CORNELL 
 
 UNIVERSITY 
 
 LIBRARY 
 
Cornell University Library 
 RB 24.D33 1885 
 
 A handbook of pathological anatomy and h 
 
 012 506 881 
 
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/cu31924012506881 
 
A HANDBOOK 
 
 PATHOLOGICAL ANATOMY 
 
 AND 
 
 HISTOLOGY 
 
 WITH AN INTRODUCTORY SECTION ON 
 
 POST-MORTEM EXAMII^ATIOE'S 
 
 AND 
 
 THE METHODS OF PEESEEYING AKD EXAMINING- 
 DISEASED TISSUES 
 
 FEANOIS PELAFIELD, M.D., 
 
 PROFESSOR OF PATHOLOGY AND PRACTICAL MEDICINE, COLLEGE OF PHYSICIANS AND SURGEONS, 
 
 NEW YORK, 
 
 T. MITCHELL PEUDDEIsr, M.D., 
 
 DIRECTOR OF THE PHYSIOLOGICAL AND PATHOLOGICAL LABORATORY OP THE ALUMNI ASSOCIATION OP 
 
 THE COLLEGE OF PHYSICIANS AND SURGEONS. NEW YORK. LECTURER 
 
 ON NORMAL HISTOLOGY IN YALE COLLEGE 
 
 NEW YORK 
 
 WILLIAM WOOD & COMPANY 
 
 56 & 58 Laeayette Place 
 
 18S5 
 
R j^ 
 7-4 
 
 /I -1.9^70 
 
 '^CORNELL 
 
 UNfVERSSTY 
 
 LIBRARY 
 
 COPTKIGHT BY 
 
 WILLIAM WOOD & COMPANY. 
 
 1885. 
 
 „„USTR..l- PRINTING COMPAN' 
 
 STETTINEP, LAMBERT ft CO . 
 
 ,jS 4 ,31 CBOSBV ST., NEW YORK. 
 
PREFACE 
 
 TO THE SECOND JED I.TI ON 
 
 The first edition of this work v.'as intended to serve as a guide for 
 those persons wlio might have to perform post-mortem examinations. 
 
 In this second edition, the scope of the work has been very much 
 extended. It is now intended to supply all the needs of students and 
 practitioners who wish to add a knowledge of the lesions of disease to 
 that of its clinical symptoms. The point of view of the work, there- 
 fore, is that of the physician who wishes to find out what are the 
 lesions of the diseases which he is in the habit of seeing, rather than 
 that of the pure pathologist. 
 
 In order to accomplish this task more effectually, I have associated 
 with myself Dr. T. Mitchell Prudden, and the book represents the 
 result of our joint labors. 
 
 The work comprises instruction in the methods of making post- 
 mortem examinations, of preserving diseased tissues, and of preparing 
 them for microscopical examination, and of preparing and examining 
 bacteria ; an account of such general processes as inflammation and de- 
 generation ; a description of tumors, of the lesions of all the different 
 parts of the body, of the general diseases, of violent deaths, and of 
 deaths from poisoning. 
 
 The illustrations have all been drawn by Dr. Prudden and myself 
 from actual specimens, and the drawings reproduced and reduced in 
 size by one of the photographic processes. 
 
 FRANCIS DELAFIELD. 
 
CONTENTS. 
 
 PAKT FIRST. 
 
 THE METHOD OF MAKING POST-MORTEM EXAMINATIONS AND OF 
 PRESERVING DISEASED TISSUES. 
 
 The objects of making post-mortem examinations. Causes of death, 3. — Exter- 
 nal Inspection, 4. — Cadaveric lividity, 4. — Putrefactive clianges, 5. — Cooling 
 of the body, 5. — Rigor mortis, 6. — Contusions, 7. — Wounds, fractures, scars, 
 and tattoo marks, 8. — Internal Examination, 8.— The Head, 9. — Removal of 
 oalvarium, 9. — The dura mater, 10. — The pia mater, 10. — The brain, 11. — 
 Base of the cranium, 13. — Hardening and preserving the tissues for micro- 
 scopical examination, 13. — The Spinal Cord, 14. — Preservation of cord and 
 membranes, 14. — The Thorax and Abdomen, to. — General inspection of ab- 
 dominal cavity, 15. — The heart, 17. — The pericardium, 18. — The pleural cavi- 
 ities, 20. — Preservation of heart, 30. — The lungs, 30. — Preservation of lungs 
 and bronchi, 31.— Pharynx, larynx, and oesophagus, 23. — Preservation of 
 larynx and trachea, 33. — The Abdomen. Kidneys, 33.— Suprarenal capsules, 
 24. — Preservation of kidney, 34. — The spleen, 35. — Preservation of suprarenal 
 capsules and spleen, 35. — Intestines, 35. — Preservation of intestines and stom- 
 ach, 26 and 37. — Stomach and duodenum, 37. — Liver, 38. — Preservation of 
 liver, 38. — Pancreas, 38. — Preservation of pancreas, 29. — Genito-urinary Or- 
 gans. Male organs, 39. — Female organs, 29.— Bladder, 80.— Uterus, 30. — Pre- 
 servation of generative organs, 89 and 81, — Ovaries and Fallopian tubes, 31. 
 
 Autopsies in Cases of Suspected Poisoning, 82 and 573. 
 
 Examination op the Bodies op New-born Children. General Inspection, 33. 
 — Internal Examination, 36. — The head, 36. — The spinal cord and thorax, 37. 
 — The abdomen, 88. — Preservation of foetal and young tissues, 89. 
 
 General Methods of Preserving Tissues and Preparing them for Study 
 40. — Fresh tissues, 40. — Decalcifying, 40. — Hardening and preservation, 41. — ■ 
 Chromic acid mixture, 41. — Osmio acid, 42. — Embedding and section-cutting, 
 42. — Staining, 44. — Preservation of museum specimens, 44. 
 
 PAET SECOND. 
 
 MORBID CHANGES IN THE CIRCULATION OF THE BLOOD.— 
 CHANGES IN THE COMPOSITION OF THE BLOOD.— DEGENERA 
 TIONS.— ANIMAL PARASITES AND BACTERIA.— INFLAMMATIONS. 
 —TUMORS. 
 
 Morbid Changes in the Circulation of the Blood. Hypersemia an 
 
VI COXTEXTS. 
 
 Ansemia, 49. — Hemorrhage and transudation, 49.— Thrombosis'and embolism, 
 51. 
 
 Cha:n'ges IX THE Composition op the Blood. Coagulability of the blood, an- 
 hydrtemia and hydrsemia, •j.j. — Leucocytosis, leukasmia, melansemia, 56. 
 Foi-eign bodies in blood, 57. 
 
 Degenerative Changses in the Tissues. Necrosis and coagulation necrosis, 
 59.— Cheesy degeneration, 60. -Parenchymatous degeneration, fatty degen- 
 eration, and fatty inaitration, 60.— Amyloid degeneration, 61. Corpora amy- 
 lacea, 63.— Mucoid, colloid, and hyaliii degeneration, 63.— Calcareous degen- 
 eration and pigmentation, 64. 
 
