose dura- tion cannot in any way be gathered. It is not to be inferred that the portal blood is infected only in the way indicated. It is possible that a cancer may make its way through the walls of the veins directly, just as an external cancer sometimes penetrates a vein. "We have now to consider the case of cancerous infection of THE peritoneum by extension of cancer from the abdominal organs. The seat of the cancer may be any of the abdominal organs; the peritoneum becomes infected when the cancerous material finds its way into the cavity. There are some cancers which have comparatively little tendency to extend along the lymphatics to the glands, but prefer to in- sinuate themselves among neighboring structures, and advance by continuity of tissue. This applies especially to colloid cancer, which often grows through the wall of the stomach or intestine. CANCEEOUS INFECTION OF THE PERITONEUM. 615 while the glands are hardly at all affected. We can understand that a cancer with such a rigid stroma as this form has, and with cells which so readily swell up and become transformed, will not readily allow of transportation of its elements. But this form of cancer very readily, after growing through the wall of the stomach or intestine, infects the peritoneum, and there is no form of cancer which, in such a large proportion of cases, produces secondary tumors there. The cancers of the ovary being already very close to the peri- toneum, readily produce cancerous infection, and do so in almost every form of cancer. Cancers of the pancreas also frequently have a similar course for the same reason. The ordinary cancers of the alimentary canal more rarely pass through the walls and infect the peritoneum, but they sometimes do. It is besides not uncommon to meet with secondary cancers of the liver which have produced an infection of the peritoneum, some of the tumors of the liver having reached the surface and extended through the capsule. When the cancerous material gets into the peritoneum it is carried throughout it by the circulating fluid, aided by the move- ments of the intestine, and secondary cancerous tumors commonly spring up in the most diverse regions (Fig. 262). It is to be Pig. 262. Disseminated cancer of the peritououui, i.uiH cancer of the stomach. (Virchow.) remembered that in the peritoneum there are innumerable open stomata ready to absorb any finely divided solid matter that may be suspended in the peritoneal fliaid. The infective material will therefore be carried from the surface into the substance of the peritoneum, or into the subperitoneal tissue, and the resulting tumors may even be subperitoneal. They form usually flat growths with smooth surface, the general surface of the peritoneum being perhaps unbroken. JS'ot infrequently the tumors are continuous with one another in some parts of the abdominal wall, a layer of cancerous tissue appearing like a subperitoneal thickening. The GREAT OMENTUM is somewhat peculiarly situated in this 616 DISEASES OF LIVER, PANCREAS, AND PERITONEUM. regard. We have seen that it probahly acts as a kind of drain in the peritoneal cavity, and if this be the case it will specially absorb any material which gets into the cavity. In accordance with this there is usually in cancer of the peritoneum great new-formation in the omentum. In colloid cancer it sometimes assumes the form of a bulky heavy mass, and in other forms we have it gathered up and converted into a solid tumor lying transversely in the abdomen. We may venture the statement that this fact is too little known among physicians, and that a great omentum thus altered is fre- quently taken during life for an enlargement of the liver, or a primary tumor of some obscure kind. The relation of peritoneal cancers to the diaphragm presents some points of interest. We have seen that the diaphragmatic lymphatics communicate with the peritoneal sac on the one hand, and the pleural sac on the other. In peritoneal cancers the dia- phragm is usuall}' permeated with cancerous gi-owths, and these are often in the form of cords as if following the course of the lymphatics. Through time they extend to the pleural surface, and tumors may appear there. If there are no pleural adhesions in this region the infective material passes into the pleural cavity, and numerous tumors are often found, especially in the lower parts of the pleura. A preexisting adhesion of the diaphragm to the lung prevents this extension of the cancer. DISEASES OE THE URIITARY OEGAIfS. A.— THE KIDNEYS AND URETEES. JS'oRMAL Structure and Function. — In studying the diseases of the kidneys, it is necessary to bear constantly in mind the general facts as to their structure, otherwise the examination of the organs will lead to confusion. The functions of the kidney must also be understood in their outlines in order to a comprehension of the changes wrought by disease. When a microscopic section of the kidney, made so as to include both the cortical and pyramidal substance, is examined, the con- trast between these two regions is sufficiently striking in respect that in the cortical substance the uriniferous tubules have a markedly irregular and convoluted course. If attention be now confined to the cortex alone, as in Fig. 263, it will be seen that convoluted tubules are not the only kind present. There are straight tubules prolonged up from the pyramids in the form of tapering bundles (a) between which lie convoluted tubules {b). These tapering bundles, called medullary rays, or pyramids of Eerrein, do not reach the surface, the most superficial part of the cortex presenting a continuous layer of convoluted tubules. In this way the deeper parts of the cortex present a regular division into alternating areas of straight tubules or medullary rays, and convoluted tubules. Among the convoluted tubules lie the Malpighian capsules (e in figure). These occur somewhat frequently, and at tolerably reg- ular intervals. In addition to these arrangements of the tubules, the blood- vessels must receive attention. The larger arteries, as shown (d in figure), run between pyramids and cortex, and send up stems given o& at right angles into the cortex. These pass at intervals into the region of convoluted tubules, and as they ascend they give off lateral branches to the Malpighian tufts. It will thus appear that the areas of convoluted tubules are also the areas of the ascending arteries (which are also called interlobular arteries) and Malpighian tufts. In the Malpighian capsule the afferent vessel breaks up into a congeries of capillary vessels, called the tuft. These gather together to form the efferent vessel, which again breaks up into capillaries which surround the tubules with a rich network. We have seen that the large arteries which run between the pyramids and the cortex give off the ascending or interlobular 618 DISEASES OF THE URIKARY ORGANS. arteries to the cortex. They also give off arterial branches down- wards to the pyramids. These arteries break up into bunches of straight arterioles (arterias rectse, c in figure) which are increased by branches coming down from the afferent vessels in the deeper "Fig. 263. Section of normal kidnej, including cortex and base of pyramid, with a very low magni- fying power, u, medullary rays; b, convoluted tubules; c, region of arteri« rectos in pyramids ; d, larger vessels running between pyramid and cortex ; e, Malpighian tufts ; /, capsule. X 12. parts of the cortex. These bunches of arterioles taper as they pass down the pyramids, so that they form small pyramids with their bases towards the cortex. They correspond in position w^ith the areas of convoluted tubules, which areas they, as it were, pro- long down into the pyramids. In the normal kidney all these arrangements are very regular, and as in disease there is apt to be dislocation of the various structures in a high degree, it is important to become familiar with THE KIDNEYS AND URETER. 619 the normal appearances. Even with the naked eye the various regions indicated ahove may usually he made out to some extent in the normal kidney. There is first the distinction of pyramids and cortex, and, normally, the bases of the pyramids are strictly demarcated from the cortical substance. Then a more care- ^i»- 264. ful examination brings out in the cortex the medullary rays, as prolongations upvpards of the pyramids. Alternating with these are the more irreg- ular areas of convoluted tu- bules in which the Malpighian tufts may be visible as red dots. Then in the pyramids we may notice that as we fol- low the medullary rays down- wards there are, alternating with them, red streaks which represent the bunches of arte- rise rectse. In studying the function of the kidney, we have to remem- ber in the first place the course of each uriniferous tubule, which may be followed in the annexed diagram. It begins in the Malpighian capsule (i). Issuing thence the tubule be- comes convoluted (ii), and then it dips down in a long loop (Henle's loop) whose bend [h) is usually in the pyramidal portion. Turning upwards (iv), the loop comes back to the cortex, again becomes con- voluted (v), and then opens, sometimes at an acute angle, into a straight tubule (vi) which passes directly downwards, joined by other tubules (vii), till it opens at the apex of the pyramid (ix) into one of the calices. So far as the water of the urine is concerned, it is generally agreed that it passes from the blood at the Malpighian tufts ; it filters, in fact, from the capillaries into the ends of the tubules. According to Ludwig, the whole constituents of the urine filter through into the Malpighian capsules, but along with an excess of water. In travelling through the long course of the tubules, the water is to a considerable extent absorbed, and the urine concen- trated. According to Bowman's views, on the other hand, it is mainly the water which passes through at the Malpighian capsules, Diagram of course of uriniferous tubules from Malpighian capsule (I) to pyramid (IX). See text. (Qcain.) 620 DISEASES OF THE URINAEY ORGANS. the urea, urates, etc., being secreted from the blood by the large granular epithelium which lines the convoluted tubules. Without insisting on one or other of these views, it is important for our purpose to observe that the actual amount of urine secreted will depend on the blood-pressure in the Malpighian vessels, or on the speed with which the blood passes through the vessels, these two, as a rule, strictly corresponding with each other. The amount secreted will be increased by increase of pressure in the Malpighian vessels, as, for instance, by relaxation of the renal arteries, and it will be diminished by any cause which diminishes the pressure in these vessels. Considering the close relationship of the renal vessels to the sj'stemic arteries and veins, it is clear that the blood in the former Avill be liable to considerable variations in pressure and in the speed of the current from circumstances affecting the general circulation, such as disease of the heart and lungs, preg- nancy, and so on. We shall see afterwards that serious results may follow from the action of deleterious agents brought to the kidneys by the blood, and it is important to consider at the outset how lesions brought about in this way will be distributed. In the first place, such diseases will probably affect both kidneys at the same time. But, further, considering that it is in the cortical portion of the kidney that the secretion of the urine takes place, it is not remark- able that these lesions occur mainly in connection with the Mal- pighian tufts and the convoluted tubules of the cortex. MALFORMATIONS AND MISPLACEMENTS OF THE KIDNEY. Congenital Malformations. — These are frequently such as to present comparatively little interference with the function of the organs. This does not apply to the extreme cases where both organs are absent or extremely small, but as this only occurs with serious malformations of the foetus as a whole, the child does not survive. Defect of One Kidney is not infrequently met with in well- formed adults without any of the signs of disease of the kidneys. It is mostly the left kidney that is defective, and it may be entirely absent, its vessels and a diminutive ureter ending in a piece of con- nective tissue. The other kidney in these cases undergoes a com- pensatory hypertrophy, as we shall see immediately. The kidney also not infrequently shows some trace of the original lobulation which exists in the foetus and is retained throughout life in some animals. Coalescence of the Two Kidneys across the middle line is one of the most frequent malformations. Various degrees of it are presented. It may be a simple elongation of the inferior extremi- ties of the kidneys which are united by a fibrous band passing across the vertebrse. Or there may be a proper isthmus of renal MALFORMATIONS AND MISPLACEMENTS OF KIDNEY. 621 tissue uniting the two kidneys into one and forming the well- known HORSESHOE KIDNEY (Fig. 265). From this we have various grades on to complete coalescence of the kidneys into an elongated or square body across the vertebrae. In almost every case there are the regular two ureters or they may even be increased in number, and they pass down in front of the isthmus. This form Fm. 265. Outline sketch of horseshoe kidney. (Roberts.) of kidney is often depressed in position, even coming as low in some cases as the hollow of the sacrum. When depressed the arteries usually have abnormal origins, as from the common iliac, hypogastric, etc. Variations oe Position. — These may be congenital or acquired. In the former case and in some of the latter the kidney is fixed in its unusual situation. In congenital malposition it is generallj' the left kidney which is concerned. It may be depressed so as to lie as low as the brim or even the cavity of the pelvis. It is not infrequently seated opposite the sacro-iliac synchondrosis. Such kidneys have usually the hilus presenting forward and are flat- tened, while their vessels are branches of the lower end of the aorta and the iliac veins or even entirely the iliac vessels. The kidney may also lie nearer the middle line than normal or in the middle line. The malposition may be acquired by the pressure of tumors or of the liver, by the dragging of a hernial sac, and so on. In a case observed by the author the kidney was fixed near the middle line, apparently on account of the abnormal shortness of the renal vein. Of great interest here is the movable or floating kidney. In connection with the etiology of this condition it is very important to remember that it occurs in the great majority of cases in females (according to Roberts in forty-six out of fifty-one cases) and mostly on the right side. This connects the lesion with dis- placement and malformation of the liver caused by wearing stays, and perhaps also with the displacements of the organs generally. G22 DISEASES or the urinary organs. incident to the rise of the uterus in pregnancy. In the case of the movable kidney the organ is so loosely bound down by the peri- toneum that it can pass forward out of its position, carrying the peritoneum before it till it lies at the edge of the liver. It is said in some cases to possess a kind of mesentery. During life it is often to be detected at the border of the liver, although it is not constantly there. The movable kidney is not very liable to secondary changes, although sometimes the abnormal position interferes with the How through the ureter, and leads to hydronephrosis, or even inflam- mation of the pelvis. Of more importance is the fact that by dragging there may be serious nervous disturbances, in the form of excruciating cramps, often of very obscure origin during life. The kidney may, however, be movable without any such nervous symptoms presenting themselves. COMPENSATORY HYPERTROPHY OP THE KIDNEY. This condition develops sometimes when one kidney is lost or congenitally defective. In the case of congenital absence of one kidney the other will be found homogeneously enlarged, and probably weighing nearly the same as the two normal kidneys together. The different regions of the kidney bear the same rela- tions to each other, each being enlarged in its due proportion. The function of the kidneys is also completely carried out by the single one. It has been determined by experiments in animals that compen- satory hypertrophy develops after excision in full-grown animals, although it is more complete when the operation is done in the new-born. It is remarkable how soon after such excision com- plete restoration of the renal functions occurs, the secretion of urea reaching its normal in one case about two days after the operation, and the animals remaining from the first apparently unaffected in health. This would indicate that the kidney does not, like a gland, secrete the urinary constituents, but that these come to it performed and are simply excreted by it. Measurements have been made of the structures in the kidney to determine whether there is in compensatory hypertrophy an actual new formation of glomeruli and tubules or merely an en- largement of these. The results are by no means conclusive, and some observers hold to one view and some to the other. Gudden, on the basis of observations, in which he excised one kidney in new-born rabbits and examined the remaining hypertrophied one when the animals were full grown, concludes that there is no actual new formation of glomeruli, but a simple enlargement of them. In relation to what follows it may here be noted that hypertrophy of the heart does not usually follow extirpation of one kidney. DISORDERS OF THE CIRCULATION IN THE KIDNEYS. 623 DISOEDEES OP THE CIECULATION IN THE KIDNEYS. Active Hyperemia is caused by dilatation of the renal arteries. This may be from traumatic injury to the vaso-motor centre in the medulla oblongata. In a case observed by the author of this kind there was the most intense hj-pei'semia with enlargement of both kidneys, the injection affecting all the vessels. During the few hours that the patient survived, large quantities of urine were twice removed by the catheter, and after death the bladder was again found distended by a watery urine. Again, we may have an active hyperemia from removal of pressure, as after excision of large tumors from the abdomen or the removal of ascitic fluid, or even the removal of pleuritic fluid. Under these circumstances there is often for a day or two excessive secretion of urine lasting till the renal vessels resume their normal state of contraction. The hypersemia which follows on the administration of certain poisons, such as cantharides, arsenic, and carbolic acid, is to be regarded as really inflammatory. Passive Hypek^mia results from obstruction to the venous cir- culation, and is most frequently met with in valvular disease of the heart and in diseases of the lungs, in which the circulation is seriously interrupted, as in severe emphysema. The naked-eye appearances of the kidney are usually very sug- gestive of over-fllling of the vessels. There is a general redness, but this is generally most manifest in the pyramids where the arterife. rectse often show very special dilatation indicated by ex- aggeration of the red streaks which pass from the bases of the pyramids in the direction of the apices. The Malpighian tufts are also visible in the cortex as small red spots. When hypersemia has subsisted for a considerable time, as in so many cases of heart disease, a more definite change occurs in the kidney. The connective tissue here, as in other organs (see passive congestion of the heart, p. 299), becomes hypertrophied, and the organ assumes a distinct increase in density. The organ, while harder to the feel, is sometimes slightly enlarged, and the capsule can be peeled from the surface even more easily than normal. Sometimes there is fatty degeneration of the epithelium, and this may result in collapse of some of the tubules, leading to slight de- pressions of the surface. Under the microscope, the kidney shows overfilling of the vessels, the epithelium presenting little alteration, at most some fatty degeneration. The hypertrophy of the connective tissue is not accompanied by any considerable formation of round cells; it is simply seen that the interstitial tissue is more prominent and perhaps more definitely fibrous than normal. Thrombosis of the renal veins is sometimes a result of passive hypersemia, but it usually occurs just before death and when the patient is very much debilitated. 624 DISEASES OF THE UBINABY ORGANS. Embolism of the kidney has heen already referred to with some degree of fuhiess (see p. 60). Remembering that the renal arteries are strictly end-arteries, it will be understood that when an artery is obstructed the infarction always occurs. The arteries of the kidney being distributed primarily to the cortex, the infarction is Fig. 266. Embolic infarction of kidney. The white appearance and wedge-shape of the infarction is represented. (After Bayer.) more or less wedge-shaped (Fig. 266), with the base of the wedge at the surface. If the wedge be of larger size it will extend also into the pyramids. As a rule, the infarction is of a pale color and of dense consist- ence, the tissue having undergone coagulation necrosis. In some cases, and especially in small infarctions, hemorrhage occurs, and we may have the regular hemorrhagic infarction, or a partial red coloration. Around the infarction, whether red or pale, there is commonly a zone of hypersemia. As already seen, the infarction gradually undergoes absorption, and is replaced by a cicatrix. In this way deep depressions of the kidney may occur, and if there are several of them the kidney may assume a lobed appearance. In cases of old mitral or aortic disease it is verj' common to find' deep cicatrices, indicating that probably at the time of acute endocarditis, embolism of the Iddney had occurred. The kidney is not infrequently the seat of septic embolism in pyaemia, ulcerative endocarditis, etc. The result is the formation of miliary abscesses, which will come up for consideration hereafter. BKIGHT'S DISEASE, OE NEPHRITIS. This is a subject of great complexity and difficulty, and one con- cerning many points in which differences of opinion exist. bright's disease, oe nephritis. 625 General Considerations. — At the outset it may be said that we include here cases in which there are undoubted inflammatory manifestations in the kidneys, but we exclude those in which there are no such manifestations present. The domain of Bright's disease, therefore, is not coextensive with that of albuminuria, as the latter may include such conditions as amyloid degeneration and passive hypersemia. In studying the causes of Bright's disease, we have to look for an irritant, and it is here important to observe in the first place that the inflammatory manifestations occur in both kidneys, and although, on examining the kidneys in detail, these manifestations will be found to present themselves in innumerable minute foci, and to confine themselves for the most part to the cortex, yet they do not affect a few definite areas, but are diffused over the length and breadth of the organ. These facts indicate that the irritant is carried to the kidneys by the blood, and is distributed with the blood homogeneously over them. As the blood is primarily distributed to the cortex, and as the cortex contains the more active secreting tissue of the organ, it so happens that the inflam- matory manifestations occur almost exclusively there. In the various cases of Bright's disease we do not find the various constituents of the kidney tissue equally engaged, and it is necessary, in studying the causation, to refer to this matter. In the kidney we have, as the main constituents, the bloodvessels, the secreting tissue (consisting of the glomeruli and the tubules with their epithelium), and the connective tissue. It is not impossible that an irritant brought to the kidneys by the blood may show a predilection for the renal epithelium on the one hand or the connective tissue on the other. But it seems more likely that in the majority of cases it will act on both at the same time. "We have already had several opportunities of observing that chronic inflammations very commonly produce inflammatory new formation in the connective tissue, and the kidney forms no exception in this respect. It may be said, therefore, that for the most part irritants which act through a long period and with little intensity produce a chronic inflammation mainly of the connective tissue. On the other hand, irritants which act intensely so as to produce acute inflammation, while they produce the usual changes in the bloodvessels which we have, seen occur in acute inflam- mations, affect mainly the epithelium of the uriniferous tubules. It may, therefore, be said that acute inflammations are mostly PARENCHYMATOUS, while chrouic inflammations are mostly inter- stitial. This distinction, however, cannot be rigidly carried out. There are some acute inflammations which affect the interstitial connec- tive tissue even more than the secreting epithelium, and in all acute inflammations which are somewhat prolonged the connective tissue is involved. On the other hand, inflammations which begin acutely frequently become chronic or subacute, and in them, 40 626 DISEASES OF THE URIXAEY OEGAXS. while the epithelium continues to show mai'kecl changes, the interstitial tissue always shows distinct inflammatory proliferation. After these observations, we are now in a position to consider what may be the nature of the irritants which produce Blight's disease. In the first place, as to acute nephritis, a very common cause, and indeed in children the commonest, is the specific poison of SCARLET FEVER. It may also be produced by the poison of measles and other specific febrile diseases. In adults the disease is mostly ascribed to cold, and we have to consider how exposure to cold should give rise to an irritant of such a nature as to cause acute inflammation of the kidneys. It is of interest in this regard that, as Dickinson so well points out, cold mostly produces these eft'ects when the person is exhausted or asleep, and when the exposure has occurred immediately after profuse perspiration. It is as if, the functions of the skin being suspended, some deleterious material accumulated in the blood and irritated the kidneys. It appears that nephritis hardty occurs in persons exposed to cold in the arctic regions, probably because, the respiration being more vigorous, the deleterious material is carried ofi:" by way of the lungs. In warm climates also nephritis is uncommon, probably because the body is less liable to sudden exposure to cold than in temperate regions. Turning to the causes of chronic nephritis, it sometimes remains after an acute attack. For the most part, however, when the dis- ease begins as acute nephritis it remains subacute with repeated exacerbations, and the anatomical condition is a combination of that seen in acute Bright's disease and chronic, or, in other words, of parenchymatous and interstitial nephritis. Sometimes, however, the disease, even after scarlet fever, becomes definitely chronic, and the anatomical features are those of interstitial nephritis, although the changes in the tubules may still be such as to suggest an earlier, mainly parenchymatous, inflammation. On the other hand, in a large proportion of cases, the disease is chronic from the outset, and is to be ascribed to a cause which has been acting with slight intensity for a long period. Of all these causes the most definitely determined is gout. The pathology of this disease is not very apparent, but there is an obvious alteration in the blood in consequence of which salts of uric acid are deposited in certain joints, generally with signs of acute inflammation. The same condition of the blood frequently induces chronic nephritis, and it is remarkable that when it attacks the kidneys it is less likely to affect the joints, and vice versa. Among the working classes gout largely arises from chronic lead-poisoning (see stat- istics in Dickinson's work on Albuminuria), and in these cases the disease is particularly hable to attack the kidney, so much so that a large proportion of painters and others who work with lead" die of chronic nephritis. Where the gout is due to the constant use of alcohol the disease is hiore liable to attack the joints. Chronic nephritis is also sometimes induced by the poison of bright's disease, or nephritis. 627 SYPHILIS. In this case it is apt to be associated with amyloid dis- ease, but may also occur as a simple inflammation. Pregnancy not infrequently leads to a chronic nephritis, in all probability by obstructing the vessels of the kidney by the pressure of the uterus. In recent cases there is extreme hypersemia of the kidney, which, with repetition of the cause, may go on to assume the regular characters of chronic nephritis. Lastly, there are cases in which there is no special cause apparent, and we can only say that the person has been exposed to some influence whose nature we do not know. In many cases the dis- ease has been very prolonged, and all through, the actual active disease at any particular time has been very slight. With this vejy insidious march, there may be the most serious permanent changes in the kidneys before any prominent symptoms have called attention to these organs. Among the causes which are some- times mentioned, it is proper to refer to prolonged mental disturb- ance. It is not impossible that the deterioration of the body, and the defective condition of the alimentary functions in such cases, may render the kidneys peculiarly liable to chronic inflammation. The Anatomical and Histological Conditions in Bright's Dis- ease. — AYe shall consider these changes under three heads, namely, inflammation mainly afiectiug the Malpighian bodies, or glome- rulo-nephritis, that in which the tubules are chiefly concerned, PARENCHYMATOUS NEPHRITIS, and that wMch affects chiefly the con- nective tissue, INTERSTITIAL NEPHRITIS. We have already seen that no absolute line of distinction can be drawn between these, and especially that when parenchymatous nephritis becomes chronic, the interstitial tissue is more and more involved. The term glombrulo-nephritis has been applied by Klebs to a condition in which the Malpighian tufts show the chief signs of inflammation. This he describes as being present in the kidneys of persons who have had scarlatina, and have died in consequence of the post-scarlatinal nephritis. It seems strange that the actual pathological condition in the nephritis of scarlatina has been so little determined till of late years. It has been customary to state that the condition is a par- enchymatous nephritis. Recent observations, however, have shown that in the earliest stage of scarlatinal nephritis there is an accumu- lation of round cells in the glomeruli and connective tissue around. This observation, originally brought into prominence by Klebs, has been confirmed by the author, Klein, Charcot, and others, and may now be generally accepted. Looking on scarlatinal nephritis as a typical acute inflammation of the kidney, we are not surprised to find that the occurrence of leucocytes in the Malpighian tufts is the most prominent appear- ance at the outset, and it is this condition apparently which is specially designated glomerulo-nephritis. The exudation is not usually confined to the glomeruli, but exists around them, and 628 DISEASES OF THE URINARY ORGANS. may extend to the general connective tissue. In the case of the author, in which the patient died on the ninth day from the outset of the fever, there was an enormous infiltration of the interstitial tissue, as well as the glomeruli, with leucocytes (Fig. 267). It is Fig. 267. Griomerulo-nephritis from a case of scarlet fever. The Malpighian tuft in tlie middle of tte figure is crowded with round cells, which are also present very abundantly in the inter- stitial substance between the tubules, whose epithelium is granular. X 300. stated by Eosenstein that, in the nephritis caused artificially in animals by cantharides, there is a similar appearance of leucocytes around the glomeruli and elsewhere. Besides these changes, there is very commonly, in the acute stage of scarlatinal nephritis, blood in the uriniferous tubules. The blood is in the convoluted tubules, and it is sometimes seen also inside the glomerulus. In a favorable section an appearance such as that shown in Fig. 268 may be found. There is seen to be blood (6) in the glomerulus, between the tuft of vessels (a) and the capsule, and there is also blood in a tubule (c), which is so related to the glomerulus as to be evidently its prolongation, although the section did not happen to be made so as to show the actual communication. Sometimes the changes in the kidney do not consist so much of exudation of leucocytes or extravasation of the whole blood, but rather in alterations in the epithelium. In scarlatina the changes in the epithelium also centre in the glomeruli. The epithelium lining the glomerulus is distinctly enlarged (Fig. 269), and whereas normally this epithelium is hardly visible, it may become remark- ably prominent, as in the figure. It sometimes increases very greatly, as in Fig. 270, accumulating inside the glomerulus in such a way as to crush the tuft. In the case from which this figure was taken there were many tufts very seriously encroached on by the' growing epithelium. Similar changes occur in the epithelium of the tubules, but there is a remarkable concentration of the lesion in that of the glomeruli. BRIGHT S DISEASE, OR NEPHRITIS. 629 In cases where there is little more than a glomerulo-nephritis, such as we have described above, there are sonaetimes severe Fig. L'fl^. ■v^:^"';^^^M? ..^j?)^ -^■^'J Hemorrhage from a Malpighian tuft in a case of scarlet fever, f/, tuft; /), blood between tuft and capsule; f, blood in uriniferous tubule extending from tuft. X 350. Fig. 269. Glomerulo-nephritis in scarlet fever. The epithelium lining the c.Tp.?ule is unduly large and abundant. X 3y0. ursemic symptoms leading, rapidly it may be, to death. It is to be remembered in this connection that the urine is secreted essentially by the glomeruli, and if in many of these the vessels are suddenly 630 DISEASES OF THE URINARY ORGANS. obstructed by the pressure of leucocytes, as in Fig. 267, or of epi- thelium, as in Fig. 270, or even by blood inside the capsule, then the secretion of urine may be much reduced. Under these cir- FiG. 270. Glomerulo-nepbritis in scarlet fever. The epithelium lining the uujisule is greatly increased so as to crush the tuft. X 350. cumstances suppression of urine and urfemia are not very extra- ordinary occurrences. The kidnej's in these cases may be very little changed to the naked eye; they are sometimes enlarged with considerable injec- tion of the vessels. The glomeruli maj' be visible as red points, and there may be on the surface and on section red streaks and spots, indicating the intratubular hemorrhage. Sometimes, on the other hand, the exudation of leucocytes may be sufficient to pro- duce great enlargement, and the kidney (as in the author's case, from ■which Fig. 267 is taken) has all the appearance of the large white kidney. Parenchymatous nephritis is characterized by the occurrence of changes in the renal epithelium. From what has been already stated it will be understood that these changes hardly ever occur without coincident signs of inflammation in the interstitial con- nective tissue. The changes consist in the first place mainly in cloudy swelling of the epithelium, with a tendency for the cells to become loosened and to discharge. The tubules are often found greatly distended, and as if choked with desquamated epithelium. Fatty degenera- tion occurs in the epithelium, and is often present in a high degree, not uniformly, but usually in a considerable stretch of tubule at a time. In the tubules, besides desquamated and frequently fatty epithelium, there may be blood, in the form of brown granular matter or fresh red blood. Tube-casts are also to be found, often bright's disease, or nephritis. 63i in great abundance. The tube-casts lie in the calibre of the tubules as transparent hyaline cylinders, and they may be traced for a con- siderable distance. The changes in the epithelium are almost entirely confined to the convoluted tubules of the cortex, although the disintegrated epithelium may be carried downwards into the loops of Henle and the straight tubules. The tube-casts are found in the straight tubules as well as in the convoluted. The kidney as a whole is considerably enlarged, audit may reach twice its normal weight. The bloodvessels are intensely injected, so that the surface presents a red color after removal of the capsule, which comes off easily. On section the cut surface is also seen to be red, and blood ilow^s freely from it; the mucous membrane of the pehns is injected. If the cut surface be washed so as to re- move the blood, it may appear as if the tissue, apart from the bloodvessels, were unduly pale, and there may even be opaque streaks if fatty degeneration is considerable. The enlargement of the organ is seen to be mainly due to increase of the cortex, which may be very much thickened, and it is in the cortex that the paler color mentioned above appears. It is not common for death to occur in this exceedingly acute stage, and as the inHammation subsides into a subacute or chronic Fig. 271. Section of large white kidney in a clilld of seven. The tubules contain irregular epi- thelium, and are distorted; in one a tube-cast is present. The interstitial tissue is greatly increased and contains abundant round cell.«. (Dickinso.\.) condition w^e have developed the lar«e white kidney. It is neces- sary here to mention that amyloid degeneration produces enlarge- 632 DISEASES OF THE URINARY ORGANS. ment and paleness of the kidney, and confusion has no doubt frequently occurred between that condition and the one now under • consideration. In the large white kidney the tubules are still distended with epithelium, which is enlarged and desquamated (Fig. 271). There is here usually considerable fatty degeneratian of the epithelium. The epithelium, and debris resulting from its disintegration, are often packed to a considerable extent into the straight tubules. Tube-casts are present usually in large numbers, and present the hyaline appearance already described, or else contain debris of epithelium and fat. The changes in the tubules are so 2:)rominent that they are apt to obscure the condition of the connective tissue. In every case probably there are round cells in the tissue, and sometimes they are present in great abundance. In the accompanying woodcut (Fig. 271), taken from .Dr. Dickinsoii's work, the condition of the interstitial tissue is shown in the case of a child seven years of age, in which each kidney weighed four and a quarter ounces. An illustration of the appearances of a similar section from a healthy child is given along with it for comparison (Fig. 272). It Fig. 2' Section of noriniil kidney for C'in|iMrison with preceding. (Dickinson.) is seen that in addition to the changes in the epithelium, already described, there are numerous round cells in the interstitial tissue. The longer the case lasts the more pronounced is the change in the interstitial connective tissue. As time goes on also the disten- tion of the tubules with epithelium becomes less. The disinteg- rated epithelium is discharged and there is less reproduction. In this way the condition shades towards that of interstitial nephritis, and may pass into that of the contracted kidney. A case which bright's disease, oe nephritis. 633 has begun acutely, however, generally even in the later stages pre- sents traces of the epithelium being specially involved. We shall see afterwards that in the typical chronic interstitial nephritis the epithelium is also involved, but the connective tissue in this case is increased to such an extent that the alteration of the tubules is apparently secondary. To the naked eye the enlargement and paleness of the kidney are the striking features in this condition. The weight of the organs is often double the normal or more. The increase in bulk is almost altogether in the cortex, and its exceedingly pale color contrasts with that of the pyramids, which are often unduly red. The color of the cortex is opaque white or buff, and it is often possible with the naked eye to distinguish yellow streaks and spots on the surface of the kidney after reraovAl of the capsule or on the cut surface, indicating fatty degeneration of the epithelium. It will be clear that from the large white kidney to the contracted form there are all gradations, and a kidney which is normal in size, but which presents paleness and irregularity of the cortex, will show under the microscope already a very marked increase of the connective tissue. Interstitial nephritis is the name applied to inflanmiation of the connective tissue of the kidney. From what has gone before it will be understood that this scarcely occurs independently of inflammation of the epithelium of the tubules, and that in almost all cases the inflammation is really diffuse. We have even seen that in acute nephritis there may be such an exudation of leuco- cytes as to give the^ appearance of an intense interstitial inflam- mation. Even subacute nephritis is sometimes mainly interstitial, that is to say there is a persistence of the exudation of leucocytes which infiltrate the entire connective tissue of the cortex, and find their way also into the uriniferous tubules. In such cases leucocytes appear in the urine in considerable abundance, and they may even be so numerous as to give rise to the supposition that pus is present in the urine. It is, however, in very chronic cases that we find the most typical interstitial changes, resulting in the so-called granular contracted KIDNEY, or cirrhosis of the kidney. The disease begins with a formation of round cells in the cortical part of the kidney, so that a kind of granulation tissue is formed. These cells, as in the other chronic infiammations, go on to the formation of connective tissue, so that there is a great increase in the interstitial tissue of the organ. This connective tissue tends more and more to assume a fibrous condition, and to contract, so that by its cicatricial shrinking it seriously interferes with the secreting tissue and the bloodvessels. The formation of round cells does not take place homogeneously in the cortex. There are frequent areas in which it is present alternating with areas in which it is absent. It is usually most 634 DISEASES OF THE URINARY ORGAN'S. apparent at iirst near the surface of the cortex, and the cells often accumulate specially round the Malpighiau glomeruli. As time goes on, tlie increase of dense fibrous tissue produces very marked secondary results. The capsules of many of^the GLOMERULI Undergo a marked thickening, as shown in Fig. 273 a, Pig. -273. Interstitial nephritis. Sclerosis of glomerulus. ", thickenel capsule; i, condensed vessels of tuft ; (1, abundant round cells in interstitial tissue ; c, dwarfed tubules remaining. X 350. and the tuft of vessels {b) solidifies into a dense homogeneous nodule. In this Avay the glomerulus is greatly contracted (com- pare with normal glomerulus in Fig. 272, which is magnified a third less) reduced often to less than half its normal size, and com- posed of white glancing connective tissue, in which can still he recognized as a rule the thickened capsule presenting a concentric fibrous arrangement (see figure), and the more homogeneous cen- tral part composed of the condensed and impervious vessels. This SCLEROSIS of the tufts is often very striking, as the small glancing bodies attract the eye. The URINIFBROUS TUBULES unclcrgo still more striking changes. In the midst of the new-formed tissue they are to a great extent destroyed, so that large districts of cellular connective tissue may be found with no tubules at all [d in Fig. 273). "When they per- sist in the rnidst of the new-formed tissue they are greatly atro- phied (e in figare), and their epithelium is rudimentary^ in appear- ance. This great destruction of tubules in conjunction with the contraction of the connective tissue causes the remaining struct- ures to be drawn together, and the altered glomeruli are often crowded together in a very extraordinary M'ay (see Fig. 274). Where the tubules are not directly destroyed by the contracting tissue, their epithelium presents alterations somewhat similar to those mentioned as characteristic of subacute parenchymatous nephritis. There is accumulation of epithelium and debris, often Avith great distention and distortion of the tubules [b in Fig. 274), and the epithelium frequently presents fatty degeneration. It will BRIGHT S DISEASE, OR NEPHRITIS. 635 thus occur that parts where nothing but the merest traces of tu- bules are present will alternate with parts where they are greatly distended. As there is a general shrinking of the cortex the dis- tended tubules are gathered together into folds as if crowded to- wards the bases of the pyramids. Fig. 274. MiWLT :i\. Section of contracted kidney with a very low magnifying power. (Tliis figure should be compared with the next, which is similarly magnified.) a, medullary rays; b, convoluted tubules crushed together and dilated ; c, region of arterial recta3 and loops of Henle, the latter dilated and forming cysts; d, large artery between pyramid and cortex, showing en- darteritis obliterans : the space between this and surface represents the cortex, and may be compared with similar space in nest figure; e, glomeruli, closely set and contracted, they also present a white homogeneous appearance ; /, capsule. X 12. Cysts form not infrequently in the contracted kidney. There may be some visible to the naked eye, yet in most cases they are to be distinguished mainly by microscopic examination. They are round or oval in shape, and often lie in rows, especially in the pyramidal portion where they probably originate from the loops of Henle (see Fig. 274, c). These small cysts are thin-walled and contain clear fluid. They arise by obstruction of the tubules from the contraction of the interstitial tissue, which constricts them and causes the ui'ine to accumulate and distend the tubules. The glomeruli may give origin to cysts of a similar nature, the fluid accumulating in the capsule and separating the tuft of vessels from the capsule. Cysts in the kidney sometimes contain a colloid material as if from degeneration of the epithelium in the tubules 636 DISEASES OF THE UEINARY ORGANS. which have heen cut off by the constriction of the connective tissue. The great alteration and dislocation which the structures ot the kidney undergo in advanced cases may be gathered frona Fig- ^7*, which was drawn under the camera lucida with the same apparatus that used in Fig. 275, with which it should be compared, the as lettering indicating similar structures in each. m. siKf ilWIliP Section of normal kidney for comparison with preceding figure. The letters indicate similar regions, and the magnifying power is the same. X 12. The bloodvessels are .often much aifected in the contracting kidney. The vessels of the glomeruli are greatly obstructed and destroyed by the sclerosis already mentioned, and when the kidney is injected many remain empty or only show a very slight injection. The capillaries also, which normally form such an abundant net- work around the tubules, are greatly destroyed by the new-forma- tion, as appears abundantly when a colored injection of gelatine bright's disease, or nephritis. 637 with carmine is thrown into the renal arterj^ It is clear that the interference with the tufts and the capillaries must seriously obstruct the circulation in the kidney, and experiments by Thoma show that when a solution of gelatine and common salt is injected Mmm iM'i ^lliBi Endarteritis obliterans from a contracted kidney Two arteries seen in transverse section, and one in longitudinal. i<, thickened and fibrous internal coat b middle coat. X 350. into the renal artery at a fixed pressure the outflow from the veins is greatly diminished in the contracted kidney as compared with the normal. Besides this, however, the branches of the renal artery frequently show considerable alterations. There is thickening of the muscular coat probably in all cases of interstitial inflammation. But in addition to that there is, in many cases, though not at all, a marked thickening of the internal coat. This is sometimes very striking, as shown in Fig. 276, almost resulting in obliteration of the smaller arteries (endarteritis obliterans). It would even appear that this endarteritis may be an early lesion in some cases, occur- ring before the definite onset of the interstitial changes. "We have still to refer to the naked-eye appearances which are to be connected with the minute changes alreadj^ described. The most definite change is loss of bulk. If the disease has begun with enlargement, then the reduction in bulk may only bring the kidney back to the normal size. But in ordinary chronic cases it is greatly reduced in size, so that it may weigh only 3 ounces or less. The capsule is adherent to the surface, strikingly so in the very chronic cases, so that in attempting to remove it pieces of kidney tissue come with it, and it may be thickened and opaque. The proper surface of the kidney is markedly uneven, being studded with small rounded granulations. The prominent granu- lations are often somewhat pale in color, representing the parts where the tubules are to some extent preserved, while the inter- vening depressions have a reddish color. Very often the general color is red with only a pale mottling from the granulations. Cysts are often visible on the surface and on section. On section 638 DISEASES OF THE UBINAEY ORGANS. the cortex is very manifestly changed. It is much less regularly defined from the bases of the pyramids than normal, and the regular markings which we see in the cortex indicating the medul- lary rays are greatly obscured. Its color is gray or bujE", and its texture is much more dense and tough than normal. It is also greatly thinned, sometimes so that it forms merely a thin rind, perhaps only a twelfth of an inch in thickness between the bases of the pyramids and the surface. The great loss of cortex may be inferred from the comparison of Fig. 274 with Fig. 175; the arteries which run between cortex and pyramids (c c) are seen to be very little removed from the surface in the former figure as compared with the latter. We have now to consider certain very important points in the pathology of Bright's disease, in regard to which it is necessary to bear in mind the anatomical conditions already described. These points are (1) the causation of albuminuria, (2) the formation of tube-casts, and (3) the condition of the heart and other arteries throughout the body in Bright's disease, chiefly in relation to the increased arterial tension which is so important a result of chronic Bright's disease. Albuminuria is well known to be the most important clinical sign of Bright's disease. By the term is meant escape of albumen from the blood serum along with the urine. It is probable that the albumen undergoes slight modifications in its chemical reactions (Kirk), but its source is undoubtedly the serum albumen. We have to consider under what circumstances albumen makes its escape. It may perhaps be a necessary preliminary to inquire why it does not make its escape under ordinary circumstances, why the urine is not normally albuminous. We know that the other transudations from the blood contain albumen, and it seems at first sight strange that the urine does not. Some have even supposed that the urine as it is separated from the blood at the glomeruli is normally albuminous, and that in its subsequent passage through the tubules the albumen is absorbed by the epithelium just as the water is taken up and the urine concentrated. But ,this view is completely opposed to known facts. We have already seen that in chronic Bright's disease there is great destruction of the secreting epithelium, so that the glomeruli are, as it were, more near to the outlets of the tubules than normal; the urine secreted in these cases is very watery, and has, in fact, characters which are pre- sumably those of the urine as it is separated at the glomeruli. But it is exactly in this class of eases that albumen is frequently absent from the urine. Again, in acute Bright's disease the renal epithelium is unduly active, and might be supposed to be peculiarly ready to absorb albumen as nourishment, but it is in these cases in which the quantity of urine is small that albumen is peculiarly apt to be present. bkight's disease, or nephritis. 63& It might be supposed that increased blood-pressure in the vessels of the glomeruli might lead to albuminuria, but this also does not seem to be the case. AYe shall afterwards see that in chronic nephritis the blood is at an excessive pressure, the excess of urine being partly due to this, but here albumen is frequently absent. Then in active hyperaemia there is increased pressure in the vessels of the glomeruli, but the urine although excessive in quantity contains no albumen. The occurrence of albumen seems, in fact, definitely related to the structural changes in the kidney. We have seen that the inliammation in its acute form affects the glomeruli primarily, and it is probably because the structure of the glomerulus is altered that the albumen escapes. In this view of it we infer that it is due to the structure of the glomerulus that the albumen does not get through in the normal kidney, and when this structure, especially the epithelium, is tampered with then albumen passes through as in ordinary transudations. It is to be presumed that other causes besides inflammation may interfere with the epithelium of the glomeruli. In acute febrile diseases it may partake in the general parenchymatous degeneration of the organs generally, and so allow of the passage of albumen. In passive hyperpemia also its nutrition will suffer and we may have albuminuria. Tube-casts. — In cases of Bright's disease these are usually vis- ible in all parts of the tubules, in the convoluted tubules of the cortex, the loops of Henle, and the straight tubules, and they are sometimes present in veiy large numbers. Those in the convo- luted tubules and in the straight tubules of the pyramids are of larger dimensions than in the loops of Henle. For the most part the casts are translucent and homogeneous in appearance, forming HYALINE casts. But there may be epithelium or fatty debris in- closed in them, and so we have epithelial and fatty casts. Very frequently, as it lies in the tubule, a cast presents a transverse fracture, as if by shrinking it had parted in the middle. In regard to the origin of these casts, they are probably for the most part of the nature of fibrinous exudations. They are mostly present in the more acute forms of Bright's disease, and in these forms we have the conditions requisite for the formation of fibrine (see p. 93). The albumen in the urine indicates an exudation of blood-plasma containing fibrinogen, and there are also leucocytes exuded in these acute cases. The coagulation will occur the more readily if the tubules have already lost their epithelium. But, besides this origin, tube-casts may apparently be composed of altered epithelium. Epithelium may be broken down and dis- charged from the convoluted tubules and impacted into the loops of Henle, where it may form cylinders. The epithelium may also, as we have formerly seen, undergo coagulation necrosis, and even hyaline cylinders may have this origin. It will be observed, how- ever, that such casts are hardly different from the proper fibrinous ones, the fibrinogen has the same source, while the epithelium 640 DISEASES OF THE URINARY ORGANS. furnishes the fibrino-plastic substance and ferment instead of the leucocytes. It is well known that tube-casts are of common occurrence in THE URINE, being washed out of the tubules. In this connection it is to be remembered that they are composed of a soft plastic substance, and will be readily floated along, accommodating them- selves to the various bends of the tubules. Looking to the large size of the convoluted tubules as compared with the loops of Henle which immediately succeed them, it has been supposed that tube- casts often become impacted in the latter and cause obstruction to the exit of the urine. It is very doubtful, however, whether this takes place to any considerable extent, the casts are so soft and compressible that they probably pass these smaller tubules very readily. It seems likely that tube-casts are often present in much larger numbers in the kidneys after death than they have usually been during life. Just before death the blood-pressure is generally low, and the secretion of urine diminished, so that the casts are not washed out as they are during the more vigorous period of life. "We have next to consider the changes in the heart and arte- ries which are frequent concomitants of Bright's disease. Of the structural changes, the most important are hypertrophy of the left ventricle of the heart and of the walls of the vessels, while the increased tension in the arteries is the most important func- tional alteration. We have already referred to the hypertrophy of the left ven- tricle of the heart, and ascribed it to increase of the arterial ten- sion. It has been held that the hypertrophy of the heart is itself the cause of the increased arterial tension, or at least that it is a concomitant, but it is now generally acknowledged that the in- crease of the muscular tissue of the heart is due to an effort to overcome an excessive resistance in the peripheral bloodvessels. There are several difficult questions which here come up for con- sideration. One of these is whether the Ipions in the kidney are sufficient of themselves to produce increased blood-pressure in. the general systemic arterial system. If this question be answered in the negative, then it has to be decided whether the changes in the arteries throughout the body are consequent on the kidney disease, or coincident phenomena due to the irritant which produces the lesions in the kidney. Here, at the outset, it is important to remark that in these dis- cussions we have to do with chronic Bright's disease, that is to say, with cases in which interstitial changes have occurred. The changes occur most typically with the pronounced cirrhotic kidney, but they are also present with the large white kidney if the inter- stitial change be at all considerable. The hypertrophy of the heart does not occur unless the general health of the patient be suffi- ciently good to allow of the muscular substance of the heart being well nourished. Hence it is absent in cases where the presence of bbight's disease, oe nephritis. 