 Animal Parasites. Protozoa, 66.— Amoeba, psorospermife, Cercomouas mtes- 
 tinalis, Trichomonas vaginalis, 66. — Ciliated infusoria, 67. — Worms, 67. — Tre- 
 matoda (flukes). Distoma hepaticum; D. lanceolatum, D. sinense, D. hae- 
 matobium, 67. — Oestoda (tape-worms), 67.— Teenia solium, 67.— T. medioca- 
 nellata, T. ecchinococcus, 68.— Echinococcus multilocularis, 70.— Tsenia nana, 
 T. flavopunotata, T. madagasoariensis, T. cucumerina, 71.— Bothriocepha- 
 luslatus, '71.~Xematoda (round- worms), 71.— Ascaris lumbriooides, 71.— A. 
 maritima, A. mystax, 72.— Oxyuris vermicularis, Strongylus gigas, Dochmius 
 duodenalis, Tricocephalus dispar, 72.— Ti'ichina spiralis, 73.— Filaria medi- 
 nensis, 74.— Filaria sanguinis hominis, 75.— Ehabdonema strongyloides, 75. 
 —Methods of study and preparation of internal parasites, 7.5.— Bibliography 
 of animal parasites, 76. 
 
 Parasitic Fungi. Moulds and yeasts, Achorion Schonleinii, Trichophyton ton- 
 surans, Microsporon furfur, Aspergillus, 76. — Oidium albicans, Actinomyco- 
 sis, 77. 
 
 Bacteria. Morphology and physiology, 77. — Classification of bacteria, 79. — 
 Sphero-baeteria, Micrococcus, Diplococcus, Chromogenous micrococci, 79. — 
 Zymogenous micrococci. Pathogenous micrococci, SO. — Micro-bacteria, 81. — 
 Chromogenous, Zymogenous and Pathogenous bacteria, 81. — Desmo-bacteria, 
 82. — Zymogenous bacilli, 82. — Pathogenous bacilli, 82, 83. — Leptothrix, 84. — 
 Spiro-bacteria , 84. 8.5. 
 
 Eelations of Bacteria to Disease, 85, 86, 87. 
 
 Methods of studying bacteria, 88. — Staining bacteria in fluids, 89. — Staining bac- 
 teria in sections of tissues, 90. — Artificial cultivation of bacteria, 91. — Prepa- 
 ration of culture substances, 92. — Sterilized potatoes, 92. — Sterilized gelatin 
 bouillon, 93. — Gelatinized blood-serum, 94. — Agar-agar or Japanese isinglass, 
 94. — Bibliography of vegetable parasites, 95. 
 
 Infl.\mmation, 96. — Inflammation of connective tissue, classification, 96. — Cellu- 
 lar inflammation, 97. — Inflammation with production of serum, fibrin, and 
 pus, 98. — Abscesses, 99. — Inflammation with production of serum, fibrin, pus, 
 and new connective tissue, 100. — Granulation tissue, 100. — Inflammation with 
 production of connective tissue, 103. — Tubercular inflammation, 102. — Syphi- 
 litic inflammation, 103. 
 
 Inflammation of Mucous Membranes, 106. — Catarrhal inflammation, 106. — Puru- 
 lent inflammation, 107. — Croupous inflammation, 108. — Tubercular inflamma- 
 tion, 109. — Syphilitic inflammation, 109. — Inflammation of the Viscera, 110. 
 — Parenchymatous inflammation, 110. — Interstitial inflammation, 110. — Dif- 
 fuse inflammation. 111. 
 
 Tumors, 112. — General characters, 112," 113, 114,115. — Cause of tumors, 116. — 
 Classification of tumors, 117. — Cysts, 118. — Xomenclature of complex tumors, 
 120. — Special form^ of tumors, 121. — Fibroma, 121. — Myxoma, 122. — Sarcoma 
 
CONTEXTS. Vll 
 
 124— Endothelioma, 132.— Lipoma, 133.— Chondroma, 133.— Osteoma, 134.— 
 Glioma, 135.— Myoma, 136.— Neuroma, 138.— Angioma, 188.— Lymphangi- 
 oma, 140,— Epithelial tumors, 140.— Adenoma, 143.— Carcinoma, 144.— Bibli- 
 ography of tumors, 153. 
 
 PART THIED. 
 MORBID ANATOMY OP THE ORGANS. 
 
 The Nervous System, 157.— The Membranes op the Bhain, 157.— Dura 
 mater, 157. — Hemorrhages, 157.— Thrombosis of venous sinuses, 157.— In- 
 flammation, 158.— Tumors, 161.— Pia mater, 161.— Structure, 161.— Hyperee- 
 mia, oedema, and hemorrhage, 163. — Inflammation, 163. — Acute meningitis, 
 164. — Cellular meningitis, 164. — Exudative meningitis, 165. — Chronic menin- 
 gitis, 167. — Tubercular meningitis, 167. — Syphilitic meningitis, 171.— Tumors 
 and parasites, 171. — Ventricles of the brain, 171, — Ependyma and choroid 
 plexus, 171. — Acute ependymitis, 172. — Chronic ependymitis, 173. — Congeni- 
 tal hydrocephalus, 173. — Secondary hydrocephalus, 173. — Primary hydro- 
 cephalus in adults, 174. — Tumors, 174. — Pineal gland, 174. — Pituitary body, 
 175. 
 
 The Brain, 175.— Thrombosis and embolism, 175. — Hyperssmia, 177.— Anaemia, 
 oedema, and hemorrhage, 178. — Apoplectic foci, 179. — Secondary degenera- 
 tions, 180. — Inflammations, 181. — Inflammatory softenings, 181. — Abscesses, 
 181. — Chronic interstitial encephalitis (sclerosis), 183. — Wounds, 183. — En- 
 cephalitis in new-born, 183. — Holes or cysts in brain, 184. — Syphilitic and tu- 
 bercular encephalitis, 185. — Lesions of brain in chronic paralysis of insane, 
 186. — Hypertrophy, 186. — Atrophy and pigmentation, 187. — Tumors, 187.— 
 Parasites, 188. — Malformations, 188. 
 
 Spinal Cord, 190. — Dura mater spinalis, hemorrhage and inflammation, 190. — 
 Tumors and parasites, 190. — Pia mater spinalis, 191. — Hemorrhages, inflam- 
 mations, and tumors, 191. — The cord, 193. — Hemorrhage, injuries, and sec- 
 ondary degenerations, 193. — Descending gray degeneration, 193. — Ascending 
 gray degeneration, 193. — Inflammation, 194. — Acute myelitis, 194. — Poliomy- 
 elitis anterior, 195. — Chronic myelitis, chronic interstitial myelitis, 196. — 
 Chronic transverse myelitis, 196. — Multiple sclerosis, 196. — Posterior spinal 
 sclerosis, 196. — Solitary tubercles, gummata, and cysts, 198. — Tumors, 198. — 
 Malformations, 199. 
 
 The Peripheral Nerves, 300. — Changes after division, 300. — Acute neuritis, 
 201. — Chronic neuiutis, 201. — Syphilitic, lepl^ous, and tubercula,r neuritis, 201. 
 —Tumors, 301. 
 
 Preparation of nerve tissue for microscopical study, 202. 
 
 The Respiratory System. Larynx and Trachea, 305. — Malformations, 305. — 
 Acute catarrhal laryngitis and tracheitis, 205. — Chronic catarrhal and crou- 
 pous laryngitis, 306. — (Edema glottidis, 306. — Perichondritis and syphilitic 
 laryngitis, 306. — Tubercular laryngitis and tumors, 207. 
 
 Structure of lungs, 207. — The Pleura. Hydrothorax and hemorrhage, 208. — Clas- 
 sification of inflammation, 209. —Pleurisy with production of fib)-in, 309. — 
 Pleurisy with production.of fibrin and serum, 209. — Pleurisy with production 
 of fibrin, serum, and pus (Empyema), 313.— Chronic pleurisy, 314.— Tu- 
 bercular pleurisy, 315. — Tumors, 216. 
 
 The Bronchi, 317.— Acute catarrhal bronchitis, 317.— Capillary bronchitis, 317.— 
 
TUl CONTENTS. 
 
 Chronic catarrhal and croupous bronchitis andbronchiectasia, 218. — Tumors, 
 219. 
 The Lungs, 320. — Malformations, injuries, and perforations, 220. — Congestion, 
 oedema, and hemorrhage, 23h — Emphysema, 222. — Atelectasis, 233. — Gan- 
 grene, 224. — Inflammation, classification, 224. — Acute lobar pneumonia, 225. 
 — Secondary and complicating pneumonia, 230. — Pneumonia of heart disease, 
 231. — Broncho-pneumonia, 332. — Interstitial pneumonia, 235. — Syphilitic 
 pneumonia, 236. — Acute mUiary tuberculosis, 237.— Chronic miliary tuber- 
 culosis, 241. — Acute phthisis, 243. — Chronic phthisis, 245. — Tumors, 350. — 
 Parasites, 251. 
 Mediastinum, 251. — Inflammation, 251. — Tumors, 353. 
 
 This Vascular System. The Heart. Pericardium, 354.— Injuries, dropsy, 
 hemorrhage, 254. — Pneumonatosis and inflammation, 855. — Pericarditis 
 with production of fibrin, serum, and pus, 255. — Tubercular pericarditis 
 and tumors, 256. — The Heart. Malformations, 256.- -Changes in position, 
 wcunds, and ruptures, 258. — Atrophy, 259. — Hypertrophy, 260. — Dilatation, 
 261. — Degeneration, 262. — Inflammation, 264. — Acute endocarditis, 264. — 
 Malignant endocarditis, 265. — Chronic endocarditis, 366. — Tubercular endo- 
 carditis, 867. — Degenerations and myocarditis, 267. — Changes in the valves, 
 ^ 268. — Aneurism and thrombosis of the heart, 269. — Tumors and parasites. 
 The Blood-vessels, 270. — Atrophy, hypertrophy, and degeneration, 270. — The 
 arteries. Inflammation, 271. — Acute arteritis, 271. — Chronic arteritis, 273. — 
 Dilatation and aneurism, 375. — Aneurism of the different arteries, 276. — Sten- 
 osis, 277. — Ruptures and wounds, 278. — The veins. Dilatation, 280. — Wounds 
 and rupture, 281. — Inflammation, 283, — Tumors and parasites, 383. — The 
 capillaries, 283. — The Lymph-vessels, 283. — Inflammation, 284. — Lymphan- 
 giectatasis ; Tumors, 285. — The Lymph-GLAnds, 285. — Inflammation, 286. — 
 Acute inflammation, 286. — Chronic inflammation, 287. — Pigmentation, 287. 
 — Inflammation with cheesy degeneration, 288. — Tubercular inflammation, 
 389. — Syphilitic inflammation, 290. — Degenerations, [390. — Hyperplasia, 291. 
 —Tumors, 293. 
 The Alimentary Canal, 2dS.—The Mouth[; Malformations, 393.— Hypertrophy of 
 cheeks and lips, 394. — Inflammation, 394.— Stomatitis; stomatitis ulcerosa, 
 8'4.— Gangrene, 395.— Syphilitic and tubercular stomatitis, 295. — Tumors, 
 295.-7/16 Tongue ; malformations, 296.— Hypertrophy and inflammation, 
 296.— Tumors, 297.— The Pharynx and Oesophagus, 398.— Malformation and 
 inflammation, 298.— Ulceration, 399.— Dilatation of CEsophagus, 399.— Ste- 
 nosis, 300.— Tumors, 300. 
 The Stomach; Malformations, 303.— Post-mortem changes; injuries and hemor- 
 rhage, 303.— Inflammation, 304.— Ulcers, 306.— Dilatation, 309.— Tumors, 309. 
 —Degenerations, 312.— The Intestines ; Malformations, 312.— Incarceration. 
 333. — Intussusception, 314.— Transposition, wounds and ruptures, Slo. — The 
 Small Intestine ; inflammation , 315 . — Lesions of solitary and agminated glands, 
 316.— Emboli, 317.— Large Intestines; Inflammations, 317. — Tumors, 319.— 
 Concretions, 320. — Parasites, 321. 
 The Peritoneum, 331.— Malformations, 323.— Inflammations; acute peritonitis, 
 322.— Cellular peritonitis, 323.— Exudative" peritonitis, 324.— Chronic cellular 
 peritonitis, 325.— Chronic peritonitis with adhesions, 326.— Chronic peritonitis 
 with thickening of peritoneum, and with production of serum, fibrin, and 
 pus, 328.— Hsemorrliagic peritonitis, 328.— Tubercular peritonitis, 329.— 
 Tumors, 329.— Parasites, 333. 
 
♦ CONTENTS. IX 
 
 The Liver ; Malformations, 333. — Acquired changes in size and position, 333. — 
 Anssmia and hypersemia, 334. — Wounds, rupture and hemorrhage, 336. — Le- 
 sions of hepatic artery, 336. — Lesions of portal vein, 336. — Lesions of hepatic 
 veins, 338. — Atrophy of liver; degenerations, 338. — Pigmentation, 341. — 
 Acute yellow atrophy, 343. — Inflammation; acute hepatitis (abscess), 343. — 
 Chronic interstitial hepatitis (Cirrhosis), 844. — Syphilitic hepatitis, 348. — Tu- 
 bercular hepatitis, 349. — Perihepatitis, 350.— Hyperplasia of lymphatic tissue 
 in the liver, 351. — Tumors, 351. — Parasites, 353. 
 
 Tlie Biliary Passages and Oall-Bladcler; Catarrhal inflammation, 356, — Suppura- 
 tive and croupous inflammation, 356. — Constriction, occlusion, and dilatation, 
 357.— Biliary calculi, 357.— Tumors, 359.- 
 
 The Spleen ; Wounds, rupture and hemorrhage, 360. — Disturbances of the cir- 
 culation, 361. — Inflammation; acute hyperplastic splenitis, 362. — Suppui-ative 
 and indurative splenitis, 363. — Syphilitic splenitis, 364. — Tubercular splenitis, 
 365. — Perisplenitis, 365. — Alterations of spleen in leuksemia and pseudo- 
 leukaemia, 865. — Degenerations, 366. — Tumors, parasites, malformations, and 
 displacements, 367. 
 
 The Pancreas ; Hemori-hage and inflammation, 869. — Degenerations, 370.— 
 Tumors, 371. — Malformations and displacements, 373. 
 
 The Salivary Glands ; Inflammation, 373.— Tumors and parasites, 374. 
 
 The Thyroid Gland ; Hyperaemia, inflammation, degenerations, and tumors, 
 375.— Parasites, 376. 
 
 The Supra-renal Capsules ; Malformations, hemorrhage, thi-ombosis, inflam- 
 mation and degeneration, 877. — Tumors, 378. 
 
 The Urinary Apparatus, 879. — The Kidneys; Malformations and changes in 
 position, 879. — Bright's Disease, classification, 380. — Congestion, 380. — Acute 
 parenchymatous nephritis, 381. — Chronic parenchymatous nephritis, 383. — 
 Acute diffuse nephritis, 383. — Chronic diiiuse nephritis, 383. — Acute inter- 
 stitial nephritis, 886. — Chronic interstitial nephritis, 387. — Fatty infiltration ; 
 suppurative and pyelo-nephritis, 888. — Chronic pyelo-nephritis and nephro- 
 phthisis, 889. — Emboliism and thrombosis, 390. — Hydronephrosis, 390. — 
 Cystic kidneys, 391.— Perinephritis, 393.— Renal calculi, 393.— Tumors, 393.— 
 Parasites, 394. 
 