641 amyloid disease indicates that the blood is deteriorated. It is also absent in cases where a profuse albuminuria has rendered the blood highly watery. Of late years there has been a tendency to regard the increased arterial tension as due to changes in the smaller arteries through- out the body, the changes in the kidney being merely a part of a general vascular lesion. This view has received its most systematic formulation in the descriptions by Gull and Sutton of the so-called AKTERio-CAPiLLARY FIBROSIS. Their vicw is that in the finer arte- ries and capillaries a development of fibrous tissue occurs, and that, though this may begin in the kidneys, it may also take origin in other organs. The contraction and atrophy of the kidneys, in this view, are but part and parcel of the general morbid change. We have here, then, represented a general disease of the vessels as the essential basis of chronic Bright's disease. Still more lately, Mahomed has asserted the existence of increased arterial tension with hypertrophy of the left ventricle without any considerable disease of the kidney, and he even speaks of a stage of " chronic Bright's disease without nephritis." As to the arterio-capillary fibrosis of Gull and Sutton, there are many very competent observers who, after careful investigation, have denied its existence altogether. The arteries usually chosen for investigation are those of the pia mater, and while hypertrophy of the muscular coat is generally acknowledged to be present, the thickening of the external coat is much more doubtful. It may be acknowledged that the walls of the arteries are thickened, how- ever, and the degree of thickening may be inferred from the accompanying figures (Fig. 277) from Dr. Dickinson's work on Clncm..jL. Arteries of the pia mater in case of granular kidney and in liealth. In the former the middle coat and, to some extent, the external are thickened. (Dickinson.) Albuminuria. It may quite well be, however, that these condi- tions are really the result of increased tension. If the blood is present in theiiner arteries at an increased pressure, then in order to prevent a permanent active hypersemia the muscular coat must contract more vigorously, and this will produce a hypertrophy of it. The thickening of the external coat will fortify the middle coat and assist in keeping the circulation in proper condition. This raises the important question whether there is any proof 41 642 DISEASES OF THE URINAET ORGANS. that lesions of undoubted renal origin ever produce increased arterial tension and hypertrophy of the heart. In order to answer this question it is necessary to leave out of account all cases in which the origin of the kidney disease is obscure, because it may be said that in these cases arterial changes have occurred simul- taneously elsewhere, and had a similar cause. In answer to this question various facts may be adduced. Dick- inson refers to cases in which distention of the pelvis of the kidney from stone has led to the contracted kidney with all the vascular and cardiac lesions. Then there are on record a considerable number of cases of double hydronephrosis in which extreme hyper- trophy of the left ventricle has been present. Eecently Gravitz and Israel have produced nephritis in animals by ligaturing the renal artery on one side for one and a half to two hours, and then letting the ligature loose. The consequence w-ds similar to that already referred to in regard to ligature of the arteries in the ear of the rabbit, namely, an acute inflammation. If the animal sur- vived long enough the inflammation resulted in contraction of the kidney, and in many cases there was hypertrophy of the left ven- tricle of the heart. Here is an undoubted case in which disease artificially induced in one kidney has resulted in hypertrophy of the left ventricle. When we consider that hypertrophy of the left ventricle results not only from the ordinary chronic nephritis, but also in cases which have begun acutely after scarlet fever, and where the con- dition presented is that of the large white kidney ; when we see also that a disease such as double hydronephrosis which obstructs the circulation in the two kidneys, as well as a shrinking of the kidney artificially produced, are followed by hypertrophy of the heart, then we seem forced to the conclusion that the increased arterial tension and hypertrophy are really due to the disease in the kidneys. The general statement may indeed be made that, given a disease which seriously obstructs the capillaries and smaller arteries of both kidneys, you wall have hypertrophy of the left ventricle, provided the person is in a tolerably vigorous state of health. That there is a serious obstruction of the capillaries and small arteries of the kidney in interstitial nephritis does not admit of question. The mere anatomical details indicate this. We have seen that the uriniferous tubules, with their surrounding capilla- ries, are greatly destroyed, and the glomeruli to a large extent reduced to solid clumps. In addition to this the result of injection with colored material shows that there is great impermeability of the capillaries and of the vessels of the glomeruli. This has been proved in a different way by some important observations of Thoma. He has injected at a constant pressure dilute solutions of common salt and gelatine into the renal artery in normal and con- tracted kidneys, and observed the amount which flowed out by the veins in a given time. In the ease of the contracted kidney the bright's disease, ok nepheitis. 643 outflow per minute was considerably reduced, evidently pointing to an obstruction in the finer vessels. "We have now to point out that the effect of this obstruction in the capillaries and glomeruli will be to increase the blood-pressure in the remaining arteries of the kidney, provided there is no serious obstruction in them. The endarteritis which we saw to exist in interstitial nephritis narrows the calibre to some extent, but careful measurements by Thom^ show that on the average the size of the arteries is but very slightly diminished, and that in comparison with the weight of the kidney the arteries are greatly larger than the normal. Under these circumstances, with a normal pressure in the aorta, there will be an excessive pressure in the general renal arteries and this pressure will tell on the vessels of the glomeruli which remain unobstructed. There are several facts which indicate that the pressure, in the vessels of the glomeruli which remain pervious, is very excessive. The author, in a paper published in 1875, recorded some observa- tions on injections of the kidneys in Bright's disease. When a solution of gelatine colored with carmine was injected into the renal artery, in cases of chronic Bright's disease, it was found that while the capillaries were largely uninjected, the mass ran to a considerable extent from the glomeruli into the convoluted tubules. This would indicate an excessive pressure in the vessels of the glomeruli. Then the occurrence of blood-corpuscles in the tu- bules in interstitial nephritis is not infrequent, the blood being present in the first part of the tubules and obviously coming from the glomeruli. The excessive pressure in the glomeruli is also indicated during life by the large amount of urine secreted by the contracted kidney. The increase in the general arterial tension, with the hypertrophy of the heart, doubtless has to do with this increased flow of urine, but when we consider that in cases of contracted kidney there are frequently only a few glomeruli still pervious, we may infer that a very excessive pressure must exist in their vessels in order to produce this exceedingly abundant flow. One of Thoma's observations is of considerable importance here. In his various experiments, in which gelatine and salt solu- tion were injected into the renal artery, he used a constant pressure. He desired to obtain the pressure in the renal artery, and in order to obtain this approximately, he connected the canula inserted into that artery with a manometer. He found that while in the normal kidney the pressure was 14.5, in the contracted kidney it amounted to from 15 to 15.7 cm. of mercury. There was thus, even in the main renal artery, an abnormally high pressure in the contracted kidney', and in the finer arteries the excess of pressure must have been still greater. We have now to consider what bearing these. facts have on the question of increase of the general arterial tension. It is clear that, though the obstruction in the renal circulation is suflicient to raise the pressure in the renal arteries, it alone is not enough to 644 DISEASES OF THE URINARY ORGANS. raise it in the general systemic- arteries, considering that there are such means of varying the tension in the arteries by relaxing or contracting the muscular coat. Ligature of the renal artery or extirpation of the kidney has not been found as a rule to raise the tension, and even ligature of the aorta at its bifurcation does not raise it for any considerable time. Even the view of Cohnheim cannot meet with general acceptance, at least in its original form. According to this view aneemia of an organ must be compensated either by hypersemia in another organ or else by loss of a corre- sponding amount of blood, otherwise a rise in the blood-pressure occurs. "When one kidney is excised or its artery ligatured a col- lateral hypersemia occurs in the other kidney and it undergoes compensatory hypertrophy. But when both kidneys are simul- taneously diseased, as in Bright's disease, there is no organ to compensate, and if the arteries of the kidney are to admit as much blood as normal there must be a rise of blood-pressure in them. Looking now at the matter more closely, we have seen that, in the case oi^ the contracted kidney, with a normal pressure in the general arterial system there is a greatly increased pressure in the liner renal arteries, and a considerable increase even in the main renal artery. This increase will be communicated to the general systemic circulation, as the renal arteries are in communication with the aorta. Let us suppose that it is at once compensated by a relaxation of many arteries throughout the body, and the pressure falls to normal. But even at the normal pressure there is a com- parative increase of pressure in the renal arteries which is again communicated to the general circulation. So that as soon as there is a fall of pressure there will be a fresh renewal of the excessive pressure from the renal arteries, and it Avill be again raised. But if the rise of pressure is not immediately compensated by relaxa- tion of the peripheral arteries throughout the body, then the blood passing into the renal arteries at an excessive pressure will, in the arteries of the kidney, be raised to a pressure still further above the normal for these vessels. We have seen that the arteries proximal to the glomeruli are hardly at all reduced in calibre, and with the great obstruction ahead we may suppose these arteries distended and their walls re- acting against the excessive pressure of the blood. It is as if at a part of the arterial system there were the continuous action of an apparatus engaged in raising the general pressure within this system. On these principles we can even understand how, under certain circumstances, excision of one kidnej^ may produce permanent in- crease of tension. After excision of one kidney the arteries of the other undergo a considerable relaxation and there is a collateral hyperemia. An excessive amount of blood reaches the glomeruli, and it is conceivable that these and the capillaries may "be unable to allow of the passage of this excessive blood quite freel3^ There will be thus a comparative obstruction in the glomeruli and capil- laries with increased pressure in the arteries. As a rule, this is SEPTIC INFLAMMATIONS OF THE KIDNEY. 645 not sufScient to affect the general circulation, but according to the experiments of Gravitz and Israel extirpation of one kidney does lead to hypertrophy of the heart when the other does not fully compensate. By some it may be supposed that, considering the small capacity of the renal arteries as compared with that of the entire arterial system, the effects of such a local increase of pressure must be very limited and insufficient to account for the general rise in pressure. If this argument be well founded then we have to look for some permanent obstruction in the systemic circulation, either in the arteries or in the capillaries, to explain the increased tension. From what has gone before it is manifest that such changes, if they exist, must be secondary to the lesions in the kidney, and are to be probably referred to changes in the constitution of the blood causing morbid effects in the arteries and capillaries. We may even suppose that the altered blood has greater difficulty in pass- ing through the capillaries generally than normal, and this would produce increase of tension in the arteries. SEPTIC INFLAMMATIONS OP THE KIDNEY. These are such as are induced by the presence in the organ of septic organisms. There .are two important classes of cases; in one the source of the organisms is outside the urinary organs, the septic material being brought by the blood ; in the other the source of the organisms is decomposition of the urine in the bladder, and they are propagated up from the latter. We have already seen that in pyaemia and ulcerative endo- carditis pieces of fibrine or other material may be carried to the kidneys and produce embolism there. In this way arise meta- static ABSCESSES. For the niost part the emjDoli are small and are carried to the ascending arteries or the glomeruli before they stick. Hence the abscesses are mostly in the cortical substance, although they are not infrequently seen in the pyramids along the course of the arterise rectse, and there may even be large ones taking in portions both of pyramids and cortex. The abscesses are usually elongated in the direction of the arteries, and they often project slightly from the surface when the capsule is removed. They are frequently present in considerable numbers in both kidneys. Under the microscope it can be seen that the abscesses arise by obstruction of the arteries (see Fig. 278). Where the embolism has been recent, the wall of the vessel and the tissue in the imme- diate neighborhood of the embolus present evidences of necrosis, while around there are multitudes of leucocytes occupying the interstitial tissue. In the embolus there are colonies of bacteria in the midst of remains of the transported fibrine. When the abscess has fully formed, these characters may be lost in the great multiplication of leucocytes. Besides in the arteries, colonies of 646 DISEASES OF THE URINARY ORGANS. bacteria are to be found in the vessels of the glomeruli, sometimes filling many of them out with a dark, granular mass, and also in the capillaries. It is sometimes to be seen that these colonies are present in the glomeruli and capillaries without signs of inflam- mation around. In such cases they are of recent growth and ha%'e From a section of the kidney in ulcerative endocarditis. An artery is plugged with davk material which contains micrococci. In the neighborhood of the plug the wall of the artery is necrosed. Leucocytes are infiltrating the tissue around, and extending through the vessel wall. X 90. not had time to produce inflammation by giving off irritating products. To some extent the bacteria may multiply in the glom- eruli and capillaries after death. The bacteria found in these cases, as probably in all septic inflammations, are micrococci (see Fig. 279). In cases of scarlet fever colonies of bacteria are sometimes to be seen in the capillaries and uriniferous tubules of the kidney (Fig. 280). They are not evidently accompanied by local inflam- mation, and it is not improbable that we have here to do with the specific organisms of the fever, which have been sparsely present in the kidney at the time of death — perhaps in process of excretion — and have multiplied into colonies after death. SEPTIC INFLAMMATIONS OF THE KIDNEY. 647 Pyelonephritis. — The other kind of septic inflammation arises in connection with inflammation in the bladder, ureter and pelvis of the kidney. As the inflammation of pelvis and kidney is con- tinuous, the condition is often designated pyelonephritis, v^^hieh means a combined inflammation of these tvro. The inflammation Fig. 279. Miorocooei in a capillary {b) of the kidney from a case of pyaemia. There is a tubule on either side, the nuclei of whose epithelium (a, a) are visible except in the neighborhood of the micrococci, where they seem to be destroyed. X 650. in all these parts is septic, due to the action of bacteria producing decomposition of the urine. "We shall have to study afterwards the condition of the bladder, ureters, and pelvis in these cases, but meanwhile we have to note that the organisms may propagate themselves into the kidney tissue. For the most part they enter the tubules from the pelvis of the kidney, and are to be found Pig. 280. Bacteria distending a capillary bloodvessel in a case of scarlet fever. X 350. forming the usual colonies inside the tubules, although sometimes the alterations in the tissue are such that it is ditEcult to determine whether the organisms are in the tubules or in capillary bloodves- sels, especially as the epithelium is often necrosed and overwhelmed with bacteria. 648 DISEASES OF THE' UBINAET ORGANS. Besides this regular path of entrance, the organisms may pene- ti'ate from the ureter or bladder into the loose connective tissue around, and as this is continuous with that around the kidney, they may propagate up to the capsule of the kidney, producing abscesses there (perinephric abscesses), as well as penetrating into the kidney from the surface, and forming abscesses in it. This mode of travel has been followed out by Dr. Steven in a case which came under observation here. The septic material in the tubules affects the renal epithelium most directly, causing necrosis and disintegration of it. But the dissolved products extend beyond the tubules and set up an acute inflammation of the kidney substance. The inflammation may be tolerably homogeneous, the leucocytes intiltrating the whole inter- stitial tissue, and appearing also in the uriniferous tubules. But, as a rule, there are special foci, in which it goes on to suppuration, resulting in the formation of small abscesses. When the abscesses have formed, it is usually diflicult any longer to find the bacteria. The appearance of the kidneys in such cases is usually suffi- ciently distinctive. It often happens that only one kidney is affected, the septic process having extended up one ureter and not the other. In this respect this disease differs from the preceding one, where the metastatic abscesses are always present in both kidneys. The kidney is greatly enlarged, and, generally with signs of inflammation of the pelvis, there are numerous small yellow points and abscesses in the kidney tissue. The abscesses are in the form of elongated streaks in the direction from pelvis to surface, and they are present as well in the pyramids as the cortex. They are sometimes in groups, and Ave may have such groups visible, projecting from the surface, when the capsule is removed. As a general rule the patient dies with these miliary abscesses in the kidney, but if only one kidney is involved he may survive and the process assume a further development. The abscess, by fresh invasion of bacteria, may multiply and coalesce. In this way abscesses of large size may form, finally, perhaps, involving the entire kidney out to its capsule. The abscess may even increase in size after the whole kidney is destroyed, and form a bulky tumor. The suppuration may extend beyond the kidney and lead to perinephric abscess. Perforation sometimes occurs externally, or into a neighboring loop of intestine. Sometimes these abscesses have no communication with the pelvis throughout their course. But not infrequently they are associated with and originate in suppuration in the pelvis. In that case the destruction of the renal tissue proceeds in a more regular manner out from the pelvis, following the arrangement of the calices to a large extent. In this Avay the abscess may be divided by partial septa, and the kidney may come to have an appearance like that in hydronephrosis, but in this case pus fills the cyst — pyonephrosis. With this great production of pus, or after it has attained its EETEOGEADE CHANGES IN THE KIDNEYS. 649 height, there may be production of cicatricial connective tissue, limiting the abscesses, and by its contraction producing sometimes considerable deformity. K the production of pus ceases the abscesses may dry in, and we may have the cavities filled with a pultaceous material from fatty and calcareous deposition. Some- times the cavities of the abscesses contract greatly, and there may remain simply a shrunken kidney with some cavities in which are pieces of chalky substance or pultaceous material. It will be understood that these abscesses very often do not communicate with the pelvis, and that when they do the shape of the kidney is much better retained. In the shrunken kidneys there is often considerable obliteration of the pelvis from inflammatory adhesion. Pyelitis. — This name is given to inflammation of the pelvis of the kidney, and it is very frequently associated with inflammation of the kidney itself. Even in acute Bright's disease there is often some inflammatory congestion of the pelvis of the kidney, and inflammations originating in the pelvis frequentlj' spread to the kidney proper. Inflammation of the pelvis is very frequently septic, and in that case, as we have seen, it may associate itself with a septic inflammation of the kidney, and go on to pyelone- phritis. Sometimes the inflammation of the pelvis is particularly violent, so as to assume a necrotic character, going rapidly on to suppurative nephritis, and perinephritis. Pyelitis is sometimes set up by the irritation of calculi in the pelvis. It is here for the most part a chronic inflammation. Chronic inflammation may also occur as the result of stagnation of urine from obstruction in the urinary passages. The mucous membrane is thickened, sometimes showing even irregular pro- jections, and is not infrequently incrusted with phosphates from the stagnating urine. In this way calculi may form, and it may be ditJicult to say whether an existing calculus is the cause or the effect of the inflammation. EETEOGEADE CHANGES IN THE KIDNEYS. Some of these occur, as we have seen, in the renal epithelium in Bright's disease, chiefly cloudy swelling and fatty degeneration, but we have here to do with such as are met with more inde- pendently. Simple atrophy occurs mostly as one of the phenomena of old AGE. The whole structures of the kidneys undergo diminution in size, but very often this aflfects especially the secreting epithelium of the convoluted tubules. If this be the case there may be a special shrinking of the cortex, and the kidneys may be like those of chronic Bright's disease. Sometimes also the surface is granular and the capsule adherent. Parenchymatous infiltration, or cloudy swelling, must be remembered as liable to occur in acute febrile diseases. There is 650 DISEASES OF THE URINARY ORGANS. a general enlargement of the renal epithelium with infiltration of fine granules in the midst of which fine fat-drops are scattered. (Fig. 281.) The pyramidal tubules as well as those of the cortex Cloudy swelling of renal epithelium. The cells are enlarged and filled with fine granules, in addition to which there are occasional minute oil-drops. X 350. are involved, the affection being usually homogeneous. It is important to note that this condition may produce considerable enlargement of the kidney without obvious change in its structure to the naked eye. Fatty degeneration of the renal epithelium is not infrequently present in cachectic conditions such as advanced phthisis pul- monalis, in which, however, it is often associated with amyloid disease or interstitial nephritis. In severe angemias it is also met with along with fatty degeneration of the muscular substance of the heart. It occurs, too, in acute yellow atrophy of the liver. Amyloid degeneration of the kidney develops, as we have already seen, along with amyloid disease in other organs in conse- quence of certain altered states of the blood. As in other situa- tions, so here it is chiefly the walls of the bloodvessels which are affected. Even in very early cases, in which the amount of amyloid dis- ease is slight we usually find it in two distinct and separate structures, namely, the Malpighian tufts and the ai'terise rectse of the pyramids. The vessels of the tufts, generally along with the arteries leading to them, are swelled up and hyaline. The rose color developed with methyl-violet is so striking that in sections stained with this dye it often looks as if the tufts were injected. They are also considerably enlarged, and even without the addition of iodine or methyl-violet they form very prominent, transparent and glancing clumps in the cortex. The arterise rectse run, as we have seen, in bunches, and their appearance with methyl-violet is AMYLOID DISEASE OF THE KIDNEYS. 651 that of a series of rose-eolored tubes. They are also sufficiently pronounced, as a rule, without any reagent, appearing as pearly glancing tubes. While these structures are first and chiefly involved, others usually follow. There is amyloid disease extensively present in the arteries of the cortex, the ascending and afferent arteries. Very often there is here and there a capillary of the cortex affected, and sometimes these are extensively so even in comparatively slight cases. Lastly the basement membrane of the tubules may become amyloid, chiefly in the cortical substance. (See Fig. 282.) Pig. 282. Amyloid degeneration of the basement membrane of uriniferous tubules. The thickened and translucent basement membrane is shown with the renal epithelium inside. X 350. Along with the amyloid disease of the vessel there is usually fatty degeneration of the epithelium of the tubules, apparently the result of anaemia from the obstruction of the vessels. There is also very often interstitial inflammation present, and it is frequently so great as to present a combination of the amyloid and contracted kidney. Fig. 283 shows a microscopic section of such a kidney in which the amyloid glomeruli are brought close together by contraction and destruction of the tubules. This combination of contracted and amyloid kidney is some- times met with in syphilis, the virus of which may be the cause of the interstitial inflammation. Again in phthisis pulmonalis, and in extensive suppurations from diseased bone, there may readily occur an absorption of irritating materials which are capable of setting up inflammation. The contracted amyloid kidnej^ is not accompanied by hypertrophy of the heart, the reason apparently being that, as the blood is deteriorated, the compensatory growth of muscular tissue can scarcely occur. 652 DISEASES OF THE URINAEY ORGANS. In regard to the nakbd-ete appearances, the simple amyloid kidney is enlarged, and sometimes greatly enlarged, so that the organ weighs nine or ten ounces. The surface is pale and the capsule comes off easily. On section, the cortex is seen to be thickened and pale in color. The general appearance, therefore, resembles that of the large white kidney, and doubtless many cases have been mistaken for that. But the organ in amyloid dis- ease has a lirm elastic feeling and a transparent bacony appearance on section, which is distinctive enough. The thickpale trans- parent cortex usually contrasts with the redder but still tolerably Pig. 283. ■iiS>;^»S^^5-.'.' ')ff? Amyloid and contracted kidney. The liighly amyloid and therefore greatly enlarged Malpighian tufts are shown, their capsules being somewhat thickened. The tufts are very unduly close together, owing to contraction of the intervening tissue. Between them there is round-cell tissue with remains of tubules. X 85. firm pyramidal substance, and the appearance has been somewhat aptly compared to the section of bacon ham. The name lakda- CEOUS KIDNEY is ofteu applied from the transparent appearance of the tissue. In the midst of the transparent basis, opaque yellow streaks are often visible, from the fatty degeneration of the epi- thelium. The addition of a solution of iodine to the cut surface of such a kidney brings out the affected glomeruli as brown dots, and the arterise rectse as brown streaks. If the kidney be con- tracted, the granulations on the surface show the usual transparent waxy appearance of the amyloid kidney, and on section the cortex, though greatly thinned, shows a similar condition. The amyloid substance apparently allows fluid to pass through it more readily than ordinary albuminous structures. Injection of the amyloid kidney shows that the vessels of the glomeruli and the arteries of the cortex are largely obstructed. It may well be that this leads to increased blood-pressure in the remaining arteries, but with the general narrowing of the smaller arteries this can hardly tell with much force on the glomeruli which remain per- vious. The excessive secretion of urine, like the diarrhoea which CONCEETIONS AND CALCULI IN THE KIDNEY. 653 is a prominent symptom in amyloid disease of the intestine, is probably to be accounted for by a greatly increased transudability of the vessels. CONCRETIONS AND CALCULI IN THE KIDNEY. Two very interesting forms of deposition in the tubules are met with in new-born children. In the common icterus of the new-born the biliary coloring matter (bilirubin) is excreted, as in the adult, by the kidneys, but in the new-born it very readily passes into the crystalline form, so that round or rhombic orange- colored crystals are found in the pj'ramidal tubules, sometimes in such numbers as to warrant the designation bilirubin-infarction. Similar crystals are found in the blood and tissues of the body. Uric acid is found in the tubules of new-born children, in about half the cases of those which die within the first few weeks. It is mostly in children who have breathed that the crystals are met with, but they have been observed in still-born children, although very rarely. The concretions consist of salts of uric acid (mostly urate of ammonia), and they are deposited mainly in the tubules near the apices of the pyramids, giving the appearance of opaque yellow or reddish streaks, converging to the apex of the pyramid. Under the microscope, amorphous urates are seen in the tubules, and when acetic acid is applied these dissolve and form crystals of uric acid. Urates are also deposited in the substance of the kidney in GOUT. In that disease, salts of uric acid (urate of soda) are de- posited, as we have seen, in the fibrous and cartilaginous strictures in the joints, but they may also appear in ci'ystalline masses in the kidney. These lie in the thickened connective tissue of the contracted kidnej'. Lime salts are sometimes deposited in the straight tubules of the pyramids, especially in cases where from disease of bone there is excessive absorption of lime salts and excretion of them by the urine. The appearance presented is that of white streaks usually near the apices of the pyramids. It is to be observed, however, that a deposition of urates occurring after death in the straight tubules may produce a somewhat similar appearance. Calculi are of frequent occurrence in the pelvis of the kidney. As we have seen, they may originate from chronic pyelitis, espe- cially with stagnation of urine, but they may apparently originate in the uriniferous tubules, and having passed into the pelvis grow larger there. They sometimes attain very large dimensions, moulding themselves into the shape of the pelvis and calices, so that we may have branches extending out into elongated recesses formed by dilated calices. By obstructing the flow of urine these calculi may lead to the occurrence of hydronephrosis, and as the cavity of the pelvis and calices enlarges so may the calculus. A 654 DISEASES OP THE URINARY ORGANS. small calculus will often pass into the ureter and obstruct it, in this way leading to hydronephrosis. SYPHILIS AND TITBEECULOSIS OP THE KIDNEY. Stphilitic Disease is rare in the kidney, unless it be that some cases of contracted kidney from interstitial nephritis are due to this cause. Gummata have been found in a very few cases. Tuberculosis occurs as part of a general tuberculosis or as a local disease. In acute miliary tuberculosis there are usually numerous tubercles scattered throughout the kidney. These mostly occur in groups visible to the naked eye, and they may even assume considerable dimensions. They are most abundant in the cortex, and they are prone to become caseous. Local Tuberculosis gives rise to the condition frequently called renal phthisis. The tuberculosis here is often propagated from the bladder and ureter, and may even originate in the passages of the organs of generation, as the vas deferens and vesiculfe semi- nales. On the other hand, it very often originates in the kidney, and extends down the ureter. The disease is usually of one kid- ney, or at least involves one much more than the other. It may begin in the pelvis of the kidney, in the calices, or at the apices of the papillfe, and there are the usual phenomena of tubercular ulceration. Tubercles are formed which become case- ous and break down so as to form an ulcer. Fresh tubercles form outside the ulcer which undergo the same process and produce an extension of the ulcer. There is thus a continually extending ulceration, and a continually growing irregular cavity. But the extension of the' ulcers occurs mainly into the kidney tissue, ad- vancing here apparently by reason of the less resistance of the tissue. We have already seen that the papillae are often attacked at the very first, and the ulceration extends into the pyramids, sometimes eating its way a considerable distance in. If several papillae have been attacked, then we may have several ragged pouches extending out from the pelvis like prolongations of the calices, or even the whole kidney may be converted into an irreg- ular cavity divided by partial septa. This condition is to be dis- tinguished from pyelonephrosis, chiefly by the irregular ulcerated surlace and the presence of broken-down caseous material. Under the microscope, the kidney tissue around the ulcer will be found infiltrated with round cells, in the midst of which tuber- cles in various stages of alteration will be discovered. The proper secreting tissue within this area will be pushed aside and greatly destroyed. The tubercular ulceration affects the pelvis of the kidney, and usually the ureter. Their walls are thickened and infiltrated. In the case of the ureter, the caseous material, instead of softening and discharging, may remain as a dense yellow layer lining the HTDRONEPHEOSIS. 655 greatly thickened tube. The wall of the tube shows multitudes of inflammatory round cells in the midst of which tubercles appear, but their outlines are frequently obscured by the round cells. The existence of giant-cells at intervals may indicate their presence. HYDEONEPHEOSIS. In this condition there is a dilatation of the pelvis and the calices of the kidney, as a result of obstruction of the ureter or urethra. The obstruction occurs in a considerable variety of ways. It may be congenital, and is then usually in the urethra, in which case there is dilatation of bladder, ureters, and pelves. Acquired stricture of the urethra is a less frequent cause, as it tends rather to produce dilatation and hypertrophy of the urinary bladder. A very frequent cause is obstruction of the ureter, and this itself is brought about very variously ; as by a calculus descending from the pelvis, a tumor pressing on the ureter in some part of its course, a hydatid cyst bursting into the pelvis of the kidney, even a renal artery taking an abnormal course and crossing in front of the ureter below the pelvis. Sometimes the ureter does not, as in the normal condition, form a continuation of the pelvis, but starts from it at an acute angle, passing obliquely through its wall, very much as the lower end of the ureter passes into tlae bladder. In that case, distention of the pelvis valves the upper orifice, and the valve may be only relieved when great dilatation is reached. This obstruction will be intermittent. Again, an abrupt bend in the ureter sometimes causes obstruction ; this may be from a congen- ital convolution in its course, or the ureter may turn more abruptly than usual over the brim of the bony pelvis, if the edge here be unusually sharp. Such a sharp edge may be formed by the iliac arteries at the brim of the pelvis, when the tissues which naturally pad them are atrophied, as in cases of general emaciation. It appears from this last instance that a comparatively small external pressure may obstruct the ureter, and that the urine in the pelvis and ureter is at such a low pressure as to be incapable of over- coming a comparatively slight resistance. As already seen, the result of the obstruction is dilatation of the pelvis and calices (Fig. 284), but, in addition, there is frequently a considerable destruction of renal tissue. That is to say, the calices in dilating cause atrophy, first of the papillae which project into them, and then of the pyramidal portion of the kidney, ad- vancing into the deeper parts of the organ. "We thus sometimes find the pyramids as if cut abruptly across transversely. But the condition frequently advances still further. The dilated calices increase in volume till, in the most extreme case, the kidney is replaced by a cyst which represents dilated pelvis and calices, partitions existing in it corresponding to the divisions between the calices. When this has occurred, the cyst may go on enlarg- ing so as to form a tumor of great bulk. The ureter is also 656 DISEASES OF THE URINAET ORGANS. dilated, often very greatly, so as to look like a piece of small intestine. It sometimes becomes convoluted in its course as well. It is not in every case quite apparent what circumstances deter- mine the degree of hydronephrosis. "With complete obstruction we may have a moderate dilatation, and with an apparently trivial obstruction it may be much more ^^•^^ 28*- considerable. In order to under- stand how this may be, it will be necessary to refer to the course of events when the ureter is obstructed. The ureter has been ligatured in animals and the processes observed. The iirst result is dilatation of the pelvis and of the ureter above the ligature. The tension of the urine in the ureter also rises up to a cer- tain point, which, however, is far below the blood-pressure. When this point is reached, the full extent of the distensile force derived from the secretion of the urine is attained. The secretion of urine, consisting in the transudation of a watery fluid through the vessels of the glomeruli, is due to the difference in pressure between the blood in the tufts and the fluid in the tubules, and, when the pressure in the tubules is raised, the secre- tion of urine ceases as soon as a state of equilibrium is brought about. There are, however, two elements in the problem still to be considered. In cases where the ureter has been ligatured in animals, the actual dilatation of the pelvis and calices has been comparatively slight, the state of equilibrium of tension being easily reached. In cases met with in the human subject, it appear's also that, where the obstruction is complete, the hydronephrosis is generally much less considerable than where the obstruction is incomplete or is relieved at intervals. The extreme dilatation which constitutes a complete hydronephrosis may be met with, for instance, in cases where the ureter has an abnormal insertion into the pelvis, and the urine only gets out when the dilatation has reached a certain point, or where the ureter has a sudden bend in it, and the obstruction is overcome when the dilatation is sufficient, as it were, to round out the bend; or, again, where the pressure of a tumor causes an occasional obstruction. The explanation of this seems to be that, when the obstruction is complete, the press- ure of the fluid in the dilated pelvis soon causes considerable obstruction of the renal vessels, and the power of secretion is reduced. But if at times an outlet is formed for the urine, and the pressure is suddenly reduced, there will be a relief of the Kidney in hydronephrosis The pelvis and calices are greatly dilated, and the renal tissue reduced to a thin layer. (ViRcnow.) TUilOliS OF THE KID:N'Ey. 657 vessels in the kidney and a violent hyperfemia leading to an ex- cessive secretion of urine. As a matter of fact, the sudden relief of an obstruction of the ureter has been found to be followed by an excessive secretion of urine which contained albumen. "Where then there are such repeated sudden collapses and dilatations the advance of the hydronephrosis is much more complete. At first the dilated pelvis and calices contain urine, but as the condition gets fully established the urinary constituents become absorbed, and a watery, albuminous fluid is found. Sometimes the dilatation is due to a calculus in the pelvis of the kidney, and in that ease there may be inflammation, possibly with suppuration. If pus flUs the cyst, then the condition is designated pyonephrosis. It sometimes happens that, where a prolonged obstruction has existed, the external fatty capsule of the kidney is greatly thick- ened, while only a moderate hydronephrosis exists, the external outline of the organ being not at all increased. It is not unlikely that an oedema of the capsule following the obstruction of the ureter may be the cause of this great new formation of fat by afibrding an extra supply of nourishing fluid, or perhaps by acting as a prolonged irritant. We sometimes meet with cases resembling hydronephrosis, but in which some of the cysts, representing dilated calices, do not communicate with the pelvis, but form independent cysts. This occurs when from inflammation there has been partial or complete obliteration of the pelvis. The inflammation may be caused by the presence of calculi in the pelvis, and some of the cysts may contain calculi. Again, an inflammation of the pelvis may extend to a dilated calyx, which, with others, is afterwards shut off by adhesion and obliteration of the pelvis. In that case we may have a cyst full of pus, or of the pultaceous material which we have seen to result from changes in the pus in pyonephrosis, and such cysts may be alongside others which have serous contents, these latter having been shut off before inflammation has extended ta them. TUMOES OF THE KIDNEY. Cysts are of peculiarly frequent occurrence and of several kinds. We have already seen that in the contracted kidney it is common to meet with small cysts which are the result of dilatation of the uriniferous tubules and Malpighian capsules from obstruc- tion of the tubules. Simple Cysts are frequently met with in kidneys which are otherwise perfectly normal, and the cysts themselves do not, as a rule, seriously interfere with the functions of the organ. They are larger or smaller well-formed cysts, which not infrequently project from the surface of the organ. They contain usually a clear fluid, but the fluid is sometimes colloid in character. The wall of the cyst is composed of connective tissue lined with a proper tessellated epithelium. These cysts sometimes grow to a 42 658 DISEASES OF THE URINARY ORGANS. Fig. 285. large size, and may push aside the renal tissue to a large extent. It is probable that they are of congenital origin, arising by fcetal obstruction of one or more uriuiferous tubules. The obstruction and the beginning of the cyst are congenital, as those formed in after-life do not apparently form such perfect cysts. Cystoid Degeneration of the kidneys is also a condition of congenital origin, at least in many cases, and probably in all. The whole kidney is converted into a congeries of cysts of larger and smaller size. The cysts form rounded promi- nences from the surface, and on section (Fig. 285) they are seen to replace the renal tissue. The wall of the cyst is composed of tunica propria with well- formed tessellated epithelium lining it. It contains usually a clear fluid, but the fluid may be brownish or even hemori'hagic, and it is noteworthy that it contains the constituents of the urine, often with albumen, and some- times throws down a granular precipi- tate of uric acid. Between the cysts there is very little space, but there arfe traces of remaining renal tissue, and the pelvis and ureter are present. The outline of the organ is greatly enlarged, measuring sometimes in the new-born child as much as eight inches by four. Kidneys of this kind have been fre- quently met with in new-born children, and from their size they may seriously interfere with parturition, even requir- ing evisceration before delivery can be effected. It is of importance to note that this condition often coexists with other congenital defects, such as hydrocephalus, defective urinary bladder, and horse-shoe kidney. But cystoid degeneration is also met with in the adult, and it is remarkable that the functions of the organs may be preserved for a long time, although both kidneys are composed of a congeries of cysts. The author met with a case in which the patient died at the age of forty-three. For eighteen years before his death there had been recurring attacks of hsematuria, and he at last died with ursemic symptoms. The kidnej'S were much enlarged and cystic, but with some renal tissue remaining between the cysts. The cystoid degeneration in all probability arises by obstruction of the uriniferous tubules. Virchow has found in some cases an obstruction of the papillae apparently from a foetal inflammation. The fact that these cysts contain the urinary constituents is also much in favor of the view that they arise by obstruction of the tubules. Those met with in the adult are also most probably of Cystic degeneration of kidney. The organ is shown in section, and is made up of a congeries of cysts of various sizes. (Virchow.) SECONDAKY CANCER. 659 congenital origin, although they may have grown on into adult life. In the author's case there was a congenital malformation of the aortic valve, indicating perhaps a proclivity to malformations. Primary Cancer. — This is not of very frequent occurrence, and is usually unilateral, although there have been cases of bilateral cancer. The tumor is virtually a cancerous degeneration of the organ. The kidney may be completely converted into a tumor which sometimes attains a very large size, retaining the general shape of the organ and covered by its capsule. But in some cases only a part of the kidney is involved, and in that case, while the affected part retains the general shape of the organ, although enlarged, the remaining piece of kidney has quite its normal appearance. To the naked eye, it is as if a portion of kidney were transformed ; and with the microscope it can be seen, at the margin of normal and pathological, that the tumor is advancing by a conversion of the proper kidney tissue. The epithelium of Pig. 286. A uriniferous tubule at the border of an advancing cancer. The epithelium is undergoing transformation. X 300. the tubules is multiplying so as to form the cancerous epithelium, and is becoming irregular in form (Fig. 286), while the cancerous stroma is being formed of the connective tissue of the organ. These tumors are usually very soft, but may be firmer. They present a remarkable tendency to break down the walls of the pelvis of the kidney and of the renal veins, so as to project in a fungating fashion into these. Hence arise hsematuria on the one hand and thrombosis of the veins on the other. The thrombosis may be very extensive, the clot propagating itself in various directions. Pulmonary embolism may result, and cancerous elements may be present in the obstructing material. In a case observed by the author cancer cells were found in coagula in the pulmonary artery, and in the heart. Secondary Cancers occur not infrequently when the cancerous elements have got into the systemic circulation. They form multiple tumors. Sarcoma, as a primary tumor, is rare in the kidney, but sec- ondary tumors of this kind are tolerably common. Of the primary sarcomas reference has already been made to the myo- sarcoma, which is usually a small tumor not larger than a pea, but may be of large dimensions. The lymphosarcoma sometimes forms bulky infiltrations of the kidney, and leuksemic lymphoid infiltrations may be very similar. 660 DISEASES OF THE URINARY ORGANS. FiBROMAS of small size are common in the kidney, and some have occurred of large size. Lipomas have also been met with. PARASITES. The ECHiNOcoccus is of occasional occurrence, sometimes along with a simultaneous hydatid cyst of the liver. There is here, as in the liver, a large mother-cyst surrounded by a distinct connec- tive-tissue capsule, and containing the usual daughter-cysts and broad-capsules. The cyst not infrequently bursts into the pelvis of the kidney, and the daughter-cysts and heads may be evacuated by the urine ; or rupture may occur into the pleura. Sometimes the parasite dies, and the cyst comes to be occupied by a pultaceous material in which the remains of the chitinous membranes are found (Fig. 287). The stratified character of this membrane is here, as in the case of the liver, of assistance in distinguishing the Fig. 287. Section of a stratified chitinous membrane from an old hydatid cyst of kidney. X 90. nature of the cyst, especially as all other trace of the parasite, even the booklets, may have disappeared. The kidney tissue may be considerably opened up and pushed aside by this parasite. The EiLARiA SANGUINIS occurs probably in the adult form in the lymphatic vessels of the kidney. The embryos have been met with in the parenchyma of the kidney and in the chylous urine which seems to be the result of the presence of the parasite. B.— THE UEINARY BLADDER AND URETHRA. Congenital Malformations. — These are chiefly represented by EXTROVERSION OE THE BLADDER. In tMs the anterior wall of the bladder and the corresponding portion of the abdominal wall are wanting, so that the posterior wall of the bladder fills the gap, and is continuous at its margins with the skin. The symphysis pubis is also usually incomplete, the rami ending in rounded lateral THE URINAKY BLADDER AND URETHRA. 661 prominences ; the urethra is also laid open on its superior aspect, the bladder being continued in the forna of a gutter into the urethra. There are also generally other coincident defects in the organs of generation. The abdominal viscera bulge out the wall of the bladder which forms a red convex surface in the lower part of the abdomen. On this exposed surface the openings of the ureters may be seen with the urine trickling from them. The mucous membrane is usually inflamed and bleeds readily, and as the urine escapes involuntarily the skin around is irritated and frequently excoriated. Occasionally the urachus remains open, generally from obstruc- tion in the urethra. If the patency be complete, the urine will come away from its aperture at the umbilicus. Perforation and Rupture op the Bladder. — Rupture may be produced in various ways. It may be by a direct wound, by fracture of the pelvis, by injuries during parturition. Then ulcera- tion not infrequently produces perforation, ulceration from stone on rare occasions, but most frequently the ulceration of a cancer. Lastly, the bladder may be ruptured by a blow, or by a catheter being pushed through its wall, but this will hardly occur unless its wa,ll has already been greatly thinned by dilatation or ulceration. These conditions are important chiefly in their consequences, leading as they commonly do either (1) to extravasation of urine in the surrounding tissue, or (2) to the formation of fistulous com- munications with the surface or neighboring canals. Simple extravasation of urine is not in itself serious. The normal urine is a bland fluid, and it may flow from a severed ureter or a ruptured bladder into the peritoneal cavity without producing any peritonitis, the urine being absorbed by the perito- neum and again excreted by the kidney. It is when the extrava- sated urine undergoes alkaline decomposition that it acquires excessively irritating characters. The urine being an exceedingly decomposable fluid, and being kept at the temperature of the body, it rapidly decomposes if the proper organisms flnd access to it. The products of decomposition lead to the usual violent septic inflammations associated with necrosis and suppuration. Fistulous openings from rupture of the bladder may be into the uterus or vagina, into the rectum, or on to the surface of the skin. From these iistulse the urine passes involuntarily as it reaches the bladder, there being no sphincter to retain it. They occur also as a result of perforation of the bladder from without, especially from the uterus and vagina, the cause of perforation being some- times cancer of these parts, sometimes sloughing from injury during parturition. Dilatation and Hypertrophy of the Bladder. — A simple DILATATION may occur from a sudden obstruction to the urethra, or from paralysis of the muscles concerned in emptjdng the bladder. In this way a very extreme general dilatation may result. 662 DISEASES OF THE URINARY ORGANS. Hypertrophy of the MU!^CI]LAR coat is of very frequent occur- rence as a result of some obstruction either at the neck of the bladder or in the urethra. The commonest cause is enlargement of the prostate leading to the prominence of the so-called middle lobe at the internal orifice of the urethra. The muscular coat of the bladder is in the form of bundles of muscular fibre-cells which run in special directions. The muscular coat is therefore not a homogeneous layer, but more like a network of interlacing bands. It is so at least when the bladder is distended, the bands coming closer together as the bladder contracts. When hypertrophy occurs these bundles increase greatly in size, and the internal ones raise the mucous membranejnto elongated prominences. As the bundles interlace, the result is that the internal surface of the bladder presents a network of prominent trabeculse which suggest the appearance of the internal surface of a ventricle of the heart. As these trabeculse interlace, little spaces are left between them in the form of small pouches. Sometimes these pouches undergo considerable enlargement, and we may have diverticula formed in this way, which sometimes attain to a considerable size. The diverticulum is originally formed of the mucous membrane pushed out between the thickened muscular trabeculse. When small it will be contained in the thickened wall of the bladder and emptied during micturition. But as it deepens and projects outside the wall of the bladder it becomes free of the muscular coat, and as it possesses no muscular coat of its own the effect of contraction of the bladder during micturition will be to force the urine into it, just as it is forced into the urethra. The diverticulum is liable in this case to periodical dilatation. The urine also will stagnate in it, and if decomposition occurs, then there will be inflammatory disturbances in the wall of the diverticulum. New formation of connective tissue occurs, and as this tissue is at first soft the recur- ring dilatation during micturition causes it to yield so that a con- tinuous enlargement goes on. In this way we sometimes meet with a large sac, -usually behind the bladder and communicating with it by a narrow neck (Fig. 288). The sac may be larger than the bladder itself, and it presents a somewhat thick fibrous wall with signs of recent inflammation internally. In diverticula of moderate or large size calculi are liable to form from the stagnation of the urine. Or a calculus may slip into such a pouch and escape detection with the sound. Disturbances of the Circulation in thk Bladder. — Passive Hyperemia occurs in consequence of obstruction in the veins by tumors or otherwise. Sometimes in such cases the veins of the mucous membrane undergo great dilatation and become varicose, especially in the floor of the bladder, giving rise to vesical hemor- rhoids. The dilated veins may even obstruct the orifice of the urethra, and there is sometimes hemorrhage from them. Hemorrhage from the bladder may occur also in consequence of the irritation of calculi, from tubercular ulcers, from papillary INFLAMMATION OF THE BLADDER. 663 and cancerous tumors. There may be hemorrhages from the mucous membrane in scurvy, hemorrhagic smallpox, etc. If the bleeding into the bladder be considerable the blood may coagulate, Fig. 288. Large diverticulum of urinary bladder j u, bladder with greatly thickened wall; e, prostate and prostatic urethra; &, diverticulum with fibrous wall; c, aperture between bladder and diverticulum ; d, rectum. and may be discharged with some difficulty. Or it may mix itself with the urine, and no consistent coagulum be formed. Inflammation of the Bladder. — This occurs as a consequence of various kinds of irritation. Stone may produce it, and the ex- tension of gonorrhoea, but by far the most frequent cause of it is alkaline decomposition of the urine. This decomposition of the urine is due to the growth of bacteria, and we have to consider how the bacteria find entrance. They are introduced from without, and mostly by the passage of the catheter, which, as it were, inoculates the contained urine with the micro-organisms. The question still remains, however, how it is that in the great majority of cases, although the catheter be used without taking the precaution of rendering it free of bacteria, no decomposition results. The answer to this question will be found in the kind of cases in which decomposition does occur in consequence of passing the catheter. It very readily occurs in cases of paraplegia in which the urinary bladder is paralyzed, also, although much less readily, in persons with dilatation of the bladder in consequence of enlargement of the prostate gland, or obstruction of the urethra. It occurs also readily when any amount of inflammation already exists, as from the irritation of a stone. In these cases the mucous membrane of the bladder is abnormal. In the case of spinal paralysis its muscle is paralyzed, and probably the mucous membrane is affected in its nutrition. In cases of dilatation the raucous membrane is stretched, and in inflammation it is directly altered. "We may infer, therefore, that 664 DISEASES OF THE URINAET OEGANS. while the normal mucous membrane is able to prevent the multi- plication of bacteria, like other living tissues, the altered mucous membrane is less able to do so. In addition to this, in most of the cases there is stagnation of the urine, and the organisms get leave to multiply, whereas normally they are carried out at the first micturition. Besides being carried in by the catheter, the bacteria may find other means of entrance, as by fistulous openings. It is not impossible that in the case of the short female urethra they may propagate along that passage from the vagina. The products of decomposition produce the usual inflammatory manifestations with various degrees of violence. In very acute cases there is great swelling of the mucous rnembrane, it may be with superficial or deep sloughing. In more chronic cases the mucous membrane gets thickened and very frequently becomes the seat of ulceration, so that with thickening and ulceration there is very great irregularity of the surface, sometimes with polypoid projections. The surface is occasionally incrusted with phosphates deposited by the alkaline ui'ine. The muscular coat is often thickened, especially ^vhen there is at the same time obstruction to the passage of the urine, and there is the usual trabecular ap- pearance, but obscured by the thickening of the mucous mem- brane. The bladder may undergo great contraction in conse- quence of this chronic inflammation, the new-formed tissue in the mucous membrane shrinking. The urine contains the inflammatory exudation as well as the products of decomposition. In acute cases there may be con- siderable quantities of pus. In more chronic cases the urine is thick and gelatinous like a mucous secretion. The toughness does not, however, depend on the presence of mucin, but is occasioned by the albumen of the inflammatory exudation being acted on by the alkaline salts in the urine. It is well known that the presence of pus in the urine may be detected by adding an alkali; the urine assumes a gelatinous character. The pus and other inflammatory products in the bladder are similarly acted on when the urine be- comes alkaline, and we have the viscid character referred to. Under the microscope the urine presents abundant pus-corpuscles and epithelium, with immense numbers of bacteria and crystals of phosphates. Tuberculosis of the Bladder. — This condition is usually only a part of much more extensive tuberculosis. There is often a coincident tuberculosis of the kidney and ureter, the disease having originated there and extended downwards to the bladder, or more rarely it has begun in the bladder and passed upwards. Then the vesiculse seminales, vas deferens, and testicle are not infrequently affected, and the bladder affection may be due to propagation from an organ as far off" as the testicle. The tuberculosis is in the form of ulcers of the mucous mem- brane which at first are circular, but acquire various shapes by coalescence (Fig. 289). The ulcers are mostly superficial and their TUMOES OF THE BLADDER. 665 edges very slightly raised, the latter having a pale color, so that the ulcer is surrounded by a whitish zone. The disease begins by the formation of tubercles in the mucous membrane. These break down and form ulcers, which continuously extend by the infiltra- tion of their walls and the breaking down of the infiltration. The Via. 289. • \ Tuberculosis of the bladder. Many round or Feipiginous ulcers are shown. These are superficial, but are defined by their white edges which represent recent tubercles. There are several white spots indicating tubercles which have not yet ulcerated. (Viecbow.) J general appearances of these ulcers are vevj well shown in the annexed figure from Yirchow's work on tumors. Their super- ficial character renders them liable to be overlooked. Tumors oi' the Bladder. — A few cases of fibroma and myoma have been described, but they are rare. A much commoner form is the PAPILLOMA. This is met with for the most part in the inferior parts of the bladder, and forms either a prominent mass with pro- jecting papillae or else a surface covered by villi. The tendency of these villi to bleed is an important fact. Sometimes the villi break down and an ulcer forms. In any case they discharge abundant epithelium, which is to be found in the urine, and is not to be taken as evidence of the existence of cancer. Cancer of the bladder is mostly met with in the form of villous cancer, the wall of the bladder beneath the villi being infiltrated with the cancerous structures. In some cases the structure gives way and a cancerous ulcer with raised edges is the result. There are also cancers without any villous projections of the surface. 666 DISEASES OF THE URIXAET ORGANS. The cancer may extend to neighboring structures, but it is much more common for a cancer originating in the uterus or rectum to extend into the bladder than for the reverse process to occur. We have ah-eady seen that fistulous communications occur in this way. Cysts have been found, especially in the posterior wall of the bladder. Parasites. — If we except the bacteria already referred to, para- sites in the bladder are of secondary importance. We have already seen that the echinococcus may burst into the pelvis of the kidney, and portions of the parasite will pass into the bladder. Ascarides and oxyurides have been found to wander into the bladder. The distoma haematobium, as we have seen, by the penetration of its ova may produce considerable irritation and hemorrhage. The filaria sanguinis is also found in the bladder as in the kidney and its pelvis. Sarcinse have been found in the urine by no means infrequently. From what has already been stated as to their development from the blood, their occurrence here will be understood. They are met with in cases of inflammation of the bladder. CONCRETIONS AND CALCULI IN THE BLADDER. These consist of the urinary constituents, normal or abnormal, deposited in bulk so as to form distinct smaller or larger stones. We have to consider what determines this abnormal precipitation of the urinary constituents, and we may begin by considering how these same constituents come to be precipitated in the urine after evacuation. The most frequent constituents of urinary calculi are phosphates, uric acid, and oxalate of lime. Phosphates are precipitated from alkaline urine, uric acid and oxalate of lime from acid urine. The phosphates are deposited abundantly when the urine undergoes its usual alkaline decomposition, uric acid and oxalates are thrown down in ciystals when the urine, at the time of evacuation or afterwards, becomes unduly acid, the deposition of oxalates occur- ring usually some time after the urine has been passed, so that this precipitate often, as it were, powders the surface of other deposits. Inside the bladder or the pelvis of the kidney, phosphates may be deposited because of undue alkalinity, especially in the case of alkaline decomposition of the urine. These often form an external coating on other stones when, from decomposition, the urine has become alkaline. Phosphates are also frequently deposited on foreign bodies which have found their way into the bladder, such as broken bits of catheters. In the case of uric acid and oxalate of lime it seems that some- times their precipitation is due to. an excess of them in the urine. This applies especially to the oxalates, and there are undoubtedly cases in which there is almost continually an excess of oxalate of CONCRETIONS AND CALCULI IN THE BLADDER. 667 lime in the urine (oxalic acid diathesis). But in both cases the substances are deposited from an acid urine, and in the case of uric acid it must be strongly acid. The cause of this abnormal acidity is not always clear. In some cases it may be due to excessive development of acid in the stomach. The formation of calculi of uric acid and oxalate seems always to begin in the kidney, and even in some cases in the uriniferous tubules. In these and in the pelvis it is very common to iind small concretions of uric acid, forming the so-called sand and GRAVEL, composed of aggregates of uric acid crystals, usually rounded in shape and of a brownish-red color. There may even be large concretions of uric acid in the pelvis of the kidney. In connection with the formation of the uric acid and oxalate calculi it is interesting to observe that the two bodies are often combined in one calculus, the mulberry stone especially having frequently a nucleus of uric acid, and perhaps layers of it alternating with the oxalate. It may now be convenient to give a brief description of the different forms of calculi, with an indication of the chemical methods for determining their constitution. As a rule it is con- venient to have the calculus sawn through the middle with a lapidary's saw, so that the arrangement of its layei-s may be seen and the character of its nucleus. The uric acid calculus is the most frequent. It is usually a small oval stone with small rounded prominences regularly dis- tributed over the surface. The color varies from a light fawn to a deep brick-red. It is heavy for its size, and of hard consistence. Uric acid is insoluble in water and dilute acids, but very soluble in caustic alkalies and weak solutions of alkaline carbonates. A convenient test is the murexid reaction. A fragment of the calculus is treated with a drop of strong nitric acid and heated. Efl'er- vescence occurs, and the heat is continued till a dry yellowish-red residue remains. When caustic ammonia is added a bright violet- red hue is developed. Calculi formed of urates are rare, the salts being urates of ammonia and magnesia. They are small soft concretions formed in the kidney, and are distinguished by their solubility in boiling water. They hardly deserve to be reckoned among the vesical calculi. The oxalate of lime or mulberry calculus is a very important form. Sometimes small stones are discharged as gravel, forming smooth, round, grayish balls like hemp seeds. The calculus proper is mostly of an irregularly spherical shape, tuberculated on the surface like a mulberry, and of a grayish or nearly black color. On section it is seen to be in layers, some of them generally com- posed of uric aid, which usually forms the nucleus. The calculus contains abundant organic material which holds the coloring matter, so that when the oxalate is dissolved out the organic basis often retains the shape of the calculus. Oxalate of lime is insoluble 668 DISEASES OF THE UEINAEY ORGANS. in the alkaline cai'bonates and organic acids, but soluble in nitric and hydrochloric acids. If a fragment be heated on a piece of platinum before the blow-pipe it becomes black, swells up, and leaves a bulky white ash of caustic lime which renders litmus blue. Calculi of BASIC PHOSPHATE OF LIME alouc are very rare. They form comparatively small yellowish or grayish-white stones, rather hard and smooth on the surface. The MIXED OR TRiBASic PHOSPHATic CALCULUS is Very common, at least many calculi are partly formed of these salts, although few are so entirely. The phosphates are deposited from alkaline urine as a light, bulky, white siibstance, which is commonly very brittle. The salts are insoluble in water and alkalies, but are very soluble in acids. When a fragment is heated in the blow-pipe flame, the salts melt and form a hard enamel ; hence this form is often called the FUSIBLE CALCULUS. The CARBONATE OF LIME CALCULUS is rare. It forms small, round, soft stones. The salt dissolves with effervescence on adding an acid, leaving an organic matrix of the shape of the stone. Cystine forms calculi in persons who are subjects of cystinuria. It appears as if by a congenital derangement of the nutritive pro- cesses such persons form cystine, to a certain extent probably in place of uric acid; and this peculiarity occurs frequently in several members of the same family. The urine, continuously or fre- quently, contains flat hexagonal crystals of cystine, and these may be already pi-esent in the urine at the time of evacuation, or may be deposited after the urine has stood for a time. The cystine may begin to be deposited in the uriniferous tubules so that calculi are formed in the pelvis of the kidney, or it may be deposited in the bladder. The stones are oval in shape and have a waxy con- sistence. The surface is brownish or greenish-yellow in color, and crystals can often be separated from it. The stone may be buried in a shell of phosphates. Cystine is soluble in alkalies, mineral acids, and oxalic acid. Xanthine calculi are exceedingly rare. The substance is allied to uric acid, and the stones are like those of uric acid but of a redder color. On applying the murexid test to a fragment of such a stone, it is found to dissolve in nitric acid but without effer- vescence ; the addition of ammonia gives an orange color. DISEASES OE THE URETHEA. Of these the most important are the inflammations. Gonorrhcba is a specific inflammation accompanied by redness and swelling of the mucous membrane with purulent exudation, sometimes mixed with blood. The inflammation is thus at first acute, and it may result in suppuration around the urethra, in the prostate or in the testicle, the virus in the last-mentioned case probably propagating itself along the vas deferens. There may be DISEASES OF THE URETHRA. 669 an ulceration of the mucous membrane as a consequence of the inflammation. If the acute stage subside there often remains a chronic inflam- mation, characterized mainly by a persistent mucous or muco- purulent discharge. As in other chronic catarrhs there is new formation of connective tissue, and in the male urethra this fre- quently leads to stbicturb. The new-formed connective tissue contracting narrows the tube, and sometimes quite a hard cicatri- cial tissue occupies the mucous membrane and submucous tissue. Or the thickening may be mainly in the mucous membrane which bulges inwards and forms folds which obstruct the calibre in the male urethra, or form projecting or prolapsed folds in the female. Besides gonorrhoea we may have inflammations produced by other causes. A simple catarrh may arise, especially in the female urethra, sometimes from propagation of an inflammation from neighboring parts. DISEASES OF THE FEMALE G-EFERATIVE ORGANS. Introductory. — It is hardly necessary to state that these organs are specially liable to disease from their functional relations. At the times of menstruation and pregnancy very extraordinary changes occur, some of which, although strictly physiological, border on the pathological. The anatomical relations of the internal organs of generation in the female have also to be taken carefully into account in connection with the changes in position to which the uterus is especially liable. It will be necessary to take up the individual portions of the organs of generation sepa- rately, but for purposes of convenience the malformations of the whole set of organs will be taken together. MALFORMATIONS OF THE FEMALE OEGANS. In treating of this subject it is necessary to bear in mind that the internal and external organs have no connection with each other in their origins, and so the malformations of the one are not necessarily connected with the malformations of the other. Hermaphroditism. — This name implies the union of the two sexes in the same individual. So far as the internal organs are concerned, such a condition is rendered possible by the fact that in every foetus the embryonic structures for both sexes are present at a certain period of development ; the "Wolffian ducts go to form the male organs, and the Miillerian ducts go to form the female organs. It is by the subsequent retrogression of one of these and the preponderance of the other that the sex of the child is deter- mined. It is well known that in the adult the testicle is repre- sented in the female by the parovarium, and the ovary is repre- sented in the male by the hydatid of Morgagni, which lies beside the epidydimis, while the vesicula prostatica represents the uterus. These facts indicate that we may have a true hermaphroditism, in which ovary and testicle are both represented. Cases have been recorded in which, on both sides, both of these glands have been present, one of them, however, generally ill-developed. This would form a true bilateral hermaphroditism. On the other hand, there_ may be a testicle on one side and an ovary on the other, forming a true lateral hermaphroditism. It is necessary, however, in such cases to be careful, and not to conclude that an JIALFOEMATIOKS OF THE FEMALE OEGANS. 671 organ is testis or ovary from its mere position, but to subject it to microscopic examination. It is clear that the sex of an individual is determined by the existence of the testicle on the one hand or the ovary on the other, and no case is truly bisexual unless both these glands are present. But there are cases in which, with the sex determined by the pres- ence of ovaries or testicles, the other parts present the structures belonging to different sexes. In such cases the designation pseudo- hermaphroditism is used, and, according as the ovaries or the testicles are the glands present, they are male or female. _ In cases of male pseudo-hermaphroditism, three different com- binations may be recognized, but in all there are testicles present. (1) Internal. In this case the external organs are those of the male and the testes are present, but from the prostatic urethra a canal arises which represents an elementary vagina with a uterus at its extremity, sometimes with Fallopian tubes. The uterus may be of the regular form but small, or it may be two-horned, or with one horn and a Fallopian tube. We have already seen that the vesicula prostatica is the representative in the male of the vagina and uterus, and the condition Ave are now considering is an exag- geration of that pouch due to an unusual persistence of the lower part of Mtiller's ducts. There may be all degrees of this persist- ence, but the case is not one of pseudo-hermaphroditism unless there is something that can be called a vagina and uterus, even if very rudimentary. (2) Complete male pseiiao-herinaphroditism is the condition in which, while the glands are the testes, all the remain- ing organs, both internal and external, approach to those of the female. This arises by a persistence of Miiller's ducts and an imperfect closure of the urethra. It may here be remarked that, as the external generative organs arise from the same foetal struct- ures in both sexes, they cannot really represent both the female and the male sexes in the same person. But as the male organs present, as it were, a further development, chiefly consisting in enlargement of the clitoris and closing in of the urinary passage to form a urethra, we may have, by arrest of development, more or less approach to the condition of the female organs. (3) JEx- ternal male pseudo-hermaphroditism is characterized by the external organs presenting the characters of those of the female, while the entire internal organs are those of the male. The cases are to be excluded in which there is simply an opening up of the urethra (hypospadias) from arrest of development. There must, in addi- tion, be an approach in the form of the organs to those of the female. At the same time the general form of the body is that of the female. Several such cases have been married as females, and the true sex only discovered on post-mortem examination. Female pseudo-hermaphroditism is of much more rare occur- rence than male and is susceptible of similar division. In all these forms there are ovaries, and the variations are in the other organs. There is (1) the internalin which with well-developed female organs. 672 DISEASES OF THE FEMALE GEig"ERATIVE OBGANS. both external and internal, there are male organs present in the persistence of the "Woltfian ducts, tubes passing from the par- ovarium to the uterus or vagina. This condition is excessively rare, although in ruminating animals it is a normal condition. (2) Complete female pseudo-hermaphroditism presents the male form of the external organs as well as a portion of the male internal organs, while the ovaries are the glands present. In one case the male organs were complete as far as the prostate, but from this sprang vagina, uterus, and Fallopian tubes. (3) In external female pseudo- hermaphroditism the external parts have the characters of the male while the internal have those of the female. It will be understood that an elongation of the clitoris will cause the parts to approach to those of the male, and some cases present nothing more than this. The name hermaphrodite can hardly be applied unless there is as well a type of body approaching that of the male. A case is recorded in which the real sex was only suspected when the person became pregnant. Other Malformations of the Female Organs. — -"We have DEFECT of various parts and in various forms. The ovaries may be wanting or may remain rudimentary. The uterus may be wanting, and with it the Fallopian tubes; or it may be quite rudimentary (Fig. 290), presenting perhaps a solid rudiment, or merely two diverging horns. "With this the vagina is often de- ¥m. 290. Rudimentary uterus. (Graily Hewitt, from KussMAnL.) fective. Then the uterus may remain in the adult of the Icetal or infantile form. Again, the uterus or vagina may be imperforate, or the hymen imperforate. There are also various defects of the external organs, as absence of the vulva, the vagina and urethra opening by a small aperture in the region which the vulva should occupy. The hymen may be absent, or it may present fimbriated processes sometimes so large as to project externally. A very interesting and important malformation is the double UTERUS. This arises by reason of the two Miiller's ducts uniting imperfectly, and there may be several varieties. We may have MALFORMATIONS OF THE FEMALE ORGANS. 673 the uterus forming two distinct diverging horns, and each with a separate vagina. Or the two horns may unite below to a greater or lesser extent (Fig. 291), the cavities remaining separate, and Fig. 291. uterus bicornis. The two horns, wiich are distinct above, are coalesced in the lower, part. The cavities, however, are separate, and there are two vaginas, as shown in figure. (Geaily Hewitt, from Kussmatjl.) with the vagina single or double. Or the two horns may be so united that the cavity of the neck or even a portion of the body is single. Fig. 292. Uterus unicornis. The parts are viewed from behind, and the distended bladder occupies the background. The right horn is large and runs into the Fallopian tube whose fimbriated extremity is shown. There is no proper left horn, the Fallopian tube and round ligament springing from the base of the right horn. (Graily Hewitt from, Kussmaul.) There are cases, again, in which, without any indication of separate cornua, the uterus is divided up the middle by a septum, each half with a separate cervix and sometimes a separate vagina. 43 674 DISEASES OF THE FEMALE GEXEEATIVE ORGANS. Or the division may be only partial, the body of the uterus having usually a septum, while the cervix has none. The UTERUS UNICORNIS occurs when one Mliller's duct is unde- veloped. This uterus is a long thin structure which curves to one side, while the other horn is absent or rudimentary (Fig. 292). Pregnancy may occur in all these forms of malformation, the foetus developing in one half of the uterus. Even the single horn in the case of uterus unicornis, although usually imperfectly formed, may be the seat of a developing foetus, which, however, usually causes rupture of the ill-developed organ in the third to the sixth month. A —THE UTERUS AND VAGINA. MISPLACEMENTS OE THE UTEErS. The arrangements by which the uterus is supported are of im- portance to the understanding of the misplacements of the organ. In the virgin the vagina forms a tolerably solid column, on the summit of which the uterus is supported and so prevented from descending. The vagina is also attached, by means of the pelvic fascia, to the bladder in front and the rectum behind. The uterus is further supported by its ligaments, and these assist in preventing its descent, although not so directly as the vagina. By the liga- ments passing off from its lateral aspects, the uterus is kept from inclining to one side or the other. While capable of very limited movement from above downwards and from side to side, the body of the uterus is very movable, within certain limits, from before backwards. When the bladder and rectum are full the uterus will be tolerably erect. AVhen the bladder is empty it will be inclined forward, and a certain amount of anteversion may be regarded as the normal condition with an empty bladder. Prolapse or Descent of the Uterus. — This occurs for the most part as a result of the loosening of the attachments of the organ, combined frequently with increased weight from chronic inflam- mation. It may also be produced suddenly by a severe exertion, as in raising a heavy weight. In this case the abdomen is fixed in the expiratory position, and by the pressure of the abdominal muscles and diaphragm the viscera are forced downwards and so may carry the uterus down, although here also there may have been some preliminary looseness of vagina and ligaments. JBesides increased weight of the organ itself, a tumor by its weio-ht may assist in dragging it downwards. It will be apparent that preg- nancy, with its various circumstances, will have great effect in loosening the attachments of the uterus, and prolapse is conse- quently much more frequent in married women than in virgins. The degree of descent is very various; it mav simply amount' to MISPLACEMEXTS OF THE UTERUS. 675 a lowering of the position of the uterus an inch or so, or it may be to any extent up to the presentation of it in the vulva or out- side, this latter condition being designated procidentia. The vaginia must be inverted in proportion to the descent of the uterus, and in cases where it is completely procident the vagina will form an external covering continuous with the skin around. As the uterus descends, it is held more by the posterior attach- ments to the rectum than by the anterior ones to the bladder, and there is accordingly a certain amount of retroversion along with the prolapse. The mucous membrane of the uterus is mostly in a state of catarrh in prolapse, with a profuse mucous discharge, and the organ itself is enlarged. There is often a special enlargement of the cervix which may be so elongated as to present externally without much misplacement of the body of the uterus. The mucous membrane of the inverted vagina is thickened, and its epithelium, where exposed, acquires characters like those of the epidermis. Prolapse of the Vagina. — This occurs mostly in connection with pregnancy, and seems to be caused by the walls remaining hypertrophied when they ought to undergo the regular involution. The thickened and loose vagina is thrown into folds, and these may project outside the vulva. As a consequence there may be prolapse of the uterus. Again, looking to the close connections of the vagina ■with the rectum and bladder, it is not surprising that prolapse of the former causes dragging on these latter struct- ures. The connection of the vagina with the neck of the bladder and trigonum is much more intimate than with the rectum, and so we have more frequently descent of the former than of the latter. In. this way cystocele and reotocele occur, pouches or diverticula, from these organs respectively, passing downwards with the pro- lapsed vagina. Inversion of the Uterus. — This is of very rare occurrence. It can only happen when the uterus is somewhat enlarged, or when, either by its own contraction or by the exercise of traction on its fundus, the organ is turned outside in. These conditions are best fulfilled during or after parturition, especially when the umbilical cord is pulled on while the placenta is adherent. It may also occur in connection with a tumor growing inside the uterus and attached to its internal wall. The inverted uterus projects from the vulva as a bleeding mass, the hemorrhage being frequently so severe as rapidly to cause death. If the patient survives, and the organ is not restored, inflammation results, and the uterus acquires attachments in its new situation, so that resort has sometimes to be had to amputation. Anteflexion and Retroflexion. — By these names are desig- nated the bending of the uterus on itself, the lower part forming 676 DISEASES OP THE FEMALE GENERATIVE OBGAXS. an open angle with the upper. The flexion talces place at a point corresponding with the internal os, and the explanation of this seems to be that the portion of the uterus corresponding with the cervix is, in front at least, closely attached to the wall of the bladder, the pouch of peritoneum between bladder and uterus not reaching below the level of the internal os. The cervix therefore being comparatively fixed, the rest of the uterus may be bent either forwards or backwards. Abnormal looseness of the texture of the uterus, occurring especially after delivery, renders it more liable to bend, and the flexion is always at this place. But again, if the fundus or body of the uterus acquires adhesions to the parts in front or behind, then these adhesions will tend to give it a permanent bend in their direction. There is another circum- stance which tends to make the flexions permanent; the uterine tissue is apt to waste in the concavity of the bend, and so there is all the more tendency to doubling up. All that has been stated applies equally to anteflexion and retro- flexion, and they are both of frequent occurrence, the former being usually regarded as the common form. Antevbksion AND Retroveesion. — In these conditions there is displacement of the entire organ forwards or backwards. The organ comes to lie more horizontally than usual, and the cervix and OS will be displaced backwards or forwards in the opposite direction to the fundus. These changes in position occur for the most part as a result of pregnancy, the uterus remaining loose and unable to support itself properly in some cases. Anteversion and retroversion rarely occur without a certain amount of the corresponding flexions. These flexions and versions sometimes produce serious results in the uterus itself. We have already seen that, in the concavity of the bend, the uterine tissue frequently wastes and becomes less able to retain the uterus in the upright position. Then the bend, if at all sudden, compresses the vessel, and may lead to a chronic congestion, by and by resulting in hypertrophy. Again, the curve may obstruct the canal of the cervix, thus leading to dysmenor- rhcea. The flexions and versions not infrequently predispose to prolapse. The fundus of the uterus projected backwards or for- wards is apt to irritate the bladder or rectum, and so induce re- peated straining eflbrts which tend to force the uterus down. ATKOPHY, HTPEKTROPHT, AND DILATATION OF THE UTEEUS. Atrophy. — We have already seen that the uterus may retain in adult life the undeveloped condition of that of the child. On the other hand the organ becomes smaller at the close of the period of sexual activity, a kind of physiological atrophy. There may be, however, a premature atrophy, in some cases ascribed to long-con- tinned catarrh, frequent pregnancies, pressure of tumors, etc. INFLAMMATIOiSrS OF UTEBUS AND ITS APPENDAGES. 677 Hypertrophy. — This sometimes occurs as a result of imperfect involution after the physiological enlargement of pregnancy, and in this case the increase in size is from excess in the muscular substance mainly. Hypertrophy of a similar kind occurs, though very rarely, without apparent cause. There may be hypertrophy from congestion and chronic inflammation however caused. A special hypertrophy of the cervix has been observed in many cases. It occurs as a result of imperfect involution after pregnancy, but also as a consequence of prolapse of the vagina, the cervix being dragged down and greatly elongated. With very little descent of the uterus the cervix may be so elongated as to present externally. Dilatation. — This occurs in consequence of the retention and accumulation of material in the cavity of the uterus. It results, therefore, from obstruction of the vagina or of one of the orifices of the uterus. There may be congenital closure of the external or internal os (generally the external) or imperforate hymen. When the period of puberty is reached and menstruation begins the blood accumulates in the uterus, and there may be enormous distention, the contents having a tarry or pulpy character. This condition is designated h^ematometra. The uterus may assume the size of the pregnant organ, and there is thickening of its walls, which, however, are loose. If escape is not provided artificially the uterus may actually rupture, not usually into the peritoneum, but, after the formation of adhesions, into some neighboring organ. The rupture is by a process of ulceration from within, unless external violence bursts the distended organ. There may be an acquired obstruction of the os uteri as from chronic catarrh, or even from inflammation occurring after deliv- ery. In such cases also we may have dilatation with the menstrual blood. It is more common, however, to have such closure after menstruation has permanently ceased, and as a result of chronic catarrh. In that case the catarrhal secretion may accumulate and distend the uterus. After a time the contents, which are at first mucous in character, become serous. This condition is sometimes called hydrometra. Lastly, the organ is sometimes distended with gas. This may be the result of decomposition of the accumulated fluid in hydrometra, or from decomposition of retained clots, etc.; but cases have occurred in which the cavity has been dilated with gas and assumed considerable proportions without apparent cause. INFLAMMATIONS OP THE UTEEUS AND ITS APPENDAGES, These are somewhat various, and they are differently named according to the locality specially afliected. In this way ^ve have to consider endometritis, metritis, parametritis, and perimetritis. The condition of the uterus and vagina after delivery lays them open to the occurrence of septic inflammations, and many of the conditions here have often this origin. 678 DISEASES OF THE FEJIALE GEXERATIVE ORGANS. (1) Endometeitis. — This is an inflammation of the mucous lining of the uterus. "We may have an acute inflammation set up by catching cold at a menstrual period, or by the extension of a gonorrhceal inflammation from the vagina, or in the course of an acute fever. The inflammation may go on to suppuration or even to sloughing of the mucous membrane and the formation of ulcers. Chronic Endometritis or chronic catarrh is a very frequent disease, and as a whitish discharge is a characteristic feature the condition is often called leucorrhcea. Apart from the excessive secretion the mucous membrane is apt to become thickened, and it may be thrown into folds or give origin to mucous polypi. The cervix especially is often thickened, and the os may present ulcer- ations. These ulcerations are for the most part little more than superficial excoriations, and are important chiefly as indicating the existence of catarrh of the cervix and interior of the uterus. Chronic catarrh sometimes arises without any apparent exciting cause except a general ansemia, which may be related to scrofula or chlorosis. During j^i'egnancy inflammations sometimes arise giving occasion to abortions, adhesions of the placenta, and other lesions. The catarrh may also have its origin in a tumor, a flexion, or a version of the uterus. (2) Metritis. — This name is given to inflammation of the wall of the uterus, but it hardly occurs as an independent affection, being commonly the result of extension of inflammation from the mucous membrane. Acute inflammation, even with infiltration of the muscular substance with blood, maj^ follow gonorrhoea. We may have also, from various causes, a chronic inflammation leading to induration, it may be with enlargement of the uterus. This is sometimes related to imperfect involution of the uterus after parturition, or to the various causes which bring about endometritis. The terms Perimetritis and Parametritis are used to designate in- flammations occurring in the peritoneum around the uterus (peri- metritis), and in the connective tissue around the organ between it and the peritoneum (parametritis). As, however, the whole of the peritoneum of the pelvis is apt to be involved in the one and the whole of the connective tissue of the pelvis in the other, the names pelvie peritonitis and j^dvic cellulitis are at least equally appro- priate terms. It will be understood also that with inflammation of the pelvic peritoneum, there will frequently be an inflammation of the sub-peritoneal connective tissue, so that these two conditions frequently go together. (3) Pelvic Peritonitis or Psrijietritis includes inflammations produced by all sorts of causes. Most frequentlv it is an inflam- mation of the uterus occurring after delivery or from gonorrhcea, which extends through the substance of the organ to its serous coat. Or it may be inflammation in the neighborinsi; intestine or PUERPERAL FEVER. 679 bladder that has led to it. Or a tumor in the uterus or outside it may so far irritate as to cause a chronic inflammation. In some of these cases the inflammation is acute and there is danger of a general peritonitis, but even when acute or subacute it may be circumscribed by adhesions, and an abscess may form which remains confined to the pelvis. Such an abscess may after- wards burst into the rectum, or vagina, or externally. When the inflammation is more chronic the result is adhesion of the pelvic organs, the adhesion being efiEected here as in the pleura, peri- cardium, etc., by new-formed vascular connective tissue. The adhesion and contraction sometimes lead to great matting together of the pelvic tissues and considerable fixity of the uterus, frequently with misplacement and deformity. (4) Pelvic CBLLULiTrs or Parametritis. — This consists in a sub- acute inflammation of the pelvic connective tissue, generally oc- curring after delivery, but also sometimes as a result of operations on the uterus, the introduction of pessaries, the uterine sound, etc. The inflammation is no doubt septic, being propagated through the uterine wall, being in this respect comparable with erysipelas and phlegmonous inflammations generally. The inflammation extends from the uterus, finding its way apparently by the lym- phatic spaces. There are the usual results of inflammation, but the exudation is here the most important. The spaces of the con- nective tissue get filled up with a serous exudation which may be partly fibrinous. There is in this way a great tumefaction of the subperitoneal tissue, especially of the broad ligament, but also that in front of and behind the uterus and in the pelvis as a whole. The uterus is thus, as it were, fixed in the midst of tumefied con- nective tissue, which may be felt as a firm swelling on examination per vaginam. Suppuration generally ensues, but it may do so very gradually, so that it may be long after parturition before it occurs. The pus sometimes extends a considerable distance from the neighborhood of the uterus. In this way the inflammation may extend and the suppuration follow into the iliac or even into the lumbar region. The abscesses which result open in very various localities, into the vagina, the rectum or the bladder, or at the surface in the iliac or inguinal region. In these latter cases the condition may simulate that of lumbar abscess, and mistake is the more likely as the sup- puration has perhaps occurred long after the originating cause. The pus discharged has usually the characters as of having been long retained, the corpuscles are largely fatty, and there is usually a fe'culent odor due to the proximity of the abscess to the rectum. PUERPEKAL PEVEE. We have in this case not merely a local inflammation but a general affection of the system. The disease is really a septic in- fection with or without pysemic abscesses. 680 DISEASES OF THE FEMALE GEXEEATIVE ORGAXS. We have here to deal with the entrance into the body of patho- genic bacteria. From what has gone before, especially in studying pysemia, it will be apparent that it is probably a special kind of bacterium which is concerned. It is not necessary to suppose that the organism is so special as that which causes splenic fever, or in fact that it is always the same organism. But it must be a patho- genic form capable of living and multiplying inside the body. There are probably organisms of this kind in many putrid fluids, but they are greatly multiplied in the body of a person infected with them, and are much more likely to be carried to another person from such a one. The infective material of other diseases, especially erysipelas, may be the cause of puerperal fever. Hence, although puerperal fever is not to be ranked as one of the specific fevers, we can understand how it is highly communicable, and how it occurs in groups of cases so as to simulate the epidemic form. In regard to the form of the organism, it is here as in other septic diseases a micrococcus, and in the peritonitis which is a frequent feature of a puerperal fever, there may be myriads of these organisms in the peritoneal cavity. The disease occurs in connection with the puerperal state, and in most cases there has been some wounding of the soft parts by the passage of the child. The protecting epithelium being re- moved, the bacteria may penetrate into the submucous tissue. The result is usuallj^ a very violent local inflammation, generally with a distinctly gangrenous tendency. The inflammation, with sloughing and suppuration, extends over the internal surface of the uterus, and extensive ulceration may occur. The fibrinous exudation, covering and involving the mucous membrane, may have the appearance of the diphtheritic exudation in the fauces. Sometimes, however, the local inflammation is not very consider- able. From its local seat the process extends, and results in a more general infection. The path of extension and the resulting con- ditions are various. The septic inflammation may extend along the Fallopian tubes, and septic pus find its way into the peritoneum. The resulting peritonitis is rarely localized, but we have rather a general septic peritonitis with resulting absorption of the products, and septic poisoning. In other cases the organisms get into the uterine veins, and by the ordinary process of thrombosis, etc., we may have a pyaemia having the usual characters, with suppuration in the joints and miliary abscesses in the lungs and elsewhere. The thrombosis here nearly always starts from the veins of the placental part of the uterus. In some cases there appears to be a septic infection of the blood without any local abscesses from embolism. In other cases the infiammation extends to the con- nective tissue of the pelvis. We have a violent parametritis with acute suppuration. The inflammation extends by and by to the peritoneum, and there is a violent septic peritonitis, just as when the extension is by the Fallopian tubes. The inflammation may extend through the diaphragm, and lead to a pleurisy. PERIUTEEINE HEMATOCELE. 681 It will be seen that in all these cases there is a vigorous multi- plication of the micrococci, and that there must consequently be a great formation of chemical products. An acute septic poison- ing is the result, and it is probably this which leads to the more pronounced symptoms of puerperal fever. PHLEGMASIA DOLENS. This is an affection in which great cedema occurs in one or both legs, usually as a sequel to the puerperal state. There is throm- bosis of the uterine veins, the thrombi growing, as we have seen thrombi readily do, into the iliac veins, and onwards into the femoral and its branches. The starting-point of the thrombosis is the placental surface of the uterus, and it is most apt to occur when, through imperfect contraction of the uterus, the veins are left with gaping mouths. It may be a question whether the intro- duction of septic material induces the coagulation, but in the usual absence of the general symptoms of septic poisoning, it may be doubted whether this has to do at least with the extension of the coagulation. The thrombosis may also have its starting-point apart from the puerperal state, as in tumors of the uterus, dysen- tery, disease of the rectum, typhoid fever, etc., but as causes these are exceedingly rare. "We have already seen that there may be extensive thrombosis in the veins of the leg without cedema, and so in this case oedema is by no means coincident in its occurrence with the thrombosis. As, however, the femoral vein takes by far the greater part of the blood from the leg, and as the other veins of the leg also join the iliac, and are consequently liable to thrombosis as well, there is often ultimately a very complete plugging of the veins of the leg. This results in a very marked oedema. It is not improbable that the lymphatics may be also to some extent obstructed. "We have formerly seen that thrombosis of a vein induces a chronic inflammation in its wall and around it (phlebitis and periphlebitis), so that there is often considerable adhesion of the vein to its sheath and of the sheath to the parts around. The lymphatic vessels may be affected by this adhesion and partially obstructed. The disease occurs most frequently in the left leg, and this is ascribed by some to the fact that the parts on the left side of the pelvis are more liable to bruising during delivery than those on the right. PEEIUTEEINE HEMATOCELE. This name is given to the condition in which blood accumulates around the uterus, usually in Douglas's space. The bleeding occurs nearly always at a menstrual period, and it is natural to look for the source of the blood in the processes occurring then, namely the bursting of the Graafian vesicle and bleeding from the uterine mucous membrane. If there is an obstruction to the exit 682 DISEASES OF THE FEMALE GEXEEATIVE ORGANS. of blood from the uterus it may pass backwards by the Fallopian tubes into the peritoneum. This is probably the commoner source of the hemorrhage, which also occurs from rupture of one of the veins of the uterine plexus, especially if these be varicose. At the menstrual period there is hypersemia of these veins, as of the whole vascular system of the uterus, and they may rupture. There may also be hemorrhage by rupture in extra-uterine pregnancy, but this falls to be considered afterwards. It is also stated that rupture of the vessels forming adhesions in perimetritis may cause the hemorrhage. For the most part the blood falls by gravitation into Douglas's space behind the uterus, where, as the serum is pressed out by the contracting clot and absorbed, the coagulum becomes condensed and assumes a kind of permanent position, from which the desig- nations HiEMATOMA and HEMATOCELE have been given. The uterus is pushed forward by the tumor which can be felt filling Douglas's space on vaginal examination. But the blood is probably not in every case within the perito- neum, although in most cases it is so. "When the blood escapes from a ruptured vein it may accumulate either in the peritoneum, or else in the subperitoneal connective tissue, thus forming a PARAMETRIC Or extra-peritoncal hematocele. It must be said, however, that as the blood when in the peritoneum sets up inflam- mation with multiform adhesions, it may be difficult in some cases to say whether it has been originally intra or extra-peritoneal. The blood acting as a foreign body sets up a chronic inflamma- tion. Connective tissue is produced around it forming adhesions of the neighboring loops of intestines and the ligaments of the uterus. The blood thus becomes inclosed in a capsule, and it may be slowly encroached on by the connective tissue ancl undergo a gradual absorption. After absorption there will usually remain more or less serious adhesions causing misplacement and deformity of the uterus, tubes, or ovaries. In some cases the inflammation is more acute, and suppuration occurs in and around the blood. Thus an abscess may form which bursts into the vagina, rectum, or bladder, or even into the peritoneal cavity with probably a fatal issue. EXTRA-TJTEEINE PEEG-NANCY. In this condition the foetus does not develop in the uterus, as usual. It is not necessary to describe particularly the various forms here, as these are taken up in works on midwifery. The ovum may be impregnated in the ovary itself, and, probably after the rupture of the Graafian vesicle, may remain in the ovary and develop further. In this case we have an ovarian pregnancy, which is exceedingly rare. Or the ovum may drop into the peri- toneal cavity, and having been impregnated either before or after its escape from the ovary, it may develop in the abdomen, forming an ABDOMINAL PREGNANCY. Or it may fail to reach the uterus, only SYPHILIS AND TUBBECULOSIS OF THE UTERUS. 683 travelling a certain distance along the tube — lodging at any part of the tube — tubal pregnancy — which is the commonest form. Sometimes it is in the last part of the tube so close to the uterus as to be imbedded in the substance of the organ — interstitial PREGNANCY. In all these situations the foetus develops and is surrounded by its regular membranes, the whole being usually inclosed in a cap- sule formed of connective tissue from the parts around. The placenta forms and attaches itself to some of the parts around^ although cases occur in which the placenta is in the uterus, while the foetus is in the tube or even in the abdomen. After developing for a time the cyst usually ruptures, this occurring earliest, as a rule, in the tubal cases. The result is profuse and generally fatal hemorrhage. If the hemorrhage does not cause death, peritonitis usually develops and proves fatal. But the person may even survive this, and in that case, as a general rule, the foetus softens and an abscess forms, which by and by bursts externally, dis- charging the more solid parts which have escaped the process of softening. In some cases, however, after rupture of the cyst the foetus may produce little inflammation and become quietly encap- suled, or even without rupture it may die and lie quiescent as a foreign body. In these cases the foetus shrivels and becomes mummified, being surrounded by a capsule formed of connective tissue and adherent to surrounding organs. In the mummified foetus the various tissues may be recognized years after. The cap- sule usually becomes infiltrated with lime salts, so that a kind of shell forms around the foetus. In cases of extra-uterine pregnancy the uterus enlarges, usually becoming two or three times as large as in the unimpregnated condition. SYPHILIS AND TUBEKCULOSIS OP THE UTERUS. Syphilis manifests itself in the vagina and vulva in the form of the hard chancre, which may even occur at the os uteri. It does not present in these situations any peculiarities distinguishing it from chancre of the skin elsewhere. Condylomata of consider- able size also occur in the vulva and vagina, often forming warty projections. Tuberculosis hardly occurs in the vagina; it is met with in the uterus, but is probably always secondary, being propagated from the Fallopian tubes (see p. 693). It may produce extensive de- struction of the uterus, ulcers forming, on the surface of which there tuslj be considerable caseous masses. Tubercular nodules form outside the ulcers in the mucous membrane and muscular substance, and the ulcers enlarge by caseous necrosis and breaking down of these tubercles. The ulcers thus enlarge in depth and superficies, and may involve the whole interior of the uterus, whose surface is exceedingly irregular. There is nearly always 6^4 DISEASES OF THE FEMALE GENERATIVE ORGAIS'.S. associated tuberculosis of the tubes, and sometimes of the ovaries and peritoneum. tu:mors op the utebus and vagina. Polypoid H^ematoma of the Uterus. — This form of tumor con- sists of coagulated and condensed blood, and strictly speaking is not a proper tumor. It is of importance, however, as it consider- ably resembles the much commoner myoma of the uterus. It is sometimes desiarnated the fibrinous uterine polypus. It consists Pig. 293. Polypoid hsematoma of uterus after an abortion in the second month; u, projecting part of maternal placenta and wall of uterus; b, remains of foetal placenta; c, stratified coagula around the foetal placenta. Natural size. (Virohow.) of a mass of blood-clot which by shrinking has become dense and hard. It may attain considerable dimensions, hanging it may be into the vagina. Consisting of blood-clot, it has originated in hemorrhage, but there must be some reason for the adhesion of the clot to the uterine wall. This is mostly afforded by the pla- centa which has been retained after delivery or abortion. The whole placenta may be retained, as in Fig. 293, or it may be only TUMORS OF THE UTEEUR AND VAGINA. 685 a portion. On the other hand, the rough surface, after removal of the placenta, may induce the coagulation of blood, which, if retained, may grow by fresh coagulation. As the heematoma originates in hemorrhage, it is usually associated with it through- out its course. The blood mostly escapes into the vagina, but some of it may coagulate and increase the size of the polypus. Myoma of the Uterus. — This is an exceedingly frequent form of tumor ; it is said to occur in about every tenth woman. JSTotMng can be said definitely as to the cause of the formation of these tumors, but as they grow for the most part in the form of isolated pieces of muscular tissue, it may be supposed that in the foetus there have been bits of the embryonic muscular tissue left over in the formation of the organ. The structure of the myoma has already been sufficiently de- scribed in the part devoted to this form of tumor in general (see p. 188, and Figs. 70 and 71), and we have here mainly to do with certain local peculiarities. The tumor is very often multiple, and there may be as many as fifty attached to the same uterus. We may have a single small tumor no larger than a pea, or a large growth weighing as much as fifty pounds, or a group of tumors surrounding the uterus and burying it. The SUBSEROUS myoma, originating in the external layers of the uterus, passes outwards as it gi'ow's, and pushes the peritoneal coat before it. In this way it frequently becomes pedunculated. The subserous form is often multiple, and as from its situation it is pro- tected, the tumor may grow for many years undisturbed, and reach very large dimensions. Such large myomas may be mistaken for ovarian tumors and excised as such, and this is the more likely to occur as the formation of cysts, to be referred to presently, not infrequently occurs in them. A subserous myoma has been known to part company with the uterus and become attached to a neigh- boring part of the peritoneum where it has grown. Of course the separation and the acquirement of new attachments would be gradual. The INTERSTITIAL Or INTRAPARIETAL MYOMA ariscs in the middle layers of the uterus. In its growth it involves the wall of the uterus, and may cause enormous enlargement of the organ. This form develops mostly at the fundus. The tumor and greatly enlarged uterus may form together a very bulky mass, which as a whole is liable to be mistaken for an ovarian or other tumor. The author has met with several cases in which the tumor and uterus were excised under this belief In one of these the tumors seemed to be multiple and the uterine wall could not be distin- guished from tumors, the greatly enlarged cavity of the uterus being surrounded by irregularly lobulated masses of muscular tissue. In this case it looked as if the uterus as a whole had un- dergone an irregular hypertrophy, or had grown into a massive tumor. The SUBMUCOUS myoma is the form which most frequently comes 686 DISEASEvS OF THE FEMALE GENERATIVE ORGANS. under the notice of the practitioner. Arising in the internal laj ers ■of the uterus, it readily passes inwards, pushing the mucous mem- brane before it, and from the action of gravity it tends to become pendulous. The submucous myoma, therefore, very often presents itself as a polypus (the so-called fibroid polypus), and it may have a very narrow neck. It very often arises at the fundus, and may grow to such dimensions as to fill the uterus, and hang down through the cervix into the vagina. The mucous membrane covering the tumor is subject to irritation, and there is frequently hemorrhage and ulceration, even with sloughing in some cases. The myomas present considerable varieties in the details of their structure. They vary in the proportion of muscular to fibrous tissue, as we have already seen, but the muscular bundles always occupy such a preponderating relation that when attention is paid to the arrangement of the nuclei (Fig. 294) there can never be any •doubt as to the nature of the tumor. It is true that the hardness Pig. 294. E^i4''/ - ^■^'^ "^ ^'-^wMps' '''^^ -^ , .^Miii^i^py^ ■Section of a myoma of uterus stained with carmine so as to show the multiple nuclei. X 350. of many myomas, and the glistening character of the cut surface, as well as the concentric arrangement of the trabecule as seen with the naked eye, suggest the characters of a fibrous tumor. But even in the hardest of them the muscular elements are perfectly pronounced, and the name uterine fibroid is misapplied. There is always a certain amount of connective tissue in myomas, as in all TUilOES OF THE UTEEUS AND VAGINA. 687 tumors, this tissue accompanying and supporting the bloodvessels just as in other tumors. It sometimes undergoes increase and causes INDURATION of the tumor, but the hardness of myomas is by no means always in proportion to the amount of connective tissue which they contain. (Edema occurs in myomas, especially when thej^ are polypoid, and have a narrow neck. The osdema consists in a distention of the lymphatic spaces with fluid, and it causes the tumor to be re- markably soft, so as even in some cases to resemble a mucous polypus. The formation of cysts may be a further development of the oedema, but it also occurs by breaking down of the tumor tissue. This occurs for the most part in large subserous myomas. The cysts are very irregular in form, and have no proper layer of epithelium lining them. Their origin in connection with the lymphatics is often indicated by the fact that the fluid, when with- drawn, frequently coagulates spontaneously. Fig. 295. •Cjs ■'%»^'»j^ ^itc»'; Calcareous infiltration of a myoma of the uterus. The muscular fihre-cells and a bloodTessel are infiltrated. X 350. Dilatation of the bloodvessels occurs not infrequently, and especially in the uterine polypi. This dilatation, occurring at the expense 'of the muscular tissue, may lead to a cavernous condition of the tumor, there being large irregular spaces filled with blood. In that case there may be considerable hemorrhage in the sub- stance of the tumor, as well as externally. As we have already seen, the connective tissue of the tumor may undergo calcabeous infiltration, so that the tumor has externally a hard shell, and. is divided internally by septa, between which there lies the muscular tissue. The muscular tissue itself 688 DISEASES OF THE FEMALE GENERATIVE ORGANS. also sometimes undergoes calcification, as we have seen, and as Tig. 295 shows. Cancers of the Uterus and Vagina. — In the great majority of cases the cancer begins just about the junction of the uterus and vagina, and involves both as it extends. The disease scarcely occurs before the age of thirty, and is most prevalent between forty and fifty. It appears also from the statistics of "West that, contrary to what is sometimes stated, it occurs much more fre- quently in women who have borne children than in those \\ho have not, and most frequently in those who have had more than the usual number of pregnancies; as if the disease developed most readily when the uterus is deteriorated by repeated conceptions. Fifi. -I'm;. Section of cancer of uterus under a very low power, showing mode of advance into wall of uterus; a, muscular substance of uterus, interrupted frequently (as at 6) by masses of can- cerous structure. At lower part of figure (at c) the muscular substance is still more frequently interrupted, and the tissue has quite an alveolar appearance, the muscle partly forming the stroma. X 22. There are various appearances presented by cancer of the uterus, but the commonest form is that usually described as soft or medul- lary CANCER. The individual elements are not essentially different to those in what is called epithelial cancer, but this form tends much more to infiltrate deeply, while the epithelioma is more superficial in its mode of growth. The medullary cancer begins as an infiltration of a limited part of the portio vaginalis of the TUjyiOBS OF THE UTEEUS AND VAGINA. 689 Pig, 297. cervix, and thus extends more or less round the external os. By and by the whole portio vaginalis is converted into a hard, irreg- ularly prominent tumor. At first the infiltration is confined to the mucous membrane and submucous tissue, but by degrees it spreads both deeply and laterally. It insinuates itself into the muscular substance of the uterus, separating and breaking up the muscular trabecules, which come to form a kind of rough stroma for it (see Fig. 296). It also passes into the vagina, infiltrating its wall. Very soon ulceration of the surface sets in, and in the subsequent progress there is a progressive ulceration and infiltra- tion, the former following the latter. The infiltration passes into the body of the uterus, but does not usually reach the fundus before the death of the patient. If the parts be now examined post- mortem (Fig. 297), it will be seen that an irregularly excavated ulcer occupies the adjacent parts of the uterus and vagina, rendering their respective limits inappreciable. Then outside this there is the whitish can- cerous tissue, which extends into the uterine substance some lines beyond the ulcer. This disease affects neighboring structures. There are cancerous masses usually in the ligaments and under the peritoneum. The bladder is frequently adherent to the uterine cancer, and its mucous membrane red and irregular, or else it presents cancerous nodules. The ulceration even extends sometimes into the bladder, which forms thus a com- munication with the vagina. The rectum is much less closely related to the cervix uteri than the bladder, and it is less frequently involved. Those parts of the uterus which are not engaged in the cancerous disease are inflamed, and adhe- sions are formed to the rectum and urinary bladder. Although thus extending locally, the cancer tends very little to form secon- dary tumors in the lymphatic glands, and still more seldom does it become generalized. It sometimes happens that the new formation of cancerous tissue is more vigorous than the ulceration, and in that case we may have prominent ragged masses hanging into the vagina. The microscopic examination of this form of cancer shows masses of epithelial cells, usually of considerable size, arranged irregularly in alveoli, the stroma being largely formed by the re- mains of the structures into which it has infiltrated. Epithelial Cancer is hardly to be distinctly delimited from the 44 Cancer of uterus, the parts shown in section. To the right is the urinary bladder. To the left are vagina and uterus, both of them to a large extent converted into irregular cancerous masses. (Graily Hewitt, from Mar- tin.) 690 DISEASES OF THE FEMALE GEXEBATIVE OEGANS. former, but is characterized by a more superficial outgrowth of prominent warty projections, while the deeper infiltration is slower and less in degree. The disease begins, as in the other case, in the portio vaginalis, and at first there is little more than a prominent warty outgrowth. But the warty growth increases while the base becomes infiltrated till a bulky prominence results, whose surface, consisting of masses of papilliform projections, gives the character of the CAULIFLOWER EXCRESCENCE (Fig. 298). jFig. 298. Cauliflower cinoer of posterior lip of os uteri. A probe is passed through the os, and the anterior lip in front of it is seen to be norma], while a cauliflower growth projects from the posterior. (Simpson.) This form of tumor is also liable to ulceration, and there may be a combination of ulceration with papilliform projections, although, after a time, the papillse may be destroyed and the appearances approximate to those of the other form of cancer. Under the microscope the structure here is more that of flat- celled epithelioma. The prominent papillse are covered with pave- ment epithelium, and the deeper infiltration consists of masses of flat cells. A few cases have been observed in which colloid cancer has been the form occurring in the uterus, the situation being the same as in the other more common forms. In rare cases also a cancer may arise from the fundus uteri. Mucous Polypi of the Uterus. — These are met with mainly as the result of chronic inflammation of the mucous membrane, and may spring from the body of the uterus or the cervix. Sometimes there is a general irregular prominence of the mucous membrane, but usually there are definite polypoid outgrowths. The mucous OVARIAN HEBNIA. 