 The Urinary Bladder ; MsiKovnisitions, 395. — Changes in size and position; rup- 
 ture and perforation, 896. — Disturbances of circulation, 397. — Inflammation ; 
 acute catarrhal cystitis, 897. — Chronic cystitis, 898. — Croupous and tubercular 
 cystitis, 398. — Tumors, 399. — Parasites, foreign bodies, and calculi, 400. 
 
 The Urethra; Congenital malformations, and changes in size and position, 401. — 
 Strictures, wounds, ruptures and perforations, 403. — Inflammation; catarrhal 
 urethritis, gonorrhoea, 403. — Croupous, syphilitic, and tubercular urethritis, 
 404.— Tumors, 404. 
 
 The Organs op Generation, 405.— Female. The Vulva; malformations, hemor- 
 rhage, and hypersemia, 405. — CEdema, inflammations, gangrene, lupus, and 
 tumors, 406.— Cysts, 407. 
 
 The Vagina ; Malformations, 407.— Changes in size and position ; wounds and 
 perforations, 408 ; Inflammations and gangrene, 409. — Tumors and parasites, 
 ilO.— The Uterus; Malformations, 410. — Changes in size, 411.— Changes in 
 position, 413. — Rupture, perforation, hypersemia, and hemorrhage, 414. — In- 
 flammation, 415.— Puerperal inflammation, 417.— Ulceration and degener- 
 ation, 418.— Tumors, 419.— Parasites and cysts, i23.— The Ovaries; malfor- 
 mations, 423. — Changes in size'and position, hypersemia, hemorrhage, and 
 
X CONTENTS. 
 
 inflammation, 424.— Tumors, 425.— Cysts, 426, 439.— TAe Fallopian Tubes ; 
 Malformations, changes in size and position, and liemoirliage, 430. — Inflam- 
 mation and tumors, 431.— Extrauterine pregnancy, 432.— The Placenta ; 
 hemorrhage and inflammation, 438. — Degenerations, 4B4. 
 
 Male. The Penis; Malformations, 434.— Inflammation, 435.— Tumors, 436.— 
 Tlie Scrotum, iSl.—The Testicles; Malformations, 437.— Hydrocele, 438.— 
 Spermatocele, hasmatocele, and inflammation, 439. — Tumors, 441. — Cysts and 
 parasites, 442.— r/ie Seminal Vesicles, 44=2.— The Prostate ; hypertrophy, 
 atrophy, and inflammation, 443. — Tumors, parasites, and concretions, 444. 
 
 The Mamma; Malformations, 414. — Hemorrhage and inflammation, 445. — 
 Tumors, 446. The male mamma, 449. 
 
 The Bones ; disturbances of circulation, 450. — Wounds, fractures, and disloca- 
 tions, 451. — Inflammation; periostitis, 451. — Osteitis, 453. — Congenital syphilis, 
 457.— Osteomyehtis, 459.— Necrosis, 460.— Caries, 461.— Rachitis, 462.— Osteo- 
 malacia, 464. — Altei-ations of marrow in leuksemia and pseudo-leukaemia, 464. 
 — Alterations of marrow in anaemia, 465. — Atrophy, 466. — Tumors, 466. — 
 Parasites, 469. 
 
 The Joints ; Inflammations, 470. — Tumors and foreign bodies, 473. 
 
 Muscle; Voluntary striated, 475. — Hemorrhage, embolism, wounds, and ruptures, 
 475. — Inflammation, 475. — Degenerative changes, 478. — Tumors, 481. — Para- 
 sites, 483. 
 
 PAET FOUR 
 
 THE LESIONS FOUND IN THE GENERAL DISEASES; IN POISONING, 
 AND IN VIOLENT DEATHS. 
 
 Typhoid Ffveb. J. Primary or Characteristic Lesions, 485. — The Intestines, 
 485. — Lesions of the lymph follicles, 485. — Gangrene, 487. — Croupous inflam- 
 mation, peritonitis, infarctions in the organs and hemorrhages, 438. — 3/e.seu- 
 teric glands and spleen, 488. — Secondary Lesions, 489. — The mouth, pharynx, 
 parotid, pancreas, liver, and heart, 489. — The arteries, veins, larynx, lungs, 
 kidneys, ovaries, testicle.s, brain and voluntary muscles, 480. — The akin, 491. 
 — Bacilli of typhoid fever, 491. — Staining the bacilli, 493. 
 
 Typhus Fever, 498. 
 
 Relapsing Fetee, 494. — Spirochsete Obermeieri, 495. 
 
 Epidemic Cerebro-spinal jMexingitis, 496. — Relations of bacteria to the disease 
 and literature, 497. 
 
 Diphtheria, 498. 
 
 Yellow Fever, '500. 
 
 Cholera. Lesions in skin, brain, lungs, heart, peritoneum, stomach and intes- 
 tines, 501. — Lesions in liver, spleen, kidneys, viterus and ovaries, 502. ReLi- 
 tions of bacteria to cholera, 502. — Method of staining and cultivating the 
 bacteria of cholera, 508. 
 
 Tuberculosis, 504.^General and localized tuberculosis, 505. — Lesions of tuber- 
 culosis, 506.— Tubercle bacilli, 507. — Methods of staining the tubercle bacilli, 
 509. — Cultures of tubercle bacilli, and references to literature, 511. 
 
 Pyaemia; its nature and varieties, 513. — Micrococci of pysemia, 514. 
 
 Glanders (Farcy), 515. — Bacilli of glanders, 516. 
 
 Hydrophobia, 517. 
 
 Lcpus, 518. 
 
CONTENTS. XI 
 
 Leprosy, structui-e of its lesions, 530. — The bacilli of leprosy, 521. 
 
 Erysipelas, the character of its lesions, and the micrococci present in them, 533, 
 533. 
 
 Anthrax ; its lesions and bacilli, 534, 585. 
 
 The Malarial Feteks ; their lesions and relations to bacteria, 536, 537. 
 
 Diseases Characterized by Alterations in the Composition op the Blood ; 
 Chlorosis, Pernicious Anemia, and Addison's Disease, 538. — Addison's 
 Disease, the lesions in skin, brain, heart, sympathetic nerves, supra-renal 
 capsules, and blood, 539. 
 
 LeuKjEMIa, 530. 
 
 Pseudo-Leukemia {Hgdghin's Disease), 580.— Scorbutus, 581.— Purpura, 531. — 
 HjEmatophilia, 583. 
 
 Gout, 538. 
 
 Diabetes, 534. 
 
 Sunstroke, 585. 
 
 Death from Burning, 536. 
 
 Death from Lightning, 537. 
 
 Death from Suffocation, Asphyxia, 538. — Death from Strangulation, Hang- 
 ing, 539. — Death from Drowning, 540. — External examination, 540. — Internal 
 examination, 541. 
 