691 polypus may consist of a limited hypertrophy of the mucous mem- brane, the tumor being a tolerably firm one unless, as sometimes happens, it becomes soft by oedema or by the excessive develop- ment of its vessels. In this latter case we may have a tumor ap- proaching to the cavernous character. Or polypi may consist largely of glandular structures, mucous glands being apparently new formed so as to provide the tissue of the tumor. These polypi are comparatively soft, and may grow to a considerable size, especially when they become cystic. We have already seen that tumors consisting of glandular tissue are peculiarly apt to become cystic, and these form no exceptions. These larger polypi may somewhat distend the uterus. Other Tumors are seldom met with. Sarcomas are of rare occurrence, and of those recorded the majority have been spindle- celled sarcomas, although the round-celled form has also been seen. The sarcoma may develop in a myoma, or a muscular tumor in its rapid growth, soft consistence, and looser structure may assume the characters of a myosarcoma. Papillomas are also met with at the portio vaginalis, and may resemble cauliflower cancers. Parasites are rare in the uterus and vagina. Thread worms may pass over from the rectum. Bacteria are frequently met with in the vaginal secretion, and the fibres of leptothrix also occur frequently. The o'idium albicans is found in connection with thrush. "The cysticercus cellulosse has been doubtfully seen in the uterus, and the echinococcus with exceeding rarity. B.— OVARIES, FALLOPIAN TUBES, AND LIGAMENTS. OVARIAN HERNIA. In this condition one or both ovaries descend into a regular sac. The ovary sometimes forms part of the contents of an ordinary hernial sac, but there are cases in which the ovary alone is present, and its descent constitutes the primary condition. These cases are mostly inguinal and have a congenital origin, and there seems reason to infer with Englisch that they are produced by a descent of the ovary comparable with the normal descent of the testicle. "When the testicle has descended, the sac forms the tunica vaginalis, and is shut off from the peritoneum except in the case of congenital inguinal hernia when the sac remains open. In ovarian hernia the sac remains open also, so that it is like congenital inguinal hernia in the male, but generally without the presence of intestine in the sac. The sac usually appears in the upper inguinal region, but may pass into the labium majus. Like the testicle, the ovary is fixed in the wall of the sac except in so far as its Ugaments allow of a certain mobility. Hence it is usually irreducible, although. 692 DISEASES OF THE FEMALE GENERATIVE ORGANS. if the ligaments are long, they may allow of the ovary passing into the abdomen while still attached to the bottom of the sac. The ovary in its abnormal position undergoes the usual changes at the menstrual periods, and being in a confined position its en- largement may cause pain. Sometimes the condition is discovered by attention being directed to it by pain and inconvenience during menstruation. The ovary may also become the seat of tumors while in the sac or may be inflamed. Sometimes it has given rise to such inconvenience in its abnormal situation that excision has been resorted to. Besides these cases of inguinal hernia the ovary may enter a crural or an abdominal hernia, but these are not congenital and are not in the same relation to the descent of the testicle as the case just considered. INFLAMMATIONS OP THE OVARIES AND TUBES. The Fallopian Tubes sometimes inflame when the uterus is the seat of acute inflammation, but they and the ovaries are most frequently aflected with acute inflammation in connection with the puerperal conditions already considered. An acute perimetritis or a puerperal fever is very often accompanied by suppurative inflam- mation of the tubes, which may be distended with pus so as to form abscesses, their apertures having become obstructed. In addition to that the tubes are often adherent and distorted by chronic inflammations of the uterine peritoneum and of the ovaries. These chronic inflammations, by contorting and obstruct- ing the tubes, often lead to dilatation by the secretion being retained. Acute Oophoritis, or acute inflammation of the ovaries, occurs also as a sequel of the puerperal state. It may be a part of a peri- metritis, or a pelvic abscess may be associated with abscesses in the ovaries, and as these conditions rarely occur apart from pregnancy so is it with the ovarian inflammation. The ovary becomes swollen and hypersemic and suppuration usually ensues. The pus at first forms in _ elongated streaks from the hilus to the periphery, but after a time there are more distinct abscesses. The Graafian vesicles a,lso frequently become filled with pus. The peritoneal surface will also be inflamed and probably coated with a fibrinous or semi-purulent exudation. Chronic Oophoritis is a condition concerning which consider- able variety of opinion is held. We know that at each menstrual period the ovaries undergo changes which present many analogies with inflammation. They become hypersemic and enlarged, and a G-raafian vesicle bursts, leaving a wound which has to heal by granulation. At these periods then it seems likely that a chronic inflammation may be readily set up by exposure to cold, cold baths, TUBEECULOSIS OF THE OVARY AND TUBES. 693 Pig. 299. or sexual excitement. But it is not to be inferred in all cases where ovarian disturbances are thus produced that there are present the actual anatomical phenomena of inflammation. _ Chronic inflammation is manifested by an interstitial new forma- tion of connective tissue, and is comparable to cirrhosis of the liver or kidney, and like these accompanied by shrinking of the organ. The capsule is thickened, and the contracting tissue in the organ produces irregular depressions of the surface. The thickening is often peculiarly manifest around the Graafian vesicles, and this with the thickening of the capsule may prevent the vesi- cles bursting. Sometimes a ripe vesicle instead of bursting ex- ternally ruptures into the substance of the ovary, and so produces further inflamma- tory disturbance. "With these changes in the ovary itself there is usually adhesion of the capsule to the parts around, the chronic inflammation causing the forma- tion of vascular connective tissue which unites opposed surfaces. In this way there may be displacement of the ovaries. If the Graafian vesicles are prevented from bursting, the fluid which naturally exists in them may become augmented, and the vesicles thus be converted into CYSTS (Fig. 299). A limited number of small cysts may thus be formed, and it is not impossible that cysts having this origin may grow to some size, having always the character of simple cysts with serous contents. It is to be remembered that in old age the ovaries are often shrunk and the capsules thickened, but this is not to be set down as the result of chronic inflammation. Cjstio formation in ovary from dilatation of Graafian vesicles. (Virchow.) TUBEECULOSIS OF THE OVAEY AND TUBES. This aflfection occurs with exceeding rarity in the ovaries, in the form of caseous masses. It is more common in the tubes, and here the appearances are very like those in tuberculosis of the ureters. The tube is enlarged, sometimes very greatly so, and it forms varicose sausage-like convolutions (Fig. 300). Internally there is a caseous layer with, it may be, some accumulation of pus, mucus, and debris. The caseous layer is somewhat consistent, forming a continuous lining to the tube. Outside this the wall is greatly thickened, mainly by inflammatory new formation in which tubercles are to be found. Along with the tuberculosis of the tubes and the very rare tuberculosis of the ovaries there is usually similar disease else- where, such as phthisis pulmonalis, tuberculosis of the urinary organs, or tuberculosis of the peritoneum. The disease commonly affects both tubes, generally beginning near the abdominal ex- 694 DISEASES OF THE FEMALE GENERATIVE ORGANS. tremity, and often extending the whole length of the tube even into the uterus. Fig. 300 Tuberculosis of Fallopian tubes seen from behind, n, uterus; i, b, fimbriated extremities of the tubes; c, right ovary. The right tube is seen to be very greatly dilated and con- voluted. The dilatation disappears just before the uterine termination of the tube. The left tube is much less affected, being most dilated at its distal part. There was also tuber- culosis of the lungs and mesenteric glands. TUMOES OP THE OVARY. Tumors of the ovary have the peculiarity that they commonly grow to large dimensions. "We may perhaps associate this with the functions of the organ, which imply, at least in the Graafian vesicles, a remarkable fitrmative power. The cysts are the most frequent and important forms, and they are here taken first. Simple Cysts occur which afe in many respects comparable with the simple cysts which are so frequent in the kidney, and like them have no very special significance. They are produced, as already indicated, by dropsy of the Graafian vesicles, as was proved by the discovery by Eokitansky of an ovum in such a cyst. Simple cysts may be of congenital origin, having been observed in new-born children. As a general rule there are several cysts simultaneously developed, usually from ten to twenty, but one or a few may attain a preponderating size. The cysts have a distinct smooth lining membrane, with a single layer of epithelium. The contents are mostly clear serum, but from hemorrhage they may be dark, or from inflammation turbid. The enlargement of the ovary is not generally great in this form of cystic disease ; it rarely reaches the size of the fist, and still more rarely that of the head. If there are several cysts, they take shape by mutual pressure. TUMORS OF THE OVARY. 695 Colloid Ovarian Cysts. — These are of mach more frequent occurrence and vastly more important. To this class of cysts the name cystoma is properly applied, because they arise by a distinct new-formation, there being first produced a preparatory tissue, which goes right on to the formation of the cysts. These cysts form very bulky tumors, and while the tumor itself is formed of a number of larger and smaller cysts, there is always Fig. 301. Section of tissue in wall of an ovarian cyst. There is a congeries of glandular structures lined with cylindrical epitheliuru. X 1^0. in the walls of these more or less solid material which shows various stages in the process of cystic formation. It is to be noted also that the tumor, sometimes of enormous size, represents the ovary as a whole, and is not merely something added to it, the external covering of the cyst being strictly analogous to the surface of the ovary. Fig. 302. Portion of wall of colloid ovarian cyst. The lining epithelium is mostly in the form of goblet-celis. X 350. It has been said that in the wall of the cysts there is solid tissue which shows the various stages in the process. If this be examined microscopically, there will be found a glandular structure (see Fig. 301) in the form of tubular canals lined with cylindrical epi- thelium. These gland-like structures often project into cysts in a 696 DISEASES OF THE FEMALE GENERATIVE ORGANS. somewhat papilliform manner, and altogether they show a very striking power of new-formation. We have in this way glandular tubes on the one hand, and villous or papillary outgrowths on the other. The transformation into cysts is readily seen in many cases. The glandular tubes become constricted at their necks, or, the villi being pressed together, unite at their apices. The cylindrical epi- thelium presents very markedly the goblet form seen in mucous glands (Fig. 302), and it secretes a colloid material, which accumu- lates in the cavity and distends it more and more into a globular cyst. "We have therefore in the walls of the cysts, very commonly large numbers of smaller cysts which take their shape by mutual pressure as in Kg. 303. Cysts formed in this way project into the Fig. 303. Section of portion of a projection on interna] surface of ovarian cyst. It consists of a congeries of variously sized smaller cysts. X 20. already existing cysts as they grow, and may afterwards burst and become flattened out on the wall of the older cyst. As all the cysts have had a similar origin, they are lined with epithelium, whose function it is to secrete a colloid or mucoid fluid, and so the cysts, once formed, have an almost continuous tendency to increase. TUMORS OF THE OVARY. 697 There arises here the question as to the origin and significance OF THIS GLANDULAR TISSUE, and in Order to understand this we must go back to the original development of the ovary. The primordial ovary consists of a layer of epithelium on the surface of a connec- tive-tissue projection. The ova form by the penetration or redu- plication inwards of this superficial epithelium, which at first forms a series of communicating channels, which Waldeyer com- pares to a cavernous tissue. By the constriction of these canals the ova are formed, it being doubtful whether the cells of the membrana granulosa which line the Graafian vesicle are derived from this epithelium or from the connective-tissue stroma. The glandular formation in ovarian cystoma may be regarded as a pathological and exaggerated recurrence of the foetal condition. It may be that some of the glandular structure which originally forms the ova is left over from the foetal state, or else that even in adult life there may be a fresh development of the glandular structures, originating in the Graafian vesicles. The probability is that the real origin is in a persistence of the original glandular tubules. Having studied the mode of formation of the cysts, it now remains to consider the appearances of the tumors as a whole. The tumor represents an ovary, and its outer covering is the outer covering of the ovary with its layer of endothelium. The surface is usually smooth and very often free from adhesion to neigh- boring structures. In shape the tumor is more or less globular, and its external configuration may not suggest that it is com- posed of many cysts. The size of the tumor may be very great in some cases, much larger than that of the uterus at Sill time. On cutting into it there escapes from the cysts a sticky brownish or yellow fluid, which is tolerably clear unless some of the secondary changes to be presently described have occurred in it. There may be one cyst or a few of greatly pre- ponderating size, but even when at first sight there is only one larger cyst, examination will show the existence of others. These may be fiatteued out in the wall, or they may be collected here and there in clusters. Generally towards the base of the tumor, but in many cases at various places, there are solid or semi-solid masses in which cysts are in process of development in the way already described. Sometimes the glandular tissue presents a tendency to form papilliform projections into the cysts, and we may have in this way dentritic or shaggy projections in the internal wall. If, as is usually the case, there are many cysts, they take shape by mutual pressure against each other, while the general globular outline of the tumor as a whole is preserved. The cysts are liable to undergo certain changes which concern chiefiy their contents. It seems almost a normal condition in large cysts that the internal wall should present collections of cells in a state of fatty degeneration, these cells being often in many layers. The cells also pass into the fluid, so that in all ovarian fluids cells are to be found of round shape and with oil-drops in 698 DISEASES OF THE FEMALE GEXEEATIVE ORGANS. them. So universally are these present in the fluid from ovarian cysts that Dr. Drysdale has insisted on their discovery as an im- portant diagnostic indication. In addition to small cells having a few minute oil-granules in them there are usually larger ones with more oil-drops, up to large cells having the regular characters of compound granular corpuscles. The number of these fatty cells may be greatly increased, and as man}' of them in that case break down we may have a fluid which is turbid from the presence of numerous fatty cells and free oil. The fluid is also pale like a fatty emulsion, and in many cases it resembles pus in its physical characters. The change is most likely to occur in old and large cysts, but it is not infrequent in younger and smaller ones, and it is important to bear this in mind because this condition is apt to be mistaken for actual suppuration of the cysts, a much more rare occurrence. The free fat if long retained is very apt to form crystals of cholestearine, and in fact these crystals are frequently found in the fluid of cysts which otherwise are not strikingly altered. Hemorrhage occasionally occurs into the cysts, especially when there are papilliform projections. This will cause the fluid to be turbid and deep brown or red in color. There may also be masses of softened flbrine in the cavity. Sometimes, however, the fluid has a dark-brown color without hemorrhage. Inflammation of the cyst-wall is not of very frequent occurrence. There may be an acute suppurative inflammation, so that the con- tents become mixed with pus and assume more and more of the purulent character. "With this there is generally an acute inflam- mation of the surface with fibrinous exudation and adhesion to neighboring structures. If the suppuration continue, there is apt to be perforation of the pus into the abdominal cavity with re- sulting fatal peritonitis. A chronic inflammation is more common, causing adhesion of the cyst to neighboring parts, and these ad- hesions may be verj' extensive and firm. Perforation of the cyst- wall is usually the result of suppuration or gangrene, but may be a consequence of the papillary growths impinging against the wall and causing atrophy. A case "is men- tioned by Klebs in which the cyst had opened into the rectum in this way. The result is usually peritonitis, but if there has been no inflammation or gangrene, then the simple existence of the fluid in the abdominal cavity need not cause peritonitis. It is here to be remarked that the colloid ovarian cyst sometimes occurs in combination with the dermoid cyst on the one hand and cancer on the other. Dermoid Cysts. — These have already been referred to in de- scrihing the teratoma. They are of comparatively frequent occur- rence in the ovary, and considering the function of this organ it may perhaps be inferred that they arise from the ova by a kind of equivocal generation. The cysts are usually single, but there may be several in the same ovary. They grow slowly and form globular TUMORS OF THE OVARY. 69& tumors with a dense connective-tissue capsule. Internally there is an epithelial lining which, in some parts, develops a more Pro. 304. Section of wall of dermoid cyst of ovary. A congeries of sebaceous glands with open mouths {a, it, a) occupy the Avail. The cyst contained large masses of buttery material with hairs. X 20. complex structure. "We have already mentioned how sebaceous glands (Fig. 304), hairs (Fig. 305), bones and even teeth may enter into the constitution of the wall, and a buttery material with hairs and sometimes teeth form the contents. These cysts not infrequently inflame and may rupture, most frequently into the bladder and rectum, their peculiar contents being discharged and so re- vealing the nature of the case. Cancer oe the Ovary occurs mostly as a cyst with cancerous growths in its walls. There may be a combination of the colloid cyst with cancer, or a partial transformation of the former into the latter; considering the glandular Fig. 305. Hair in its follicle with sebaceous gland, from wall of same cyst as the former figure. X 20. 700 DISEASES OF THE FEMALE GENERATIVE ORGANS. character of the structures forming the colloid cyst, this cannot be regarded as very remarkable. In the ordinary colloid cyst the epithelium has a regular and normal arrangement, and we may call the tumor in that aspect an adenoma; in the cancer the epithelium is distinctly abnormal in its arrangement, being aggre- gated into indefinite masses. It may even happen that in the midst of the cancer the epithelium is undergoing metamorphosis, so that cysts are developing from it as from the more regular glandular tissue. Besides these cancerous cysts we may have a solid cancerous tumor in the ovary, presenting the usual characters, but like the ovarian tumors showing a very excessive growth. Sarcoma is a rare tumor in the ovary. Spindle-celled sarcoma is the more usual form, but round-celled sarcomas also occur. These tumors may also assume very large proportions reaching the size of the head sometimes, and they are not infrequently bilateral. Cysts are frequently present in the midst of them, and these may be simple serous cysts or they may have colloid contents. These latter may arise from glandular structures, and the disease may form a combination of the colloid cystoma and the sarcoma, or they may originate in a softening of the sarcoma- tous tissue. For the rest, fibromas and enchondromas have been met with in the ovaries on rare occasions. CYSTS OP THE BROAD LIGAMENTS— PAEOVAEIAN CYSTS. These cysts deserve special mention, especially from a practical point of view, in relation to their diagnosis from ovarian cysts. The probability is that most of the cysts of the broad ligament develop in connection with the remains of the "Wolffian body, commonly called the parovarium. The exact relations of this body are of importance in regard to the relations of the resulting cyst, and the principal points will be gathered from the accom- panying figure (Fig. 306). The parovarium lies between the two folds of the peritoneum constituting the broad ligament, and under the arch of the Fallopian tube, between the latter and the ovary. When the broad ligament is held up against the light bj' catching the Fallopian tube, the parovarium can be seen as a series of tubules, converging towards the ovary. In the figure a little tube with a knob at its end (A) represents a frequently occurring so-called hydatid, which is one of the tubules with a cystic dilatation at its extremity. This cyst may undergo slight enlargement, but it does not come practically into account as-forming the proper parovarian cyst; probably if it enlarges much its very narrow neck is apt to get broken or twisted and the cyst will then shrink. In connection with the anatomical details it is to be further noted that a firm ligament unites the CYSTS OF BROAD LIGAMENTS. 701 ovary to the upper angle of the uterus just below the origin of the Fallopian tube (see figure). The ovary is also united (see figure) to the firnbriated extremity of the Fallopian tube, so that the par- ovarium is as it were surrounded by a girdle of structures, Fallopian tube above, and continuous with it the ligament passing to the ovary, the ovary itself and the proper ovarian ligament. Pig. 300. Diagrammatic view of uterus and appendages, po, parovarium ; od, Fallopian tube ■ fi its fimbriated extremity ; o, ovary, with a ligament to the right proceeding to the fimbriated extremity, and one to the left to the uterus near the origin of the Fallopian tube. (QcAiu.) One or more of the tubes of the parovarium sometimes undergo great enlargement and constitute the parovarian cyst. Whether originating in one tube, or in more than one, the cyst is nearly always a single one, and it assumes a typically globular form. From the anatomical relations just referred to, it comes about that the cyst as it enlarges stretches the structures named as forming a girdle round it. There is frequently great elongation and dilata- tion of the Fallopian tube, which may be fourteen or fifteen inches in length, and arches over the convexity of the cyst, its fimbriated extremity being spread out on the surface, considerably exagger- ated and drawn out. One part of the fimbriated mouth is drawn downwards towards the ovary, which again is found flattened and greatly elongated on the under surface of the cyst. The ligament of the ovary is also elongated and thickened. The cyst itself is a perfectly homogeneous bladder, consisting of a connective-tissue wall, lined with epithelium. Besides this proper cyst- wall there is an external coat of peritoneum, which is quite distinct from the proper cyst-wall. So loose is the connec- tion between the two that the peritoneal coat can usually be stripped from the cyst-wall, so that two globular cysts can be separated, like the external and internal layers of a football. As the parovarium is covered on both sides with peritoneum, forming the folds of the broad ligament, we can understand how in en- larging the cyst retains a distinct peritoneal coat. The elasticity 702 DISEASES OF THE FEMALE GENERATIVE ORGANS. of the peritoneum doubtless allows of its distention, hut there must also be some increase of peritoneal tissue, as the coat is not thinner than the ordinary peritoneum. The contents of the cyst are a clear, limpid fluid, of low specific gravity, sometimes as low as 1003, and not exceeding 1008. It is very rare to find any considerable secondary alteration of the cyst- wall or its contents, but inflammation may occur. By RUPTURE or perforation (paracentesis), the cyst, being a single one, will be completely emptied, and it is noteworthy that there does not seem to be much tendency to refilling. In one examined by the author with Dr. Gairdner, the cyst, to judge from the symptoms, had been of large size, and ruptured sixteen months befoi'e death. It was found lying in the abdomen collapsed and flattened, and a cicatrix represented the point of rupture. The cyst could be blown up to the size of a child's head, but the cor- rugated appearance of the internal wall showed that it had been much larger. Here the peritoneal coat, which could be easily stripped, had contracted to suit the diminished size, and was smooth on the surface, while the proper cyst-wall, being devoid of elasticity, was thrown into ridges. It may be useful here to compare the parovarian with the ovarian cyst. The former is a single cyst, the latter never really single, although it may simulate the unilocular character; accordingly, the former is completely emptied by tapping, the latter only par- tially. The parovarian fluid is limpid, and its speciflc gravity never above 1008, while the fluid of the ovarian cyst is mostly more or less glutinous, usually brownish in color, and of a specific gravity over 1020. It is important also that the parovarian cyst, after being emptied, may not refill, while in the case of the ovarian cyst, if that which has been emptied does not refill, others grow to take its place. When the cyst itself is examined, the stretching and enormous elongation of the Fallopian tube are usually very characteristic in the parovarian cyst, although it may happen that an ovarian cyst will grow mainly from the upper part of the ovary, and so cause stretching of the tube. Then there is, in the case of the parovarian cyst, the ready separation of the peritoneal coat, whereas in the ovarian cyst there is no such isolable layer. This arises from the fact that the peritoneum over the ovary is only represented by a layer of endothelium, and not by a membrane distinct from the capsule. The ovarian cyst being the ovary itself with cystic development, it has its external covering formed simply of the exaggerated ovarian capsule. One can sometimes tear this capsule into layers for a certain distance, but no continuous sepa- ration of the coats is possible. There is, lastly, the fact that the parovarian cyst is a single simple bladder, whereas even in the case of dropsy of the Gfraafian vesicles there are several cysts, and in the common colloid cyst there are multitudes of developing cysts and solid glandular tissue. THE MAMMARY GLAND. 703 C— THE MAMMARY GLAND. Malformations of the Breast. — One or both mammae may be absent. It is more frequent, however, to have supernumerary breasts or nipples, sometimes three, four, or even five, instead of two. The supernumerary breasts are usually situated near the axillae, or under the normal ones. But there are cases in which they have had a very abnormal situation, as in the inguinal region, on the thigh, or even on the back. Thej^ are usually small in size, but in some cases they have produced milk during lactation. It may be noted that the occurrence of additional mammae is not altogether extraordinary, considering that in the lower animals the mammae are usually more in number than in man. Inflammation of the Mamma. — This rarely occurs except in con- nection with lactation. During this process, and especially at its commencement, the structures in the mamma are the seat of very active processes ; there are hypersemia and an active secretion of milk. Under these circumstances inflammation is more readily induced than usual. It may happen that contraction of the arteries from accidental circumstances, such as exposure to cold, may induce inflammation. We know that an inflammation may be induced in animals by ligaturing an artery for a time and then loosening it, and we may believe that partial contractions of the arteries may act in this way. Even a general irritation of the vaso-motor centre by reflex action, when the skin is exposed to cold, may, in the case of the highly excited vascular system of the mamma at the commencement of lactation, induce inflammation. Again, disease of the nipples, such as cracks and ulcers, often induces inflammation in the breasts. We may believe that here the irritant which has caused the lesion in the nipple may extend along the tubes and cause inflammation in the mamma. At the time of pubertj', the female breast undergoes a special develop- ment, and is also in an active state, and at this period inflamma- tions are also apt to be induced. Th"e inflammation is usually an exceedingly acute one, and is accompanied by exudation, the interstitial tissue being packed with leucocytes and the breast hardened. This hardening is often local, as the inflammation is usually to some extent limited to certain parts of the breast. But very often the exudation of leuco- cytes goes on to actual suppuration and the formation of abscess, sometimes with sloughing of the tissue. The abscess so formed may have extensive ramifications in the mamma, especially if the pus does not get vent externally. After evacuation the cavity fills with granulation cells, and finally closes, and a cicatrix is formed. A CHRONIC INFLAMMATION resulting, after the usual manner of interstitial inflammation, in induration of the organ, has been described, but is not of frequent occurrence. 704 DISEASES OF THE FEMALE GENERATIVE ORGANS. TUMOES OP THE MAMMA. Adenoma of the Mamma. — This form of tumor is of somewhat common occurrence. It is met with chiefly as an isolated tumor, either in the midst of the gland or in its neighborhood. There is preserved in the museum of the Western Infirmary a tumor the Section of an adenoma of mamma. Glandular structures of well-formed outline are shown in the midst of fibrous tissue. X 90. situation of which was behind the gland, which had to be cut through in order to remove it. The tumor was thus almost like a supernumerary mamma. Tumors of this kind are surrounded by a distinct connective-tissue capsule which isolates them from the gland or from the neighboring tissue. Under the microscope the tumor (see Fig. 307) presents a per- fectly regular glandular structure, with acini and ducts, but of course without any external communication. Between the gland- ular elements there is connective tissue which is sparsely nucleated like that of the normal gland. Adenoid Sarcoma and Sarcoma. — The adenoid sarcoma is a form of tumor in which there is glandular tissue with sarcoma- tous tissue between the glandular structures. Doubts have been expressed as to the actual new-formation of gland-tissue in tumors presenting sarcomatous elements, but as we meet with tumors pre- senting all gradations between the simple adenomas and the typical sarcomas, we can hardly refuse to believe that glandular new-formation does take place in the cases under consideration. "When much glandular tissue is present, as in Fig. 308, the tumor is usually isolated, and partially separated from the surrounding TUilORS OF THE MAMMA. 705 mammary tissue, and there is sometimes more than one distinct tumor present. The glandular structures are as in the adenoma, acini and smaller tubules, but they do not conform so strictly in their arrangement to the type of the normal mamma. The sarcomatous tissue evidently arises from the interstitial tissue, and is usually spindle- TiG. 308 Section of an adenoid sarcoma of the mamma. Grlaudular structures are shown with spindle-cell tissue between. X 90. celled. In regard to this tissue great varieties are presented. The cells may be comparatively limited in number, so that the tissue is a connective tissue with an excess of spindle-cells. Prom this we have all gradations up to a complete spindle-celled tissue separating the glandular elements. From cases in which there is a new formation both of glandular and sarcomatous tissue, it is difficult to distinguish those in which the new formation is entirely sarcomatous, and any glandular tissue is simply the remains of the normal mammary structure. Tumors are of frequent occurrence in the mamma, in which it may be said at least that the glandular element is very subordinate, and these tumors warrant the designation of true sarcoma. Such tumors are not usually isolated or defined from the neigh- boring mammary tissue. They sometimes involve a limited part of the mamma, that portion undergoing what may almost be called a sarcomatous degeneration. That is to say, its interstitial tissue becomes converted into spindle or round-celled tissue, while its glandular structures are variously contorted. But not infrequently the disease affects the whole mamma ; there is a diffuse sarcoma- tous growth. In that case the mamma is greatly enlarged, and may attain a weight of ten or twenty pounds. The tumor may involve the skin and ulceration may occur. There may thus be a deep ulcer in the midst of a massive tumor. 45 706 DISEASES OF THE FEMALE GENERATIVE ORGANS. Under the microscope the sarcomatous elements are seen most prominently, while the glandular elements are somewhat sparse or entirely absent; but here and there a duct lined with epithelium or a misshapen acinus may be found. For the most part the glandular structures seem to be drawn out, so that tubes are much more frequent than acini. In these sarcomas cysts are very frequent, and sometimes the cystic formation is so marked that the name cystosaecoma is given. The cysts take origin in the glandular structures. Perhaps because of obstruction of the latter they may dilate and form distinct cavi- ties in the midst of the sarcomatous tissue. A minor degree of this is very common, glandular structure being represented by elongated spaces lined with epithelium, which is mostly cylindrical (see Fig. 309). Even in these incipient cysts we can often see that Fig. 309. Semidiagrammatic view of dilated glandular spaces in a cystosarcoma of the mamma. The spaces are lined with cylindrical epithelium. The tendency to intracystic growth is shown, especially in the upper one. These were drawn under the camera lucida, so that the outlines are correct. X 62. the sarcomatous tissue is, as it were, pushing its way into them (see figure), a kind of papillary growth presenting itself in the wall of the space, the growth being covered with epithelium like that lining the space. Sometimes this intracystic growth is very marked, and we may have large cysts filled with ingrowing masses of sarcoma. In fact, it sometimes appears as if the main growth of the tumor were into greatly dilated gland-ducts. It need hardly be added that the sarcomas and adenoid sarcomas present malignant characters, chiefly in the form of a tendency to local recurrence. K an adenoid sarcoma is excised, it will prob- TUMOES OF THE MAMMA. 707 ably recur as a pure sarcoma, but the author has seen, in a case ot recurrence, an arrangement of the spindle-cells as if around dis- tinct centres, which suggested glandular structure. These tumors, oh recurrence, also become softer, and the cells more loose. There are also sarcomas in the mamma which are not related to the glandular structure either directly or indirectly. These are Fig. 310. Section of cartilaginous part of a tumor of mamma which contained besides spindle-celled and fibrous tissue. X 200. usually spindle-celled sarcomas, but they may be considerably mixed, cartilage even occurring as part of their structure, as in the case from which Pig. 310 was taken. Cancer of the Mamma. — According to what has been stated in the general section of this work, we have in cancer an aberrant growth of epithelium as the foundation process, and in the first place we may consider the finer details of the overgrowth. In the more ordinary form of cancer of the breast the process begins in the glandular acini. As a rule, it is a chronic process, and, along with new formation of epithelium in the acini, there is formation of round cells in the connective tissue around. The epithelium of the acini grows through the basement membrane, forming pene- trating processes, and the round cells develop connective tissue which frequently causes great contraction of the tumor (Scirrhus). It is as if the epithelium, growing outwards, acted as an irritant, causing inflammatory new-formation in the interstitial tissue of the gland. Where the case is very chronic, the connective-tissue for- mation may be very pronounced, but when more acute the epithe- lial elements preponderate. Cancers which take origin in the glandular acini may be called parenchymatous cancers. But cancers may take origin rather in the ducts of the gland, forming a class called duct cancers (Thin). These very often begin in the large ducts in or near the nipple. In this case the growing epithelium often distends the ducts, forming cavities which are sometimes lined with cylindrical epithelium, with more irregular epithelium inside. Such dilated ducts may even have the appearance of cysts, so that the tumor may appear cystic. This process in the ducts is also associated with irritation of the 708 DISEASES OF THE FEMALE GENERATIVE ORGANS. surrounding connective tissue, so that there are round cells and new-formed connective tissue. The special characters of duct cancer are usually most manifest in the parts near the nipple, where it generally begins. On passing into the substance of the gland the appearances are more like those of the other form. Duct cancer is sometimes associated with the condition known as Paget's DISEASE or ECZEMA OF THE NIPPLE. Eczema, as indicated in the section on Diseases of the Skin, is an inflammation of the skin, in which both the epidermis and the superficial layers of the cutis are engaged. In case of duct cancer, the affection of the ducts seems to induce an inflammation of the skin of the nipple and parts around, characterized by the usual formation of round-cell tissue. The superficial or papillary region of the skin may then be replaced almost entirely by round cells with nests of epithelium in their midst, and the condition is somewhat like that of a granulating wound. The epithelium of the surface takes little part in the process, and it may be lost, so that the granulation tissue is exposed. As the cancerous process begins commonly in the nipple, this con- dition of eczema may be a very early one, and may precede, it may be for many months, the actual appearance of a tumor in the mamma. It is to be remembered also that a simple eczema may occur in the nipple, due to an ordinary irritant. In connection with this subject, the views recently enunciated by Creighton deserve notice. According to the observations of this author, there is, during the process of evolution of the gland preparatory to lactation, a great new formation of glandular epithelium, which gradually, after a number of generations, assumes the condition in which it forms milk. In the involution after lactation there is a reverse process, successive generations of epithelium being produced till it assumes the resting state. All these stages between the resting state and the milk-producing state are characterized by the production of epithelium which is in itself useless, and has to be disposed of It is disposed of by the lymphatic system, into which the cells pass, and are carried to the lymphatic glands. Creighton regards cancer as the exaggera- tion of a condition comparable to one or other of the stages of evolution or involution, and therefore primarily a disorder of function. There is an excessive production of epithelium, which bursts through the basement membrane and is grouped outside the acini. In like manner the cells pass to the lymphatic glands, where they give rise to secondary tumors, not by themselves growing and proliferating, but by inducing the lymphatic gland- ular tissue to assume the characters of cancerous tissue. These views are somewhat theoretical, and stand in need of confirmation. "We have now to consider cancer of the mamma according to the more ordinary division into its several forms. The commonest form of cancer is scirrhus. The description of scirrhous cancer in the general part of this work is chiefly based on scirrhus of the mamma, and need not be repeated here. It TUMOES OF THE MAMMA. 709 will be remembered that the epithelial masses often form elongated processes (Fig. 311) in the midst of an excessive stroma composed of dense contracting fibrous tissue. The cells are often atrophied, so that in some parts of the tumor there is little beyond dense connective tissue. The cancer commonly forms rather a limited infiltration of a part of the gland than a proper tumor, and as the tissue contracts there is commonly an actual diminution of bulk with great induration. The gland is distorted and puckered towards the affected part. Very often the disease is continuous with the nipple, and by the dragging of the tissue the nipple is Fig. 311. Section of cancer of mamma from a recent nodule. Epithelial cells in spaces formed by connective tissue; these are sometimes in single rows, and by multiplication form larger masses. X 200. (Cornii, and Eanvier.) drawn in, sometimes even forming an umbilicated depression. The tumor is very irregular in its extension in the gland, and it very often happens that in the midst of hard scirrhous tissue some ADIPOSE TISSUE appears, being the remains of some of the fat which normally surrounds the gland. In like manner, pieces of the gland-tissue may crop up amidst the contracting tumor. ISTot infrequently scirrhus goes on to ulceration of the skin, which usually occurs about the site of the nipple and areola. The ulcer is crater-shaped, with dense prominent Avails. Sometimes after formation of the ulcer the growth of the cancer becomes more rapid. 710 DISEASES OF THE FEMALE GENEEATIVE ORGANS. When a mamma which is the seat of scirrhous cancer is cut into, either the whole gland or a portion of it is seen to be occu- pied by a hard mass of a grayish color on the cut surface. It is very hard to cut, and the cut surface is commonly concave, the elasticity of the dense connective tissue producing retraction. In the general gray basis there are various whitish or yellowish pieces which represent the remains of mammary or adipose tissue, or the cancerous epithelium in a state of fatty degeneration. If the cut surface be scraped a thickish juice is obtained, which micro- scopic examination shows to be composed of epithelial cells and their debris. Many of the cells are large and well formed, while some may contain secondary cells within them or double nuclei (see Pig. 312). There are also free nuclei which have escaped Cells in the juice scraped from a scirrhus of mamma. They are of very irregular shape. Most of them contain several nuclei and some daughter-cells. X 200. from cells as a result of the mechanical interference in the process of preparing the specimen. Many of the cells contain fatty de- generation — in fact, very often nearly all contain fatty granules — and there are some completely degenerated, showing nothing but an aggregation of fat-drops like the compound granular corpuscle. The lymphatic glands commonly become secondarily affected in scirrhus of the mamma, and the tumor produced here is also a hard cancer with excessive development of the stroma. It is to be observed, however, that in the glands the stroma usually forms a more distinct meshwork than in the mamma, and the epithelial cells form more definite groups. Medullary Cancer forms the opposite extreme to scirrhus, and there are all intervening grades. In the medullary cancer we have a bulky tumor of soft consistence and rapid growth. There is a well-formed alveolar stroma, and the cells are somewhat loosely contained in it. The tumor involves neighboring tissues, very readily infiltrating the skin, subjacent muscle, and even the osseous ribs and the pleura. This form is not uncommonly present simul- taneously in both breasts. On section the tumor presents a gray brain-like appearance. The juice furnishes numerous cells, mostly TUMOES OF THE MAMMA. 711 small in size but with prominent oval nuclei, also abundant free nuclei which have escaped from the delicate cells. As the tumor commonly extends to the skin, we may have ulcers with fungating prominence of the tissue. The lymphatic glands are early affected and they also may ulcerate. Many large tumors of the mamma of comparatively rapid growth do not correspond with the description either of the medullary cancer or the scirrhus. In their minute structure they are more like the scirrhus, and perhaps may be designated acute scierhus. They have a remarkably firm fibrous stroma, but it forms distinct meshes in which the epithelial masses are contained with consid- erable regularity. The cancer cells are also large and essentially like those in scirrhus. The tumor as a whole also is hard, this depending on the abundance and density of the stroma. Colloid Cancer is, as compared with scirrhus, an exceedingly rare form of tumor, but it does occur not infrequently. The col- loid degeneration may affect the cells of an ordinary cancer, pro- ducing a partial metamorphosis. Or the cancer as a whole may present, from the first, a tendency in this direction, and the whole tumor have the characters of colloid cancer. The entire mamma is commonly affected, and it is greatly enlarged, while it presents a hard feeling like that of acute scirrhus. On section the tumor presents a flickering gelatinous appearance. Under the micro- scope there is the usual pronounced stroma with colloid material in the meshes. In the midst of the colloid masses there are often seen groups of cells, the remains of the epithelium. It is to be added that sometimes cancers occur having a close re- semblance to colloid cancers, but in which the metamorphosis is in the stroma, which is the seat of mucous degeneration. We may thus have a large gelatinous tumor which, on microscopic examina- tion, shows epithelial masses embedded in a gelatinous flickering stroma. To this form may be applied the term mucous cancer. Other Tumors of the breast are of uncommon occurrence. We may have an excessive growth of the adipose tissue around the mamma, forming a lipomatosis or lipoma capsulare. Even iso- lated lipomas have been met with. Isolated fibromas have also been seen. Myxoma of the mamma has been observed in a con- siderable number of cases. It forms a tumor of considerable size, the interstitial tissue of the mamma generally being converted into mucous tissue, while the glandular structures have atrophied ; this form of tumor is apt to be mistaken for colloid or mucous cancer. The Myoma has been met with in the nipple. DISEASES OF THE MALE GENERATIVE ORGANS. A.— THE TESTICLES. Malformations and Misplacements of the Testicle. — The testicle may be absent on one or both sides, while the vesiculse seminales and vasa deferentia are perfect. Or the vas deferens may be deficient while the testis is well developed. Impeefect descent of the testis, or cryptorchismus, is a very frequent and important condition. The descent of the testis occurs laormally before birth, but in a considerable number of cases the organ has not yet appeared externally at birth. In the majority of such cases it comes down within the first week, but it is sometimes delayed for months or a year, or even till puberty. When thus delayed the descent is very^ often imperfect, so that the gland remains in the inguinal canal or at the ring. On the other hand, the testis may be retained throughout life in the abdomen. The testicle retained in the abdomen or on the way down is usually imperfectly developed, and although apparently of normal size, it does not generally contain spermatozoa in its tubules. It is also more prone to inflammation and the formation of tumors than the normally placed testis, especially when in the inguinal canal where it is exposed to external violence. When it is late in descending the accompanying pouch of peritoneum, which forms the tunica vaginalis, is apt to remain open and so to induce a congenital HERNIA. Besides these congenital misplacements, we may have the testis descending into the crural canal, or into the perineum. Inflammation op the Testicle. — This condition presents itself under a considerable variety of forms, certain of which are diflicult altogether to separate from syphilis and tuberculosis. It is to be remembered that the testicle is bounded externally by a dense fibrous capsule, the tunica albuginea, and that the products of inflammation are apt to be closely confined within this. Acute Orchitis is mostly secondary, although occasionally resulting from a blow or other injury. It occurs as a secondary result in gonorrhcea, the specific irritant being apparently prop- agated along the vas deferens; also in cases of irritation of the urethra by calculi, the passage of instruments, etc., the inflamma- tion in such cases being called sympathetic, and probably brought THE TESTICLES. 713 about by reflex irritation of the vaso-motor centres. In mumps there is also, in a certain proportion of cases, orchitis as a secondary result, the specific irritant attacking the testicles as well as the parotid gland. The inflammation very often begins in the epididymis, and may remain confined to that region or pass on to the testis. There are hypersemia and serous exudation producing great swelling, so that the tunica albuginea is tightly stretched, and the organ feels hard and tense. At the same time there is often serous fluid in the tunica vaginalis. There may be resolution without suppuration, the testis returning to the normal condition, or the disease may become chronic, or suppuration may occur. In the latter case an abscess or abscesses form in the testicle, and these may burst exter- nally. In that case the tense albuginea often forces the tissue of the testicle through the opening, so that it projects in a fun gating form. This, which forms the benign fungus, and is not to be mis- taken for cancer, has a red color and looks like protruding granulations. But it really contains the seminal tubules, and after the subsidence of the inflammation these may be replaced and resume their function. On the other hand, the abscess may dry in and form a caseous mass, which becomes surrounded by a fibrous capsule. This mass may ullimately become calcareous. Chronic orchitis rasij arise out of an acute attack, remaining after the formation of abscess, or else supervening without that. There is also a spontaneous chronic orchitis which in most cases is either syphilitic or tubercular. The ordinary chronic orchitis is characterized by new formation of connective tissue in the stroma of the organ, and consequent induration of it. The tubules atrophy and the whole organ is reduced in bulk and hardened. Generally on section it can be seen that the albuginea and the septa which proceed towards the mediastinum, are greatly thickened. At the same time there is frequently adhesion of the tunica vaginalis which may obliterate the sac. The other form of chronic orchitis which is described is char- acterized by the occurrence of yellow caseous masses. Such masses may arise from the drying in of abscesses, or in connection with syphilis or tuberculosis, and probably have no independent origin. Syphilitic disease of the testicle sometimes occurs as a gen- eral induration, having the usual characters of chronic orchitis. The albuginea is thickened and the trabeculse are enlarged as they converge towards the mediastinum. These thickened structures may be largely composed of granulation tissue, and we may have in addition definite gummata. The gummata may undergo caseous necrosis, and by coalescence of neighboring tumors we may have considerable masses of caseous material. In the midst of this caseous material the outlines of the seminal tubules can sometimes be made out, indicating that the necrosis has overtaken the proper tissue as well as the new formed. 714 DISEASES OF THE MALE GENERATIVE ORGANS. Tuberculosis of the testicle is characterized by the formation of caseous masses, sometimes of considerable size, and these are surrounded by a gray inflammatory tissue in which tubercles are to be found. The tuberculosis is very often associated with similar disease in the prostate and vesiculse seminales, and this coincidence points to propagation from the one to the other. The starting- point may be at the testis or at the other extremity of the vas deferens. There is also, not infrequently, tuberculosis elsewhere, as in the form of scrofulous glands or phthisis pulmonalis. As a general rule, the tuberculosis begins in the epididymis, mostly in its tubules. The result is great thickening and the formation of a caseous mass, enclosed very often in a firm fibrous capsule. Thus a firm elongated tumor may form behind the testicle. In the testicle also caseous masses form, at first isolated, but afterwards running together into considerable conglomerates. The caseous masses are very dense, but after a time they generally break down, and having burst externally, tedious fistulas are the consequence. "When the testicle is examined in section the caseous structure is seen to be surrounded by a transparent gray tissue, in which, as already mentioned, tubercles are present. This inflammatory and tubercular structure by its pressure destroys the tubules for the most part, but not altogether, as bits of tubules are sometimes ex- pelled along with the softened caseous material. Tumors of the Testicle. — These are mostly somewhat malig- nant in their characters, and there is a peculiar tendency to a mixed structure. Sarcomas occur frequently mixed with tissue of other tumors, as the myxoma, enchondroma, etc. Even when the tumor is a pure sarcoma there may be combined the structures of various forms of this tumor, spindle cells, round cells, and mucous tissue. There may, however, be a simple round-celled sarcoma. The sarcomas form usually large tumors of soft consistence and rapid growth. They occur in comparatively young persons, and are prone to metastasis, the secondary tumors occurring mainly in the lungs. The relation of the sarcomas to the seminal tubules deserves special consideration. The tissue of the tumor, like that of other sarcomas, originates in the interstitial tissue. In many cases the glandular structures undergo atrophy; but in others, changes occur comparable with those we have already considered in sarcomas of the mamma. Cysts are thus of frequent occurrence, and they are so characteristic in some cases that the name cystosarcoma is given. These cysts often contain a gelatinous material, although in the larger ones the contents are usually serous. Sometimes the contents undergo fatty degeneration, and we may have choles- tearine in the fluid, or even an atheromatous substance. As in the mamma, there may be a papillary ingrowth of the sarcoma into the cyst, forming peculiar intracystic projections. It appears also that there is sometimes an actual new formation of glandular tissue THE TESTICLES. 715 along with the sarcomatous, in this respect resembling the adenoid sarcoma of the mamma. Cancer of the testicle connects itself with the cystic and adenoid sarcomas. It appears that not infrequently the glandular tissue in these tumors has more of the irregular atypical cancerous character than of the strictly glandular, and in particular the epi- thelial masses do not possess a membrana propria. These char- acters are also expressed in the fact that sometimes these tumors extend to the neighboring lymphatic glands, while others penetrate more readily into the veins. Proper cancer of the testes is mostly a large, quickly growing, soft tumor — medullary cancer. It involves the whole organ as well as the epididymis, converting them together into a massive tumor. It may also extend along the vas deferens, and on to the lymphatic glands, inguinal, lumbar, and prevertebral. From these glands it may extend to the radicles of the portal vein and so pro- duce tumors in the liver, or more frequently to the radicles of the vena cava, producing tumors in the lungs. In the midst of the tumor we may have cysts formed b}"^ mucous or fatty degeneration. The cancerous tissue is derived from the epithelium of the seminal tubules, and the stroma from the interstitial tissue. It is necessary, however, to. mention that tumors may arise in connec- tion with the bloodvessels which have a resemblance in their structure to cancers, but which are properly plexiform angio- sarcomas. Other tumors of the testicle are uncommon. We meet with CTSTS, but the chief of them, the spermatocele, will be described afterwards. The testis is also sometimes the seat of the dermoid cyst. It may be a simple dermoid in the midst of the gland, arising apparently by inclusion of a piece of embryonic skin. But sometimes there is a more complex cyst, like that of the ovary, and deserving the name of teratoma. Such tumors probably owe their origin to the inclusion of a whole fcEtus. For the rest, the occasional occurrence of fibromas, lipomas, enchondromas, myomas of the striated variety and even osteomas, has been observed. Hydrocele. — By this name is meant the accumulation of fluid in the tunica vaginalis. The fluid is serous and the cause of its accumulation is inflammation. It is not properly a dropsy of the tunica ; a general dropsy, affecting the skin of the scrotum very greatly, causes little fluid to accumulate in the tunica vaginalis. The inflammation may be acute, in which case there is fibrine de- posited on the surface as well as serous fluid in the sac. More commonly it is chronic, and there is a gradual accumulation of serum. The fluid distends the sac, and so a bulky tumor is formed which is pear-shaped with its blunt end downwards. The fluid is usually a clear serum, but sometimes it is slightly opalescent. In the true hydrocele this is not from the presence of spermatozoa, but from the existence of tine fat-drops, resulting from degeneration of the 716 DISEASES OF THE MALE GENEEATIVE ORGANS. leucocj'tes floating in the fluid. Tliere may even be cholestearine crystals formed in this way. ISTot infrequently hemorrhage occurs, most commonly as the result of a blow or other injury, and the hydrocele becomes a HEMATOCELE. The blood mostly coagulates, and the coagulum through time undergoes various changes, softening into a brown pultaceous material or into a brown turbid fluid, in which are enormous numbers of cholestearine crystals. The blood seems to act as an irritant to the tunica vaginalis, causing often a ver^!- great thickening of it. The interior also is rough and sometimes presents considerable projections. The thickened cyst may contract some- what so that the tumor is reduced in size. This thickening of the wall, even when the contents are fluid, may cause the hpematocele to be mistaken for a solid tumor, and castration has often been performed under this belief. A hydrocele or hsematocele may be cured by the fluid being absorbed, the result usually being adhesion of the opposed surfaces of the tunica vaginalis and obliteration of the sac. In the condition named congenital hydrocele the tunica vagin- alis retains its communication with the peritoneal cavity. The fluid may come from the peritoneal cavity, or may originate as in an ordinary hydrocele. It can be pressed into the peritoneum through the neck. It will be understood that a congenital hernia may occur along with or alternate with this form of hydrocele. Spermatocele. Encysted Hydrocele. — In this afiection there is a cyst having in many cases much the external appearance of hydrocele, but containing a fluid in which spermatozoa are abund- antly present. In other respects also the condition differs from that in hydrocele, for we have here not merely an accumulation in an existing sac, but a proper new-formed cyst. Hence the name Encysted Hydrocele is often used as equivalent to spermatocele. The cyst arises in connection with the epididymis for the most part, and probably takes origin in one or more aberrant tubules which have formed blind diverticula from the seminal tubules. They usually arise near the upper end of the epididymis, but it may be at the lower end or from the rete testis. The cysts grow often to a large size, and they sometimes push themselves into the sac of the tunica vaginalis, inverting one layer of the wall against the other. As a rule, the tunica vaginalis is found below and in front of the cyst, this position being connected with the origin of the cyst in the neighborhood of the testis. The fluid from these cysts has a peculiar opalescent appearance, which is due to the presence of multitudes of lively spermatozoa. The existence of these shows that the cyst has retained its con- nection with the seminal tubules. The cyst is usually lined with a ciliated epithelium, but in large ones the pressure of the fluid may cause it to assume the pavemented form. It will be observed that these spermatic cysts are comparable in their origin to the parovarian cysts. THE PENIS AND SCROTUM. 717 Other forms of hydrocele have been described, but they re- quire only a passing notice. There may be an encysted hydrocele without spermatozoa in the fluid. Then there is encj^sted hydro- cele of the cord, sometimes arising by a portion of the communi- cation between the tunica vaginalis and the peritoneum remaining unobliterated and becoming the seat of an accumulation of fluid. There is also diftuse hydrocele of the cord, in which there is an cedematous condition of the connective tissue around the spermatic cord. There may even be a hydrocele from a hernial sac, which has got emptied of its contents, and shut off from the peritoneum by adhesion»of the neck. B.— THE PENIS AND SCROTUM. In the PENIS, the ulcers or chancres are the commonest forms of disease. The simple chancre is an ulcer which has its usual seat on the glans or frenum. Sometimes we meet with a deeply penetrating or phagedenic ulcer. The hard chancre is the primary syphilitic sore, and as such we have already considered it. Another syphilitic manifestation is the condyloma, which forms warty outgrowths sometimes of considerable size. There may be large groups of papillae forming a cauliflower-like tumor. Cancer of the penis occurs in the form of epithelioma. It begins usually in the glans, and the tumor is often covered with prominent papillae, which give it a highly characteristic warty appearance, like the cauliflower excrescence. It may remain long without ulceration, but usually sooner or later breaks down, and there are sometimes deep ulcerating fissures or fistulse between the groups of papillfe. In the SCROTUM, cancer is somewhat common, and it is so often chimney-sweepers who are affected that the disease is often called chimney-sweepers' cancer. In Glasgow it has been found that workers in paraffin refineries are also liable to this disease. It generally forms a flat tumor from whose surface prominent papillee protrude. Through time ulceration occurs, and the testicle may be exposed. Elephantiasis of the scrotum has been sufiiciently treated of in the genei'al part of this work. Lymph scrotum has already been referred to in connection with the filaria sanguinis. In it there is a varicose condition of the lymphatic vessels of the scrotum with the formation of vesicles in the skin. These frequently burst and discharge a fluid in which the embryo filaria is usually to be found. In some such cases the filaria is also present in the blood, but sometimes not. The lym- phatic glands of the groin are indurated, and the dilatation of the lymphatics seems to be due to the obstruction of these vessels in the glands by the embryo filarise. According to Manson, elephan- tiasis sometimes develops from lymph scrotum, and depends on 718 DISEASES OF THE MALE GENERATIVE ORGANS. the same parasite, but this view can hardly be accepted pn the present evidence. In lymph scrotum, the adult female filaria, and probably the male also, inhabits a lymijhatic vessel in the groin, and their embryos or ova pass off and stick in the glands, thus obstructing the lymphatics. The PROSTATE, as we have already seen, is subject to hyper- trophy. The common enlargement of old age is due to increase of the muscular substance. This enlargement exists in about thirty per cent, of men above sixty years of age. It develops slowly without any apparent cause, and in this respect has the characters of a tumor. Sometimes the whole prostate enlarges, and it may reach the size of the fist. But sometimes there is a more partial hypertrophy, forming the so-called third lobe of the prostate, which projects inwards at the neck of the bladder, and is sometimes so large as to act like a valve to the orifice of the urethra. The efi'ect of enlargement of the prostate on the urethra is to be noted. If there is a general enlargement, the urethra is necessarily elongated in its prostatic portion, and whereas normally this portion measures one and a half inches in length it may come to be four inches. At the same time the tube may be narrowed and even distorted. If, for instance, the central part of the pros- tate is specially hypertrophied, then the urethra, being pushed upwards, has on section a crescentic shape with the convexity upwards ; or if one side is larger than the other, there will be a convexity towards the opposite side. Besides this muscular hypertrophy, the much rarer hypertrophy of the glandular structure is to be mentioned. The glandular structure does not commonly increase with the muscular, but sometimes enlarges by itself, so that we have an adenoma of the prostate. Cancer of the prostate is not of frequent occurrence. The gland enlarges, and the disease is apt to extend to neighboring structures. TuRERCLE occurs uot infrequently in the prostate and vesiculse seminales in conjunction with similar disease in other parts of the urino-genital passages. There is caseous necrosis with ulceration as usual, and this may cause even perforation into the rectum or bladder. Concretions are of frequent occurrence in the prostate in old persons. They are formed in the gland ducts, and are of various sizes, from very minute to the size of a grain of corn. When small, they are colorless, but as they enlai'ge they frequently be- come blackish or reddish-brown in color. They are round or oval in form, and frequently present concentric stratification (Fig. 44, p. 135). They have usually a 'central cavity. Yery commonly these bodies present the character of amyloid bodies, giving a bluish or mahogany-red color with iodine. Sometimes they con- tain lime salts in their substance. They may pass into the urethra and escape with the urine. While in the prostate they do not appear to produce much disturbance. DISEASES OF THE BOl^ES AND JOINTS. A.— THE BONES. Introduction. — In considering the diseases of the bones, it is necessary to bear in mind certain matters regarding their structure and life. It is to be remembered that bone grows, not like ordi- nary tissues by interstitial expansion, but by addition of new tissue to the old. An attempt has indeed been made, on the basis of the architecture of the fine lamellse of the spongy bone at the ends of the long bones, to show that growth occurs by interstitial expan- sion ; but this attempt is not generally accepted as successful, and it may be said that in the growth of bone, deposition and absorp- tion go on simultaneously, so as to preserve the architecture while the size is increased. Bone is therefore to be regarded as a solid, comparatively unalterable structure. When hypertrophy of bone occurs, this takes place by the action not of the bone itself, but of the periosteum or endosteum. For the most part also, when destruction of bone takes place, it is by agents acting from with- out. It is to be noted, however, that the bone corpuscles are not altogether inactive cells. They doubtless look after the nutrition of the bone, and although they do not, in pathological processes, as a rule, present any great increase in activity, they are certainly capable of degeneration, in which case they induce changes in the solid intercellular matrix. In studying the diseases of boue, and more especially in regard to rickets and inflammations, it is important to bear in mind certain facts as to the relation of osseous tissue to cartilage and connective tissue. These three tissues appear to be fundamentally one, and they are to some extent mutually' convertible. This fact is some- times expressed in the term metaplasia, and may be illustrated by the accompanying figures (313 and 314), from a case of fracture of a rib. As we shall see afterwards, an inflammatory process is concerned in the healing of fractures, the so-called callus being an inflamma- tory new-formation. As a rule in the human subject, this callus is formed of bone, but in animals cartilage enters into its constitu- tion, and in the section of which the figures are representations, the callus was variously composed of bone, cartilage, and fibrous tissue, the existence of one or other being apparently determined 720 DISEASES OF THE BONES AND JOINTS. by circumstances. In some parts, as at 6, b, in Fig. 313, cartilage and bone exist side by side, and it is sometimes even difficult to f^ say which is actually present, there being obviously transition forms. In this as in other inflammations, the new-formed tissue RICKETS OR RACHITIS. 721 has originally the structure of granulations, and the granulation tissue may develop bone, or cartilage, or hbrous tissue.^ From same section as Fig. 313, showing continuity of cartilage and bone in the callus. At a there are cartilage-eells, and at 6 bone-corpuscles, the matrix being continuous and appar- ently of the same structure. X 350. EICKETS OK BACHITIS. This disease occurs in children during the earlier periods of growth, and so far as the bones are concerned it is a disease of de- velopment, the normal process of ossification being interfered with. Cases have been observed of congenital rickets, but these are rare, and in the majority of cases it begins in the first or second year, its commencement being very rarely delayed beyond the fourth or fifth year. In a large proportion of cases its onset seems to be in the latter half of the first year or the first half of the second. An endeavor has been made lately to make out that rickets is merely a manifestation of hereditary syphilis. This view has not received acceptance in this country. It has been pointed out again and again that rickets is very common in cities where syphilis is uncommon. In the city of Glasgow, for instance, rickets is very common among the poorer classes, but syphilis is very uncommon. It is so also in Aberdeen, Edinburgh, Belfast, and elsewhere. We 46 722 DISEASES OF THE BONES AND JOINTS. Fig. 315. ib^.pcu shall see afterwards that syphilis produces changes in the bones in some respects analogous to rickets, and atrophy of the cranial bones, sometimes designated craniotabes, although formerly re- garded as rachitic, is probably in most cases syphilitic; the two dis- eases, however, are essentially separate. Rickets occurs amongst children who are injudiciously fed and badly housed, and the disease in the bones is to be regarded as part of a general loss of health. The body is weakened, and, besides the bones, there are other parts that sufi'er. The state of malnu- trition may be the efl'ect of an un- healthy state of the mother during utero-gestation, or it may be pro- duced by unhygienic conditions after birth. According to Mac- ewen, it supervenes in a considera- ble number of cases on an attack of one of the acute fevers, such as measles or scarlet fever, such an attack leaving the child in an ill- nourished condition. There are usually symptoms of indigestion and intestinal catarrh, sometimes with fever, and in a certain pro- portion of cases there is enlarge- ment of the spleen and sometimes also of the liver and lymphatic glands. The bones, being per- haps the most actively growing parts at this period of life, may be specially affected when the general nutrition suffers. Rickets has been produced arti- ficially in growing animals by feed- ing them with.small doses of phos- phorus, or b}' giving them lactic acid, by the mouth or subcutane- ously. In both cases the diet must be deficient in lime salts. In the latter case it has been supposed that the lactic acid, being a ready solvent of lime, prevents its depo- sition in the bones, and it has been inferred that in the human subject the gastric derangement causes the formation of an excess of lactic acid, which is the cause of the dis- ease in the bones. There is, how- ever, the objection to this view, Longitudinal section of bone ossifying from cartilage; a, commencement of pro- liferation of cartilage-cells; b, cells ar- ranged in longitudinal groups; c, matrix of cartilage impregnated with lime, this calcified matris is continued beyond the ossifying border (e on right sidej ; d, me- dullary spaces containing round cells re- placing cartilage-cells; e, e, formation of bone at borders of calcified matrix, the os- teoblasts each forming a piece of bone and remaining as the bone-corpuscle. X 90. (After THIERrELDER.) RICKETS OR RACHITIS. 723 that rickets is not always accompanied by any considerable gastric disorder, and such a view does not explain its occasional occurrence in the foetus. Besides, the disease is clearly an error in develop- 724 DISEASES OP THE BONES AND JOINTS. ment, and were it clue merely to absence of the lime salts, we should expect the bony matrix to be formed without the lime salts. The very opposite frequently occurs ; we have often an impregna- tion of the cartilage with lime salts, a calcification of the cartilage (see Fig. 316, b, b), while true ossification lingers. Rickets can in most cases be cured by supplying suflicient food and proper lodging, and this points to its origin in the ojpposite of these. In order to comprehend the processes presented to us in rickets it is necessary to bear in mind the main points in normal ossifi- cation. If in a growing child a long bone be divided longitudin- ally, and the cartilage and ossifying border examined, it will be seen that the transition from cartilage to bone with medullary spaces, occurs somewhat suddenly. With the naked eye it can be seen that the deepest layer of the cartilage has a bluish color, this zone being very narrow. It is succeeded by a still narrower yellow zone which is scarcely more than a line in breadth. On micro- scopic examination of a longitudinal section the conditions can be made out as shown in Fig. 316. At the upper part of the figure (a) is the normal appearance of hyaline cartilage. As the ossify- ing margin is approached the cells multiply, and at first they form irregular groups, as at b. Still nearer the margin the multiplying cells become arranged in rows parallel to the long axis of the bone, the elongated groups being separated by narrower elongated pieces of hyaline matrix. The beginning and end of this zone of multi- plying cartilage-cells are quite abrupt, and form nearly straight transverse lines. This zone is that which, to the naked eye, is blue. 'Ees.t occurs an infiltration with lime salts of the hyaline matrix between the groups, the matrix becoming opaque and granular, c in figure. This forms the yellow zone as seen with the naked eye. This zone is also suddenly interrupted, and at a definite level the groups of cartilage-cells give place to cavities filled with foetal marrow, consisting of round cells and bloodves- sels [d). These cavities are still bounded by the calcified carti- laginous matrix. Some of the marrow cells are osteoblasts, and these fix themselves on to the surface of the calcified matrix and begin to develop the bony matrix around them. Each osteoblast forms a piece of bone around it {e. in figure), retaining a cavity for itself, which is the lacuna. In this way the cartilaginous matrix is encroached on and destroyed by the new-formed bone, while, at the same time, it is partly destroyed without the new formation of bone so as to make the medullary cavities larger. On the surface of the bone we have beneath the periosteum a layer of cells similar to those in the medullary cavities. Here also the osteoblasts form bone around them and add to the thickness of the bone. Turning now to rickets, the condition of the ossification from CARTILAGE may be studied with the assistance of the accompanying excellent figure copied from Thierfelder's atlas. The most pro- RICKETS OR RACHITIS. 725 nounced difference from the normal is the enormous exaggeration of the zone of multiplication of the cartilage-cells (a, a). These seem to be proliferating without any purpose and without the regular arrangement. There are groups of cells as in the normal case, but they are in much larger numbers and occupy a much greater space ; at the same time they have not always the normal arrangement in rows parallel to the long axis of the bone. The cells of the groups also vary considerably in size. In the normal bone the cells in the deepest part of this zone are large, but in rickets while some are large, as at b, there are others even at the same level, or deeper, of small size. ISText, in regard to the zone in which the cartilaginous matrix becomes calcified, this also is represented here in the most irregular fashion. Calcification of the matrix occurs, and calcification of the cartilage-cells (as at b on left), but this occurs quite indiscrim- inately. There will be calcification of the cartilage high up, as at b, while there are numerous groups lower than that uncalcified. In many cases also, whether calcified or not, the cartilage-cells lose to a considerable extent their grouping into rows (as below b on left). Then as to the formation of medullary cavities and development of bone, the figure shows how irregularly this occurs. Blood- vessels appear with considerable frequency in the midst of the cartilage, and towards the deeper parts there are medullary spaces with osteoblasts in them. These may even be seen forming new bone, as at d. But the medullary cavities do not occur with any greater regularity than the other stages in the process, and it is not always apparent that they have always to do with the formation of the bone. It will be seen in the figure that at a certain somewhat indefinite level, which is lower at the left side than the right, bony trabeculse appear (e, c). But it will also be seen that the bone is directly continuous with cartilage, the difference in the two being signalized chiefly by the difference in the cells. It appears also that in the cartilage, which is thus immediately continuous with the bone, the individual cartilage-cells are separated by a matrix just as the bone corpuscles are (see figure). In fact it looks very much as if a conversion of cartilage into bone were occurring, and there are even appearances suggestive of the gradual transformation of cartilage-cells into bone-corpuscles. The examination of such sections as that figured can leave hardly any doubt that an actual transformation of this kind occurs, this being consistent with what has been stated above in regard to metaplasia. It will be seen in various places, but especially at d, that pieces of cartilage survive in the midst of the new-formed bone. The carti- lage may be calcified or not. To the naked eye the changes described above are indicated in a longitudinal section of a rickety long bone. The blue zone which forms a straight narrow transverse line in the normal bone is here greatly increased and its boundaries are irregular. The yellow zone of calcification of the cartilage is still more irregular, and 726 . DISEASES OP THE BONES AND JOINTS. yellow pieces crop up in the midst of the blue zone. Bloodvessels appear also at different levels. In the area of the blue zone the cartilage is greatly swollen, as the enormously multiplying cells take more space than normal. Under the Periosteum we have a process which may, like that in the cartilage, be described as an enormous preparation for ossification while the process of ossification lags behind. The thin layer of osteoblasts is increased till it forms a layer of considerable thickness. By this layer bone is formed to a very limited extent and very imperfectly. Instead of a proper dense bone, such as should be formed on the surface of the shaft, there is a loose irregular spongy bone. But even the trabecule of this spongy bone are not properly formed. Immediately under the thick subperiosteal layer the ncAV-formed bone does not show in its matrix the homogeneous character of the matrix of bone ; it is granular, and the lime is obviously deposited without combining with the matrix in the normal manner. It is a calcification rather than an ossification, and the trabeculse are rather osteoid than osseous. On passing inwards the tissue becomes more strictly osseous however, although hardly acquiring the regular arrange- ment of the dense bone of the shaft. Corresponding with the structure described are the naked-eye characters. The subperiosteal layer is seen in the form of a red vascular layer of some thickness. This is so obvious in some cases that, at one time, it was described as if a blood-clot were formed under the periosteum. Beneath this the spongy character of the bone can be seen, while the shaft is considerably thicker than nor- mal and obviously more easily bent. Deformities op the Bones due to Rickets. — In considering the deformities so often produced by rickets, it is to be remembered that the two chief changes in the bones are, in the first place, enlargement and softening of the epiphyseal extremities of the bones from the affection of the cartilages, and, in the second place, thickening with loss of resistance of the shafts from the periosteal lesion. These conditions do not always go strictly parallel, one or other being frequently the more prominent in a particular bone. The various bones of the body also present very commonly different degrees of rickets although the disease is a general one, and usually affects many bones. Even in bones affected to a similar extent, however, the resulting deformities present very great variations; the deformities consist largely of curvatures of the bones from, the application of external forces, and the bones are diflierently placed in relation to such forces. Deformities of the Long Bones. — The most obvious change at the outset is swelling op the cartilaginous ends of the long bones, giving a clubbed or knobbed appearance to the limbs. This is common to all the long bones, and is the condition generally taken EICKETS OR RACHITIS. 727 in practice as evidence of the existence of the disease. The bones are also arrested in their growth, so that they are stunted while at the same time they are unduly thick. The remaining deformities occur in the majority of cases in the lower limbs, and are the result of the weight of the body acting on the bones in their weakened condition. Similar deformities are met with in the bones of the arms in cases where external force is frequently applied to them, as where a child in creeping leans on the arms, or where a nurse frequently lifts a child by one arm (Macewen). The deformities consist mainly of curvatures of the shafts of the bones, along with shifting of the epiphyses in some cases. In regard to the latter, the extended blue zone at the car- tilaginous border being soft allows the epiphysis to change its position according to the direction of pressure, and so at the ankle, the epiphysis is sometimes displaced inwards, and, as it were, overhangs the joint on its internal aspect. The same may occur at the knee-joint, and the internal condyle may exceed in length the external even after the disease has been cured. The familiar curvatures of rickets are due mainly to the weight of the body acting on the softened shafts, and as the pressure acts mainly on the lower limbs the two principal forms are genu valgum and genu varum. GrBNU VALGUM, or knock-knec, is a condition in which the thigh and leg form an angle at the knee opening outwards. This deformity depends usually on several alterations. There is gener- ally a curve of the lower third of the femur, with its convexity inwards, the effect of this being that the internal condyle is lower and the external higher than normal. Along with this there is usuallj' the lengthening of the internal condyle already referred to. As a rule the tibia is not bent, the two conditions named taking the chief part in producing the deformity, but sometimes the shaft of the tibia is at an angle with the epiphysis, as if the latter were to some extent overhanging the former. In addition the femur or tibia sometimes shows an anterior curvature, which of course does not increase the valgum condition. GrBNU VARUM, or bow-legs, is the converse condition to genu valgum. The shafts of the femur and tibia are curved, with the convexity outwards, but these bones take part in the deformity in very different degrees, the tibial curve being more frequent and usually more pronounced than that of the femur. The long bones being soft and flexible are not so liable as normal bones to complete fractures, but they are specially liable to partial FRACTURES or INFRACTIONS. If the bone is suddenly bent it does not break across, but is partially torn as when an attempt is made to break a green stick. In this case the concave surface of the bent bone gives way and the convex surface does not. The marrow is torn by the broken concave portion, and the broken edges may be projected through the marrow to the opposite internal wall. This kind of fracture has been aptly compared by Virchow to the breaking of a quill. These infractions occur most frequently 728 DISEASES OF THE BONES AND JOINTS. at the lower part of the tibia, also in the pelvis and ribs, and less frequently in the bones of the arm. Deformities of the Chest. — The junction of the cartilaginous and bony ribs is analogous to the ossifying cartilage of a long bone, and undergoes a similar thickening in rickets. These parts of the ribs are therefore knobbed, and there is thus a row of knobs on each side of the chest — the so-called rachitic rosary. The chest is also liable to deformity from the flexibility of the ribs. During inspiration the lateral aspects of the ribs are drawn inwards from being unable to withstand the atmospheric pressure, so that instead of the natural arch with the convexity outwards, these lateral por- tions are flattened or even rendered concave. As the ribs take thus a straighter course the sternum is pushed forward, and the characteristic pigeon-breast is produced. It may even be some- times seen how, in inspiration, the lateral wall of the chest is visibly carried inwards. Deformities of the VERTBBRiE. — The vertebrae very often escape in the milder forms of rickets, but in many cases they also are com- posed of abnormally spongy bone, and allow of the occurrence of curvature. Such curvatures are mostly exaggerations of the normal antero-posterior curves, but lateral curvature also occurs. Any considerable curvature will cause narrowing of the chest, and if this be associated with the pigeon-breast the interference with the circulation and respiration may be serious. Derfomitibs of the Pelvis. — These are of great importance in the female in relation to the possible occurrence of pregnancy in after-life. The chief deformity is produced by the weight of the body acting through the vertebral column on the sacrum. This bone is pushed forward and the pelvis undergoes a corresponding displacement of its parts, the antero-posterior diameter being diminished. The growth of the bones here also is stunted, and the pelvis therefore remains unduly small. The BONES of the head frequently undergo very marked deform- ities. The bones of the face, like the other bones generally, are stunted in their growth, so that the face is small. It is also stated that the jaws by the action of the muscles undergo changes in shape by which the lower jaw is shortened and the upper jaw lengthened, so that the teeth of the latter overlap very much those of the former. While these are the conditions in the face, the bones of the cranium present striking peculiarities. The flat bones ossify from membrane, and in rickets we have the ossifi- cation lingering behind, so that at their borders these bones pre- sent somewhat broad areas in which there is soft tissue like that under the periosteum. The effect of this is to cause an apparent widening of the sutures and extension of the fontanelles. The closure of the fontanelles is also delayed. The cranium is enlarged in rickets, at least its circumference is greater, and at the same time it is commonly flattened on the summit. The enlargement of the cranium, with the stunted condition of the face, causes the well-known overhanging of the brows so often seen. OSTEOMALACIA. 729 Another occasional consequence of rickets is the condition designated craniotabes. As we shall see afterwards, this is probably most frequently a consequence of syphilitic disease of the bones, but it occurs also in rickets. The bone in rickets is soft, possessing less power of resistance than normal bone. If the child be lying constantly on one spot, or if the contents of the skull be increased, as in chronic hydrocephalus, then the pressure on the bone may cause it to waste. This occurs most frequently when both these conditions are present, and the bone is, as it were, between two pressures. In this way may occur thinning and actual perforation of the skull, so that in the midst of the bones there will be holes, where the brain is covered by the soft parts alone. From the nature of the case it will be under- stood that these apertures are mostty in the occipital or the parietal bone, according as the child lies mostly with the back or side of the head downwards. Eecovbry takes place in rickets by the removal of the insani- tary conditions, or by the termination of the period of growth. The ossification advances in the cartilage and under the periosteum. The spongy bone produced under the periosteum becomes dense, and so the bone may be unduly heavy and thick, while it is stunted. The deformities having occurred in a rigid structure are rendered even more fixed by the completion of the ossification. There is, however, in the course of time, an effort on the part of nature to restore the normal architecture of the bones ; where they are bent, absorption occurs on the convex surfaces, and increased new formation on the concave ; there may be considerable restor- ation of the proper shape in the long bones, but usually much less in the pelvis, head, and thorax. OSTEOMALACIA AND MOLLITIES OSSIUil. This disease contrasts with rickets in respect that it affects the bones after their complete ossification. Like rickets, it produces a softening of the bones, but it is a softening which supervenes after they have acquired the normal resistance of fully formed bone. It rarely occurs in children, although at least one case has been reported by Dr. Rehn, in which it was present without a trace of rickets. It is to be stated at the outset that several distinct conditions are often included under the designation osteomalacia. "We must, in the first place, eliminate cases of mere senile atrophy, or others of a similar kind. It often happens in old persons that the medul- lary spaces increase in size at the expense of the bone, and the bone becomes in consequence less resistant. But the remaining bone is not softer than normal ; it often contains even more lime salts than it should do, and is therefore abnormally brittle. Put- ting aside such cases, however, there are two distinct forms of 730 DISEASES OF THE BONES AND JOINTS. mollities ossium in which the calcareous constituents of the bone are reduced. It is not possible to separate these two absolutely in their causation, but it may be said that both forms are rare in this country, and that one of them, while it is sometimes met with here, seems hardly to occur on the Continent. The disease seems to be caused for the most part by defective nutrition, but there are two conditions which specially predispose to it, namely, pregnancy and insanity. It not infrequently comes on during pregnancy, and runs a rapid course. It has also been frequently observed in insane persons, and here the softness of the bones may lead to fractures under comparatively slight violence. Turning now to the diflerent forms of the disease, there is one which appears to occur most frequently in England, and the class- ical description of which is that given by John Hunter. It appears to consist in a fatty degeneration of the bone-corpuscles with soft- ening of the matrix. The condition, so far as the naked eye is Fig. 317. A fragment of bone from a case of osteomalacia. The central part shows the usual ap- pearance of bone, while the marginal parts are transparent, being devoid of lime salts, although still showing bone-corpuscle. X 90- concerned, is thus described by Hunter : " The component parts of the bone were totally altered, the structure being very different from other bones, and wholly composed of a new substance re- sembling a species of fatty tumor, and giving the appearance of a spongy bone deprived of earth and soaked in soft fat." In these cases the medulla forms a bright yellow, pink, or deep INFLAMMATIONS OF BONE. 731 crimson material, and, when examined microscopically, presents free oil in great quantity with crystals of margarine as well as ordinary adipose tissue. The other form of the disease is that described by writers on the Continent as osteomalacia, but it is not so infrequent in this country as has been supposed, the mollifies ossium of insanity being probably always of this form. In this form, as shown in Fig. 317, there is a direct absorption of the lime salts from the bone. The solution of the lime salts occurs primarily in the por- tions of the bone next the medullary spaces and Haversian canals, so that, if the bone be examined, the central parts of the trabeculse are seen to be opaque like normal bone, while the peripheral parts are transparent because deprived of their lime salts. The condi- tion of these parts is like that of bone which has been decalcified by steeping in an acid, the bone-corpuscles are preserved, and the matrix has a homogeneous or fibrous appearance. As the disease advances, the decalcified matrix is encroached upon by the medulla, and the decalcification advances further. The medulla itself is altered ; the adipose tissue is largely replaced by round cells some- times with several nuclei. The eflfect of these changes is, of course, to make the bones much softer and more flexible, so that they can often be cut with a knife, or crushed with the fingers. And so in the living body the bones are often bent or crushed. The disease has a particular tendency in some cases to attack the pelvis and vertebrse, but the long bones are also affected. Serious deformities result, especially in the pelvis and vertebral column. The pelvis is narrowed by the acetabula being pushed in on either side, so that the pubes are pointed and prominent. The vertebral column is curved. The sternum sometimes undergoes sharp bendings, and the ribs may be fractured. INFLAMMATIONS OF BONE. We have already seen that the proper bony tissue is somewhat inert, and for the most part conducts itself passively in patho- logical processes. On the other hand, in its development and nutrition it is intimately connected with the periosteum on its surface, and with the tissue lining its various cavities and canals, whether forming proper medullary cavities or narrower canals (Haversian) and spaces. The periosteum, endosteum, and contents of the various spaces in bone, form thus integral parts of the osseous tissue, and in studying inflammation our principal concern will be with the changes in these structures, and their inter-rela- tions with the proper bony tissue. In most cases the inflammations of bone are propagated from neighboring structures. Many of them originate in connection with disease of the joints, and many from inflammation of the periosteum. If the inflammation be acute there may be suppura- tion, but whether acute or chronic, so far as the bone is concerned 732 DISEASES OF THE BONES AXD JOINTS. the most important result is the formation of granulation tissue which, coming into relation with the osseous substance produces various changes there. This granulation tissue replaces the proper medulla of bone, and is often in great abundance under the peri- osteum, as we shall see in studying periostitis and the healing pf fractures, and its effect on the bony tissue is either to destroy it, or to add to it by the new formation of fresh bone. It is possible, in theory to separate these two processes, and to speak of a rare- fying or DESTRUCTIVE, and a formative or condensing osteitis, but the processes so frequently go on together that it will be better to consider them in connection. In order to understand these processes it is necessary to refer to the state of matters in the original formation and growth of bone. We find in a growing bone that (as already mentioned at p. 724) the medullary spaces are occupied by cells, and that cells of a similar character are present under the periosteum. Many of these cells are evidently busy forming the new bone. They are to be found applied to the surface of the existing bone, and gradually becoming buried in a bony matrix which is apparently formed around them, while they take up the position of bone-corpuscles. The cells thus engaged in the formation of bone are properly designated osteoblasts. But in order to preserve the architecture of the growing bone, there must be at some parts destruction of the already formed tissue. It used to be supposed that this de- struction occurred by the bope-corpuscles enlarging and causing the surrounding tissue to melt down, but it has now been shown that a special form of cell is engaged in the destruction of the bone, and these cells are properly called osteoclasts. They are very large cells with a granular protoplasm and many nuclei, or in other words, they are giant-cells or myeloplaques (see Fig. 320, p. 735). Wherever absorption of bone is going on these cells are to be found, and they appear to adhere to the surface of the bone and cause absorption of the matrix. In this way they dig themselves into the bone and form gaps, in which they are often to be found lying. These rounded gaps in the bone have long been known, and they are usually designated Howship's lacuna. In the granulation tissue of an inflamed bone both osteoblasts and osteoclasts are frequently present. By the action of the osteo- clasts in the Haversian canals and medullary spaces, the bone becomes opened out and dense bone is made spongy or spongy bone more open. At the same time the osteoblasts are often at work, and perhaps under the periosteum there are spiculse of new- formed bone, at the marginal parts of which processes exactly similar to those beneath the periosteum of a growing bone can be seen (see Fig. 318). It happens not infrequently that after the bone has been opened out by the rarefying process, the osteoblasts subsequently set to work, and the bone is restored, or even con- siderably condensed as compared with its original condition. ABSOKPTIOi^ OF BOXE. 733 It is to be added that besides the rarefaction of the bone by the process already described, it appears that the bone sometimes gets channelled for the accommodation of new-formed bloodvessels. We know that the bone-corpuscles, with the canaliculi, convey nutritious fluid through the dense bone, and according to require- ments these may expand into bloodvessels apparently by the lacunse enlarging and running together. This, however, as compared with the other, is an insignificant factor. Pig. 318. .^.£,-«fe?^^ New formation of bone in connection with inflammation. The osteoblasts are getting surrounded by bony matrix and becoming hone-corpuscles. X 85. Caries. — This subject may be conveniently considered here, especially in connection with rarefying osteitis. "We have seen that in this latter condition the bone is encroached upon by the osteoclasts, and the lamellae are thinned. I^Tow, this process may go on to the complete destruction of the bony lamellffi, so as to produce, in fact, a progressive destruction of the bone. This con- dition is usually associated with either a very acute inflammation or one which has an infective .character (tuberculosis, syphilis). As the place of the bone is taken by sofb inflammatory tissue, this structure is not able to resist the mechanical wear to which bone is naturally exposed, and so there is an ulceration of the soft tissue generally associated with suppuration. As the soft tissue gives way, the invasion of the bone advances, and so, beyond the actual ulcerating and suppurating surface, the bony lamellae are greatly thinned and ready to break down. In the majority of cases the caries is connected with disease of the joints, as we shall see after- wards, but a periosteal inflammation, especially when connected with syphilis, may lead to it. Before leaving the general subject of osteitis, it will be proper to make some observations on the absorption of bone. We have already seen in the case of rarefying osteitis and caries that ab- sorption of bone takes place by means of the osteoclasts or giant- cells, and it appears further that whenever bone is absorbed, 784 DISEASES OF THE BOXES AXD JOINTS. whether it be dead bone or living, the same agents are at work. When, in a simple fracture, a considerable piece of bone is separated from all its attachments and all its bloodvessels torn across, then it will probably die. Necrosis does not occur in every case, as the observations of Macewen on transplantation 01" bonb show that pieces of bone removed from one person to another may survive and become incorporated in their new position. But in order to their survival, the pieces must be small, so as to allow of ready penetration of bloodvessels into their medullary spaces. When pieces of considerable size are broken off they do not survive. Similarly in compound fractures pieces of bone are frequently separated from all their vascular connections and may be seen lying in the wound, with a dead white color and a hard feeling when touched, being evidently dead. Or again, at the end of stumps necrosis of a piece of the bone may occur from osteo- myelitis or otherwise. Or, as we shall see afterwards, periostitis may lead to extensive necrosis. Pig. 319. isSi/J' oh " 'i „ a "a" ''a , Section of a piece of necrosed bone wliich liad been undergoing absorption. Tlie margins of the bone at the medullary spaces and Haversian canals have an eaten-out appearance from the presence of Howship's lacunse. X 85. IS'ow, in all these cases, if acute suppurative inflammation be averted, and especially if septic inflammation be kept off, the dead bone may be absorbed. This is sometimes seen very plainly in cases of compound fracture where a piece of dead bone may be- come visibly eaten into and replaced by vascular granulations. It must occur frequently in simple fractures and at the ends of stumps. It is also not uncommon in necrosis from periostitis but it will not occur unless the inflammation be moderate in intensity, just as new formation occurs only in chronic inflammations. ABSORPTION AND TE AXSPL ANT ATION OF BONE. 735 The absorption is effected by the osteoclasts. If a piece of dead bone which has been partially absorbed be examined, its surface will be seen to have a worm-eaten appearance, and under the microscope this is found to be due to the existence of innumerable Howship's lacunse (see Fig. 319). In these lacunse, or lying beside them, giant-cells are to be seen, and sometimes a regular row of such cells is visible as if feeding on the bone. Sometimes they are nearly buried in flask-shaped spaces (see Fig. 320). Pig. 320. 'yk.^ Howship's lacunae with giant-cells (osteoclasts) in them, and free giant-cells ; from same piece of necrosed bone as preceding figure. X 350. The process of absorption occurs not only in pieces of bone which have died in the body, but in pieces of ivory or bone intro- duced for therapeutic purposes, as in ivory pegs for ununited fracture, bone drainage-tubes, etc. Here also the bone or ivory is eaten into, and Howship's lacunae with osteoclasts are visible. Such pieces of dead and macerated bone may thus be completely absorbed. By a similar process living bone is absorbed. Where an aneurism advances against a bone, as the sternum or vertebrae, and erodes it, the destruction of the bone is produced, as in the other case, by osteoclasts. So it is also when a tumor advances against a bone and erodes it, although it is necessary to exclude from the category the case of certain turners which, as we shall see afterwards, may originate in the bone itself, and cause destruc- tion of the bone by softening occurring around the bone-corpuscles which give origin to the tissue of the tumor. It is necessary to add to all this that although osteoclasts in the form of giant-cells appear to be the chief agents in the destruction of bone, both dead and living, and both in the physiological growth of bone and under the command of pathological processes, yet that absorption may be produced by other agents. We have seen how 736 DISEASES OF THE BONES AND JOINTS. in osteomalcia there is destruction without giant-cells, and we have also seen how by canalization there may be rarefaction of the bone withoxit giant-cells. We may now enter more specifically on the individual Forms OF Inflammation in which the bone is involved, and it will perhaps illustrate the matter if we take up first the processes concerned in the healing of fractures. Healing of Simple Fractures. — As we have seen, this occurs mainly by the formation of callus, and we have to consider how this callus is formed. At the time of fracture the periosteum is torn and, to some extent, raised from the surface. The marrow is also torn across. Blood is effused, but it generally gets diffused, and if it exercises any influence on the further course of events it is by keeping the parts separate and interfering with the healing process. The blood, however, usually offers little obstacle, and is either absorbed or displaced by the new-formed tissue. The peri- osteum around the broken ends becomes vascular and swollen, and by an inflammatory process is converted into granulation tissue. A similar process occurs in the medulla, and here too the tissue is replaced by inflammatory structures. More slowly, a rarefying osteitis causes the enlargement of the Haversian canals and medullary spaces, and these also are filled with granulation tissue. The next process is the new formation of mature tissue, and the amount of tissue formed and its kind are determined by circum- stances. If the bones are kept very fixed then there is compara- tively little inflammation, and the amount of granulation tissue produced is small. The granulation tissue under these circum- stances forms new bone, in the way already described (formative osteitis). In the periosteum, in the marrow, and between ends of the bone, the osteoblasts set to work and produce bone. This bone is at first in the form of narrow trabeculse, and the callus thus foi'med consists of soft tissue in which are narrow trabeculse of bone. According to its situation the callus is called external, INTERNAL, Or INTERMEDIARY. The external callus encloses the broken ends in a sheath, the internal forms a rod uniting them, the intermediary, formed in the widened canals and spaces of the bone itself, passes from one broken end to the other and so unites them in detail. If the bone has not been kept rigidly fixed, the amount of graimlation tissue and of callus is large, and especially the external callus, in which a large number of narrow trabeculse of bone are formed. When the rigidity is very imperfectly pre- served, then, instead of the granulation tissue forming bone, it develops into fibrous tissue and cartilage. This occurs almost uniformly in the fractures of animals, but is sometimes seen also in man, especially in fractures of the ribs where it is difficult to prevent a certain amount of movement. Fig. 313, p. 720, was taken from a case of multiple fractures in an insane person, in PERIOSTITIS. 737 whom the existence of the fractures was unknown, and no attempt made to keep the bones at rest. We have ah'eady seen that carti- lage, connective tissue, and bony trabeculse are all represented. When the bone has become fully united the parts of the callus not necessary for the preservation of the continuity of the bone are disposed of. The intermediary callus becomes, for the most part, the permanent bond of union, Avhile the external and internal disappear except I'ig- 321. in so far as they are needed to fill up gaps where the bones have not been exactly in apposition. Sometimes the bones are con- siderably out of position, and a large amount of new bone remains permanently as the bond of union. Periostitis. — The periosteum is inflamed under somewhat various circumstances. Chronic periostitis is a frequent circum- stance of inflammation in joints and of necrosis of bone; it occasionally results even from ulcers of the skin when situated immediately over a bone which has little more than the skin covering it, as, for in- stance, the tibia. The periosteum is the seat of granulation tissue which, as time goes on, is developed into mature tissue. In some cases, and especially in old rheu- matic aflPections of the joints and under ulcers of the skin, the new tissue formed is cicatricial connective tissue, so that the bone is covered with a dense hypertrophied peri- osteum. In the majority of cases, however, and this applies to most inflammations of the joints, the inflamed periosteum pro- duces new bone and the osteoblasts add irregular outgrowths of bone to the surface. In this way we have localized thickenings of the bone which are sometimes designated hyperostoses, or periostoses (see Fig. 321). The new formation of bone may even extend out a considerable distance from the bone, and we may have the joint locked by projecting bony outgrowths, which sometimes coalesce, forming a synostosis. Suppurative Periostitis occurs in two forms. There is a rare form in which a rapid suppuration occurs with gangrene of the periosteum and acute inflammation around. With this malignant periostitis there are sometimes associated pysemic lesions in the lungs and elsewhere. In this disease micrococci are found in the pus which forms beneath and around the periosteum, as well as in 47 Hyperostosis in the bones of the leg and foot in ele- phantiasis. (ViRCHOW.) 738 DISEASES OF THE BONES AND JOINTS. the bloodvessels in the metastatic inflammations. The disease is thus an infective one, although the mode of entrance of the organisms is just as obscure as in the case of ulcerative endo- carditis. Simple Acute Periostitis occurs mostly in weakly children as the result of a blow or other injuiy, and it takes place most fre- quently in the bone which is most exposed to such injuries, namely, the tibia. The inflammation afi:ects the subperiosteal layer and the subjacent bone chiefly. At first there is swelling from inflam- matory infiltration of the periosteum, and, if the inflammation does not resolve, then suppuration ensues.. The pus collects between the periosteum and the bone and raises the former over a certain area. The bone thus denuded of its periosteum dies, as the nutrient vessels passing into the bone are severed. The sub- sequent events connect themselves with the necrosis of the bone, and will be considered afterwards under that heading. Osteomyelitis. — This name is given to inflammation of the bone-marrow, and it occurs very rarely as a spontaneous or in- dependent disease. There are cases of malignant osteomyelitis which are strictly comparable to malignant periostitis, and in which also micrococci have been found. A general pysemic con- dition may develop also in this disease. Teaumatic osteomyelitis arises as a septic inflammation in connection with compound fractures and amputations. The m'arrow becomes swollen from inflammatory hypersemia and inflltration, and ultimately abscesses may form. This disease is of importance for two reasons. The suppurating marrow may induce necrosis of the bone, or it may be the starting-point of a pyjemia, the infective organisms getting into the open-mouthed veins of the bone and extending inwards. NECROSIS OP BONE. This name implies the death of a portion of bone, and we have already considered some of the ways in which it may be brought about. It may be by periostitis or osteomyelitis, or by direct violence. We have seen also how in some cases the piece of dead bone is absorbed. But in many cases absorption does not occur, chiefly where an acute inflammation exists around. Whether ab- sorption occurs or not, the first occurrence is the separation of THE DEAD BONE FROM THE LIVING, and this is effected by an inflam- matory process. The dead bone by its mere mechanical presence sets up an inflammation around it. By means of a rareiying osteitis the Haversian canals and medullary spaces enlarge, and the bone immediately around the dead piece being replaced by granulation tissue, the necrosed portion becomes a sequestrum. The process of absorption may, as we have seen, proceed to attack the dead piece, which may completely disappear. But this pre- sumes that the sequestrum is itself non-irritating, and that the NECROSIS OF BONE. 739 granulation tissue is not stimulated to suppuration. In many cases these conditions are not fulfilled. The acute inflammation which caused the necrosis may continue, or a septic inflammation may extend from a wound communicating with the dead piece of bone, it may be after the opening of an abscess in periostitis or otherwise ; in either case suppuration may occur in the granula- tions around the sequestrum, and this is fatal to the absorption of the dead bone. In these cases we have a considerable area of inflammation around the sequestrum, and in this area of inflammation we have both new-formation and destruction of bone. The surrounding bone is opened out by rarefying osteitis. At the same time the periosteum or endosteum produces new bone, so that the bone as a whole is thickened and the sequestrum is covered in by a mass of soft bone like callus. The commonest cause of necrosis is peri- ostitis, and the sequestrum in that case is on the surface of the bone, and the periosteum is raised in the original suppuration. This raised periosteum produces a shell of new bone as just mentioned, and if the necrosis be considerable this shell of new bone may exercise the function of support instead of the bone. In this shell there are very commonly apertures through which the pus of the original suppuration has passed, and through which the pus of the existing suppuration finds exit. Such an aperture is called a cloaca, and it is usually by enlarging the existing cloacae that the sequestrum is removed. Phosphorus-necrosis. — This condition occurs chiefly in persons who are employed in workshops where lucifer matches are manu- factured, and who are thus exposed to the vapor of phosphorus. The vapor acts locally, on the jaws chiefly, and it is said that persons with carious teeth are particularly liable to be aifeeted. The phosphorus produces an inflammation mainly of the perios- teum, resulting in a great new-formation of cancellated bone on the surface of the jaw. This bone may afterwards become con- densed by the ossification encroaching on the medullary spaces. After a time the inflammation leads to suppuration, and the pus forms between the new-formed bone and the original bone of the jaw. From this results a necrosis of the jaw which may involve the entire bone, and be accompanied also by necrosis of the new- formed bone. The resulting suppuration is usually fatal in their results, but after removal of the sequestrum healing may occur. From the observations of Wegner it appears that phosphorus acts as a general stimulant to the structures concerned in the for- mation of bone. The phosphorus vapor acting directly stimulates so violently as to produce the inflammation and necrosis just described, and this result has been produced also in rabbits exposed to the vapor of phosphorus. When given in small doses internally, phosphorus produces in growing animals a distinct stimulation of the process of formation of bone. In such cases the bone produced at the ossifying border of the cartilage is not a spongy bone, but a dense layer, and there is also an unusually 740 DISEASES OF THE BONES A:N-D JOINTS. dense bone produced beneath the periosteum. It is noteworthy that in growing animals to whom small doses of phosphorus were given, while insufficient quantities of lime were supplied, there was a great production of osteoid tissue, somewhat like that pro- duced in rickets. SYPHILITIC AFFECTIONS OF BONE. These lesions have nearly always their seat of origin in the peri- osteum, although the subjacent bone may be simultaneously involved. The condition may be briefly described by stating that gummata are produced, while inflammation occurs around. The existence of the gummata is sufficient indication that the lesions are of the tertiary stage. Gummata of the usual structure are produced in the internal layers of the periosteum, and there is thickening of the periosteum around. This membrane being tightly stretched over the tumor, the swelling is hard to the feeling, but often with a certain elastic resistance. The gumma undergoes caseous metamorphosis in its central parts, but advances peripherally, and as it advances against the bone it causes erosion of it. The advance is in the flrst instance along the vessels, and as erosion occurs around them a worm-eaten appearance is produced in the bone. Beneath the gumma, which has most frequently its seat on the bones of the skull, especially the frontal bone, there may be thus considerable loss of substance, so that even the entire thickness of the skull may be penetrated. The caseous material often undergoes softening and suppuration ensues. If great care is not taken in evacuating the abscess at an early date, there may be very obstinate and even extending ulcers produced. "Without ulceration the gumma may undergo resolu- tion, and a cicatricial depression result, or after ulceration healing may occur. Along with these processes immediately related to the gumma, there are in the neighborhood conditions referable to inflammation. The bone around is condensed by new-formation filling up the medullary spaces, and there is sometimes a thickening of the bone by inflammation of the periosteum. This is much less common in the skull than in the long bones, especially those of the legs,.where it sometimes leads to a very striking hypertrophy of the bone, whose surface is exceedingly rough from the loss of substance in some parts, and the irregular new-formation in others. The bone around the syphilitic defect or ulcer is dense bone, and in this respect con- trasts very markedly with that around the ulceration in caries. Heebditary syphilis leads to certain important changes in the bones which have been described chiefly by Wegner. These changes consist mainly in a stimulation of the ossifying structures of the bone, while the proper process of ossification is imperfectly effected. In certain respects, therefore, they show some analogy SYPHILITIC AFFECTIOXS OF BOXE. 741 to the changes in rickets, but differ from them, as we shall see, in detail. They also differ in respect that the principal changes in syphilis are congenital, and are to be seen in their typical form in the long bones of still-born syphilitic foetuses. These changes may even be used to diagnose the existence of congenital syphilis. In the cranial bones there are frequently changes, mainly affecting the periosteum, but they are by no means constant, and are to be distinguished from those in the long bones, which are more distinctive of syphilis. These changes in the periosteum consist in slight inflammatory processes, leading to thickenings with softening of the bone. They are of importance as being probably the cause of craniotabes, which appears to be a frequent concomitant of hereditary syphilis. This condition is brought about when a child with bones affected as above is in the habit of lying with one part of its head resting on a support ; in that case the bone is apt to give way, and the brain to be covered merely by soft parts. In the long bones the changes occur at the ossifying margin of the cartilage. "We have already seen that in the normal bone the border of ossification is a narrow line, the transition zone occupying little space and forming a straight transvere line. In congenital syphilis this is altered, and for convenience of description Wegner distinguishes three stages; these may be followed in the bones divided longitudinally, ' so as to show cartilage, ossifying border, and bone, in section. In the first stage the ossifying border is not linear, but forms a zone about the twelfth of an inch in breadth, and of a whitish or reddish-white glancing appearance. In this zone microscopic examination shows an excessive proliferation of the cartilage-cells, which, with the matrix, have become calcified as if in preparation for ossification, but this process has not been completed. In the second stage the zone is about twice the breadth of that in the first stage, being occupied as before by calcified and prolif- erated cartilage. The boundaries of this zone in both directions are very irregular, the calcified cartilage on the one hand sending papillary-like projections into the hyaline cartilage above, and being encroached upon by the irregularly ossifying margin below. Bloodvessels occur in the midst of the cartilage, and these are often surrounded by fibrous tissue instead of the proper foetal marrow. In this dense tissue a direct ossification may occur, a formation of bone without the agency of the foetal medulla. _ In the third stage we have again the calcified zone, which, however, is more brittle than formerly. Above it the cartilage is swollen and blue as in rickets, and beneath it there is a zone not represented in the previous stages. It has a graj'ish-red ov yellow appearance, resembling granulation tissue or pus, and is exceed- ingly soft so as almost to dissolve the continuity of the bone. This zone actually consists of granulation tissue, and appears to be the result of a reactive inflammation induced by the condition of the zone above. This, the calcified zone, shows no longer well- 742 DISEASES OF THE BONES AND JOINTS. formed cartilage-cells; these have shrunken and become ill-shaped like the cells in caseous material. It appears, indeed, as if the calcified cartilage had become necrosed, and by its irritation had set up the inflammation in the medulla beneath. This condition has suggested the question, whether the separation of the epi- physes, which is sometimes met with in young children, may not be due to congenital syphilis. It is to be noted that, so far as known, these affections of the bones have their origin during intra-uterine life, although they may continue and perhaps develop further after birth. It is even possible that future observation may show that they can originate after birth. In regard to the bones affected, the order of frequency given by Wegner is, lower end of femur, lower ends of bones of leg and forearm and upper end of tibia, upper ends of femur and fibula much more seldom than upper end of radius and ulna; and most rarely the lower end of the humerus. It may be inferred that the disease is usually multiple, being present in several bones simultaneously ; and the various stEiges may be seen in the same person, the disease being variously aclvanced in different parts. TUBERCFLAE OE SCEOPULOFS DISEASE OE BONE. This connects itself in a majority of cases with similar diseases of joints, under which heading it will again be considered. But apart from the joints we may find it in the bodies of the vertebrae, in the bones of the carpus and tarsus, etc. The disease manifests itself as a rarefying osteitis with caseous necrosis. The opened- out spongy tissue is filled with granulation tissue, and in the midst of this tissue tubercles of regular structure are to be found. The tubercles in the midst of the granulation tissue indicate the true nature of the disease, and it is therefore proper to recur to the older designation, tuberculosis of bone, rather than to use the term scrofulous disease. In many cases the disease goes on to suppuration, but it is a chronic process, and the abscesses which result are cold abscesses; these, in the case of the vertebrae, may attain a considerable size. The destruction of the bone and substitution of soft granulation tissue cause the structure to lose greatly its power of bearing pressure. As the bodies of the vertebrae are exposed to consider- able pressure, they very often become in this disease crushed together, and an acute curvature (antero-posterior) is the result. Although the disease is tubercular, it is capable of healing, and in that case the granulation tissue forms new bone, often dense, so that the structure is firmer and heavier than it was originally. If collapse of the vertebrte has occurred, then the healing will make permanent the loss of substance, and confirm the curvature. SPINAL CURVATURES. 