 Death from Poisoning, 543. — Sulphuric acid, 543. — Nitric acid, 544. — Hydro- 
 chloric, oxalic, and tartaric acids, 545. — Potash and soda, and their carbon- 
 ates, 545. — Ammonia, potassium nitrate and phosphorus, 546. — Arsenic, 547. 
 — Corrosive sublimate, lead and copper, 549. — Tartar emetic, vegetable irri- 
 tants, cantharides, opium, and poisonous fungi, 550. — Hydrocyanic and car- 
 bolic acids, and alcohol, 551. — Chloroform and ether, 553. — Cliloral hydrate, 
 strychnia, nux vomica, conium, aconite, belladonna, lobelia , digitalis, stranio- 
 nium, carbonic oxide, and carbonic acid, 553. 
 
LIST OF ILLUSTEATIOl^S. 
 
 Fig. 
 
 1. Side view of human brain, showing its fissures and convolutions 
 
 3. Head of Taenia solium 
 
 3. Head and proglottides of Taenia mediocanellata 
 
 4. Cuticula of echinococcus cyst .... 
 
 5. Soolices of taenia echinococcus .... 
 
 6. Hooklets from scolex of taenia echinococcus 
 
 7. Trichinae, encysted in muscle .... 
 
 8. Filaria sanguinis hominis .... 
 
 9. Sphero-bacteria (genus Micrococcus) . 
 
 10. Micro-bacteria (genus Bacterium) .... 
 
 11. Desmo-bacteria (genus Bacillus), B. anthracis 
 13. Leptothrix buccalis and micrococci from mouth 
 
 13. Spiro-bacteria (genus Spirillum) .... 
 
 14. Colonies of micrococci in the blood-vessels of the kidney in pyaemia 
 
 15. Cellular peritonitis in omentum of dog 
 
 16. Emigration of white blood-cells in inflamed bladder of frog 
 
 17. Granulation tissue in wound of skin . 
 
 18. Developing blood-vessels in new-formed tissue . 
 
 19. Cicatricial tissue 
 
 30. Tubercle tissue in acute phthisis . 
 
 31; Tubercle granulum from pleura . 
 
 32. Tubercle granulum from lymphatic gland . 
 
 33. Tubercle granulum and diffuse tubercle tissue from chronic phthisis 
 
 24. Pus cells from bronchitis ... 
 
 25. Croupous inflammation of trachea 
 
 36. Fibroma of abdominal wall 
 
 27. Myxoma of subcutaneous tissue of back .... 
 
 28. Myxoma with fatty degeneration of cells ... . . 
 39. Large spindle-celled sarcoma of humerus 
 
 30. Small spindle-celled sarcoma of forearm 
 
 31. Small round-celled sarcoma of liver 
 
 32. Large round-celled sarcoma of leg 
 
 33. Melano-sarooma of submaxillary region ... 
 
 34. Giant-celled sarcoma of bone .... . . 
 
 35. Angio-sarcoma of liver 
 
 36. Myxo-sarcoma of pharynx . . .... 
 
 37. Adeno-sarcoma of parotid 
 
 Page. 
 11 
 
 69 
 69 
 
 70 
 
 73 
 
 75 
 
 80 
 
 81 
 
 82 
 
 84 
 
 84 
 
 86 
 
 97 
 
 98 
 
 100 
 
 101 
 
 101 
 
 102 
 
 103 
 
 104 
 
 104 
 
 107 
 
 108 
 
 121 
 
 133 
 
 133 
 
 125 
 
 126 
 
 126 
 
 127 
 
 127 
 
 128 
 
 139 
 
 180 
 
 131 
 
XIV 
 
 LIST OF ILLtrSTEATIONS. 
 
 Fig. 
 
 38. Endothelioraa of dura mater 
 
 39. Chondroma of subcutaneous tissue 
 
 40. Myxo-chondroma of cervical region 
 
 41. Neuroglia or "spider cells " from glioma of brain 
 43. Myoma of uterus 
 
 43. Angioma telangiectoides of skin .... 
 
 44. Angioma cavernosum of liver 
 
 45. Adenoma of mamma 
 
 46. Adenoma of stomach 
 
 47. Cancer cells infiltrating the tissue near a tumor . 
 
 48. Metastatic carcinoma in lymph-vessels of pleura 
 
 49. Epithelioma of neck 
 
 50. Epithelioma of axillary lymph gland . 
 
 51. Epithelioma of back of hand 
 53. Small epithelioma of side of nose .... 
 
 53. Epithelioma of nose, highly magnified 
 
 54. Carcinoma mammas (scirrhus) 
 
 55. Medullary carcinoma of stomach .... 
 
 56. Colloid carcinoma of rectum ..... 
 
 57. Carcinoma myxomatodes of mamma . 
 
 58. Chronic pacchymeningitis interna hemorrhagica 
 
 59. Brain sand from pacchymeningitis interna 
 
 60. Cellular meningitis ..... 
 
 61. Acute purulent meningitis 
 63. Fatty degeneration of ceils in pia mater after meningitis 
 
 63. Miliary tubercle of pla mater of child . 
 
 64. Miliary tubercle of pia mater . . . 
 
 65. Miliary tubercle around artery in brain 
 
 66. Miliary tubercles of ependyma of lateral ventricles 
 
 67. Miliary tubercle of ependyma highly magnified 
 
 68. Congenital hydrocephalus of child ... 
 
 69. Degenerated brain-tissue in embolic softening . 
 
 70. Fatty degeneration of blood-vessels in embolic softening of brain 
 
 71. Syphilitic obliterating endarteritis of cerebral vessel 
 
 72. Solitary tubercle of cerebellum 
 
 73. Degenerated tissue in acute myelitis 
 
 74. Posterior spinal sclerosis 
 
 75. Posterior spinal sclerosis, highly magnified 
 
 76. Multiple fibromata (false neuromata) of pneumogastric nerve 
 
 77. Fibroma (false neuroma) of lumbar nerve 
 
 78. Artificial pleurisy of dog, twent3'-four hours' duration 
 
 79. Artificial pleurisy of dog, fifth day 
 
 80. Tubercular pleurisy . 
 
 81. Lobar pneumonia, red hepatization .... 
 83. Acute lobar pneumonia with organized tissue in air spaces 
 
 83. Organized tissue in air vesicle . .... 
 
 84. Pneumonia of heart disease . 
 
 85. Broncho-pneumonia of child . . ... 
 
 86. Broncho-pneumonia of adult 
 
 87. Interstitial pneumonia of ch onic phthisis .... 
 
 88. Interstitial syphilitic pneumonia 
 
 PAGE 
 
 133 
 134 
 134 
 136 
 137 
 139 
 139 
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 143 
 145 
 146 
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 176 
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 184 
 185 
 195 
 197 
 197 
 301 
 203 
 311 
 213 
 315 
 326 
 338 
 229 
 231 
 333 
 334 
 235 
 268 
 
LIST OF ILLUSTEATI0N8. 
 
 XV 
 
 89. Miliary tubercle of lung 
 
 90. Miliary tubercle of lung 
 
 91. Composite miliary tubercle of lung ... . . 
 
 92. Bacilli of tuberculosis in miliary tubercle of child's lung . 
 
 93. Chronic miliary tubercle 
 
 94. Aggregation of miliary tubercles in chronic miliary tuberculosis 
 
 95. Diffuse tubercular inflammation 
 
 96. Area of coagulation necrosis in acute phthisis .... 
 
 97. Tubercle tissue around area of coagulation necrosis . 
 
 98. Fatty epithelium in air vesicle in chronic phthisis 
 
 99. Growth of connective tissue in an air vesicle in chronic phthisis 
 
 100. Growth of connective tissue in an air vesicle in chronic phthisis 
 
 101. Interstitial pneumonia of chronic phthisis 
 103. Primary carcinoma of lung . 
 
 103. Fatty degeneration of heart muscle 
 
 104. Lipomatosis of heart 
 
 105. Micrococci in colonies in malignant endocarditis 
 
 106. Chronic endarteritis of cerebral artery 
 
 107. Chronic obliterating endarteritis . 
 
 108. Atheroma of aorta ... . . 
 
 109. Diffuse sarcoma of pharynx .... 
 
 110. Acute cellular peritonitis, hunan omentum 
 
 111. Acute peritonitis, human omentum 
 
 112. Chronic cellular peritonitis, human omentum 
 
 113. Chronic peritonitis with adhesions 
 
 114. Retro-peritoneal sarcoma .... 
 
 115. Retro-peritoneal sarcoma .... 
 
 116. Chronic congestion of liver .... 
 
 117. Fatty infiltration of liver cells 
 
 118. Amyloid degeneration of liver capillaries . 
 
 119. Chronic interstitial hepatitis .... 
 
 120. Chronic interstitial hepatitis, highly magnified 
 
 121. Small syphilitic tumor of liver ... 
 
 122. Gumma of liver .... . . 
 
 123. Echiuococcus multilooularis of liver . 
 
 124. Primary carcinoma of bile-duct . 
 
 125. Acute parenchymatous nephritis . ' . 
 
 126. Acute diffuse nephritis 
 
 127. "Waxy degeneration of vessels of glomeruli of kidney 
 138. Chronic diffuse nepliritis, atrophied kidney 
 
 129. Acute interstitial nephritis . 
 
 130. Cystic adenoma of ovary (papillary form) 
 
 131. Fatty cells from ovarian cyst 
 133. Chronic inflammation of mamma 
 
 133. Intra-canalicular fibroma of mamma . 
 
 134. Rarefying osteitis, ulna of child . 
 
 135. Condensing osteitis, ulna of child 
 
 136. Cells from marrow in leukaemia . 
 
 137. Chronic interstitial myositis . 
 
 138. Pseudo-hypertrophy of gastrocnemius muscle 
 
 139. Hyalin degeneration of muscle in typhoid fever 
 
XVI 
 
 LIST OF ILLUSTKATIONS. 
 
 FIG 
 
 140. SpirochsBte Obermeieri of relapsing fever . 
 
 141. Bacillus tuberculosis in sputa of chronic phthisis 
 143. Micrococci in exudation of pysemio pleurisy 
 
 143. Lupus of face 
 
 144. Bacilli of Leprosy ....... 
 
 145. Micrococci in vessels and lymph spaces in erysipelas 
 
 146. Bacillus anthraois in vessels of liver of mouse . 
 
 PAGE 
 
 495 
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 51S 
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 534 
 
PART I. 
 
 THE METHOD OF MAKING 
 
 POST-MORTEM EXAMINATIONS 
 
 AND OF 
 
 PEESERYING DISEASED TISSUES. 
 
THE METHOD 
 
 OF MAKING 
 
 POST-MORTEM EXAMINATIONS. 
 
 The particular object of making a post-mortem examination varies in 
 different cases. It may be to determine whether a person has died from 
 violence or poisoning ; to account for a sudden deatli ; or to study the 
 lesions of disease. In any case the examination should embrace all the 
 important parts of the body, not merely a suspected organ, and it should 
 be recorded at the time it is made. 
 
 In endeavoring to ascertain the cause of death, when the clinical 
 history is imperfect or unknown, great care is necessary. Mechanical 
 causes of death, which destroy life by abolishing the function of one of the 
 important viscera, only occur in a moderate number of cases. Most of 
 the lesions which we find after death, rather indicate the disease than the 
 cause of death. We do not know how great a degree of meningitis, or of 
 pneumonia, or of endocarditis, or of cirrhosis, or of nephritis, necessarily 
 causes death. On the contrary, we find that one patient recovers with an 
 extent of lesion that is sufficient to destroy the life of another. So with 
 accidents ; there is often no evident reason why a fracture of the skull 
 or of the pelvis should destroy life, but yet they usually do. In some of 
 the general diseases, such as typhoid fever, the lesions cannot always be 
 called the cause of death ; in others, such as typhus fever, there may.be 
 no evident lesions at all. Sudden deaths of persons who have apparently 
 been in good health up to the time of death are particularly obscure. In 
 many of them we have to acknowledge that we can find no sufficient 
 cause for the death. This is of course due to our imperfect knowledge. 
 But it is much better in such cases to avow our ignorance than to attri- 
 bute the death to some trifling lesion. The brain and the heart are 
 the organs which are especially capable of giving symptoms during life 
 
* THE METHOD OF MAKING 
 
 without corresponding lesions after death. Very well-marked cardiac or 
 cerebral symptoms may continue for days or months, and apparently de- 
 stroy life, and yet after death we find no corresponding anatomical 
 changes. It is the novice in post-mortem examinations who is particu- 
 larly apt to mistake ordinary post-mortem appearances for lesions. 
 
 EXTBRSTAL HTSPECTION. 
 
 Before commencing the examination of the internal viscera, it is al- 
 ways necessary to make some inspection of the external surface of the 
 body. The minuteness of this inspection will depend upon the character 
 of the case : in the case of an unknown person, or of one suspected to 
 have died from unnatural causes, it is necessary to search for and record, 
 not only all contusions, wounds, etc., their size, situation, and condition, 
 but also deformities from disease and any physical peculiarities of hair, 
 ej^es, teeth, moles, etc., by which the person may be identified. In such 
 cases it is well, if possible, to have a photograph taken of the entire body. 
 In ordinary examinations, vve note the general nutritive condition of the 
 body and look for evidences of external injury, for skin diseases, ulcers, 
 oedema, gouty deposits, abscesses, enlarged lymphatic glands, etc. The 
 glans penis and prepnce are to be carefully searched for syphilitic cica- 
 trices. 
 
 It is usual to find certain changes in the external appearances of the 
 body which are due to the cessation of life, and the commencement of 
 decomposition. We speak now of bodies which have not been buried, 
 but which have been kept in the ordinary way lying on the back and 
 loosely covered with a shroud, or dressed with the ordinary clothes. 
 
 Cadaveric Lividity. — After life becomes extinct and before the blood 
 coagulates it settles in the veins of the more dependent parts of the body, 
 producing, usually within a few hours after death, a mottling of the 
 surface with irregular livid patches. These patches may coalesce, form- 
 ing a uniform dusky red color over the back of the trunk, head, and ex- 
 tremities, and sometimes over the ears, face, and neck. The same effect is 
 observed on the anterior aspect of the body if it has lain on the face. At 
 points of pressure, from folds in the clothes or from the weight of the body 
 on the table, the red color is absent or less marked. These changes occur 
 before putrefaction sets in. This cadaveric lividity or hypostasis should 
 not be mistaken for ante-mortem ecchymosis, from which it may usually 
 be readily distinguished by its position and extent, by the fact that the 
 surface of the skin is not elevated, and by the fact that on incision no 
 blood is found free in the interstices of the tissues. Not infrequently 
 the subcutaneous tissue in the vicinity of these post-mortem hypostases 
 becomes infiltrated with reddish serum. Very soon after death, particu- 
 larly in warm weather, the tissues immediately around the subcutaneous 
 veins of the neck and thorax and in other situations may become stained 
 
POST-MOETEM EXAMINATIONS. 5 
 
 of a bluish-red color from the decomposition and escape from the vessels 
 of the coloring matter of the blood. If the epidermis has been detached 
 at any point, the skin beneath soon becomes dry and brown. 
 