743 SPINAL CURVATURES. Introductory. — The spinal column is composed of vertebrae whose bodies are separated by elastic fibro-cartilages. The ver- tebrae articulate with each other at four other points, two on the upper and two on the lower surface of the arch. The vertebrae are also bound together by firm ligaments in front of and behind their bodies. The efifect of these various connections is that, even when the spine is separated from all its attachments except the ligaments, it retains its form to a large extent, and its natural con- formation may be studied after its removal from the body. When seen in profile the spine presents the well-known antero- posterior curves, the convexity being forwards in the cervical and lumbar regions, and backwards in the dorsal. These curves are capable of considerable variation in the movements of the body. The whole of the curves may be obliterated and converted into a general convexity backwards by stooping forwards, as when, with the arms extended and the legs straight, an attempt is made to touch the toes with the tips of the fingers. By arching the body backwards the dorsal curve may be partially obliterated, and a general convexity forwards be produced. It appears, therefore, that the spine is capable of considerable antero-posterior move- ment. These antero-posterior movements imply a considerable degree of compressibility of the intervertebral cartilages. The combined cartilages occupy about a fifth of the entire length of the spinal column, and their compressibility may be inferred from the fact that during the retention of the erect posture the entire length of the column gradually diminishes, so that the stature is usually from half an inch to three-quarters less at night than in the morning. This is believed to be due chiefly to the compres- sion of the cartilages, which recover at night Avhen the recumbent posture is assumed. The antero-posterior movement of the spine is freest in the cervical and lumbar regions, and most limited in the dorsal. The spine is capable to a much more limited extent of lateral movement. The articulating processes, being situated on either side of the arches, prevent any considerable lateral deviation, as they become locked against each other when that occurs. If the surfaces of these processes were horizontal, facing one another above and below, then they might allow of freer lateral movement, but the more they assume the perpendicular position, and the more they face inwards and outwards, the greater is the impedi- ment to lateral movement. It will be found that on passing from above downwards the articulating surfaces assume more and more of a perpendicular position. In the cervical region they are oblique, and face slightly inwards and outwards; in the dorsal they are more perpendicular and face nearly forwards and back- wards, while in the lumbar region they are nearly perpendicular, and face each other nearly inwards and outwards. In this way it 744 DISEASES OF THE BONES AND JOINTS. occurs that while lateral movement is limited in all regions it is almost impossible in the lumbar region. For a similar reason, twisting of the spine on its axis is possible to a very limited extent. The question of the existence of a natural lateral curvaturehas been matter of dispute. It is generally stated that there is a slight lateral deviation to the right in the upper dorsal region, and this is usually ascribed to the more frequent and forcible exertion made with the right arm; brt the existence of this curve has been seriously questioned (Adams). The late Dr. Foulis, in one hundred and ten post-mortem examinations, found lateral deviation in no less than fifty-eight cases. He did not observe it specially in the upper dorsal region or towards the right, and concluded that it was due to the positions habitually assumed by the persons at their various trades. We may perhaps conclude that normally there is no lateral curvature, but that a very slight permanent deviation is often assumed when a frequently repeated position of the body predisposes to it. Forms of Spinal Curvature. — The function of the spine is to support the structures attached to it, and to hold the head erect, the latter function being in man the more prominent one. Any single curvature of the spine will have the tendency to remove the head from the erect position, and tilt it backwards or forwards or to one side, and in order to preserve the erect position there is required a curvature in the opposite direction. The natural antero-posterior curves are in this sense mutually compensatory, the lumbar restores the position lost by the sacral curve, and the cervical that of the dorsal. "When abnormal curvatures occur there is a tendency to a similar compensation, so that the curvatures may be divided into primary and secondary. It will not be necessary to consider in detail the secondary curvatures ; their amount and direction may be inferred from those of the primary ones. It may be stated, however, that there are, fre- quently, several secondary or compensating curves, the spine presenting several sinuosities in order to reach the stable position for the head. 1. Antero-postbrior Curvature.— There are two quite distinct forms of antero-posterior curvature, the curve in the one form being rounded, and mainly an exaggeration of the natural curva- ture, and in the other sharp or angular. {a) Angular Curvature, or Pott's Disease of the Spine. — This depends on disease of the bodies of the vertebrae. For the most part it is a local tuberculosis of one or more of the bodies with the caseous necrosis and caries described above. The result is usually a slow suppuration with psoas, lumbar, or other abscess. The softened bodies of the vertebrae give way under the superin- cumbent weight, and the spine is bent at a sharp angle, the spinous processes becoming unduly prominent behind. The affection of SPINAL CUEVATUEES. 745 the bodies may be unsymmetrical, and if collapse be more at one side than the other the angular curvature will not be exactly antero-posterior. This form of curvature is more rarely due to traumatic causes, as crushing of the bodies by heavy weights falling on the head or back, or by a fall from a height. This may lead immediately to an angular curvature, or may be the starting- point of a necrosis and suppurative inflammation. Even tuber- cular disease of the bodies seems often to have its starting-point in an injury, such as a fall or twist of the spine, such injury leading to this result only in predisposed persons. In the majority of cases Pott's disease occurs in children, tuberculosis of bone being commonest in early life. If healing of the disease of the bodies occurs, the carious bone becomes firm, but the loss of substance by the collapse of the bodies is not recovered, and the bone is fixed permanently in its abnormal position. The new-formed bone may be even firmer than the old, and if several bodies have been diseased there may be anchylosis of them, so that a piece of the spine is absolutely fixed. It is worthy of special notice that angular curvature is much more obvious in the dorsal region than elsewhere, as it here increases the natural posterior curvature. In the cervical and lumbar regions, where the natural convexity is forwards, there may be a rounded posterior curvature produced, or even with extensive disease, there may be very little posterior curvature visible externally. The spinal cord is not generally injured by angular curvature, but in some cases it is crushed and interrupted. It may be so even during the process of healing, the sclerosis or condensation of the vertebrse sometimes causing further shrinking and increase of the curvature. (b) Kyphosis or Posterioe Curvature. — This is mainly an exaggeration of the normal curvature with the convexity back- wards in the dorsal region, and is due chiefly to muscular weakness or a habit of stooping. It is most frequent in children and old people, leading in its most exaggerated form to hump- back, and in a lesser degree to round shoulders. (c) Lordosis or Anterior Cura^aturb. — In this conditionthe convexity of the curve is forwards, and the tendency of it is to throw the head backwards. It is most common in the lumbar region, and in the majority of cases is due to rickets. Rickets when it afifects the pelvis causes the sacrum to assume a more horizontal position than normal, and in order to retain the erect position the lumbar anterior curve is exaggerated. It may also be produced by congenital dislocation of the hip-joint (stated by Adams to be of considerable frequency), and anchylosis of the hip. There may be also, but rarely, a direct lordosis in the lumbar region from rickets, the natural curvature being increased by reason of the softness of the bones. In the dorsal and cervical regions lordosis is very uncommon. 746 DISEASES OF THE BONES AND JOINTS. 2. Lateral Curvature or Rotatory Curvature. — In the intro- ductory section we have seen that the mechanism of the spine allows of exceedingly limited lateral deviation. But it often hap- pens that from habitual faulty positions at work or otherwise there is a frequently repeated tendency to lateral deviation. In that case, as a direct displacement is not possible, there may be, espe- cially in persons constitutionally weak, a deviation with partial rotation of the vertebrae. The faulty position may be merely the result of a bad habit, of standing on one leg for instance, so as to cause obliquity of the pelvis; or it may be from sitting in a con- strained position at study or manual labor, so that either the pelvis is oblique or the arms are used in one particular direction so as to displace the centre of gravity to one side; or there may be a hys- terical contraction of the muscles of the scapula lasting for a long period and altering the centre of gravity; or there may be an ob- liquity of the pelvis from one leg being shorter than the other, as sometimes in rickets. There is also softening of the bones in rickets, and very severe curvature may occur when this is asso- ciated with obliquity of the pelvis. Pm. 322. Diagram showing rotation of vertebra in lateral curvature. The various lines show the positions of the body and transverse processes in the different degrees of rotation. The axis of rotation is behind the tip of the spinous process, where the three lines meet. (Adams.) The mechanism of this rotation will be understood from the ac- .companying diagram (Fig. 322). The dark outline indicates the natural position of the vertebra, the dark straight lines indicating the natural axis and the direction of the transverse processes. When rotation occurs the body moves round so as to present to one side in the direction of the lines aa and aa, while the spinous process deviates very little. In the figure the centre of rotation is just behind the tip of the spine, and there is a slight deviation of it; but the centre of rotation maj^ be at the tip of the spine, and LATERAL OE ROTATORY CURVATURE. 747 with very marked rotation of the vertebrae, there may be no devia- tion of the spines. Lateral rotatory curvature is met with chiefly in the dorsal and lumbar regions, being, as a rule, much more extreme in the former, probably from the greater mobility there. There is usually curva- ture in both these regions, the two curves being in opposite direc- tions, and one of them in a certain sense secondary. It is not possible, however, to distinguish rigidly between primary and secondary curves, as the two form nearly pari passu; a slight de- viation to one side will result in a similar curve to the opposite side, and they will increase together. We have seen above in connection with Fig. 322 that the plane of the transverse processes is altered by the rotation of the verte- brae. An examination of that figure will show that the transverse process on the side of the convexity is considerably displaced back- wards, and in actual cases it may be felt projecting under the skin. If the curve be in the dorsal region the rib will be similarly dis- placed, and its angle especially will project. As shown in Fig. 3.23, the rib in that case commonly makes a sharp curve at its angle, so Pig. 323. Diagrammatic section of normal chest and that with rotatory curvature. In the latter it is seen that the body of the vertebra is rotated into the right side of the chest, the rib on this side turning at an unduly sharp angle. The prominence of the transverse process on this side and of the breast on the opposite side is shown. (Adams.) that it is greatly flattened laterally. The figure also shows that, in such a case, the capacity of the corresponding side of the chest is greatly diminished. The body is rotated into that side of the chest and the ribs are flattened towards the vertebrse, these condi- tions sometimes attaining to such a degree that the bodies of the vertebrse approach the internal surfaces of the ribs. There is con- sequently great reduction in the capacity of this side of the chest, the lung being correspondingly compressed and curtailed in its movements. It will be seen also that posteriorly there is prom- inence of the angles of the ribs on the side corresponding with the convexity of the curve, while anteriorly the breast on the op- posite side is prominent. 748 DISEASES OF THE BONES AND JOINTS. TUMOES OP BONE. Osseous Tumors. — In view of the fact already illustrated on more than one occasion that inflammatorj' processes in and around bone lead frequently to new formation of osseous tissue, it is not remarkable that there are certain bony growths which stand, as it were, on the border-land between tumors and inflammatory growths. Some of these have been mentioned at p. 187, under the designations hyperostosis and periostosis. In these cases there is always some form of irritation inducing the new formation, and the new bone takes origin from the periosteum, so that it is applied to the surface of the existing bone, forming outgrowths from it. The irritation may have its origin in an inflammation of the bone, of the periosteum, or of the joints, and we shall see afterwards that diseases of joints, especially chronic rheumatic inflammations, are frequently accompanied by new growth of bone. Various names have been applied, according to the circum- stances of these bony outgrowths due to irritation of the peri- osteum. The name osteophyte is given when there are numerous small elevations of the surface without any considerable thickening of the bone; these may have a figured appearance on the surface, and they are sometimes loosely adherent to the bone, coming ofl with the, periosteum when it is removed. Hyperostosis is a gen- eral enlargement of a whole bone, or a considerable part of it, with roughness and tuberculation of the surface, such as occurs sometimes in a long bone in consequence of syphilis or elephan- tiasis (see Fig. 321, p. 737). Such a hypertrophy of a long bone has hardl}' the characters of a tumor, but when a small bone is thus enlarged, it acquires much inore of the appearance of an independent separate growth. Exostosis is a more definite tumor of bone, an outgrowth with a limited basis, but even some of these have intimate relations to irritations of bone. This applies especially to multiple exostoses, which are of occasional occurrence. In the ease from which Fig. 324 is taken (Virchow), the patient, a boy ten years of age, had suffered, during the course of three years, from repeated attacks of rheumatism affecting the joints and muscles. The result was the formation of sixty-five exostoses on various bones of the body. Exostoses also occur not infrequently at the insertion of tendons, growing into the latter and sometimes even separate from the bones. These are connected in their origin with the contraction of powerful muscles, occurring chiefly where such muscles are inserted, and sometimes induced by specially violent exercises of the muscles. The more simple exostoses have been already considered at p. 185. The name osteoid chondroma has been given by Virchow to a form of tumor which merits a more special description. The TUMORS OF BONE. 749 I'iG. 324. Pig. 325. /ii Fig. 325. — Osteoid chondroma of the tibia, divided ob- liquely. At the upper extremity the tumor has surrounded the cartilages of the knee, and new-formed cartilages have been produced. Internally the bone is condensed by the new formation of bony masses. From a boy 13 years of age. (ViRCHOw.) Fig. 324. — Multiple exostoses of femur, tibia, and fibula. These are grouped towards the ends of the diaphyses. At its lower end the fibula is flattened by the exostoses growing out from the tibia. From a boy 10 years of age. One-third the natural size. (Viechow.) 750 DISEASES OF THE BONES AND JOINTS. • tumor is composed essentially of tissue such as we find in the deep layer of the periosteum of a growing bone, or in callus, its main constituents being osteoblasts. The cells are smaller than cartilage-cells and mostly round, but they do not possess a capsule. There is a dense intercellular substance which has a somewhat fibrous appearance. In the midst of the tissue bits of true car- tilage may be found. Being formed of tissue analogous to that which is preliminary to ossification, it frequently undergoes calci- fication, and even true conversion into bone. The tumors form, mostly, under the periosteum of the long bones, and their seat of election is the lower end of the femur or the upper end of the tibia, originating probably in the layer of osteoblasts there, and they may grow to large dimensions. They thus form club-shaped expansions of the long bones (Fig. 326). On section, the tissue is found to be dense, and it is found to be osseous or calcareous on passing deeply, where it is incorporated with the bone. The medullary cavity of the bone is often filled with new-formed bone. This form of tumor sometimes presents a tendency to become sarcomatous, and even without that it may recur after removal. Sarcomas in connection with bone are a very important group of tumors. As the sarcomas are of a connective-tissue structure, so they originate from connective tissue. The marrow and the periosteum being connective-tissue structures, we may have sar- comas originating from them, but the bone also is a connective tissue, and there seems no reason to doubt that it may also give origin to sarcomas. We may, therefore, distinguish sarcomas according as they have a central (myelogenous), interstitial (osse- ous), or peripheral (periosteal) origin. Of the MYELOGENOUS SARCOMAS the most characteristic is the myeloid or giant-celled sarcoma, already sufficiently considered. But we also meet with central round-celled sarcomas, or even spindle-celled sarcomas. The central sarcomas originating in the medulla of the cancellated tissue or in that of the shaft of a bone, usually destroy the external shell of bone as they grow. In this way they frequently reach the surface and may even work them- selves into surrounding tissue. In some tumors which are usually regarded as central, it is not certain that the destruction of the bone occurs entirely hy the tumor acting on it. Considering that the bone-corpuscles are but modified medullary cells, it is not unlikely that they also take part in the tumor-formation. As we have already seen in the case of the myeloid tumor, there may be a new formation of bone at the same time as the destruction, and . so the tumor may acquire a bony shell after the destruction of the proper external shell of the bone. The sarcomas of interstitial growth do not form such a definite group. It has been customary to regard sarcomas of bone as originating either in the medulla or periosteum, but Ziegler has shown that the tissue of a sarcoma may take origin directly from the bone-corpuscles. Tumors taking origin in this TUMOES OF BONE. 751 way will in tlie first instance replace the bone, and they may grow to a considerable size, simply occupying the place of the bone. In a preparation in the museum of the Western Infirmary the entire humerus of both arms is replaced by a soft sarcoma, which occu- pies the place of the bone, although larger than it in circum- ference. It is onlj^ at the extremities that any of the bone remains, and here the appearance is not as if the bone were being destroyed by a myelogenous tumor, but as if it were actually expanding into the tumor. A tumor of soft tissue replacing the bone will readily lead to fracture, and in the case referred to the first indication of any disease of the bone was a spontaneous fracture. These sar- comas are usually soft tumors whose cells are mostly round and generally small. The PERIOSTEAL sarcoma is usually composed of spindle cells, and such tumors may grow around a bone, extending outwards for a considerable distance. "We have seen also that sometimes a myeloid tumor takes origin in the periosteum of the jaw, forming an EPULIS. Of peculiar interest here is tlie tumor named the OSTEOID SARCOMA. This tumor is that which by Paget and others has been well described as osteoid cancer. It shows some relation to the osteoid chondroma in respect that its cells are like those of the ossifying layer of the periosteum. In the osteoid sarcoma, however, the cells are more abundant and less regular, and they produce bone more uniformly. The tumor, in fact, usually pre- sents the appearance of a dense mass of bone of ivory hardness, on the surface of which there is a layer of fibrous-looking tissue. This layer is often comparatively thin, and on microscopic exami- nation it presents spindle cells or round cells which are so closely adherent to each other that they are with difficulty isolated . The bone is formed by the direct transformation of these cells, and one has sometimes the opportunity of observing remarkable transition forms. The tumor, like the osteoid chondroma, mostly originates at the end of one of the long bones, and forms a bulbous swelling there, the end of the bone, with its medullary spaces, being com- pletely transformed into a hard, heavy, osseous tissue. The tumor enlarges by incorporating neighboring parts, and it not infrequently extends by metastasis. Primary cancer is very rare in bone, but tumors of a glandular or epitheliah structure have been met with, destroying the bone in their growth. In some cases this is really a penetration of a cancer into bone, but there seem to be actual cases in which a cancer has originated in bone. Secondary cancer is much more frequent. There are some cancers which, when they become generalized by the cancerous material getting into the blood, have a special pro- clivity to develop their metastatic tumors in the bone marrow. We may thus in a great number of bones have a cancerous trans- formation of the medulla, and as the tumor grows the bone is de- stroyed. A condition sometimes develops in this way not unlike OSTEOMALACIA in the manner in which the bone becomes softened. We may thus have cancerous softening of the bodies of the verte- 752 DISEASES OF THE BONES AND JOINTS, brse, of the ribs or of the long bones, the tumors being in large numbers, and everywhere growing from the medulla. The bones are sometimes the seat of cysts. These mostly occur in the jaws, where they may greatly distend the bone, but in the case represented in Fig. 426, the ^10- 326. fibula was at its end distended into a bulky cyst which contained merely a serous fluid. The CYSTS OF THE JAWS, Originating as they do for the most part near the alveolar processes, are probably re- lated to the teeth. Some of them are single, unilocular cysts, and have their origin in teeth which have not undergone the usual eruption. A tooth or pieces of hard substance (dentine) are usually present in the wall of the cyst. Others are multi- LocuLAR and develop out of a gland- like tissue, the cells of which un- dergo colloid degeneration, and in this way form cysts. In its original structure the tumor might be called an adenoma, and a considerable por- tion of it is sometimes composed of solid glandular or epithelial tissue. According to Eve the tumor arises by penetration downwards of the epithelium of the gums, and he re- lates this to the normal penetration of this epithelium in the foetus in order to form the enamel organ. These multilocular cysts are mostly innocent, but sometimes the epithe- lium is less regularly arranged, and they approach in structure and ten- dencies to the cancers. Both forms of cysts originate in the interior of the jaws and distend them; those in the upper jaw have a special tendency to pass into the antrum, which they may fill out. FiBROMAS have been occasionally observed growing from the periosteum in the neighborhood of the mouth and nose, and they sometimes project inwards into the nares or mouth as fibrous polypi. The MYXOMA is a very rare form of tumor. Parasites are very rare in bone. The cysticercus cellulose has been observed, but the echinococcus more frequently. The hydatid cyst has mostly been met with in the bones of the pelvis or in the tibia. After growing and distending the bone it may burst through it and develop further in the soft parts around. Cyst of upper end of fibuls.. The upper part of the bone is expanded into a cyst which contained a reddish serous fluid. DISLOCATIONS AND JIISPL AGE JIENTS. 753 B.— THE JOINTS. DISLOCATIONS AND MISPLACE:mENTS. Congenital Dislocations. — Children are sometimes born with the joints in faulty positions, some of these being really traumatic and others of more obscure origin. The traumatic cases arise for the most part during parturition, either from the natural forces engaged in delivery, or by dragging on the part of attendants. The HIP-JOINT is net infrequently dislocated in this way, and usually the displacement is on both sides at once. The head of the bone is usually displaced upwards so as to rest on the dorsum of the ileum above and behind the acetabulum. Through time the head makes for itself a new joint, and the acetabulum fills up. Con- genital dislocations of other joints are exceedingly rare. Talipes or Club-poot. — These names are applied to distortions of the feet, or more rarely of the hands; the bones assume certain abnormal positions in which they are retained by the contraction of muscles. A certain proportion are oonsenital, and these seem to arise in utero by a faulty distribution of the impulses by which the muscles are made to contract. One or more muscles are kept in a continuous state of more or less rigid contraction, while the others are not, and the consequence is that the foot is held in a distorted position. The NON-CONGENITAL forms are, in the great majority of cases, due to infantile paralysis. In this disease, as we have seen, some muscles are paralyzed, while others are not. It has been generally stated that the deformities are due to contraction of the unpara- lyzed muscles which are not opposed in the normal manner by the paralyzed ones. This appears to be the explanation in some cases, but it does not account for the occurrence of talipes in cases where nearly all the muscles of the foot are paralyzed. Such cases indi- cate that the faulty position may arise to some extent because the muscles are not able to keep the foot in its proper position, so that it tends to fall into the attitude it would assume if there were no muscles. These positions are also variously modified by the use made of the foot in walking, the parts being brought against the ground in the position most suitable to stability in the maimed condition of the limb. In a similar way club-foot may occur in pseudo-hypertrophic paralysis. Besides paralysis, it seems that spasm may lead to talipes, al- though the explanation of the' local spasm is often very obscure. It is stated that mimicry sometimes leads to it, or disease of the nervous centres or refiex irritation. It is undoubted that children sometimes acquire a talipes after a convulsive attack. The PORMS OP TALIPES do not call for detailed description here. There are four principal forms, some of which may be combined. In TALIPES VARUS the toes are inverted, and the inner margin of 48 754 DISEASES OP THE BONES AND JOINTS. the foot is raised upwards; the tibiales anticus and posticus are the muscles which are chiefly contracted. In talipes valgus, which is one of the rarer forms, the foot is turned outwards, and the outer border is raised, there is usually also soroe elevation of the heel; the peronei, extensor longus digitorum and gastrocne- mius are the muscles chiefly engaged. In talipes bquinus the heel is raised and the foot extended, so that the person walks on the distal extremities of the metatarsal bones; the gastrocnemius is the muscle contracted. In talipes calcaneus the heel is de- pressed and the foot flexed at the ankle, this deformity being the reverse of the preceding one; the contracted muscles are chiefly the tibialis posticus, the peronei, and the extensors. By long retention of the fixed position the bones become variously modified in shape, undergoing atrophy where exposed to prolonged pressure. Where the cartilage is no longer used in the movements of the joints it also atrophies. The bones frequently acquire ad- hesions in their new positions, and the ligaments, bj^ elongating or shortening, accommodate themselves to the new position. ISTew ligamentous attachments are sometimes formed, and the bones may become joined together by anchylosis. Traumatic Dislocations. — We have here to do with cases in which the bone is pushed out of its place by some external force acting on it. The bones are kept in their places mainly by the ligaments of the joints, but no inconsiderable aid in this regard is given by the muscles which act on the bones. As a general rule when external pressure is exercised on a bone at a joint, the mus- cles are so braced as to enable the bone to retain its place in spite of the external force. But if unexpectedly, or when the muscles are generally relaxed, as by alcoholic stupor, a force is exercised on a bone, then it may be displaced, although the force under ordi- nary circumstances would be insufficient to produce this effect. The bone may even be displaced by the action of the muscles themselves, where a certain group acts very vigorously while their antagonists are relaxed. There are indeed persons who can vol- untarily produce dislocation of almost all the more movable joints, and that by mere muscular efforts. In order to this we must sup- pose a certain laxness of the ligaments, but there is also a power acquired by education of strongly contracting certain muscles, while others which usually contract along with them are relaxed. We know that for the most part the muscles in their contractions are coordinated, and most people are unable to contract individual muscles apart from their coordinates, but there are exceptional persons who possess this power, some in a limited degree and others very remarkably. Many persons, for instance, cannot shut one eye without the other, and most persons when they shut one require to make an active effort at opening the other, in order to prevent it shutting too. But there are persons who can close the eyelids of one eye as easily as they can close the fingers of one hand. ANCHYLOSIS. 755 In traumatic dislocation there is usually tearing of the ligaments to some extent, and in the case of some joints much laceration is necessary before dislocation can occur. When the bone is dislocated, the same contraction of the muscles which normally aids in preventing dislocation, generally offers serious obstacles to the return of the bone to its normal place. If restoration does not occur soon, then the bone acquires adhesions in its abnormal situation, the adhesions being the result of chronic inflammation set up by the irritation of the bone. The displaced bone generally comes to press with its head against a neighboring part of the bone with which it formerly articulated, and the ad- hesions attach it to the periosteum in its new position. Friction by degrees wears down to some extent the opposed piece of bone, and as new bone is produced around by the irritation there may be a kind of hollow joint formed. By the wearing of the bone the cancellated tissue would be exposed, were it not that dense bone is produced on the surface so as to cover in the spongy tissue. A smooth hollow surface may thus be produced, and a tolerably perfect joint, although cartilage is not formed to cover it, but only a layer' of smooth polished bone. The head of the displaced bone also loses its cartilage, and may even get worn away considerably. If the bone remains permanently displaced the old hollow of the joint becomes filled up, bone growing when the friction of the opposing bone is no longer exercised. Spontaneous dislocations are mostly due to inflammatory changes in the joints or their ligaments, or to the contraction of cicatrices in the neighborhood. It will be understood also from what has gone before, that the sudden contraction of one set of muscles while the rest are relaxed may cause dislocation. If spontaneous dislocations are unreduced there may be changes in the joints similar to those in traumatic cases, but there are fre- quently primary inflammatory changes, which are more prominent than those secondary changes. ANCHYLOSIS. By this name is meant fixation of a joint by union of the op- posing bones by means of firm adhesions. The expression "false anchylosis " is sometimes used to designate the condition in which the joint is fixed, not by adhesion between the bones, but by rigidity and shortening of the surrounding soft parts. For the most part anchylosis is the result of inflamma,tions of joints, where the cartilage has been destroyed and healing has subsequently occurred. In the process of healing the inflammatory tissue on the opposing surfaces develops into connective tissue, and as the two surfaces have to a considerable extent coalesced, fibrous tissue unites them permanently. In this fibrous bond of union there are often bony plates, and occasionally the union is effected 756 DISEASES OF THE BOjSTES AINTD JOINTS. by bone itself. This, however, is a very unusual occurrence, as even slight movement of the joint is sufficient to prevent the formation of bone. The fixation of the joint, however, is often so firm«as to resemble an actual coalescence of the bones. An interesting discovery was made by Meier, of Zurich, in regard to the architecture of the cancellated tissue of bones. The bony trabeculse of the spongy tissue do not form an irregular network, as they seem at first sight to do, but they are arranged according to a definite architectural plan. They form, in fact, pillars, which are directed towards the surfaces on which pressure is exercised in the various movements of the joints. Each bone has its own architectural structure, and the structure corresponds exactly with what mathematicians make out as to the direction of pressure in the various bones. When anchylosis occurs, or after the healing of fractures, the lines of pressure may be changed. If these occur in growing bones, the architecture readily undergoes a corresponding change. But even in adults, by thickening of the lamellae in some parts and absorption at others, there is a gradual adaptation of the structure to the changed circumstances. INFLAMMATION OP JOINTS— AETHEITIS. This is a somewhat extensive subject, and includes the great bulk of the diseases to which the joints are liable, especially if we include scrofulous or tubercular disease of the joints. In most cases of arthritis the inflammation affects, more or less, all the structures which enter into the construction of the joint. The irritant is usually present in the joint itself, and is distributed over it with the synovial fluid by the movements of the joint. "We may expect, therefore, that the synovial membrane and the carti- lage, as they cover the surface, will in most cases be primarily aftected. The cartilage, being non- vascular, is less liable to in- flammatory changes than the synovial membrane, which in most cases is primarily and chiefly engaged, especially in acute in- flammations. But in chronic cases the irritation extends beyond these structures to the ends of the bones, to the neighboring peri- osteum, and even to the ligaments. Simple. Acute Arteritis. — This condition is produced most directly by the opening of joints and the occurrence of septic de- composition in their fluids. But it also occurs sometimes by ex- posure to cold, from injuries, and from the extension of phleg- monous inflammations from surrounding parts. The inflammation resembles closely that of the pleura and peri- cardium in its anatomical details. The synovial membrane and cartilages are covered with flbrinous exudation, and the cavity con- tains serous fluid in which flakes of flbrine are visible. This fluid is sometimes very considerable and distends the joint. In this stage the disease may resolve and the joint return to its normal INFLAMMATION OF JOINTS — ARTHRITIS. 757 condition. On the other hand, especially if the joint has been laid open and exposed to decomposition, the inflammation goes on to suppuration. The synovial membrane becomes swollen and dull, being infiltrated Avith inflammatory cells, and gradually .converted into granulation tissue. If the inflammation is very acute, we may have suppuration by the mere exudation of leucocytes without much change in the synovial membrane. "When the disease has gone on to the formation of granulation tissue it is now in a sub- acute condition and is apt to be prolonged. The inflammation also extends beyond the synovial membrane. In the cartilage the cells undergo active proliferation, and the matrix breaks down; thus softening occurs, and ulcers form. There is inflammation of the bone, a rarefying osteitis with caries. The ligaments also take part in the inflammation, they are softened and, with the synovial membrane, take part in the formation of granulation tissue. The periosteum is inflamed and new bone is formed, so that irregular projections occur near the ends of the bones. With all this there is, of course, usually an abundant purulent discharge from the joint, which may weaken the patient and prove fatal, perhaps with amyloid disease. If the inflammation subsides, the various masses of granulation tissue develop into connective tissue, and, by the contraction of this, great rigidity of the joint may be produced. The granulation tissue lining the joint does also to a great extent coalesce^ and the result is a partial or complete obliteration of the joint. The bones thus become finally united by fibrous or osseous adhesions, and a permanent anchylosis is the result. Pyemic arthritis has already been partly considered. In this disease a virus is deposited in the joint and spread over the surface by the synovial fluid. The result is an acute inflammation with fibrinous exudation, but generally going rapidly onto suppuration. It is remarkable that when the joint is full of pus there is some- times very little structural change in the synovial membrane, the whole condition being almost confined to the bloodvessels from which an excessive exudation has occurred. The inflammation usually affects several joints simultaneously. ' It is to be added that occasionally in typhus, dysentery, diphtheria, scarlet fever, etc., a similar acute arthritis occurs. Acute rheumatic arthritis is, like pysemic arthritis, due to an irritant which is present primarily in the blood and affects the structures of the joints like other connective-tissue structures. The result is an acute inflammation accompanied by serous and fibrinous exudation into the joint. The synovial membrane is in- jected and swollen, and if the inflammation is of sufiicient inten- sity and duration the cartilage, and even the bone, take part in it. The cartilage cells undergo proliferation, and may burst into the cavity of the joint. The bones show inflammatory proliferation in the medulla in the usual fashion. As a rule these changes do 758 DISEASES OF THE BONES AND JOINTS. not reach an extreme degree, and suppuration is hardly known to occur. Gouty Arthritis. — In this disease uric a:cid, in the form of urate of sodium, is deposited in the tissues of the joints. It is first de- posited in the cartilage, and, according to Charcot, always, to begin with, at the middle of the articulating surface, that being the point furthest removed from the bloodvessels. The urate is sometimes in the form of stellate crystals (Fig. 327), the cartilage cells forming the middle points of the bunches of crystals. But the salt is also deposited in the matrix and often in the form of irregular needles. It is also frequently deposited in the synovial membrane, and in the bones, ligaments, and soft parts around the joints. Sometimes the salts are deposited even under the skin, forming visible projec- tions (the so-called tophi or chalk-stones). This deposition seems to lead to an acute irritation of the structures of the joint, chiefly an intense hypersemia, often with serous exudation. It never goes on to ^iQ- 327. suppuration, however. "When recovery takes place it frequently leaves a chronic inflammation, resulting in changes analogous to those in chronic articular rheumatism. Chronic Rheumatic Arthritis. — As a rule, this disease aftects many joints, but as the changes are virtually the same as in arthritis deformans, and the two conditions run into one another, we may describe them together. In arthritis deformans the disease is partial, being confined perhaps to a single joint, and the lesions attain a much greater development than in general articular rheumatism. It is also much more a disease of old people, and is met with chiefly among the poor. In both these diseases the nature of the irritant is entirely obscure. The inflammatory phenomena appear first in the synovial membrane and the cartilages. The synovial fringes enlarge by a slow process of inflammation, and the villous projections increase in number and become more prominent. Not uncommonly pieces of cai-tilage develop in the fringes, originating in the cartilage cells which exist normally there, and these pieces of cartilage, being usually pedunculated, act very much like free bodies in the joint and may become loose. The cartilage also sometimes undergoes ossification in whple or in part. At the same time there is an increase of the synovial fluid, but without any formation of fibrine or pus. Vertical section of an articular cartilage infiltrated by urate of soda, from a gouty patient, p. Articular surface of the cartilages. V, n. Amorphous and crystallized urate of soda. u. Capsules and cartilage cells. X 200. (Cornil and Rantier.) CHRONIC RHEUMATIC ARTHRITIS. 759 The cartilage cells undergo proliferation and the matrix presents a peculiar fibrillation, so that the cartilage assumes a soft, velvety condition, and readily undei'goes destruction from the friction of the opposing surfaces. It is stated by Rindfleisch that the fibrillse of the matrix undergo mucous degeneration, and that mucus may be found in the synovial fluid. The bone beneath the cartilage also undergoes considerable alteration, especially when the cartilage gets worn away. To pre- vent the cancellated tissue from being opened, there is formed, as the cartilage is destroyed, a layer of dense bone, which is smooth and polished, and takes the place of the cartilage. This forms a much less efl3.cient covering, and the ends of the bones work roughly against each other. This layer of bone may also be worn down, and so considerable atrophy of the head of the bone may result, a layer of dense, smooth bone being always reproduced. At the borders of the articular surface there is often consider- able new formation of bone, the result of the inflammation where the parts are not exposed to friction. It appears from the obser- vations of Eanvier that the bone here develops largely from car- tilage. The synovial membrane, at the edge of the joint, covers in some of the marginal portions of the cartilage, and, being thus protected, the cells may proliferate so as to lead to new formation of cartilage, which may ossify. The periosteum may also produce new bone, and even the ligaments attached to the periosteum may be the seat of bony processes. "With all this there is considerable thickening of the ligaments by inflammatory new formation of connective tissue, and often fibrous union between opposing parts of the joints. Indeed, if the joints are kept at rest, there may be a complete union of the parts around the joints opposite each other, leading to anchylosis. Without anchylosis there is stiflEhess of the joints, whose move- ments are greatly curtailed. There is frequently great deformity from the thickening of the tissues and new formation of bone. An extreme degree of arthritis deformans is sometimes seen in the hip-joint, when it gets the special name of morbus cox^ SENILIS. Hei-e the wearing down of the head of the bone is some- times very extreme, so that ultimately the articulating surface may lie between the trochanters. As new formation of bone occurs simultaneously at the borders of the articular surface, a kind of artificial head is produced, and the appearance is presented as if the neck were atrophied and the head displaced. In like manner, an apparent widening of the acetabulum may occur. The original articular surface is worn away, but, by the formation of new bone by the periosteum around, a wall is formed, giving the appearance of the borders of a widened acetabulum. Syphilis does not frequently attack the joints, but rheumatic attacks in syphilitic persons may have some relation to the specific virus. According to Lancereaux, there may be in the secondary stage an infiammation like that of acute or subacute rheumatic 760 DISEASES OF THE BONES AND JOINTS. arthritis, and, in the tertiary stage, manifestations like those of chronic arthritis. Scrofulous or Tubercular Arthritis. — Besides these names, this disease is often called strumous synovitis, gelatinous degen- eration of the joint, tumor albus, fungous caries, etc. The disease occurs mostly in delicate children, but as it is associated with the formation of definite tubercles we must regard it as taking origin in the specific tubercular virus. It is sometimes said that the tubercular formation is secondary, and that there is first a chronic inflammation of a scrofulous kind going on to caseous degeneration, and so leading to the formation of tubercles. A case observed by the author is quite opposed to such a view. There was in this case a great thickening of the synovial mem- brane, which was converted into a bulky, soft, gray tissue, which overlapped the cartilage, and was so prominent that when the joint was opened for the purpose of excision the idea of a tumor was suggested. There was not a trace here of caseous material or of pus, and yet the thickened synovial membrane consisted essen- tially of an immense aggregate of tubercles with inflammatory tissue around them. The tubercles were of typical form, with large giant-cells. The disease begins usually in the synovial membrane, and consists in a formation of tubercles and a chronic inflammation with great production of granulation tissue. The soft, pulpy granulation tissue gives the synovial membrane a gelatinous ap- pearance, from which one of the names of the disease is taken. There is also a slow enlargement of the joint from the increased bulk of the synovial membrane. The ends of the bones constituting the joint are affected simul- taneously or soon after, and here the characters presented are those of a rarefying osteitis. The medullary spaces become filled with granulation tissue and enlarged by destruction of the bony lamellae. In this granulation tissue there are also tubercles. In this way there is, as it were, a pad of granulations under the articular cartilage. The cartilage also at the sides is partly encroached on and over- lapped by the altered synovial membrane which advances over it. In this way it is partly enclosed between two layers of granulation tissue, and it gradually becomes eaten into. The granulations, chiefly those of the medulla, extend into the cartilage, and their encroachment is assisted by proliferation of the cartilage corpuscles, which enlarge and cause softening of the matrix around. By the absorption of the cartilage the whole joint may be con- verted into a cavity lined with granulation tissue, and the liga- ments also are frequently transformed in a similar way. Generally suppuration results, and the joint becomes flUed with pus. Abscesses also not uncommonly form around the joints. Through time the pus generally finds its way outwards, and is discharged by an aperture in the skin. A fistulous canal is the CHRONIC RHEUMATIC ARTHRITIS. 761 result, forming a communication between the cavity of the joint and the surface, and this canal is also lined with exuberant granu- lations, which pout out at the opening at the skin. Among the granulations here, as elsewhere, tubercles are found. The rubbing of the two ends of the bones, which are now covered by granulations, leads to an ulcerative destruction of these soft structures. The inflammation extends more deeply in the bone as the superficial parts are ulcerated, and so we have progressive caries. For some distance beneath the surface the medullary spaces are filled with granulations and the bony trabeculse thinned. It will be understood from this how the disease is apt to recur unless the whole carious portion be removed, for tubercles are present in the granulation tissue filling the medullary spaces, and unless they be removed a fresh extension may occur. In an early period of the disease, before suppuration has oc- curred, there may be recovery ; but after the occurrence of sup- puration, there is seldom a spontaneous restoration, which at best is a slow process. If recovery takes place the granulating surfaces unite more or less, and the joint being partly or completely ob- literated, a fibrous union may come about, leading, it may be, to anchvlosis. DISEASES OE THE SXm AND ITS APPENDAGES. INTRODUCTION. The diseases of the skin are exceedingly manifold, and the names applied to them somewhat complicated. In the present section no attempt will be made to give a complete description of the appearances presented in each affection. So far as the naked- eye appearances are concerned, these are sufficiently described in the text-books on the practice of medicine or on diseases of the skin. "We shall endeavor here to summarize the pathological conditions and group together the various diseases according to the nature of the lesion. It will be necessary first to refer to the normal structure of the skin. JSToRMAL Structure. — The corium or true skin is a very vas- cular dense membrane composed of interlacing fibres of connective tissue, with numerous elastic fibres. It is richly supplied with nerves, and possesses bundles of smooth muscles. It has also a rich system of lymphatic vessels. In the corium we may distin- guish a superficial or papillary layer and a deeper one. Many of the diseases affect the papillary layer especially. The epidermis on the surface of the corium is in several layers (Fig. 328). Most superficial is the horny layer (a) composed of flat cells, which are little more than scales, and have lost their nuclei. JSText comes the stratum lucidum (6) composed of flat transparent cells. This is followed by the stratum granulosum, also composed of flat cells which are granular. Most deeply situated is the stratum mucosum or rete Malpighii, composed of cells which, in the deepest layer, are cylindrical, but towards the surface become polygonal and flattened. In the deeper layers the cells are serrated at the margins, so as to give the appearance of prickles by which the cells fit into each other. The stratum lucidum and stratum granulosum are thin, and for practical purposes the epidermis may be divided into the horny and Malpighian layers. The Malpighian layer extends between the papillae of the corium, forming inter- papillary processes. The SEBACEOUS GLANDS may be regarded as modified prolonga- tions of the Malpighian layer. They are mostly connected with hair-follicles, into which they open, but sometimes large glands are connected with small hairs, and small glands with large hairs, while there are glands not connected with hairs at all. The SUDORIPAROUS GLANDS are usually situated beneath the skin, their INTRODUCTION. 763 ducts passing through corium and epidermis, having a spiral course in the latter. The hairs are composed of horny epidermis, and are placed in follicles. In the latter, two layers of epidermis can be distinguished (Fig. 328), the outer root-sheath corresponding ■Pig. 328. Section of epidermic layer of skin with a hair and its follicle, a, horny layer; 6, stratum lucidum; c, Malpighian layer with (d) the deepest layer of cylindrical cells; e, hair, whose sheath presents two layers, one continuous with the horny and the other with the Malpighian layer. X 350. with the Malpighian layer, and the inner root-sheath corresponding with the horny layer. At the bottom of the follicle is a papilla continuous with the corium, and on this is set the bulb of the hair. The NAILS are composed of compressed horny epidermis. Beneath the nail are still two layers of epidermis, a horny layer of loose cells, and a Malpighian layer covering well-formed papillae. The exposed position of the skin renders it very liable to the in- fluence of agents acting from without. It is also liable to be in- fluenced by irritants circulating in the blood, in which case the skin aflection will probably be an insignificant part of a general condition. The skin again is liable to be affected by states of the nervous system. From these remarks it will be inferred that the inflammations of the skin are the most important morbid condi- tions, and these will call most largely for description. 764 DISEASES OF THE SKIN AND ITS APPENDAGES. HYPEEiEMIA, HBMOEEHAGE, (EDEMA OP THE SKIN. The skin is very liable to variations of its blood supply. An active hyperemia hardly occurs as a pathological condition except as part of an inflammation. Passive hypersemia, on the other hand, is exceedingly common as a result of general venous en- gorgement, especially in disease of the heart, where it leads fre- quently to CYANOSIS. Hemokrhages are frequent and of various kinds. As to their causes little need be added to what is stated at p. 56. The skin is liable to hemorrhage by traumatic rupture of its vessels, but still more, perhaps, by alterations in the state of the blood affecting its vessels. In scurvy, in purpura, in smallpox, in typhus, etc., the skin is the seat of hemorrhage much more frequently than any other structure. The blood escaping from the vessels collects in the serous spaces of the corium for the most part, but may pass to the subcutaneous tissue, where the fat is sometimes considerably infiltrated. When the blood has escaped from a small vessel and infiltrates a limited area so that a bluish spot is seen on viewing the surface, the term PETECHIA is given. As these small hemorrhages depend on the state of the blood the petechise are nearly always multiple. When the blood infiltrates a larger area, then the term ecchymosis is used. Sometimes the blood collects between corium and epidermis, and then a hemorrhagic vesicle is the result ; but this can only happen if the deeper layers of the epidermis have been killed so as to al- low of their separation from the corium. When there are numer- ous small hemorrhages forming a large number of petechise, then it is customary to use the term purpura, or to speak of a purpuric condition. The blood effused in the skin undergoes changes like those already described at p. 58. The affected area is first dark blue, and the color does not disappear on pressure. After a time, as the blood-coloring matter is dissolved, the color gets fainter and changes in hue, while the discoloration becomes more extended. If blood has collected between the layers of epidermis, it comes to the surface and is disposed of as the epidermis is shed. (Edema of the skin, apart from inflammation, is chiefly related to disease of the heart and kidneys. Its general pathology has been considered at pp. 63 and 64. The exuded fluid collects in the lymph-spaces and is carried off by the lymphatics. A condi- tion of the skin has been recently described under the name myxedema. It appears to occur in connection with Bright's dis- ease, and differs from ordinary oedema in respect that the fluid oc- cupying the spaces contains a considerable amount of mucine. The cedematous parts are much firmer than in ordinary cedema and do not pit on pressure. ATROPHIC CHANGES IN THE SKIN. 76& ATROPHIC CHANGES IN THE SKIN. Simple Atrophy is not uncommon in the skin. The most fre- quent example of it is aftbrded by senile atrophy, resulting in the wrinkled skin of old people. In this case the connective tissue of the cutis loses in bulk, especially the papillary layer. Very often the remaining fibres have a strikingly granular appearance under the microscope, but there are sometimes patches in which the fibres have assumed a glassy or colloid character, so as to give rise to the designation colloid or hyaline degeneration- The epidermi?^ is also thinner and dry, and there is often desquamation in the form of dry scales or larger membranous pieces. The hairs are atrophied, as their papillse have taken part in the general atrophy of the papillae of the skin. The hair-follicles are shortened and the sebaceous glands on this account may be brought close to the surface, almost opening directly on it. The secretion may ac- cumulate in the sebaceous glands so as to form small or large CYSTS. A general atrophy also occurs in emaciated persons, and it may closely resemble the condition in senile atrophy. There are further conditions variously named parchment skin, xeroderma, general atrophy, hide-bound skin, which are of rare occurrence, and are not very well understood in their exact rela- tions. The skin is thinned and hardened, especially the epidermis, 80 that the body seems covered with stiff parchment, which often looks as if too small for the surface to be covered, so that the movements of the limbs are impeded. It is sometimes mottled with pigmented spots, sometimes white. The disease generally begins in early life and extends gradually over the skin. This con- dition will be considered subsequently under the tropho-neuroses. Of the LOCAL atrophies, the most familiar is that which occurs after pregnancy. It is well known that white lines are found in the abdomens of persons who have been pregnant. Similar lines occur in persons whose abdomens have been distended by tumors, by ascites, or even by accumulation of fat. The white lines have a cicatricial appearance, and they seem to owe their origin to the connective-tissue fibres of the cutis being dissociated by the stretch- ing. Somewhat similar white lines or striase sometimes occur idiopathically, especially over the buttocks, trochanters, pelvis, and thighs. The HAIRS are liable to atrophy, and two forms may be distin- guished according as either the hair itself or its pigment dimin- ishes. Alopecia or baldness is atrophy of the hair itself. All through life a continuous falling out of hair is occurring, and is due, as we have seen before, to an atrophy chiefly of the bulb. But the papilla remains, and a healthy new hair is produced on the site of the old one. In old people, however, the new hairs are not usually reproduced of normal 'size, and they become grad- 766 DISEASES OF THE SKIX AND ITS APPENDAGES. ually finer and finer, till there are only the finest woolly hairs on the bald part, or even none at all. It is well known that this condition frequently occurs in comparatively early life — pkemature ALOPECIA. The cause seems to be an atrophy of the papilla, and sometimes of the skin itself. Besides being produced in this way, baldness may be secondary to syphilis, to inflammations, and to certain parasitic diseases ; in these cases it depends on interference with the nutrition of the sheath and papilla. Special attention has been paid to alopecia areata, in which baldness occurs in circular patches. These patches are not entirely bald, but are covered with fine woolly hairs, and the papillfe are not destroyed. The nature of this disease must still be regarded as obscure. Some regard it as of parasitic origin, and Eichhorst states that, as the fungus is mainly in the hair-sheath, it is usually left behind when the hair is extracted, and so is overlooked. Others assert that it is due to changes in the nerves which com- mand the nutrition of the skin, and is a tropho-neurosis. Canities or grayness of the hair is also for the most part a natural atrophy of old age. But it also sometimes comes on pre- maturely. It depends for the most part on a deficiency of pigment in the individual hairs at their original formation, so that the pigment granules between the cells in the cortical layers of the hair are diminished. But there may be a temporary blanching of the hair from air getting infiltrated among the cells of the cortex. Cases of sudden permanent blanching have received no satisfac- tory explanation. The NAILS are liable to atrophy, which may be congenital or acquii'ed. In the course of acute illnesses, such as fevers or maniacal attacks, the formation of the nails is often diminished, and the illness is marked for a time by a transverse depression, which, with the growth of the nail, proceeds from the root out- wards, and disappears in due course. The nails also atrophy sometimes in consequence of various parasitic or infiammatory skin diseases. The nail substance may be simplj^ thinner and more delicate than normal, or it ra&j be brittle and split or crumble readily. INFLAMMATIONS OF THE SKIN. These include a very great variety of disease, and the nomencla- ture is exceedingly complicated. In the skin, as elsewhere, in- flammation is produced by the action of irritants, and the form of the inflammation will depend greatly on the nature and source of the irritant. But it depends perhaps just as much on the nature and condition of the skin itself, the same irritant producing very different effects in diflierent persons. As illustrative of many points in the pathology of inflammation INFLAMMATIONS OF THE SKIN. 767 of the skin, we shall refer to the very simple case of the results of a FLEA-BITE. The results are not the same in every person, because different persons are variously susceptible to the irritant. "When a flea penetrates the epidermis, it introduces an irritant, which has an immediate effect on the sensory nerves. This is followed in certain persons by an oedema of the superficial layers of the skin, leading to the formation of a flat elevation called a wheal. By rubbing, the poison is dispersed in the serous spaces around the puncture, and the wheal is enlarged up to a certain point. The wheal is preceded by a slight hypersemia, and at its periphery there is still some redness of the skin, but this is generally insigniflcant. After a short time, all trace of the irritation subsides ; the inflam- mation has been very slight and transient. But the irritant still remains, and next day more permanent changes show themselves. At the place of the puncture there is a conical elevation, which at first is solid, forming a papule, but after a time presents a clear cavity containing fluid, a vesicle. Both of these conditions are again due to inflammatory exudation. The exudation is from the vessels of the papillary layer of the skin, and it consists of serous fluid, with leucocytes. This may confine itself to the papillae, or it may pass among the epidermic cells, loosening them out, in either case forming a solid elevation or papule. But it may so dissociate the epidermic cells as to form a cavity in which it collects, thus producing a vesicle. The vesicle does not form, as might be supposed, between the epidermis and cutis, but among the deeper layers of the epidermis itself, the softer cells of the Malpighian layer becoming separated, so as to leave a space. According to Ziegler, this is always by necrosis and destruction of some of these cells. The papules and vesicles thus formed are often very persistent, remaining vsdth trivial alterations for days or even weeks. As a rule, the vesicles dry in, and only papules are left, but the vesicles are sometimes renewed at intervals. The elevations ultimately subside, but a piece of epidermis is discharged from the surface, a DESQUAMATION, and the skin is restored to its normal condition. Causation of Cutaneous Inflammations. — From what has gone before, it will be apparent that in the base of all infiammations we have to look for an irritant. But the illustration just given shows that the same irritant produces very different effects in different persons. We have seen that in some persons a fiea-bite produces an exudation leading to the formation of a wheal, but in many persons it does not. In some persons a wheal may be produced by a very trivial irritation. A simple scratch with the finger-nail will, in some, cause a raised line such as in others is produced by the lash of a whip. Then it is remarkable that in the same person at one time a wheal will be produced by a simple scratch and at others it will not. These differences apparently depeiid on varia- tions in the state of the nervous system at different times and in different persons. In urticaria there is a formation of wheals in 768 DISEASES OF THE SKIN" AND ITS APPENDAGES. various parts of the body without any special external irritant. Such attacks are usually brought on by eating shell-fish, walnuts, or other special forms of food. These substances appear to produce their effects through the nervous system, inducing, by reflex action, a peculiarly sensitive state of the skin. The wheals occur ,espe- cially in parts of the skin which are irritated by rubbing or by the contact of the clothes, and there may be very striking oedema of the eyelids, for instance, where the feeling of itchiness has induced the person to rub them more than other parts. In almost all forms of inflammation the state of the nervous system and individual peculiarities have a most important bearing on the form and intensity of the process. But there are some forms of inflammation in which the condition of the nervous system has even a more direct bearing on the causation. Where the trophic centres of parts of the skin are interfered with, a trivial irritation may lead to necrosis or severe inflammation. Inflammations owe their immediate origin to direct or indirect irritation of the skin. The irritant may be circulating in the blood and carried to the skin as to other structures. This applies to the cutaneous eruptions in the acute specific fevers and in syphilis ; in these cases we may designate the eruptions as symp- tomatic. On the other hand, the irritant may come from without, as in the case of erysipelas, scalding, etc., and the inflammation is localized according to the extent of the irritation. FORMS OF CUTANEOUS INFLAMMATIONS. It is somewhat diflicult to classify the various inflammations of the skin, but for convenience we shall consider them in four groups : (1) Symptomatic Inflammations ; (2) Inflammatory Skin Eruptions; (3) Traumatic and jSTon-infective Inflammations; (4) Septic and Infective Inflammations. SYMPTOMATIC INFLAMMATIONS. This class embraces the inflammations occurring in the acute fevers. Of the former, some are very trivial so far as the actual lesion in the skin is concerned. Thus the eruptions in measles, scarlatina, typhoid and typhus fevers consist of little more than an inflammatory hypersemia, with slight exudation. The action of the irritant on the epidermis is evidenced in many cases by the subsequent occurrence of desquamation, which implies that the cells have been so injured as to lead to their premature necrosis and discharge. In SMALLPOX there is a much more severe inflammation. As the changes here aftbrd an excellent example of the more pro- SYMPTOMATIC INFLAMMATIONS OF THE SKIN. 769 nounced inflammatory lesions of the skin, and may be regarded as typical of the anatomical conditions in inflammatory skin erup- tions in general, they merit a more careful study. In this case the virus evidently lodges in the skin and multiplies there, leading to pronounced local changes. The fine pai-ticles, which we saw in a previous page to be the direct vehicles of the virus, are pres- ent in the smallpox eruption, especially in the earlier stages of the process, and it is evidently the products of their action that irritate the skin. The effects of the irritant are seen mainly in the epidermis, which show changes chiefly in the more plastic Malpighian layer. Many of the cells undergo a kind of coagulation-necrosis, their nuclei being lost and their substance converted into a hyaline material. These necrosed epidermic cells allow of spaces being formed among their layers, in which exuded fluid collects. In this way a vesicle is formed, but it does not consist of a single cavity. As shown in Fig. 329, the' epidermic cells or their remains form a EiQ. 329. Section of a smallpox vesicle. Superficially there is a network formed of the altered epidermis. In the meshes of this (6, b) are pus-corpuscles. For the most part the Mal- pighian layer in its deepest cells (c) is preserved, hut at gome points, as at d, it is broken through, and the pus is infiltrating the skin, a, umbilioation of the vesicle, due to a sweat- gland, the coils of which are distinguishable. X 1*0. (After Rindpleisch.) network of fibres and partitions which divide the vesicle into com- partments or loculi {b in figure), in which a serous fluid containing the fine particles already referred to is contained. As the inflam- mation increases in intensity leucocytes are exuded, and these accumulate, as seen in the figure, both in the superficial layers of the cutis {d) and in the loculi of the vesicle. By the aggregation of these the vesicle becomes a pustule. In the figureit is seen that while the papillary layer of the skin (d) is somewhat infiltrated with leucocytes, yet it is not destroyed, and the interpapillary pro- cesses of the Malpighian layer of the epidermis (c) still persist. 49 770 DISEASES OF THE SKIN AND ITS APPENDAGES. Sometimes no further destruction occurs than this; the pustule dries in and a crust is formed, and under it the Malpighian layer forms new epidermis, so that when the crust is shed healing occurs without any loss of substance. But more commonly the action of the virus causes death of the superficial layers of the cutis as well as of the epidermis. This is shown in Fig. 330, where an injection Smallpox eruption with necrosis, from an injected specimen. The normal skin at either side (a, o) has its vessels fully injected, while the necrosed part (b) is uninjected and homo- geneous. X 50. (EiNDFLEISCH.) thrown into the arteries runs into the surrounding skin (a, a), but does not penetrate into the slough (6). In this case, when the crusts are torn, little sloughs infiltrated with pus are revealed, on the removal of which ulcers appear. By the healing of the flat ulcers we have the depressed reticulated cicatrices characteristic of smallpox (the so-called pitting of smallpox). 2. INFLAMMATORY SKIN ERUPTIONS. We include here all simple inflammations of the skin which do not depend on any traumatic or infective cause. (1) Erythema and Eoseola. — These names are applied to mild inflammatory conditions in which the chief, and sometimes the only apparent, change is hypersemia. The inflammatory nature of the condition is, however, often indicated by the existence of more or less swelling, due to oedema of the superficial layers of the skin (erythema nodosum and papulosum). The attacks are frequently evanescent, but are often followed by desquamation, which also evidences the inflammatory nature of the condition. These very mild inflammations are frequently somewhat gen- eralized, and appear in many cases to be, like urticaria, related to special conditions of the nervous system, especially, perhaps, of the vaso-motor nerves. They may also be produced by external irritants, especially in susceptible persons. (2) Eczema. — This name is applied to localized inflammations of the skin, usually of a subacute or chronic character. The mere ECZEMA. 771 fact of their local nature would indicate that the irritant here comes from without ; but external irritation is hardly ever the entire ex- planation of the attacks. In no other disease do individual pecu- liarities and special states of the organism play a more important part. The external irritant may be very various, such as medicinal ointments, stuifs used by the patient in his occupation, as in dyeing, parasites which induce scratching, etc. The intensity' of the in- flammation depends on the susceptibility of the patient and the character of the irritant. The various degrees of intensity are, to a great extent, distinguished by the characters of the eruption, so that M'e have papules, vesicles, pustules, etc., characterizing dif- ferent cases of eczema. If the irritation be very mild there is little beyond a patch of redness, with raised papules, depending on infiltration of the papillary layer of the skin — eczema papulosum. In cases where the irritation is more violent, there is partial necrosis of the epidermis, and vesicles form in the manner already described — eczema vesiculosum. A greater degree of inflammation will convert the vesicles into pustules — eczema pustulosum. In the two forms last mentioned crusts are often formed, and sometimes, without any considerable formation of vesicles, scales and crusts form, so that the eczema is nearly dry and the surface scaly — eczema squamosum. On the other hand the vesicles may break, and as fresh exudation passes to the surface there may be a continual discharge — eczema madidans. The surface thus exposed is often very red and infiltrated, so the name eczema rubrum is given. These forms are not to be rigidly distinguished, and several of them maj' be present in the same case, there being papules, vesicles, pustules, crusts, and a weeping surface represented on the same patch. In what has gone before the conditions referred to have been chiefly those in subacute eczema. "When the disease becomes chronic there are more permanent changes which may be compared to those in catarrh of mucous membranes. The inflamed surface usually keeps on discharging serous fluid, not always to the same extent. The epidermis is softened, and, to a considerable extent, lost, so that the cutis is exposed or covered with irregular crusts. The cutis itself is red and it is thickened both by the serous ex- udation and by accumulation of round cells. The skin,_ in fact, shows more or less the characters of a chronic inflammation with the usual new formation of connective tissue. When the inflammation subsides, there is, in the milder forms, a complete restoration. But where considerable infiltration of the skin has occurred there may be a very imperfect restoration of the papillae, the skin, as a whole, having somewhat of a cicatricial character. Hence the smooth homogeneous appearance some- times presented. The part is also not infrequently the seat .of pigmentation. 772 DISEASES OP THE SKIN AND ITS APPEKDAGES. (3) Psoriasis.— The nature of the irritant is in this case quite unknown, but it is probably to be found in some special condition of the blood. We know, at least, that remedies introduced into the blood (arsenic, and, according to Napier, chrysophanic acid administered internally) frequently cure the disease. The lesion is mainly of the epidermis, and especially of its Malpighian layer. The papillary layer of the cutis is hypersemic and partly infiltrated with leucocytes ; the papillae are also described as enlarged, but these alterations are comparatively trifling, as, after death, very little indication of them is to be found. During life the hypersemia gives the corium a red color. In the middle regions of the Malpighian layer of the epidermis there is an abundant new formation of epidermic cells. This new formation is so great that there is no time for the cells to become horny before they pass to the surface. Hence the epidermis on the patch is entirely composed of Malpighian layer, and, these cells being soft, they adhere, as they dry much more readily into con- siderable scales than do the horny cells. For a similar reason, as they dry they shrink much more than the horny cells, and air insinuates itself in interstices between them. It is the finely di- vided air which gives the scales the peculiar silvery appearance characteristic of this disease (Eindfleisch). "When the scales are removed the papillary layer of the skin is seen to be red and readily bleeds. (4) Pityriasis Rubra. — In this disease we have a more or less general aflection, and it is not improbable that it depends on a lesion of the trophic centres of the skin. It is characterized by an excessive discharge of scales consisting of masses of epidermic cells. These scales pass ofl' from slightly raised and reddened surfaces, which in the earlier periods are limited in size, but often extend till they cover nearly the entire body. In the earlier periods the cutis presents little more than hypersemia with excess of leucocytes in its papillary layer, but when the disease has lasted for some time there is thinning of it with flattening of the papillae. The sebaceous glands and hairs as well as the sweat-glands, are usually atrophied. There is often a very excessive discharge of epidermis, and the disease may lead by debility and marasmus to a fatal issue. (5) Lichen Ruber. — The designation lichen is frequently used to denote a simple papular eruption, and in this sense lichen simplex is nothing but eczema papulosum. Lichen ruber, on the other hand, is a diffused papular eruption, depending like pityriasis rubra on some obscure general cause. There is an inflammation of the skin, generally begining in patches, but sometimes extending till nearly the entire body is covered. There are individual red papules on a red basis. As the disease goes on, the skin gets infiltrated and thickened, so that the movements of the joints are hindered, and fissures are formed at the folds of the skin. On the AONB. 773 face the lines of expression are obliterated. The nails are usually thickened. In its details the disease seems to consist in an inflam- matory infiltration of the papillary layer of the cutis and the Malpighian layer of the epidermis. The cells of the rete Malpighii are enlarged and increased in number, and the interpapillary pro- cesses are enlarged. The papillae show abundant accumulation of round cells, especially around the vessels. There is often accumu- lation of epidermic cells in the hair-follicles. (6) Peurigo. — This also is a difl'used affection of the skin, which somewhat resembles urticaria, except that it is more permanent. Like urticaria, it seems to depend on some condition of the nervous system, induced, especially among children, by neglect of sanitary conditions and defective nutrition. Numerous small papules appear on the skin, and they are intensely itchy. The papules are due to an inflammatory thickening of the papillae and rete Malpighii. There are round cells and a serous fluid exuded, so that when the head of the papule is removed by scratching a drop of fluid appears. The papules are often induced to bleed by scratching, and it is probably from this that they frequently leave a brown stain. The irritation produced by scratching may also lead to eczema. (7) Pemphigus. — This condition is characterized by the forma- tion of large vesicles or bullae filled with fluid, which is at first clear, but usually becomes more or less purulent. As the bullae usually occur at intervals over a considerable surface, the disease is to be ascribed to some general cause, and in some acute cases the existence of an irritant in the blood is suspected. There arise at first patches of a red color and slightly raised. The epidermis is then separated from the cutis by fluid accumulating beneath it. There is not here, as in smallpox, an exudation among the cells of the Malpighian layer, but for the most part the whole epidermis is raised, and the bleb is not divided by septa into loculi. If the bleb remain unruptured, a layer of epidermis forms on the surface of the cutis. But if it burst, then the exposed cutis discharges for a time; by and by, however, a crust forms, under which the epider- mis grows. In some cases the blebs are imperfectly formed and neighboring ones coalesce, so that a considerable surface is affected. When these blebs burst there is little tendency to new formation of epidermis, and the skin continues discharging fluid as well as crusts produced by the fluid drying in. This form is designated PEMPHIGUS FOLIACEUS. (8) Acne. — This name is applied to inflammations of the seba- ceous glands and their neighborhood, chiefly in connection with accumulation of the secretion in the gland. There are two forms in which the accumulation of sebum occurs, named respectively comedo and milium, but it is chiefly in connection with the former that acne occurs. 774 DISEASES OP THE SKI2Sr AND ITS APPENDAGES. In COMEDO a sebaceous follicle is filled with secretion, which forms a solid plug in the gland. The end of the plug presents at the surface, and has a black or dark-blue color. It has been usually supposed that this color is simply due to dirt, but Unna has asserted that there is a true pigment concerned, whose compo- sition is allied to that of ultramarine, and whose color is destroyed by aqua regia. The plug can be readily pressed out by squeezing the skin around the gland; it emerges as a w^orm-like structure with a dark head. The plug consists of shed epidermis and sebum, with occasionally a small parasite, the acarus folliculorum. In MILIUM there is an accumulation of the secretion with closure of the orifice of the gland. The accumulated secretion forms a pounded solid globe, which can be felt in the substance of the skin, but over which the epidermis passes unbroken. It is, in fact, a small retention cyst, and it contains the secretion of the gland mixed with epidermis, so that on cutting into it a whitish globular body is discharged. The cause of the closure of the duct is ob- scure. In acne there is a more or less acute inflammation of the sebace- ous glands, usually in connection with comedo. There are redness and swelling around, and pus is usually formed, and mingles with the substance of the comedo. Sometimes there is not a proper suppuration, but the substance of the plug is softened by the in- flammatory exudation. The inflammation is due to the irritation of the plug, especially when by long stagnation it has become foul. The name acne mkntagra, or sycosis, is given to cases where there is inflammation of the sebaceous glands in connection with the hairs of the beard. There is a sycosis of parasitic origin, but in the simple form there is suppuration in and around the hair- follicles of the nature of acne. A more chronic inflammation of the sebaceous glands of the face, with special hypersemia of the vessels around, has received the name acne rosacea. There is very little tendency to suppura- tion, but great thickening of the skin occurs, so that sometimes there are large lobulated and red protuberances, especially on the nose, on the surface of which many comedones are seen. This disease is not uncommoii in women, especially about puberty and at the climacteric period. In men it is often associated with dissi- pated habits. 3. TRAUMATIC AND NON-INPECTIVE UsTPLAMMATIONS. (1) Burns and Scalds. — "We include here the lesions produced by the application of excessive heat to the skin, whether the heated substance applied be in the solid, liquid, or gaseous form. The heat acting as an irritant damages or kills the tissue, and so we have signs of inflammation frequently associated with necrosis. Burns have been distinguished into three degrees, according to their intensity, and we have to consider the exact condition of the BURNS AND SCALDS. 775 skin in each. The three degrees are characterized by these three phenomena — hypersemia, vesication, sloughing. In the FiRs?T DEGREE the heat is only sutficient to produce a hy- persemia of the skin. Exposure to the rays of the sun, or to hot water of a temperature of 100° F. and upwards, causes such a re- laxation of the arteries as to induce congestion. The inflamma- tory nature of this hyperemia is shown by its continuance for some time after removal of the cause, and by the occasional occur- rence of some cedematous swelling of the skin. After a time there may be desquamation. The SECOND DEGREE is produccd by the action of a temperature of 140° to 185° F., or by the evanescent action of a still higher temperature. The etFect is to cause a necrosis with swelling of the epidermic cells of the Malpighian layer, and an inflanmiatory exudation from the papillary layer of the skin. The changes in the rete Malpighii are similar to those already described as occur- ring in the formation of the smallpox vesicle, but they are more rapidly produced and the layer of cells is more homogeneously atfected. The exudation, passing out from the papillae, separates the epidermic cells from the surface of the papillae, and a vesicle is thus formed. Usually the interpapillary cells of the rete Mal- pighii escape destruction, but when the action is more intense they also may be killed. The inflammation soon subsides, and from the remaining cells of the rete Malpighii new epidermis is repro- duced; there may be already a complete coating of new epidermis before the vesicle bursts. But sometimes the vesicle bursts early, and the inflamed surface of the skin is exposed ; or nearly the whole of the rete Malpighii may have been destroyed, even the interpapillary processes. In these cases the covering over of the surface with epidermis may be delayed, and the surface may even become like a granulating wound, discharging pus. In the THIRD DEGREE there is necrosis not only of the epidermis, but of the true skin to a greater or less depth. The temperature is over 140° F., and if very high may have acted for a very short time. As a general rule the necrosed tissue lies as a dry crust on the surface. An inflammatory process occurs around it, with exu- dation, going on usually to suppuration. In this way the slough is separated, and a granulating wound is left, which heals in the usual way, leaving a cicatrix, the character of which varies with the depth of the slough. Severe burns sometimes lead rapidly to death with symptoms of collapse. The explanation of this is not easy, but there are two conditions which affect the body in general which probably are the chief agents. When a part of the skin is exposed to a high temperature, the red corpuscles in the vessels perish, and they do so even in parts where the circulation persists. If the heat has acted for some time, then the blood in the vessels may have been frequently renewed and large numbers of corpuscles may have been destroyed. The red corpuscles yield their haemoglobin, which, as we have seen at p. 27, acts as a poison. Besides this, 776 DISEASES OF THE SKIN AND ITS APPENDAGES. the mere destruction of large numbers of corpuscles may seriously interfere with the respiratory functions. Again, the vessels of the skin are dilated after the occurrence of the burning. . If the surface affected be large there may be, as a result of this, a serious loss of heat and reduction of temperature in the body as a whole. At the same time the dilatation of so many arteries may reduce the blood- pressure to a considerable extent. The combined action of these conditions seems to bring about the collapse after burns. If the person survives for some time after the burning, there are frequently found inflammations of internal organs, the lungs, kidneys, serous membranes ; also fatty degeneration of the heart and of the liver. These are to be ascribed with great probability to the alteration of the blood. It is much more difficult to account for the occurrence of the DUODENAL ULCER after burns. When several weeks elapse before death, there is found in about twenty per cent, of the cases one or more ulcers, usually situated in the duodenum near the pylorus, but sometimes in the pyloric region of the stomach. It may be a superficial hemorrhagic erosion or a deeply penetrating ulcer. (2) Feostbite AND CHILBLAIN. — These conditions are' produced by the action of excessively low temperatures. "We can distinguish three degrees here also. The common chilblain is an example of the first degree. If portions of the body are exposed to a low temperature and then heated, a chronic or subacute i-nflammation is induced. This occurs especially in the fingers and toes. There is passive hy- persemia sometimes amounting almost to stasis, so that the part has a livid hue. There is also serous exudation, so that the part is swollen and oedematous ; there may be red corpuscles as well as leucocytes in the exudation. Sometimes ulceration occurs. The SECOND DEGREE includes the less severe cases of frostbite. The skin has been frozen and too rapidly thawed, the result being such an injury to the tissue as to cause an acute inflanimation. The epidermis is raised in blisters, which often contain a bloody serum. There may even be sloughing of the superficial layers of the cutis, and by the separation of the slough an indolent ulcer forms. In the THIRD DEGREE, forming the more severe cases of frost- bite, there has been prolonged exposure to very intense cold. The consequence is the complete freezing of part of the body, especially in regions removed from the heart, as the fingers and toes. The tissues are stiffened by freezing, and the blood coagu- lated, so that sometimes parts can be broken off like glass. When the parts are thawed gangrene sets in. The whole frozen part does not die, but there is partial recovery with inflammation. The gangrenous part is separated in the usual way, generally with decomposition (moist gangrene). (3) Boil and Carbuncle. — These names are applied to localized acute inflammations of the skin with partial necrosis. The boil or ULCERS. 777 FURUNCULUS occurs for the most part in persons who are debilitated or exhausted, but in addition to this we have to look for some local irritant. The fact that it begins in the neighborhood of a hair- follicle or sebaceous gland seems to suggest that accumulation of secretion may afford the irritant. The boil would thus be related to the acne pustule, the more intense inflammation in the former being related to the state of the patient. The inflammation manifests itself in hypersemia and exudation, so that a localized redness and swelling are the result. A piece of skin in the very centre of the inflamed area dies, and a small abscess having formed, the slough is by degrees discharged along with the pus. The carbuncle or anthrax is similar in its general characters to the boil, but a much larger piece of skin is involved. The slough is therefore of much larger extent. It sometimes happens that the whole piece of skin in its entire thickness dies and is separated as a dry leathery slough. More frequently the necrosis is less extensive in the superficial layers, but more extensive in the deeper parts, and the slough is discharged through numerous small apertures. (4) Wounds and Excoriations. — The phenomena connected with the healing of wounds and the formation of granulations have been considered in previous pages. When merely a portion of the epidermis is removed by an injury, forming an excoriation, it is restored with remarkable celerity. The cells at the margin, and those of the deeper layers, divide and form new cells, which fill in the gap. In the case of a deeper wound, the epidermis also shows great vigor, and it sometimes advances beyond the line of the other healing processes. Dr. Macewen has pointed out to the author that the new-formed epidermis may advance over a blood- clot filling up a wound. The epidermis here has a remarkably transparent hyaline appearance, and is continuous, not with the Malpighian layer, but with the layers superficial to that. The character of the cells here and their transparency suggest that they may be derived from the stratum lucidum. It may, indeed, be suggested that this layer in the normal skin is composed of young epidermis, and that the loss on the surface is supplied by new formation here, and not in the Malpighian layer. (5) Ulcers. — By this name we understand losses of substance in the skin which are mostly in process of enlargement. The margin of the ulcer is inflamed and infiltrated with inflammatory products. The enlargement takes place by a gradual molecular necrosis of the inflamed structures, and it implies the continuous action of an irritant. The irritant is mostly an infective virus, and the majority of the ulcers will be again referred to under the next heading. The varicose ulcer, however, does not belong to this category. The original lesion here is a prolonged venous hypersemia, leading to oedema and inflltration of the skin. The nutrition of the skin is seriously compromised, and a trivial external injury may cause the epidermis to give way. The exposed and inflamed skin forms 778 DISEASES OP THE SKIN AND ITS APPENDAGES. granulations, but these also, from the persistent venous engorge- ment, are readily destroyed by slight injuries, and the ulcer advances, while the inflammatory infiltration of the skin outside extends. The granulations will only proceed to healing in the usual way when the venous hypersemia is removed. In the case of infective ulcers there is also usually a granulating surface, which is gradually destroyed by the action of the virus. When the virus has been destroyed, the ulcer proceeds to heal like a granulating wound. 4. INFECTIVE INFLAMMATIONS. We include here those forms of inflammation of the skin wMch can be traced to the action of speciflc viruses. The syphilitic inflammations might be considered here, but they will be taken up afterwards by themselves. (1) Lesions from Cadaveric Poisons. — In the juices of the dead body, when in process of decomposition, there are innumerable bacteria of diiferent kinds. Some of these may attack the skin of the dissector or pathologist, and find a lodgement there. The organisms themselves are of very various degrees of virulence. If the subject has died of a septic disease, then the organisms which have during the life of the patient been active factors in the production of the disease may remain specially virulent after death. The fluid in the abdomen after septic peritonitis, such as that which occurs in one form of puerperal fever, teems with micrococci, and this fluid is peculiarly virulent when applied to the skin. So is it also with septic pleurisy, etc. Besides degrees of activity in the virus, there are various degrees in the susceptibility of different persons, and of the same person at different times. The frequent exposure to the cadaveric viruses creates a certain immunity, so that a person will be more secure against them when frequently engaged in post-mortem work than when making only an occasional examination. A. state of exhaus- tion of the body renders one much more susceptible, and makes the inroads of the virus when once implanted more vigorous than when in ordinary health. The inference from this is that the best treatment for this condition is to leave off work and at once seek rest and fresh air. The virus very often finds access to the skin without any breach of surface. When a wound is made during dissection it is usually washed thoroughly and sucked, while bleeding is encouraged ; in this way the viius may be washed away. But if it gets into the hair-follicles or sweat-glands, it may lodge and multiply undis- turbed. The immediate effects are usually an acute localized inflamma- tion of the skin, resulting in the formation of a small pustule. The virus may have attacked at several points, and there is a crop of pustules, usually on the back of the hand or forearm where the ERYSIPELAS. 779 epidermis is thin, the left hand being more frequently affected than the right, as it is most frequently exposed in separating and holding the organs. In many eases nothing more than the pus- tules is produced, and in the case of the regular pathologist a crop of pustules in the spring may be his annual experience. The" pus contains I'ig- 331. micrococci, some of them free, but some in the substance of the pus-corpuscles (see Fig. 331). Sometimes, however, there are more severe local effects, and sometimes the virus travels further inwards. Instead ,, ,-*,,• « 1 . ^ , T r" Fu3-eorpuSGles with micrococci of dying away ,_ the pustule, after par- in them, from a cadaveric pustule. tially disappearing, sometimes leads to x i500. an acute inflammation in a larger area around, so that a boil is the result. The inflammation is often so acute as to lead to a necrosis of a piece of skin, so that suppura- tion is set up and a slough is ultimately discharged. In this case there is a cicatrix left when healing occurs. In other cases it is what has been called a blind boil which develops after the pustule. There is a more chronic inflammation of the skin with considerable thickening and elevation. The surface of these elevations is often irregular and somewhat warty in appearance — the pathological WART. These, however, not infrequently develop without a pre- vious pustule, the virus acting slightly but continuously from the first. In all these cases the forces of the tissues seem suflicient to keep the virus local, although there may be some general disturb- ance of the body, perhaps from the absorption of the products. In some cases, however, the virus propagates itself upwards to- Avards the trunk. It may be that an erysipelas starts from the local inflammation, extending upwards along the lymph-spaces of the skin. In other cases, the axillary glands become inflamed without any intervening lesions, the virus passing up the vessels, and only producing mischief after lodging in the glands. Here suppuration is common. An inflammation of the skin resembling erysipelas may spread from the glands, as the virus, checked in its upward course towards the trunk by the gland, passes outwards to the lymph-spaces around. This course of events is shown in the exquisite account which Paget has given of his own case in his Clinical Lectures and Essays. The inflammation may travel along the connective tissue of the skin and subcutaneous tissue, and may even reach the pleura. In the skin its effects may be very severe, resulting in sloughing and profuse suppuration like that in ery- sipelas. It may even lead to septic infection or pyaemia. (2) Erysipelas. — This is an acute infective inflammation of the skin. The virus depends on bacteria in the form of micrococci which extend more or less abundantly in the lymph-spaces and vessels of the skin (see Fig. 332) and subcutaneous tissue. The result is a more or less severe inflammation. At first there is an 780 DISEASES OF THE SKIN AND ITS APPENDAGES. inflammatory hyperemia, whicli advances as the virus propagates along the lymph-spaces. This, vsrith a moderate exudation of fluid and leucocytes, may be all the phenomena. But spnaetimes there is much more intense inflammation. The skin is infiltrated vpith leucocytes to such an extent that it is softened and opened out FiQ. 332. From the skin in a case of erysipelas. The upper illustration shows a lymphatic vessel at the border of a sebaceous gland, filled with mierocoooi. The lower shows a straight vessel similarly filled. X 350. with pus. The epidermis is raised by exudation, so that vesicles or pustules are formed. Sometimes the lymph-spaces are occupied vpith fibrine. Besides suppuration, there is often necrosis of por- tions of the skin, so that sloughs are separated vpith the pus. (3) Phlegmonous Inflammations. — These have very much the character of the severer forms of erysipelas, for which, indeed, the name phlegmonous erysipelas is used. The term phlegmonous is applied to inflammations of the skin of a very acute character, associated with sloughing. Such inflammations may be produced directly by the presence of virulent decomposing material in the skin and subcutaneous tissue, as where urine is extravasated and decomposed. But the condition may be more directly allied to erysipelas, depending on the gradual extension of micrococci in the lymph-spaces. This occurs mostly around septic wounds, and may be followed by abscesses at some distance from the wounds. Sometimes the virus is of such an intense nature that gangrene rapidly develops, being preceded only by an oedema. To this condition the name malignant oedema is sometimes given. (4) Splenic Fever or Anthrax. — This disease, as we have seen, depends on a special bacillus. There is usually a local aflfection to begin with, and the disease may remain local. The local afiec- tion has the characters of a phlegmonous inflammation of the skin and subcutaneous tissue. Sometimes the appearances of malignant INFECTIVE TUMORS. 781 oedema are produced. From these local manifestations the condi- tion is sometimes called malignant pustule. As a general rule, the bacillus penetrates to the blood, and the patient dies from the general specific fever. (5) Infective Tumors. — Of these lupus, leprosy, and glanders have been sufficiently described in the general part of this work. Syphilitic diseases will receive special description in the next section. The name erambcesia is given to a disease which evidently depends on a virus which acts on the skin. There are prominent irregular swellings produced which have the general appearance Pig. 333. Section of skin in framboesia, from a part where the disease was not very far advanced. The papillary layer of the cutis is seen to be replaced by granulation tissue while the epi- dermis is preserved on the surface. X 75. of exuberant granulations. These have been compared in appear- ance to strawberries and raspberries. The local names yaws (African for raspberry) and pian (mulberry) also suggest these re- semblances. The disease is endemic in the West Indies and Africa ; it also occurs in Peru, where it is called verruga. It is 782 DISEASES OF THE SKIN AND ITS APPENDAGES. contagious, and in many respects so much resembles syphilis that some authors have regarded it as the same disease. It begins as a small raised spot, usually on the face, on the upper or lower extremities, or near the organs of generation. The spot enlarges and gradually assumes the red irregular appearance which has suggested its names. It may continue for months or years, and, neighboring areas coalescing, it may aft'ect a large portion of the cutaneous surface. The structure of these growths closely resembles that of the syphilitic chancre, as may be seen by comparing Fig. 333 with Fig. 48, p. 148. The cutis is converted into granulation tissue, whose bulky masses form the irregular prominences chai'aeteristic of the disease. The epidermis may be continuous over even the most prominent of these masses (see figure), and may even be ex- aggerated; but the horny layer is lost and the soft Malpighian layer alone remains. The epidermis may give way, and an ulcer form, from which a thin fluid is discharged, not usually a true pus. SYPHILITIC, LESIONS OF THE SKIN. In the first part of this w'ork it has been sufficiently indicated that syphilis depends on a virus, and that the various manifesta- tions in the skin are the results of the action of this virus. In regard to these lesions it has been stated that they are either simply inflammatory, or that they have the characters of the gumma, form- ing in the latter case more or less definite tumors composed of granulation tissue. Even the purely inflammatory lesions have a tendency, when they have persisted long, to present considerable new formation of granulation tissue. The syphilitic lesions of the skin may be divided into the primary, secondary, and tertiary. 1. The HARD CHANCRE has been already sufficiently considered at p. 148, and its structure is illustrated in Fig. 43, p. 148. 2. Syphilitic Skin Eruptions. — We may, under this heading, group together the various secondary manifestations. It is to be remembered that here the virus is in the blood, and that, as a rule, the manifestations occur over the skin as a whole, although cir- cumstances may determine a certain local selection. The eruptions are for the most part symmetrical, and they present a peculiar tendency to occur in round patches. These patches by healing in the centres and extending at the periphery, frequently assume a circular or serpiginous shape. _ The syphilitic eruptions of the secondary stage are somewhat similar in character to the simple inflammatoi-y eruptions, and they are commonly designated by similar names. There is, however, more tendency in the syphilides to the development of granulation tissue in the skin, and hence the papular forms of eruption are more frequent. The syphilitic eruptions present very various characters, and there is no form which is constantly present at a SYPHILITIC LESIONS. 783 particular stage. In the earliest periods there is usually a gen- eralized hypersemia of the skin (syphilitic erythema or roseola). A more local development of elevated papules, generally in groups, constitutes the syphilitic lichen. In these papules, the corium, especially its superficial layers, and to a certain extent the epi- dermis, are infiltrated with round cells; generally there is des- quamation of epidermis, and this is sometimes very prominent. Occurring in the palms of the hands and soles of the feet this desquamation is so characteristic as to give rise to the designation syphilitic psoriasis, the papules after a time coalescing and so merely producing a generally raised surface. The Condyloma {plaque muqueuse, mucous tubercle) is a further development of the papule. It occurs usually in situations vphere two surfaces of the skin are in contact and are thus kept moist, as in the neighborhood of the genital organs, in the axilla, beneath the mamma, etc. We have here a very marked and extensive in- filtration of the papillary layer of the skin with round cells, so that an elevated surface is formed. Sometimes there is a special elongation of the papillae, so that a warty surface is produced, giving rise to the pointed condj'loma. Sometimes the condyloma breaks down on the surface and an ulcer forms. The syphilitic papules sometimes develop into pustules or vesicles. The pustule forms by the epidermis being raised from the surface, while a fluid inflammatory exudation occurs between it and the corium, which latter remains infiltrated with round cells. The pustule or vesicle and its infiltrated basis may enlarge so as to produce a broad bleb on a red raised base (syphilitic pemphigus). The blebs often dry in and form raised crusts (rupia). In these cases the pustules are as if on the surface of condylomata. This is still more the case in pemphigus neonatorum, which is one of the manifestations of hereditary syphilis. Here the corium is affected somewhat as in the condyloma, but the infiltration has more the characters of granulation tissue. In the condyloma the structure of the skin remains to a great extent, but it is infiltrated with round cells which are mostly leucocytes. In pemphigus neonatorum, however, the tissue is replaced by a vascular tissue in which are many large cells, the condition approaching to that of the gumma. On the surface of this the epidermis is raised, form- ing a vesicle or pustule. The Gumma. — This is not of very common occurrence, and is, as we have seen, a special tertiary manifestation. It begins as a hard swelling in the cutis. It increases in size and raises the sur- face, sometimes forming a tumor of considerable dimensions. It is peculiarly prone to ulcerate, and after ulceration has occurred it may go on extending, the infiltrated edges gradually giving way. The structure of the gumma has been described and illustrated at p. 150. 784 DISEASES OF THE SEIN AND ITS APPENDAGES. TROPHO-NEUEOSES OF THE SKIN. "We include under this heading lesions of the skin in which, by reason of disease of the nervous system, such changes occur in the nutritive processes as to lead to definite anatomical results. The existence of separate trophic nerves for the skin has not been anatomically demonstrated. But there are evidences, especially in pathological processes, that trophic centres exist, and that fibres convey impulses of this kind to the cutaneous surface. The ganglia of the posterior roots of the spinal nerves and the similar Gasserian ganglion seem to contain trophic centres, and the trophic fibres are either identical with the sensory ones or run along with them. (1) Herpes. — This disease is typically of nervous origin. It is commonly accompanied by neuralgia, and in its site it nearly always follows the distribution of a single nerve-stem. It appears, for instance, in the course of an intercostal nerve, or occupies one side of the face in the area of distribution of the fifth. The eruption in' the skin is in the form of vesicles which some- what rapidly pass through a series of changes. There is first a group of slight elevations occupying a reddened patch of skin, and each of these rapidly develops a vesicle; in a few days the vesicle dries up into a crust, under which fresh epidermis is formed. In its details the eruption is inflammatory. There are hj^persemia and oedema of the papillary layer of the skin. The serous exudation collects in the Malpighian layer of the epidermis, separating its cells just as in the case of the smallpox eruption. The vesicle is divided by a network composed of the elongated and contorted epidermic cells, which often present clear spaces or vacuoles in their sub- stance. In the serous contents of the vesicles there are leucocytes, and these may accumulate till the fluid approaches to the nature of pus. The papillary layer is also frequently the seat of infiltra- tion with round cells. Occasionally there is hemorrhage, and the papillary layer of the skin may be destroyed, so that when healing occurs by granulation a cicatrix may be the result. The nervous origin of herpes has been abundantly established. Direct injury to a nerve, as by a gunshot or other wound, may cause it. It is to be presumed that, in this case, the inflammatory process iu the wound irritates the nerve, and the cutaneous in- flammation may be regarded as due to the irritation of trophic fibres. Spontaneous herpes, and especially herpes zoster, has been found associated with inflammations of the intervertebral or Gasserian ganglia, but it has been questioned whether the trophic centres have actually their seat there. The herpetic eruption may arise from disease of the spinal cord and brain. In the case of the cord it is chiefly in locomotor ataxia that we meet with herpes, and the eruption is accompanied by the severe pains characteristic of that disease. "We know that in loco- motor ataxia it is the posterior columns of the cord that are MORPHCEA AND SCLERODERMA. 785 affected, and this would indicate that the cutaneous trophic centres or fibres run in these parts, while the coincidence of neuralgic pains also indicates a sensory locality. It is here again to be pre- sumed that the lesion producing the herpes is an irritative one, as indicated by the violent coincident pains. But we may have herpetic eruptions from disease in the brain. There are cases recorded in which one-half of the body was affected, and in some of these there was a hemiplegia due to a coarse lesion in the brain. It is clear that there must be trophic fibres and centres in the brain as well as in the cord, and their irritation may lead to herpes. There are also a few cases on record of universal or nearly universal herpes, as if a general centre for the whole body were irritated. (2) Glossy Skin. — This name was applied by Paget to a condi- tion which he observed in connection with injuries or wounds of the nerves. There is here again indication of irritation of the nerves, as there is always neuralgic pain, described by Mitchell as burning pain. The condition also occurs sometimes after an attack of herpes (Paget), and it may be associated with eczema. It may also follow disease of the spinal cord (Mitchell). The disease occurs mainly in the hand, and especially in the fingers. The affected fingers "are usually tapering, smooth, hair- less, almost devoid of wrinkles, glossy, pink or ruddy, or blotched as if with permanent chilblains" (Paget). The most striking pecu- liarity is the shining, glossy appearance of the surface, as if it had been varnished. The comparison to chilblains is usually applicable, but sometimes the appearance is rather that of highly polished scars, and the condition resembles that in morphoea. In the affected part the hairs mostly disappear, and the nails undergo peculiar changes. The latter become greatly curved, much more than in cases of phthisis, while the skin at the root of the nail becomes retracted, leaving the sensitive matrix partly exposed. The dis- ease affects mainly the fingers and toes, but it may extend to the palm of the hand or the dorsum of the foot. The histological details in this condition are unknown. (3) MoRPHCEA AND SCLERODERMA. — These names are applied to denote conditions which are sometimes regarded as of a different nature, but the presumption is that they are virtually the same disease. The nervous origin of the disease has been brought prominently forward by Hutchinson on the ground that it usually occurs in defined patches, often distinctly following the distribution of par- ticular nerves. But sometimes the disease is more extensive, and it may be almost universal. The same may be said, however, as regards herpes, and it does not invalidate the supposition of its nervous origin. "When the disease is in the form of patches it is often described as MORPHOEA or Addison's keloid. The patches have the char- 50 786 DISEASES OF THE SKIN ANU ITS APPENDAGES. acters of induration and stiffening of the skin; they are mostly- white and ivory-like, but may have a yellowish or mottled appear- ance. The greatest peculiarity is the hardness, as if the skin were frozen. The skin is sometimes bound down to the parts beneath, the induration extending to the subcutaneous tissue, and even deeper, and in that ease there may be considerable interference with motion and even deformity of limbs from contraction of the skin. In the more diffuse form of scleroderma proper, extensive tracts of skin are sometimes involved, such as the greater part of the face, the arms, etc. In a case observed by the author, the face, chest, and both forearms and hands were affected, and dry gangrene had occurred in the fingers, which had a stiff" black appearance. In its anatomical details the skin presents characters which may be summarized as atrophy with chronic inflammation. The pa- pillae are mostly flattened, and the cutis thinner than normal, but it is composed of more homogeneous connective tissue than usual, having somewhat the characters of cicatricial tissue, and less fibrous than that of the normal skin. This condition extends somewhat to the subcutaneous tissue, where the fat is to a con- siderable extent atrophied, apparently by the encroachment of the connective tissue. The hairs are also atrophied in the affected areas, and there is said to be alopecia when the patches extend to the hairy scalp. The evidence of chronic inflammation is the existence of abundant nuclei in the altered skin. These are usu- ally aggregated around the bloodvessels, but they are also seen around sebaceous glands and under the rete Malpighii. It will be seen from the above that the changes here are to a great extent comparable to those which occur in muscle after destruction of its trophic centres; there is atrophy with chronic inflammation. An endeavor has been made to associate this disease with stasis of lymph, and relate it to elephantiasis. Some also regard it as allied to leprosy. "We have already seen that both elephantiasis and leprosy are diseases probably dependent on specific irritants, and that they are endemic in particular localities, whereas this is in no sense true in regard to scleroderma. Allied to scleroderma in the general characters of the lesion in the skin is the condition commonly designated sclerema neona- torum. In this disease the skin, usually of the lower extremities, is hard and swollen, so that movement of the limbs is curtailed. When it persists for some time the skin may be like parchment. In the eai'lier stages the skin is oedematous, while in the later there is thickening from new formation of connective tissue. The disease occurs, as the name implies, in new-born children, being sometimes congenital. The children are weakly and usually die in a few days. ICHTHYOSIS. 