 Putrefactive Cliav.ges. — Usually in from one to three days, depending 
 upon circumstances, a greenish discoloration of the skin appears, at first 
 upon the middle of the abdomen, over which it gradually spreads, assum- 
 ing a deeper hue and often changing to a greenish purple or brown. 
 Greenish patches may now appear on different parts of the body, earliest 
 upon those overlying the internal cavities ; this discoloration is probably 
 produced by the action on the haemoglobin of gases developed by decom- 
 position. The eye-balls now become flaccid, and if the eye-lids are not 
 closed, the conjunctiva and cornea become brown and dry. The pressure 
 of gases developed by decomposition in the internal cavities, not infre- 
 quently forces a greater or less quantity of frothy reddish fluid or mucus 
 from the mouth and nostrils ; produces distention of the abdomen ; and 
 if excessive may produce changes of position of the blood in the vessels, 
 and even a moderate amount of displacement of the internal organs. 
 
 After five or six days, under ordinary circumstances, the entire sur- 
 face is discolored green or brown. After this the epidermis becomes 
 loosened from the formation of gases and separation of fluids beneath, 
 and the tissues become flaccid. The abdomen and thorax may be 
 greatly distended, the features distorted and scarcely recognizable from 
 swelling, and the hair and nails loosened. Beyond this stage of putre- 
 faction, the consecutive changes, leading to more or less disintegration of 
 the soft tissues, can scarcely be followed with certainty. The rapidity 
 with which these changes follow one another depends upon a variety of 
 conditions, such as temperature, moisture, access of air, and the dis- 
 eases which have preceded or caused death. Thus an elevated tempera- 
 ture and the presence of air and moisture, hasten the advent and pro- 
 gress of putrefactive changes. The bodies of infants usually decompose 
 more rapidly than those of adults, fat bodies more quickly than lean 
 ones. The infectious diseases, intemperance, and the puerperal condition 
 promote rapid decomposition ; as does also death from suffocating gases. 
 Poisoning by arsenic, alcohol, antimony, sulphuric acid, strychnine, and 
 chloroform may retard the progress of decomposition. Burial in dry soil 
 and submersion in water also retard the progress of decay. 
 
 Cooling of the Body. — The internal temperature of the healthy living 
 body is about 37.5° 0. (99.5° Fahr.). But it maybe increased several de- 
 grees in consequence of disease. After death, the chemical changes upon 
 which the maintenance of this temperature depends, rapidly diminish, 
 and the body gradually cools to the temperature of the surrounding 
 medium. This usually occurs in from about fifteen to twenty hours, but 
 the time required depends upon a variety of conditions. Immediately 
 after death, there is, in nearly all cases, a slight elevation of internal tern- 
 
b THE METHOD OF MAKINa 
 
 perature, owing to the fact that the metabolic changes in the tissues still 
 continue for a time, and the blood ceases to be cooled by passing through 
 the lungs and peripheral capillaries. After death from certain diseases, 
 yellow fever, cholera, rheumatic fever, and tetanus, a considerable eleva- 
 tion of internal temperature has been repeatedly observed. This post- 
 mortem rise of temperature amounted in a case of rheumatism, reported 
 by Dr. Davy, to 7.5° C. The time occupied by the cooling of the body 
 may be prolonged after sudden death from accidents, acute diseases, 
 apoplexy, and asphyxia. A number of cases are recorded in which the 
 the body retained its heat for several days without known cause. 
 
 After death from wasting chronic disease, and in some eases after 
 severe hemorrhages, the cooling of the body is very rapid, the external 
 temperature being reduced to that of the surrounding air within four or 
 five hours. Fat bodies cool less quickly than lean ones, the bodies of 
 well-nourished adults less quickly than those of children or old persons. 
 The temperature of the surrounding medium, the degree of protection 
 of the body from currents of air, will, of course, modify the progress of 
 cooling ; and the internal organs retain their heat naturally longer than 
 the surface of the body. The rate at which cooling occurs is most rapid, 
 as a rule, during the hours immediately following death, notwithstanding 
 the post-mortem rise which may ensue. 
 
 It will thus be seen that if required to pronounce upon the time 
 which has elapsed since death in a given case, we can do so only approxi- 
 mately. It is necessary to take into account all of the above-mentioned 
 conditions which modify the rate of cooling of the body, and then we 
 may be able to state only the probabilities of the case. It is furthermore 
 unsafe in any case to infer the cause of death from the rate of cooling of 
 the body. 
 
 Rigor- Mortis. — Death is usually succeeded immediately by a period 
 of complete muscular relaxation; the jaw drops and the limbs become 
 flaccid. The muscles may retain for two or three hours, however, the 
 capacity of contracting on the application of appropriate stimuli. On 
 the average within six hours, the muscles become firm and rigid. This 
 post-mortem rigidity, called rigoi^ mortis, is due, according to Ktihne, to 
 the coagulation of myosin or muscle fibrin. This substance is coagu- 
 lated by weak acids. According to the theory of Kiihne, acids are being 
 constantly formed in and removed from the system during life. After 
 death, however, these acids accumulate in the muscles, producing coag- 
 ulation of myosin and consequent rigidity. On the occurrence of putre- 
 faction at a later period, ammonia is developed, which dissolves the my- 
 osin and the flaccidity of decomposition ensues. 
 
 On the occurrence of the rigor mortis, the muscles become fixed in 
 whatever position they may have had at the time of its occurrence. It 
 usually begins in the muscles of the eyelids, extends to those of the back 
 
POST-MOETEM EXAMINATIONS. T 
 
 of the neck and lower jaw, then to the face and neck, and thence passing 
 downwards affects the muscles of the thorax and lower extremities. It 
 usually disappears in the same order. 
 
 Although commencing on the average six hours after death, it may set 
 in almost instantly, or it may be delayed for twenty-four hours or more. 
 It may pass off very rapidly, in rare cases in from one to three hours; or 
 it may persist for two or three weeks or longer. It may be said in gene- 
 ral that the average time of its disappearance is within twenty-four or 
 forty-eight hours after its occurrence, depending on temperature, its in- 
 tensity, the mode of death, the period of its advent, etc. Caspar states 
 that in foetuses before term he has never observed rigidity, and that in 
 young children it is feeble and of short duration. 
 
 Its occurrence and phenomena may be in some cases of the highest 
 medico-legal importance; but its careful observation does not, with our 
 present knowledge of its significance, appear to , essentially further the 
 aims of the practical pathologist.' 
 
 Contusions. — It is often important to determine whether violence has 
 been inflicted in a given body before death. In regard to this point, we 
 must remember, first, that blows and falls of sufiS.cient violence to fracture 
 bones and rupture the viscera, may leave no marks on the skin, even 
 though the person has survived for several days; and second, that there 
 are post-mortem appearances which simulate ante-mortem bruises. A 
 severe contusion during life may present, at first, no mark or only a gen- 
 eral redness. After a short time, the injured part becomes swollen and 
 of a red color; this color may be succeeded by a dark blue, and this in 
 turn fade into a greenish-yellow or yellow; these later appearances are 
 ■due to an escape of blood from the vessels and to a subsequent decom- 
 position of hemoglobin. If therefore we cut into such an ecchymosis 
 after death, we find extravasated blood or the coloring matter of the blood, 
 in the form of pigment granules, free in the tissues. Post-mortem dis- 
 colorations, on the other hand, although their external appearance may 
 resemble that of ante-mortem ecchymosis, are not formed by an extrava- 
 sation of blood, but by a circumscribed congestion of the vessels, or by an 
 escape of blood-stained serum. If we cut into such discolorations, there- 
 fore, we find no blood outside the vessels. 
 