787 (4) Bedsores. — Besides the ordinary bedsores which occur in persons who lie long in one position, especially when cleanliness is not attended to, there are some which are obviously related to nervous lesions. The acute decubitus is met with in connection with lesions of the spinal cord or brain, usually in severe cases, such as cerebral hemorrhage or injury to the cord. The appear- ances presented in the skin are those of an acute phlegmonous inflammation with sloughing. At lirst there are simple oedema and hyperfemia, but vesication follows and deep ulceration. The sloughing may extend to the muscles, tendons, etc., sometimes laying bare the bones. These acute bedsores imply a grave lesion of the trophic fibres, and there are indications that these foUow the course of the sensory fibres. Bedsores have been observed, for instance, in unilateral lesions of the cord where there were paralysis of motion on one side and anaesthesia on the other; in that case the bedsores are on the anaesthetic side. HYPERTROPHIES AND TUMORS OF THE SKIN. The Callosity is an exaggeration of the horny epidermis occur- ring where the parts are exposed to unusual friction. It is a true hypertrophy, being a direct provision of nature to protect the true skin from the excessive friction to which it is exposed. The best example of the callosity is in the horny hands of workmen, but it is often seen in tlie feet, at points which are much exposed to pressure. The CORN (cLAVus) is closely related to the callosity. Here, also, there is friction, but it is associated with compression. It occurs chiefly in the foot, where there is a concentric pressure from ill- fitting boots, and friction against either the boot or a neighboring toe. There is, as in the former case, an excessive new formation of horny epidermis, but, by the concenti'ic pressure, the layers of epidermis have their directions changed, and growing against each other are projected inward towards the cutis. There is thus an ingrowing kernel of hard horny epidermis which has given rise to the name of corn. The cutis is irritated and undergoes atrophy. Around the kernel the epidermis is always thickened, the condi- tion being like that of the callosity. Ichthyosis. — This is a disease which apparently owes its origin to a congenital defect in the structure of the skin. The disease .itself is sometimes manifest at birth, but if not it begins in the earlier years of life, gradually extends over the whole body, and continues during life. It consists, anatomically, in an exaggeration of the horny layer of the epidermis, which is sometimes greatly thickened. The thickened horny layer forms scales of larger or smaller size, some- times producing merely a furfuraceous exfoliation, but in more 788 DISEASES OF THE SKIN AND ITS APPENDAGES. severe eases giving rise to large plates like jfish-scales. From this latter appearance the name of the disease is derived. The scales do not consist entirely of epidermis, hut contain sebaceous material, which is sometimes so abundant as to give the scales a polished appearance like mother-of-pearl. The large scales may be fixed in their peripheral or middle parts, and project considerably at their edges, so as to give an imbricated appearance. The milder forms of the disease, in which there is little more than an excessive scaliness of the surface, are often included under the designation ICHTHYOSIS siMPLKX or XERODERMA, while the more severe forms, in which there are prominent scales, are distinguished by the name ICHTHYOSIS CORNEA Or ICHTHYOSIS HYSTRIX. In the milder forms the cutis is not markedlj^ affected, but in some cases the papillae are greatly elongated. The substance of the corium is often atrophied, and the subcutaneous fat deficient. The COMMON WART may be variously regarded either as a tumor or a hypertrophy of the skin. There are warts which have dis- tinctly the characters of tumors, presenting specialties of structure and growth which entitle them to that designation. But the common wart, consisting for the most part of local exaggeration of the normal structures and occurring in numbers in the same persofl, has more doubtfully the characters which we ascribe to a morbid growth. A group of papillfe are elongated, and the epi- dermis over them thickened, so that the characters are those of a hard papilloma. The horn is of similar structure to the wart, but the papillae are usually more elongated, while the horny layer of the epidermis forms a more consistent mass which grows into a prominent outgrowth. The TRUE Keloid is an elevation of the skin which has in its marginal parts branching processes extending out. There are evidently considerable contraction and dragging on the part of the central tumor and of the radiating processes, so that the skin is puckered around as in the case of a contracting cicatrix. The lesion has many of the characters of a definite tumor. It is com- posed in the fully developed state of dense connective tissue which may be unduly cellular. The new formation has its seat in the deeper layers of the cutis, and it is stated that the papillary layer is intact. In the earlier stages it consists mainly of spindle cells, and Virchow therefore regarded it as a sarcoma. The analogy to the sarcomas is supported by the fact that the tumor recurs on re- moval. The most common site of keloid is the front or back of the chest, but it is found in other parts. The name false keloid is sometimes used to designate a condi- tion which occurs in scars. A localized thickening, usually in the midst of a large cicatrix, as from a burn or an ulcer, presents itself, and there are raised processes passing out from it as in the true keloid. FIBROMA MOLLUSOUM. 789 Soft Wabts and Pigmented Moles {noevi pigmentosi). — These ai-e very often congenital, or they occur very early in life, and usually remain stationary throughout life. They are smaller or larger elevations of the skin, either colorless or pigmented, and frequently beset with hairs. They present a somewhat peculiar structure, especially considering that they exist unchanged for many years. They are covered b^^ epidermis which shows little difference from the normal. But instead of the normal tissue of the cutis beneath the epidermis, there are masses of cells separated by connective tissue. The cells in these nests are usually large and resemble epithelial cells or large sarcomatous cells. The presumption is that these structures are really survivals of the foetal condition, and their importance in relation to tumors has already been referred to at p. 171. In their structure it will be observed that these warts are much more like tumors than the ordinary warts, and that their tissue conforms to that of the cellular tumors, prob- ably the sarcomas. MoLLuscuM CoNTAGiosuM. — This namfe is applied to little growths of the skin, occurring chiefly on the face and showing a preference for the eyelids, but sometimes extending so as to be almost uni- versal over the body. It will be inferred that the growths are multiple. The individual ones have been compared to pearl buttons, which they resemble in their circular shape and central depression, but they are usually pink in color. There is considei-- able elevation of the little growth, and, although generally sessile, it sometimes becomes pedunculated and may even drop off. In the centre of the elevation a depression is visible which is the orifice of a sebaceous gland, and the tumor consists of an enlarged sebaceous gland. A section of the growth shows the exaggerated lobules of the gland, while within there is an irregular cavity con- taining white sebaceous material which sends prolongations into the gland lobules. The lobules of the gland consist of epithelium, the peripheral cells of which are cylindrical. In the midst of the sebaceous material are found peculiar glancing bodies, compared to swollen starch-granules. The disease depends on some virus, and, as the name implies, it is contagious. It generally occurs in groups in the same person, as if spreading, and several members of the same family, or several persons living together, are usually affected simultaneously. It is usually seen in children, but occurs also in adults. Fibroma Molluscum.— This condition is to be carefully distin- guished from that just mentioned. We have here also multiple growths, but they are definite fibrous tumors having their seat of origin in the cutis. When small they may lie embedded in the cutis, but as they increase in size they become prominent, and may finally assume a pendulous condition. They are sometimes present in enormous numbers, the individual growths varying in & 790 DISEASES OF THE SKIN AND ITS APPENDAGES. size from very small tumors up to those having even the bulk of a man's head. The epidermis is usually unchanged on the surface of the tumor. The tumor consists of connective tissue in which there may be an excess of small spindle-shaped cells. To the naked eye all the characters of a hard fibroma are presented. It appears from the observations of Recklinghausen that these multiple iibromas of the skin are often associated with multiple fibromas of the nerves. The structure in the two cases is the same, namely, a soft connective tissue, rather more cellular than normal. The fibromas of the nerves are often described as neu- romas, but, as they contain no new-formed nerve-tissue, they are false neuromas. From these observations there seems reason to suspect that the tumors in the skin have their origin in the nerves of the skin, and that they also are primarily false neuromas. Looking to this probable origin of these tumors, they may, per- haps, along with those of the nerves, be grouped as multiple NEUROFIBROMAS. In Several cases of this kind a distinct hereditary tendency has been observed, and some of the tumors are often congenital. Elephantiasis. — This condition has been already described at p. 176. It may be added here that a condition somewhat resem- bling elephantiasis, and designated lymph-scrotum, is sometimes brought about by obstruction of the lymphatics. There are dilata- tion of the lymphatics and formation of vesicles, and there may be, after a time, a thickening of the skin, but without the attacks of acute inflammation characteristic of elephantiasis. This con- dition (which has been named elephantiasis lymphangiectodes) is usually the result of the filaria in the lymphatics, and has already been referred to (see p. 282). Xanthoma, or Xanthelasma. — This name is applied to slight elevations of the skin of a yellowish color. They occur mostly on the eyelids, where they appear as firm yellow patches, which are usually quite flat, but may be slightly tuberculated. They consist of firm connective tissue in which finely divided fat-gran- ules are abundantly present. The latter give the opaque yellow character to the lesion. Of the remaining simple-tissue tumors, the lipoma is common, originating in the subcutaneous tissue. The myxoma is not infre- quent, and the enchondroma and osteoma very unusual. The ANGIOMA of the skin is common as the congenital nsevus (see p. 193). Sarcoma. — This form of tumor is of somewhat frequent occur- rence, and we may have round-celled or spindle-celled growths, which sometimes assume considerable dimensions. We have already seen that sarcomas sometimes originate from soft warts or CANCERS. 791 moles, and, when they do so, they frequently present a similar structure to that described above, namely, masses of large round cells in a stroma. To this form the name alveolar sarcoma is applicable. Sarcomas originating from moles are peculiarly apt to be pigmented. Sarcomas rarely occur as secondary tumors in the skin, but a case is known to the author where multiple tumors composed of round-celled tissue formed at intervals in the subcutaneous tissue and some of them disappeared. These were either round-celled sarcomas or lymphosarcomas. Cancers. — The epithelioma of the skin forms the majority of the flat-celled epitheliomas, and it has been already referred to at p. 215. In the skin, two forms of epithelioma have been distinguished, one in which the cancer cylinders tend to penetrate deeply into subjacent structures, and the other in which there is rather a tendency to extend along the surface. The one form is sometimes called infiltrating cancer, the other flat cancer. The infiltrating epithelial cancer has its most familiar seat in the lower lip. Beginning as a slight thickening, it gradually Fig. 344. Section of an epithelioma at its marginal part. The epidermis is seen to be penetrating inwards into the cutis. At a a small laminated capsule is indicated. X 100. extends, producing a knotted, thick appearance. The surface ulcerates, and a scab forms. On making a section through such a tumor an appearance is presented as of a wart growing inwards, 792 DISEASES OF THE SKIN AND ITS APPENDAGES. and the material of which it is composed has a brittle, crumbling appearance. Under the microscope, it is seen at the margin that the epidermis is growing downwards, the growing cells having the characters of those of the rete mucosum (see Fig. 334). The growth is in cylinders, and as it progresses there seems to be a mutual pressure of the cylinders, causing great compression of the central cells. To this cause, and perhaps also to a tendency to degeneration on the part of the cells, is due the formation of the peculiar glistening epithelial globes, or laminated capsules, which are so prominent in many cases (Fig. 335). These globes Pig. 335. Parts from an epithelioma. a, isolated epithelial cells; h, a cylinder composed o'f epi- dermis, and with many laminated capsules ; o, a laminated capsule opened out so as to show the cells composing it. Prom a fresh preparation with the addition of dilute acetic acid. X 400. (Billroth.) consist of epidermic cells wrapped round a common centre, and, when they are disintegrated, the cells may retain their curved shapes. The epithelial cylinders may penetrate very deeply, and CANCERS. 793 usually cause great irritation, evidenced by the presence of round cells in the tissue, as in Fig. 336. In the scrotum the cancer is very much as it is in the lips, having the infiltrating character. It is met with principally in chimney- sweepers, but also in Glasgow among workers in paraffin refineries. ■FiQ. 336. Portions of three cylinders of an epithelioma, embedded in round cells produced as a result of irritation of the cutis. X 200. At the edges of the scrotal cancers there is often some enlargement of the papillae. In other parts of the skin it is generally the flat form which is met with. The epithelioma tends to spread laterally rather than deeply, so that it may come to cover a considerable surface, which is often circular in form, with raised warty-looking edges. On examining these edges under the microscope it is often seen that there are series of elongated papillae. The central parts are ulcerated, but even here there is an appearance as if papillae had been cut oiF at their bases. Sometimes these flat cancers appear to take origin in the sebaceous glands, and to grow rather by an exaggeration of them than of the surface epithelium. All flat cancers of the skin grow slowly, and sometimes they cicatrize in their central parts while slowly extending at their edges. In the flat form ulceration very often overtakes to a large extent the new formation, so that the lesion presents itself as an ulcer with infiltrated margins, and is often called kodent ulcer. Some- times healing occurs in the central parts, a cicatrix forming, while the ulcer extends peripherally. At other times the ulcer goes on 794 DISEASES OF THE SKIN AN"D ITS APPENDAGES. extending. In these cases with the ulceration there is a great new formation of inflammatory tissue, and this may greatly obscure the epithelial elements, which, however, are to be found in nests of large flat cells. The flat ulcerating form occurs mostly in old people, and does not usually lead to secondary tumors in the lym- phatic glands. The rodent ulcer occurs on the face, especially on the eyelids and side of nose. Ordinary cancer is of rare occurrence in the skin, but cases have been observed to which the names scirrhus and soft cancer have been given. Pigmented cancers are of occasional occurrence, and they are of importance on account of their tendency to form secondary tumors, first in the lymphatic glands and then through- out the body. They are, however, much less frequent than melanotic sarcomas, with which they are apt to be confused. PARASITIC DISEASES OF THE SKIN. We have already seen that certain forms of inflammation are associated with the presence of micro-organisms, especially the infective inflammations. We saw also that leprosy depends on a specific bacillus. These do not require further treatment here. Fungi are present in three forms in the skin. It has already been indicated that many are of opinion that the same fungus is at the basis of all three forms, and that this fungus is the oidium lactis. But if this be the case it seems strange that the three varieties keep perfectly distinct, and that when the diseases are communicated from person to person they do not interchange. 1. Tinea Favosa or Favus. — This is a disease chiefly of the hairy scalp, although it occurs on other parts of the skin and also Fig. 337. The fungus in favus. Short threads are shown. X 350. in the nails. On the scalp it forms crusts which at first are isolated and about the size of split-peas. They are circular in shape, pale- TINEA TONSURANS. 795 yellow in color, and dimpled in the centre through which a hair or hairs generally pass. When removed the crusts are usually seen to be somewhat cup-shaped, the convexity of the cup being next the skin, the latter presenting a corresponding depression. If the cups be divided with a knife they are seen to have a porous appearance, the interstices being filled with air, and they are brittle, so that they can be easily broken down in water. The crusts are formed of fungus along with epidermic scales and their debris. The fungus is the achoeion Schoenleinii, in the form for the most part of short tubes (Fig. 337) with rows of conidia spores. The proper mycelium is not jointed, but the receptacula are. The fungus appears to begin its growth in the hair-follicles, enveloping the hair and passing into it. It also FiQ. 338. Hair from tinea tonsurans. The shaft is penetrated and broken up by spores. X 350. passes into the hair-sheath and epidermis around, separating the cells and destroying them. It has its seat thus in the first instance beneath the horny layer, which may be continuous over it. It 796 DISEASES OF THE SKIN AND ITS APPENDAGES. does not invade the true skin, but the crust may cause inflamma- tion around it which may go on to suppuration and ulceration. As a rule, however, it only affects the epidermic structures, the hairs being largely destroyed where the crusts are developed. When it attacks the nail, it forms a yellow crust, the tissue of the nail being opened out and softened by the fungus penetrating between the horny cells. 2. Tinea Tonsurans. — This is also a disease chiefly of the scalp, but the same fungus attacks the beard and the parts of the body devoid of hair. The disease is therefore divisible into three forms, TINEA tonsurans PROPER, TINEA SYCOSIS, and TINEA MAR&INATA. In tinea tonsurans, or ringworm, there are circular patches on the scalp, in which the hairs are short and small, as if the hair had been badly cut. The fungus, called the trichophyton ton- surans, is here chiefly in the form of spores (see Fig. 388) w^hich infiltrate the hair and its sheath, as well as, to a less extent, the epidermis around. The mycelium is only represented by short threads. The hair-shaft is greatly penetrated by the spores, which break it up. In tinea sycosis, or ringworm of the beard, the fungus is again chiefly in the form of spores in the hairs and hair-follicles, but here it produces great irritation, so that pustules and papules form. In tinea marginata, or ringworm op the body, there are patches generally more or less circular or crescentic in shape, and consist- ing of vesicles on a raised surface, or simply scaly elevations. In this form the fungus develops mycelium abundantly, whose threads pass among the epidermic cells. The spores are much less abun- dant than in the other two forms. The name eczema marginatum has been given to what is really a severe form of the condition which we are now considering. FiQ. 339. Fungus in pityriasis versicolor. Threads are seen with groups of spores. X 500. (Duhkino.) 3. Pityriasis Versicolor. — In this disease there are patches of a yellowish or dark-brown color with a scaly surface, and occur- SCABIES. 797 ring chie% on the trunk in adults. If the surface be scraped, and the scaly products examined under the microscope (best with the addition of liquor potassse, both in this case and the others), there will be found epidermic cells with the elements of a fungus, the MICEOSPOEON FUEFUE. There are usually abundant mycelium threads, and the spores are in rounded masses which have been compared to bunches of grapes (see Fig. 339). Of the lesions due to animal paeasites, the most important is scabies. Scabies. — This disease is characterized by the formation of papules, vesicles, pustules, and other signs of inflammation due to the effects of the acaeus scabiei or saecoptes hominis. The female of this insect penetrates into the substance of the epidermis. It forms a tunnel for itself as it penetrates, and in this it deposits ova and feces, the latter in the form of brown granules. It usually passes through the horny layer into the rete Malpighii, sometimes approaching the si^rface of the papillae. It opens up the epidermis and causes irritation, evidenced by intense itching. The inflammatory conditions are the result partly of the irrita- tion of the acarus and its embryos, which, as they develop from the ova, begin to travel along the tunnels, and partly the effect of the scratching induced by the itching. The primary lesion is a papule on which a minute furrow is visible to the naked eye. The papule is produced by the opening up of the epidermis and swell- ing of the papillary layer, which is infiltrated with serous fluid and round cells. Vesicles and pustules are produced when the in- flammation is more severe, and are met with chiefly in children and persons with delicate skins. The ACARUS EOLLicuLOEUM is au insect sometimes met with in comedones. The LARV^ OF INSECTS are occasionally met with in the skin. The ova are deposited in the skin, and the larvae having developed, may traverse the skin and subcutaneous tissue for a considerable distance till they present at some part and are squeezed out or ex- tracted. They may produce considerable inflammations in the form of boils or swellings. ADDENDUM. ACTINOMYCOSIS. This disease should have been considered under the heading of PARASITIC FUNGI, but was Overlooked. The disease occurs chiefly in cattle, and occasionally in pigs, but it has been met with in a certain number of cases in man. It depends on the existence of a fungus whose exact botanical posi- tion is unknown. The fungus is in the form of short threads which are clubbed at their extremities. These threads, which are perhaps conidia, are arranged in a radiating fashion, many_ spring- ing from a common centre, with their clubbed extremities out- wards. They thus form peculiar radiating groups of a globular or oval form, which, being made up of club- or wedge-shaped pieces, present a peculiar glandular or knobbed surface, like that of a mulberry. The club-shaped fibres are united in the centre by a matted mass of fibres, which may be the mycelium. It is from these radiating structures that the fungus has received its name of Eay-fungus or Actinomyces (a/crif, a ray), and the disease that of Actinomycosis. The radiating clumps are individually of very small size, like grains of dust, but thej are usually united into larger masses as the heads in a cauliflower (Ponflck). These larger masses are the characteristic indications of the disease, appearing to the naked eye as yellow, sulphur-colored granules in the midst of the structures about to be described. The disease was first described and named by Bollinger, in 1877, he having distinguished it in cattle, in which it seems some- what common in certain localities. Its occurrence in the human subject has been established, chiefly by the observations of Israel and Ponflck. In cattle it mostly appears as a tumor-like swelling of the jaw, most commonly the lower jaw. It grows outwards to considerable dimensions, forming a simple or lobulated tumor. After a time the skin gives way, and a prominent projecting mass protrudes, which discharges a thick pus with pieces of slough. In this dis- charge are visible little sulphur-yellow granules, which are some- what firm in consistence, and have a greasy feeling. These are the fungous masses already described. The new formation may extend from the jaw to the tongue, pharynx, larynx, oesophagus, stomach, and intestinal wall. ACTINOMYCOSIS. 799 The disease is communicable by inoculation from one animal to another. The rabbit and dog seem to be incapable of inoculation, but cattle are highly susceptible. It may be produced by inocula- tion into the subcutaneous or intermuscular tissue, and produces its effects in a very striking manner when inoculated into the peritoneal cavity. When introduced into the blood it produces typical new formations in the lungs. _ In man the disease is induced apparently by accidental inocula- tion, usually by a wound in the mucous membrane of the mouth (as from extraction of a tooth) or pharynx, but possibly by a wound in the skin. "When so induced it produces swellings, as in cattle, but these do not usually grow to such bulky tumors, as they break down more readily so as to form abscess-like cavities Avhich open externally and give rise to fistulas. The disease may remain local, affecting, it may be, the jaws and surrounding parts. On the other hand, it may extend slowly till it involves the bodies of the verte- brae or the pleura. In such cases the introduction is probably by the pharynx. In these internal parts it produces a slow inflam- matory process with exuberant granulations and chronic suppura- tion. When it affects the vertebrae, which it seems to do with peculiar frequency, these become carious, and a chronic abscess forms which may gradually extend to the surface and open in the lumbar region or the groin. In these cases the person becomes slowly emaciated, and dies after months or years from exhaustion-, sometimes with amyloid disease. In some cases there has been a metastasis, so that abscess-like formations have occurred in various organs, and the case has been like one of pyaemia. In all these situations the sulphur-yellow granules are found, and they are to be recognized in the pus of the abscesses, etc. Looking moi-e closely at the anatomical details in this disease, it is clear that we have to do with a specific irritant. The most direct effect of the action of this irritant is the formation of granulation tissue. In cattle this is so abundant that a bulky tumor is produced, which, from its structure, might be taken for a round-celled sarcoma. In man the granulation tissue is not so exuberant, although produced abundantly, and when the abscesses find their way to the surface the granulations pout at the opening like those of a sinus leading from a scrofulous joint. Looking at this great new formation of granulation tissue and at its tendency' to break down, Pontick has suggested that the disease should be placed among the infective tumors. The granulation tissue here resembles that in the infective tumors, not only in its exuberance and tendency to break down, but also in its tendency to form con- nective tissue in an irregular way. In the midst of the masses of granulations there may be strands of coarse connective tissue. INDEX. ABSCESS of brain, 428 Acarus foUiculorum, 284, 797 (aKapi, a mite) soabiei, 283, 797 Aohorion Schoenleinii, 259 {axp6(, the kidney) Hydrophobia, lesions in brain, etc., in, 432 {Map, water, and 0o/3£u, I fear) Hydrorhachis, foetal, a cause of spina bifida, 451 {Map, water, and paxi^, the back) Hydrothorax, 523 {Mop, water, and e6pa^, the breast) Hypersemia {imep, over, and al/xa, blood) and anaemia, 25 active, of the lungs, 481 general, 25 collateral, 32 from dilatation of arteries, 38 of the lungs, 482 local, 32 active, 32 passive, 34 oedema from, 63 passive, from thrombosis, 46 Hyperostosis, 748 {vvip, over or excessive, and bareov, bone) Hyperplasia, 140 {vTr^p, over, and TrAdoif, a moulding ; from widaao, I mould) Hypertrophy, 137 {virip, over, and rpifa, I nourish) from excessive performance of a normal function, 138 from frequently recurring pressure, 140 from increased blood supply, 140 in bones, 141 in epidermis, 139 in muscle, 139 Hypertrophy, in neighborhood of inflam- mations, 141 Hypostatic engorgement of lungs, 482 {vnoaTarmd^, from vijiicTafiai, I stand under) TCHTHYOSIS, 787 {;ixek, a fish) i Icterus, 125 {iKvepog, jaundice) Immediate union, 143 Immunity, acquired, 251 natural, 249 in zymotic diseases, theories of, 252 Indurated chancre, 148 Infantile paralysis, 397 Infarction from embolism, 48 {infarcio, I cram in) hemorrhagic, of lungs, 485 Infective inflammation, 103 tumors, 147 Inflammation {inftammo, I set on fire), 80 active hypersemia in, 84 artificial production of, 80 changes in the tissues and new forma- tion, 95 characters of the inflammatory ex- udation, 94 disposal of exudations, 95 emigration and diapedesis in, 90 etiology of, 80 exudation cells, 89 {exsudo, I sweat out) fibrinous exudation, 91 formative cells, origin of, 99 formation of fibrine in, 93 individual forms of, 103 inflammatory exudation, 89 internal pavementing of veins, 86 its mode of occurrence, 91 nervous system, its influence in causa- tion of, 81 new formation of bloodvessels, 98 new formation of bone and cartilaee, 101 ^ ' paralysis of tissues in, 85 path of entrance of irritants, 82 principal phenomena, 82 processes observed in wounded web of frog, 83 produced by irritants, 81 retardation and stasis of blood-current, 86 retrograde changes, 95 the serous exudation — inflammatory oedema, 91 state of the vessels in, 84 syphilitic, 149 temperature of inflamed parts, 87 Insane ear, 60 Intestine, catarrh of, 563 catarrhal ulcers of, 564 condition in dysentery, 567 cholera, 568 typhoid fever, 669 cysts of, 564 follicular ulcei's of, 564 INDEX. Intestine, hernia or rupture, 556 introduction to diseases of, 554 intussusception or invagination of, 561 in leukaemia, 70 malformations of, 555 mucous polpi of, 564 obstruction to calibre of, 576 post-mortem changes in, 555 prolapse of, 563 results of obstruction of, 577 simple inflammations of, 563 specific inflammations of, 567 tuberculosis of, 572 secondary to phthisis pulmonalis, 515 tumors of, 574, 576 twisting of, 560 Introduction, 17 Intussusception of the intestine, 561 {intus, within, and suscipio, I receive) Iodine as a, test in amyloid degeneration, 131 Irritants, their nature, 80 JOINTS, anchylosis of, 755 U dislocations and misplacements of, 753 inflammations of. See arthritis syphilis of, 759 KELOID, true and false, 788 (/o?Aif, a spot) Kidneys, active hyperaemia of, 623 acute miliary tuberculosis, 654 amyloid degeneration of, 650 Bright's disease of, 624 calculi and concretions in, 653 coalescence of (horse-shoe kidney), 621 compensatory hypertrophy of, 622 cirrhosis of, 633 cystoid degeneration of, 658 cysts of, 635 embolism, 50, 624 tatty degeneration of epithelium, 650 granular contracted, 633 hydronephrosis, 655 independent cysts of, resembling hy- dronephrosis, 657 in leukaemia, 70 in scarlet fever, 646 lardaceous, 652 local tuberculosis of, 654 malformations and misplacements of, 620 metastatic abscesses in, 645 micrococci in, 646 movable or floating, 621 normal structure and functions of, 615 parasites in, 660 parenchymatous inflltration of, 649 passive hyperaamia of, 623 perinephric abscess, 648 Kidneys, primary cancer of, 659 retrograde changes in, 649 septic inflammations of, 645 simple atrophy of, 649 simple cysts of, 657 syphilis of, 654 thrombosis of veins, 623 tubercular ulceration of, 158 tumors of, 657 Kyphosis, 745 {icvfdc, bent forwards) LARDACEOUS degeneration, 131 Large white kidney, 631 Larvaj of insects in the skin, 797 in the tissues, 284 Laryngeal phthisis, 463 Larynx and trachea, acute catarrh of, 460 diphtheria and croup, 458 diseases of, 457 Larynx, condylomata of, 462 chronic catarrh of, 461 inflammation of the perichondrium, 461 malformations of, 457 oedema glottidis, 460 phthisis of, 463 subglottic inflammation, 461 syphilis of, 462 tumors of, 464 Late rigidity in descending sclerosis, 387 Lead poisoning, atrophy with paralysis in, 116 Lepra ansesthetica, 167 {lenp6g, scaly) tuberculosa, 167 Leprosy, 166 {\enp6(, scaly) bacillus in, 167, 246 nerves in, 379 Leptomeningitis, 444 [Xe%t6q, fine, fifviy^, a membrane) Leptothrix buccalis, 259 (Txnrdq, slender, 6pl^, a hair, and bucca, the cheek) Leucocytosis, 28 (Aerndf, white, and kvtoq, a hollow, a cell) Leucomyelitis, 390 [levK6g, white, and fiveU^, marrow) Leukaemia, 66 (Aewjciif, white, and aliia, blood) Charcot's crystals, 67 intestines in, 70 kidney in, 70 liver in, 70 skin in, 70 lymphatic glands in, 68 medulla of bone in, 68 relations to lymphoma, 222 spleen in, 67 Lichen ruber, 772 [\eixffv, a tree-moss, a scabj and ruber, red) Lipoma, 178 [Xlnog, fat) diffuse, 179 pendulous, 179 Liver, acute yellow atrophy of, 586 acquired deformities of, 579 adenoma, 597 amyloid degeneration of, 585 810 INDEX. Liver, atrophy of, 583 atrophy of cells in passive hypersemia, 580 cancer of, 598 cirrhosis of 589 congenital syphilitic disease of, 594 deformity in females, 579 embolism in, 582 fatty degeneration of, 583 fatty infiltration of, 123, 584 folds of, 580 hypertrophic cirrhosis of, 591 hypertrophy of, 583 inflammations of, 587 introduction to diseases of, 578 in leukaemia, 70 malformations of, 579 nutmeg, 580 parasites of, 600 passive hyperaamia of, 580 parenchymatous infiltration of, 583 perihepatitis, 593 pysemic abscesses of, 588 red atrophy of, 580 retrograde changes in, 583 syphilitic disease of, 594 thrombosis and embolism in, 582 tropical abscess of, 587 tuberculosis of, 595 tumors of, 596 Locomotor ataxia, 393 [locus, a place ; moveo, I move; a, priv., and rd^ig, order) lesion in, 393 physiology of, 394 trophic lesions of skin, muscles, and joints, 395 Lordosis, 745 (%opS6Q, bent supinely) Lungs, active hyperajmia of, 481 acute pneumonia, 489 anthracosis, 519 atelectasis, 471 ' brown induration of, 484 cancer of, 517 carnification of, 472 collapse of, 472 causes of collapse, 472 collateral hypersemia of, 481 diseases of, 469 disorders of the circulation in, 481 embolism of the pulmonary artery, 487 emphysema of, 474 gangrene of, 498 hemorrhage from, 488 hemorrhagic infarction of, 485 hypertrophy (compensatory) of, 473 induration of. See pneumonia, chronic inflammations of, 489 inhalation of foreign substances, 518 malformations of, 471 oil embolism in, 487 passive hypersemia and cedema of, 482 passive hyperaemia from heart disease, 484 Lungs, phthisis pulmonalis, 500 pigmentation of, 125, 518 syphilitic disease of, 516 tumors of, 516 Lung-tissue in sputum in phthisis, 509 Lupus, 166 [lupus , a wolf) exedens, 166 non-exedens, 166 {non, not, and exedo, I devour) Lymphadenitis, acute, 359 {lypmpha, water, and adr/v, a gland) chronic, 360 Lymphadenoma, 222 {lympha, water, and aS^v, a gland) Lymphangeitis, 355 {lympha, v/ater, and hyyelov, a vessel) Lymphangiectasis, 356 [lympha, water ; ayye'iov, a vessel ; and inraaig, expansion) Lymphangioma, cavernous, 356 [lympha, water, and ayyelov, a vessel) Lymphatic circulation, 61 glands, acute inflammation of, 359 diseases of, 357 in leukemia, 68 pigmentation of, 359 scrofulous disease of, 162, 360 secondary tuberculosis of, 362 in syphilis, 149 syphilitic disease, degenerative changes, and tumors of, 363 growth. See lymphoma vessels, obstruction of, 61 inflammation of, 355 Lymphoma, 222 [lympha, water) Lympho-sarcoma, 222 of mediastinum and mesentery, 222 of lung, 516 Lymph-scrotum, 282, 790 MACKOGLOSSIA, 856, 530 [fiafcpdg, large, and yloaaa, the tongue) Madura foot, 257 Malarial fevers, bacilli in, 246 Malformations. See the individual organs Malignant pustule. See splenic fever Mamma, acute scirrhus of, 711 adenoid sarcoma of, 704 adenoma of, 704 cancer of, 707 colloid cancer of, 711 cysts and cysto-sarcoma of, 706 duct cancers, 707 inflammation of, 703 malformations of, 703 medullary cancer of, 710 mucous cancer of, 711 parenchymatous cancer of, 707 rarer tumors of, 711 sarcoma of, 705 scirrhus of, 708 Meckel's diverticulum, 556 Medulla oblongata, bulbar paralysis, 401 introduction to diseases of, 380 tumors of, 406 INDEX. 811 MelansBmia, 70 {fiiTiag, black, and alfui, blood) Melanotic cancer, 222 {/j.ehic, black) Membranes and cavities of brain and cord, introduction to diseases of, 441 Membranes of brain, bemorrbage from, 443 syphilitic disease of, 435, 438 tumors of, 452 Meningeal hemorrhage, 442 Meningitis, epidemic cerebro-spinal, 445 (p/vjyf , a membrane) gummatous, 436 simple acute, 444 simple chronic, 444 tubercular, 445 Meninges, tumors of, 452 Mercury, effects on mouth, 527 Mesentery, aperture in, causing obstruc- tion, 577 lymph-sarcoma of, 222 Metaplasia, 719 [fieTaTrXaaiQ, transforma- tion, from //Era, indicating change, and TrAdffou, I mould) Metastasis, 172 (ueBiaT7i/it, I change place) Metastatic calcihcation, 128 Meteorism, 577, 609 (//Ereupifu, I elevate) Methyl-violet, as a test, in amyloid de- generation, 181 Metritis, 678 UiZ/rpa, the womb) Micrococci, 226 {junpoq, small, and k^kkoq, a kernel) in kidney, 646 Micro-organisms, 224 Microsporon furfur, 259, 797 Milium, 774 (Lat., millet) Mitral insufficiency or incompetency, 319 obstruction or stenosis, 321 {arevoQ, narrow) Moles, pigmented, 789 Mollities ossium, 730 (Lat., softness of bones) Molluscum contagiosum, 789 (moUuscum, a fungus, from mollis, soft) Molluscum fibrosum, 178 Morbid anatomy, relation to pathology, 18 Morbus coxae senilis, 759 (Lat., disease of the hip in the aged) Morphoea, 785 Mouth, catarrh of, 526 effects of scurvy, 527 of mercury, 527 epithelioma of, 530 follicular stomatitis, 526 infective tumors of (syphilis, etc), 528 smallpox eruption in, 527 syphilis of, 528 thrush or aphthous stomatitis, 526 tumors of, 529 Mucous and colloid degeneration, physio- logical type of, 126 in ovarian tumors, 126 in thyroid gland, 127 in cancers, 127 Mucous cancer, 222 degeneration, 125 of intercellular substance, 127 tissue tumor. See myxoma Mummification, 111 Muscle, fatty infiltration of, 122 hypertrophy of, 139 regeneration of, 146 Muscular-tissue tumor. See myoma Myelitis, transverse acute, 390 {/iveXdQ, marrow) transverse chronic, 391 Myeloplaques, 732 (/ziJEAdf, marrow, and TrAdf , a flat surface) Myocarditis, 304 (/j.vc, a muscle, and Kapdia, the heart) interstitial, 304 Myoma, 187 (fJ-vc, a muscle) of female generative organs, 189 of nipple, 711 of uterus. See uterus retrograde changes of, 190 situations of, 189 smooth-celled, 188 strio-cellulare, 187 Myxoedema, 764 (/iifa, mucous, and oUr/fia, a swelling) Myxoma, 180 {/iii^a, mucus) characters of mucous tissue, 181 hydatid mole, 182 situation and characters of, 183 "Vr.^VI, vascular (naevus, a mole). See ll angioma Nails, atrophy of, 766 Nasal passages, acute catarrh of, 454 chronic catarrh of, 456 congenital malformations of, 454 tumors of, 456 Necrosis, caseous. 111 (veapaaic, state of death, from veKpdg, a dead body) disposal of the dead tissue in, 113 its causes, 105 limitation of, 112 of bone, 738 Nematoda, or round worms, 275 {vrjjia, a thread, dSog, likeness) Nephritis {ve(j>p6s, the kidney). See Bright's disease Nerves, chronic neuritis, 379 diseases of, introductory considera- tions, 375 effects of division of, 377 hypersemia and acute inflammation of, 378 regeneration after division of, 146, 378 tumors of, 379 Nervous system, diseases of, introduction, 372 Nervous-tissue tumor. See neuroma Neuritis, acute, 378 {vevpov, a nerve) chronic, 379 Neuroma, 190 (vevpov, a nerve) false, 191 painful subcutaneous tumor, 191 812 INDEX. Neuroma, relation to multiple fibromata of skin, 790 true, structure of, 191 Nipple, Paget's disease of, 708 Noma, 527 {vifia, I devour) Normal growth, 137 OBESITY, 122 Oildema and dropsy, 61 {oldiu, I swell, iiSpaij), dropsy ; from Mup^ water) in passive hyperfomia, 36 from hydrajmia, 64 from thrombosis, 46 from venous hypera3mia, 63 glottidis, 460 in Bright's disease, 64 inflammatory, 91 of the brain, 448 of the lungs, 482 (Esophagus, diseases of, 537 general dilatation of, 537 inflammations of, 539 obstruction of, 538 partial dilatation (diverticulum) of, 538 perforating ulcers of, 539 tumors of, 540 Oidium albicans, 260, 527 Oil-embolism, 54 Oligsemia, 28 {oMyog, small, and al^a, blood) Omentum, condition of, in tubercular peri- tonitis, 611 its relations to cancer of peritoneum, 616 Oophoritis, acute, 692 {uo^6poQ, bearing eggs, or roe, from ^dv, an egg, and (ftopca, I bear) chronic, 692 Orchitis, acute, 712 (dpxtg, the testicle) chronic, 713 Organization of thrombi, 44 Organs of respiration, diseases of, 454 Osseous tumors, 748 Ossification, normal, 724 in rickets, 724 Osteitis, rarefying or destructive and formative or condensing, 732 {oarcov, bone) Osteoblasts, 782 [bareov, bone, and /SAacmif , a sprout) Osteoclasts, 732 {barEov, bone, and KXaardc, broken in pieces) Osteoid chondroma, 748 (barhv, bone, and sldoc, likeness) Osteoma, 185 (bariov, bone) hyperostosis and periostosis, 187 {vwip, over, and bareov, bone), (Trspi, around, and boTiov , bone) ivory exostosis, 186 spongy exostosis, 185 unconnected with bone, 187 Osteomalacia, 729 {bareov, a bone, and /m?M.Kia, softness, from //aAa/cpa^, the breast) QUINSY, 535 (through French esqui- nancie, from KmdyKrj, dog-quinsy, or sore throat, from kvuv, a dog, and ayxo, I strangle) RACHITIC rosary, 728 Bachitis. See rickets, {pdxv, the spine) Eanula, 530 (dim. of rana, a frog) Red corpuscles, replenishment of, 29 Regeneration, 141 of blood, 144 after loss, 144 of bone, 146 of connective tissue, 145 of epidermis and epithelium, 144 of muscle, 147 of nerve fibres, 147 Relapsing fever, 244 Renal phthisis, 158, 654 Repair of injuries and restoration of lost parts, 141 Reproduction of lost parts, law of, 142 Retrograde metamorphosis, 105 Rhabdo-myoma, 187 (po/3(!of, a stripe, and /jvg, a muscle) Rickets, 795 deformities of bones in, 726 of chest in, 728 of head in, 728 of long bones in, 726 mode of ossification in, 724 partial fractures in, 727 shifting of the epiphyses in, 727 Ringworm, 258 Rodent ulcer, 793 Round worms. See Nematoda OAND tumor, 198 U Sarcina ventriculi, 253 (sareina, a bundle, and ventriculus, the stomach) in blood, 254 Sarcoma, definition of, 204 {adp^, flesh) division of, according to type, 205 mode of growth, 205 of lung, 516 of membranes of brain, 453 retroperitoneal, 612 structure and classification of, 205 varieties of, round-celled, 206 alveolar, 210 cystic, 208 melanoid or pigmented, 209 myeloid or giant-celled, 208 osteoid, 209 plexiform or cylindroma, 210 spindle-celled, 207 Sarooptes hominis, 797 Scabies, 797 (Latin, the itch) Scalds, 774 Scarlet fever, state of kidneys in, 646 Schizomyceta3, 225 (ffjtfu, I split, and fivK7/<;, a mushroom) Scirrhus, 218 (amppdg, hard) of the mamma, 708 of the stomach, 552 Sclerema neonatorum, 786 (aKhripdQ, hard, vio^, new, and naius, born) Scleroderma, 786 (anXripdg, hard, and dep/ia, the skin) INDEX. 815 Sclerosis, disseminated or in patches, 429 {aK2.7jp6^, hard) of spinal cord, 386 Scolex, 266 (oKokri^, a woma) Scrofula, its relation to tuberculosis, 102 {scrofa, a sow) Scrofulous tubercle of the brain, 159 Scrotum, cancer of, 717 lymph-scrotum, 717 Scurvy, condition of mouth, 527 Senile emphysema, 480 gangrene, 107 Septicsemia, 231 (^ar/nnKdc, putrefying, and alfia, blood) of mice (Kooh), 284 of rabbits, 235 pathogenic bacteria in, 236 septic poisoning, 232 septic or putrid infection, 233 Septic poisoning, 232 infection, 233 thrombosis, 46 Simple-tissue tumors, 176 Skin, cancer (epithelioma) of, 791 causes of cutaneous inflammation, 767 cysts in, 765 eruptions in fevers, 708 eruption of smallpox, 768 fibroma moUuscum, 789 fibro-neuromata of, 790 forms of cutaneous inflammations, 768 "glossy skin," 785 gumma of, 783 hemorrhages of, 764 hypersemia of, 764 hypertrophies and tumors of, 787 infective inflammations of, 778 infective tumors of, 781 inflammatory skin eruptions, 770 introduction to diseases of, 763 lesions of, due to cadaveric poisons, 778 leukaemia, lesion in, 70 local atrophy of, in pregnancy, 765 molluscum contagiosum, 789 multiple fibromata of, 790 normal structure of, 762 oedema of, 764 parasitic afifections of, 794 parchment skin, 765 phlegmonous inflammations of, 780 pigmented cancer of, 794 sarcoma of, 790 simple and senile atrophy of, 765 symptomatic inflammations, 768 syphilitic lesions of, 782 traumatic and non-infective inflam- mations, 774 tropho-neuroses of, 784 tumors of, 787 Smallpox eruption in mouth, 527 on skin, 768 Softening of the brain, 425 in the aged, 107 Softening with decomposition in gangrene, 112 Soor, 526 Spastic paralysis (Erb), 396 {avacTucSc, stretching, from CTrda, I draw, napd, beside, and /Idw, I loosen) Spermatocele, 716 {anep/ia, seed, and Ktih;, a tumor) Spina bifida, 451 condition of cord in, 452 Spinal cord, acute softening of, 391 amyotrophic lateral sclerosis, 397 (a, priv , /J.VC, a muscle, and rpkijia, I nourish) anterior and posterior root zones, 382 arrangement of gray substance,. 380 of white substance, 381 ascending gray degeneration, 388 degeneration of, after amputa- tions, 389 descending gray degeneration, 386 descending sclerosis, 386 inflammations of, 390 introduction to diseases of, 380 poliomyelitis anterior acuta, 397 poliomyelitis anterior chronica, 399 progressive muscular atrophy, 400 pseudo-hypertrophic paralysis, 403 pyramidal and cerebellar tracts, columns of Tiirck and Goll, 382 sclerosis of the posterior columns, 393 secondary degenerations of, 384 spontaneous lateral sclerosis, 396 tumors of, 406 Spinal curvatures, antero-posterior, 744 forms of, 744 introductory considerations, 743 lateral or rotatory, 746 Spirillum, 226 (dim. of spira, a coil) Spirochseta Obermeieri, 244 Spleen, active hypersemia and Inflamma- tion of, 365 acute splenic tumor, 366 amyloid disease, 369 chronic inflammation of, 367 chronic splenic tumor, 367 diseases of, 364 embolic infarction, 368 general hypertrophy and fibrous in- duration of, 367 in leukfemia, 67, 369 malformations of, and supernumerary spleens, 365 passive hyperasmia of, 367 rupture of, 369 sago spleen and diffiise amyloid spleen, 369 tuberculosis, syphilis, tumors, 371 Splenic fever, 242, 780 Sponge grafting, 102 816 INDEX. Sputum ooctum of bronchitis, 468 {spud, I spit, and coquo, I cook) Stasis, 87 (craaiQ, a standing, from laTriiu, I stand) Stercoraceous vomiting, 577 {stercus, ex- crement) Stomach, acute catarrh of, 545 acute and phlegmonous inflamma- tions of, 545 cancer of, 551 chronic catarrh of, 546 colloid cancerof, 552 dilatation and hypertrophy of, 543 epithelial cancer of, 70 hemorrhage from, 549 in ulcer, 547 inflammations of (gastritis), 545 introduction to diseases of, 541 medullary or soft cancer of, 551 mode of origin of ulcers, 548 perforation of, 547 post-mortem changes of, 542 scirrhus of, 552 simple perforating ulcer of, 546 tumors of, 550 Stomatitis, aphthous, 526 (ard/m, the mouth, a(j>6a, an eruption) follicular, 526 gangrenous, 527 Strohilus, 263 (arpdfSi^s, a fir cone) Strongylus duodenalis, 279 gigas, 279 Superior mesenteric artery, embolism, 52 Synovitis, strumous, 760 (aiv, with, and u6v, an egg) Syphilis, 148 amyloid disease in, 153 arteries in, 153 chancre, 148 congenital, 153 due to a virus, 148 effects on mouth, 529 hereditary, 153 affection of the bones in, 741 incubation period, 149 inflammations in, 149 lymphatic glands in, 149 of the brain and its membranes, 435 of the larynx, 462 secondary lesions, 149 symmetrical lesions in, 149 skin eruptions in, 782 tertiary stage of gummata, 150 ulceration in, 152 Syphilitic disease of cerebral bloodvessels, 437 Syringomyelia, 406 (avptyS, tube, and fweMg, the marrow) TABES dorsalis, 393 (tabeo, I waste, and dorsum, the back) Ta3nia echinococcus, 270 (icenia, a ribbon ; ixi-voi;, a hedgehog ; and kSkko^, a kernel) brood capsules of, 271 Tajnia echinococcus, characters of cyst wall, 275 development of cysts, 271 mediocanellata, or saginata, 268 solium, habitat and characters of, 263 sexual apparatus, 263, water vascular system, and de- velopment of, 265 Talipes, its various forms, 753 (talus, the ankle, and pes, the foot) Tapeworms. See oestoda arid tasnia Teeth, caries of, 531 constituents of, 531 inflammations of, 532 osteoma of, 533 tumors of, 533 Temperature of inflamed parts, 87 Tendon reflex, exaggeration of, 388 Teratoma of internal organs, 203 {repa;, a monster) of ovary. See dermoid cysts sacral, 203 situations and structure of, 203 Testicle, benign fungus of, 713 htematocele, 716 hydrocele, 715 imperfect descent of, 712 inflammation of, 712 malformations and misplacements of, 712 syphilitic disease of, 713 tuberculosis of, 714 tumors of, 714 Tetanus, lesions in, 434 (reravog, stretch- ing, tension) Threadworm, 279 Thrombi distinguished from clots, 43 {6p6/j.j3og, a lump or clot) in heart, 41, 327 in veins, 41 liable to grow, 42 organization, 44 red, 40 softening, 43 white and mixed, 40 Thrombosis and embolism, 39 Thrombosis, hypersemia, oedema, gangrene from, 46 of cerebral sinuses, 418 vessels, 415 Thrush, 260, 526 Thvroid gland, colloid degeneration of, 127 Tinea favosa, 794 (tinea, a worm, and favus, a honeycomb) tonsurans, 796 (tonsura, a shaving) Tongue, inflammation of, 528 Tonsillitis, acute, 536 (ionsillce, the tonsils) chronic (hypertrophy), 536 Trachea, malformations ol^, 457 Transfusion of blood, 25 of alien blood, 26 of blood about to coagulate, 26 Transplantation of bone, 146 Transverse myelitis, 390 INDEX. 817 Trematoda, 260 {TpJiftaTtJdr/g, perforated) Trichina spiralis, site and characters of, 275 {rpixivog, of hair) impregnation of capsule with lime, 129 Trichooephalus dispar, 279 Trichophyton, 259 {dpi^, a hair, and fvrdv, a plant) tonsurans, 790 Tricuspid valve, relative insufficiency of, 326 Tropho-neuroses, 115 [rpiipu, I nourish, vevpov, a nerve) of skin, 784 Tube casts, 639 from coagulation necrosis, 110 Tubercle and tuberculosis, 153 [tubercu- lum, a little lump) caseous necrosis of, 156 fibrous transformation of, 156 miliary, its structure, 155 Tubercles, their relation to bloodvessels, 155 Tubercular bacillus, characters of, IGl meningitis, 445 appearance of brain in, 446 white softening around ventricles, 447 peritonitis, 610 ulcer, 158 ulcer of intestine, 573 virus, nature of, 160 source, 163 Tuberculization and fatty degeneration, 122 Tuberculosis, acute miliary, 154 and inflammation, 157 artificial production of, 159 bacillus in, 246 by inoculation, 160 from inspired air, 160 general, 154 local, 157 of serous cavities, 158 relations to scrofula, 162 Tumor albus, 760 (Lat., white swelling) Tumors, 169 classification of, 174 Cohnheim's theory of malignancy, 173 cysts in, 202 definition of, 169 growth and extension of, 171 local malignancy, 172 metastasis or generalization of, 172 origin and development of, 169 origin from embryonic remains, 170 secondary changes of, 173 simple or innocent, 172 Twisting of intestine, 560 Typhlitis, 565 (™.^/l(Sv, the ocecum or blind gut) Typhoid fever, 569 (rvfo^, smoke, and Eirfof, likeness) lymphoma in, 222 Typhoid fever, bacillus (Eberth's) in, 245 condition of intestine in, 571 mesenteric lymphatic glands in, 572 characters of, 571 ULCER, perforating of, stomach. See stomach Ulceration, 104 (ulcus, a sore) syphilitic, 152 Ulcerative endocarditis, 241, 310 kidneys in, 645 organisms in, 246 Uloers of the skin, 777 Union by first intention, 144 by second intention, 144 Urajmia, 72 (obpov, urine, and, a'lfia, blood) Urachus, patency of, 661 Urethra, diseases of, 668 Urinary organs, diseases of, 617 Uterus, anteflexion, 675 anteversion, 676 atrophy of, 676 dilatation of, 677 distention of by gas, 677 double, 673- epithelial cancer of, 689 fibrinous polypus, 684 hypertrophy of, 676 cervix, 677 inflammations of, 677 inversion of, 075 malformations of, 674 mucous polypi of, 690 myoma, 685 cysts, dilatation of bloodvessels, and calcareous infiltration in, 687 induration and oedema of, 687 prolapse of, 674 parasites of, 691 retroflexion, 675 retroversion, 676 soft or medullary cancer of, 688 syphilis of, 683 tuberculosis of, 683 tumors of, 684 less frequent forms of, 091 unicornis, 674 VAGINA, cancer of, 688 prolapse of, 675 tumors of, 684 Valvular disease of heart, 319 Varicocele, 355 (yarix, a dilated vein, and K'f/Tiri, a tumor) Varicose ulcer, 777 [ Varix, 354 (varix, a dilated vein) I results of, 353 Vascular tumor. See angioma Vegetable parasites, 224 Vein-stones, 44 Vermiform appendix, foreign bodies in, 565 52 818 IXDEX. Vermiform appendix, retention cyst of, 565 Vertebra', rachitic deformity of, 728 WART, common, 202, 788 pathological, 779 soft, 789 Waxy degeneration, 131 White pneumonia, 516 Wood's tumor, 191 Wounds. See healing of wounds bacteria in, 230 Wounds of the skin, 777 Wound fever, 232 XANTHOMA, xanthelasma, 790 {^avBd^, yellow, and eTuia/ia, a plate) Xeroderma, 764, 788 (fw^f. dry, and depfia, the skin) Y AWS, 781 pLINT'S PRACTICE— A Treatise on the Principles and Practice OF Medicine. Designed for the use of Students and Practilioners of Medicine. By Austin Flint, M.D., Professor of the Principles and rraciice of Medicine and of Clinical Medicine in Bellevuc Hospital Medical College, N. Y. Fifth edition, entirely rewritten and much improved. In one large and closely-printed octavo volume of 1 150 pages. Cloth, ^5.50; leather, ;^6.50; very handsome half Russia, raised bands, ^7.00. whilst at the same time it shows its author to be 'T'HTS voKime is certainly one of the standard text- books on medicine; and we may safely affirm that, taken al ogetber, it exhibits a fuller and wider acquaintance with recent palhokgical inquiry than any similar work with which we are acquainted, possessed of the rare faculties of clear exposition, ihoughtful discrimination, and sound judgment. — London Lancet, July 23, 1881. pLINT'S AUSCULTATION AND PERCUSSION— A Manual of Auscultation and Percussion ; Of the Physical Diagnosis of Diseases of the Lungs and Heart, and of Thoracic Aneurism. By Austin Flint, M.D., Professor of the Principles and Practice of Medicine in the Bellevue Hosp. Med. Coll., N. Y. Third edition. In one handsome royal i2mo. volume of 240 pages. Cloth, S1.63. Just ready. T-T is safe to say that there is not in the EngHsh or of words. Professor Flint's language is precise and any other language the equal amount of clear, simple, conveying, without dubiety, the results of exact, and comprehensible information touching the his careful study and ample experience, — American physical exploration of the chest in an equal number Practitioner , June, 1883, T>RISTOWE'S PRACTICE— A Treatise on the Practice of Medi- cine. By John Syer Bristowe. M.D., F.R.C.P., Physician and Joint Lecturer on Medicine at St. Thomas' Hospital. Second American edition, specially revised by the Author. Edited, with additions, by James H. Hutchinson, M.D., physician to the Pennsylvania Hospital. In one hai:idsome octavo volume of 10S5 pages, with illustra- tions. Cloth, ^5.00; leather, ^6.00; very handsome half Russia, raised bands, ^6.50. are appropriate and practical, and greatly add to its usefulness to American readers, — Buffalo Medi- 'T'HE reader will find every conceivable subject connected with the practice of medicine ably presented, in a style at once clear, interesting and concise. The additions made by Dr. Hutchinson cal and Surgical Journal, Rlarch, 1880. LJ YDE ON THE SKIN — A Practical Treatise on Diseases of the Skin. For the Use of Students and Practitioners. By J. Nevins Hydf, M.D., Professor of Dermatology and Venereal Diseases in Rush Medical College, Chicago, In one handsome octavo volume of 570 pages, with 66 beautiful and elaborate illustrations. Cloth, ^4.25 ; leather, $5.25. Just Ready. pROF, HYDE has given to the profession a valu- able and comprehensive work upon this special subject, exposing the etiology, symptomatology, and treatment of diseases of the skin in a concise and thorough manner. The book is a valuable one for the student and practitioner, containing all the latest progress made in dermatology, and will, without doubt, attain the end expected by its author — to make the general practitioner thoroughly informed in regard to the treatment of cutaneous diseases. It will prove a valuable book of reference to the specialist.— A^. O. Medical and Surgical Journal ^ April, 1883. TDRYANT'S SURGERY— The Practice of Surgery. By Thomas Bryant, F.R.C.S.-, Surgeon to Guy's Hospital, London. Third American from the third and revised English edition. Thoroughly revised and much improved, by John B. Roberts, A.M., M.D. In one large and very handsome imperial octavo volume of 1009 pages, with 735 illustrations. Cloth, ^6.50; leather, ;^7.5o; very handsome half Russia, raised bands, $8.00. TTSriTHOUT freighting his book with multiplied details and wearying descriptions of allied methods of procedure, he is ample enough for refer- ence on all the departments of surgery, not omitting such strict specialties as dental, ophthalmic, mili- tary, orthopedic and gynsecological surgery. Some of these chapters are written by specialists in their respective branches. The labors of the American editor deserve unqualified praise. His additions to the author's text are numerous, judicious and ger- mane — Medical and Surgical Reporter, Feb. 12, HENRY C. LEAS SON & CO., Philadelphia. r^ROSS' SURGERY— A System of Sukgery : Pathological, Diag- nostic, Therapeutic and Opeiative. By S. D. Gross, M.D., LL.D., D.C.L. Oxon., LL.D. Cantab., Emeritus Professor of Surgery in the Jefferson Medical College of Phila- delphia. Sixth edition, thoroughly revised and greatly improved by the Author and Samuel W. Gross, A.M., M.D., Professor of the Principles of Surgery and of Clinical Surgery in the Jefferson Medical College. In two large and beautifully-printed imperial octavo volumes containing 2382 pages, illustrated by 1623 engravings. Strongly bound in leather, raised bands, ^15.00; half Russia, raised bands, ^16.00. Just ready. acquired The several parts have been extended, "\XrE have purposely abstained from comment or criticism of the book before us. It has for- merly been noticed more than once in our columns, and it is enough now to remark that the present edition fully maintains the reputation the work has elaborated and amplified, till it has become a com- plete and systematic book of reference alike for the student and the practitioner. — The London Lancet, Jan. 27, 1883. r^ROSS ON IMPOTENCE— A Practical Treatise on Impotence, Sterility, and Allied Disorders of the Male Sexual Organs. By Samuel W. Gross, A.M., M.D., Professor of the Principles of Surgery and of Clinical Surgery in the Jefferson Medical College. Second edition, thoroughly revised. In one veiy handsome octavo volume of l68 pages, with i6 illustrations. Cloth, $1.^0. Just ready. T^HE book is the outcome of intelligent clinical who may be called upon to treat these cases will observation and extensive experience. The find the directions both for diagnosis and treatment arrangement and classification leave nothing to be very perspicuous and %o\i.n^.— Liverpool Medico- desired in the way of clearness ; and practitioners Chirur^cal Journal, ]n\y, li^^. CTIMSON ON FRACTURES — A Practical Treatise on Fractures. By Lewis A. Stimson, B.A., M.D. Professor of Pathological Anatomy at the University of the City of New York, Surgeon and Curator to Bellevue Hospital, Surgeon to the Presbyterian Hospital, New York, etc. In one very handsome octavo volume of 598 pages, with 360 beautiful illustrations. Cloth, ^4.75 ; leather, ^5.75. Jtisl Ready. ough. His mode of treatment of the different frac- tures is eminently sound and practical. We con- sider this work one of the best on fractures ; and it 'T'HE author has given to the medical profession in this treatise on fractures what is likely to be- come a standard work on the subject It is certainly not surpassed by any work written in the English, or, for that matter, any other language. There is nothing scanty or superficial about it, as in most other treatises ; on the contrary, everything is thor- will be welcomed not only as a text-book, but also by the surgeon in full practice, — Neiv Orleans Med- ical and Surreal Journal, March, 1883. ALLEN'S ANATOMY — A System of Human Anatomy, Including Its Medical and Surgical Relations. For the Use of Practitioners and Students of Medicine. By Harrison Allen, M.D., Professor of Physiology in the University of Pennsylvania. With an Introductory Chapter on Histology, by E. O. Shakespeare, M.D., Ophthalmologist to the Philadelphia Hospital. In one large and handsome quarto volume of about 600 double-columned pages, with 380 illustrations on 109 lithographic plates, many of which are in colors, and about 100 engravings in the text. In six Sections, each in a portfolio. Section I. Histology {Just Ready). Section II. Bones and Joints [Jttst Ready). Section III. Muscles and Fascia {Just Ready). Section IV. Arteries, Veins and Lymphatics [Just Ready). Section V. Nervous System (Shortly). Section VI. Organs of Sense, of Digestion, and Genito-Urinary Organs (/« Press). Price per Section, ^3.50. For sale by subscription only, encyclopsedic, and the result shows that he has brought to it a mind well prepared for the task by extensive reading, critical judgment, and literary ability. We can cordially recommend the work to the profession, believing that it is suited not only to those of scientific tastes, but that it will be of use to the practising physician. — Boston Medical and Sur' gical Journal. — January 11, 1883. 'T'HE appearance of the book marks an epoch in medical literature. It is the first important work on human anatomy that has appeared in America ; and, more than this, its scope is new and origmal. It is intended to be both descriptive and topographical, scientific and practical, so that while satisfying the anatomist, it will be of value to the practising physician As the author points out, such a work as he has undertaken is necessarily HENRY C. LEAS SON & CO., Philadelphia.