 Blows on the skin of a body which has not been dead for more than 
 about two hours may produce true ecchymosis with extravasation of 
 blood, such as can be distinguished with great difficulty or not at all 
 from those formed during life. If putrefactive changes be present, the 
 difficulty of distinguishing between ante-mortem and post-mortem brui- 
 ses is greatly enhanced. 
 
 ' For further details concerning rigor mortis, putrefactive changes, particu- 
 larly the later stages, and the phenomena of cooling of the body, see Tidy, ' ' Legal 
 Medicine," vol. i., p. 52-120, or other works on medical jurisprudence. 
 
O THE METHOD OF MAKING- 
 
 Hanging and strangulation are attended with the formation of marks 
 on the neck which are fully described in works on forensic medicine. 
 These marks must not be confounded with the natural creases of the 
 skin of the neck. Many adults during life have creases of the skin of 
 the neck, one or more in number, running downwards from the ear 
 under the chin or encircling the neck. After death these creases may 
 be much more evident than during life, and may be rendered more de- 
 cided by the jDosition of the head, and the freezing of the body. They 
 regularly persist until the skin putrefies. 
 
 Wotinds. — "We should notice the situation, extent, and direction of a 
 wound; the condition of its edges and the surrounding tissues. If it be 
 a deep penetrating wound, its course and extent should be ascertained 
 by careful dissection rather than by use of a probe. 
 
 If the edges of a wound be inflamed and suppurating, or commencing 
 to cicatrize, it must have been inflicted some time before death. In a 
 ^ound inflicted a short time before death, the edges are usually everted; 
 there may be more or less extravasation of blood into the surrounding 
 tissues, and the vessels contain coagula; but sometimes none of these 
 changes are observed. The chief characteristics of a wound inflicted 
 after death are, absence of a considerable amount of bleeding, non-retrac- 
 tion of the edges, and the absence of extravasation of blood into the tis- 
 sues. But a wound inflicted within two hours after death may resemble 
 very closely one inflicted during life. In general, unless a wound is old 
 enough for its edges to present inflammatory changes, we must be 
 very careful in asserting its ante-mortem or post-mortem character. 
 
 Fractures. — It may be important to determine whether a bone was frac- 
 tured before or after death. This point cannot always be decided. Frac- 
 tures inflicted during life are, as a rule, attended with more extravasation 
 of blood and evidences of reaction in the surrounding tissues; but fractures 
 produced within a few hours after death may resemble these very closely. 
 Usually a greater degree of force is necessary to fracture bones in the 
 dead than in the living body. 
 
 Scars and Tattoo Marks. — The presence and character of cicatrices 
 should be noticed. Scars produced by any considerable loss of substance 
 may become very much smaller and less conspicuous, but never entirely 
 disappear. Slight and superficial wounds, however, produce marks which 
 may not be permanent. The discoloration produced by tattooing may, 
 although rarely, disappear during life. 
 
 INTEBNAL EXAMINATION. 
 
 After completing the external inspection of the body, we commence 
 the internal examination. This examination should be made both 
 thoroughly and rapidly, and, in order to eflect this, we must follow a. 
 regular method. The method should be such as will enable us to examine 
 
POST-MOETEM EXAMINATIONS. 9 
 
 the relations of parts to one another, without seriously disturbing them, 
 and to remove and inspect the organs in such an order and manner as 
 will not interfere with the examination of parts which are to follow. In 
 certain cases it may be necessary to depart from the regular method; but, 
 as a rule, the following plan will be found most advantageous. 
 
 It is important to remember the difEerence between the distribution 
 of the blood in the body during life and after death. During life, the 
 blood is in constant motion and is distributed in a regular way in the 
 heart, capillaries, arteries, and veins. Inflammations and obstructions 
 to the circulatioa may disturb this natural distribution and produce 
 congestion of particular parts of the body. After death, the blood 
 ceases to circulate; it leaves the left cavities of the heart, the arteries and 
 capillaries, and collects in the veins and the right cavities of the heart. 
 According to the character of the disease which causes death, coagulation 
 of the blood takes place more or less extensively and at an earlier or later 
 period. The local congestions which existed during life often disappear 
 after death. On the other hand, local congestions are found after death 
 which did not exist during life. Thus, after death, the scalp often con- 
 tains a large amount of venous blood. The veins of the pia mater and the 
 sinuses of the dura mater may be filled with blood. The mucous mem- 
 brane of the larynx and trachea may appear to be deeply congested. The 
 lungs are congested, if the patient has been comatose for some hours be- 
 fore death. All the tissues of the back and the membranes of the spinal 
 cord are often gorged with venous blood. The rigiit auricle and ventricle 
 of the heart may contain fluid or clotted blood in considerable quantity. 
 
 THE HEAD. 
 
 The scalp is divided by an incision across the vertex from ear to ear. 
 The flaps are dissected forward and backward, taking up the temporal 
 muscles with the skin, and leaving the pericranium attached to the 
 bone. The internal surface of the scalp and the pericranium are to be 
 searched for eechymoses and inflammatory lesions. A circular incision 
 is then made with a saw, and the roof of the cranium removed. The 
 incision in front should pass through a point about three and one-half 
 inches above the bridge of the nose, behind through the occipital pro- 
 tuberance. If fracture of the cranium be suspected, the bones should be 
 sawn entirely through; if not, it is sufficient to saw partly through them 
 and then sepai-ate the calvarium with a chisel. When the roof of the 
 cranium is thus entirely loosened, a stout hook is introduced under the 
 upper edge of the calvarium, and this is wrenched off with a jerk. Some- 
 times the dura mater is so adherent to the calvarium that the latter can- 
 not be torn from it without injury to the brain. In this case, the dura 
 mater should be cut through at the leveUof the cranial incision, and the 
 brain removed with the calvarium. 
 
10 THE METHOD OF MAKING 
 
 We should notice whether or not the calvarium is symmetrical. The 
 cranial bones increase in size by a growth of bone at the edges of the sutures. 
 If any suture become completely ossified and closed prematurely, the 
 bones will be unequally developed. The thickness and density of the 
 cranial bones vary considerably within the limits of health. There are 
 often deep depressions on the inner surface of the skull along the sagittal 
 suture, caused by the pressure of the Pacchionian bodies, and of no 
 pathological significance. We should observe the blood Content of the 
 bone, determine the existence or absence of fractures, inflammatory le- 
 sions, exostoses, etc. 
 
 The Dura Mater is now exposed to view. It will be found more or 
 less adherent to the calvarium; a moderate amount of adherence, espe- 
 cially in old persons, does not denote disease. Very extensive and firm 
 adhesions are usually produced by inflammation. Near the median line, 
 the Pacchionian bodies often project through the dura mater and may 
 produce indentations in the internal surface of the calvarium. We must 
 look for clots and for tumors and for inflammatory lesions on the ex- 
 ternal surface of the dura mater. The longitudinal sinus should be laid 
 open with the scissors, and its contents examined. A circular incision 
 is then made through the dura mater in a line corresponding to the 
 cranial incision; the falx is divided between the anterior lobes of the 
 brain, and the entire membrane drawn back. We should observe the 
 existence of abnormal adhesions of the dura mater to the pia mater, 
 bearing in mind that a moderate amount of adhesion along the longi- 
 tudinal fissure is normal. The internal surface of the dura mater is to 
 be examined for the products of inflammation and for tumors. 
 
 The Pia Mater covering tlie convex surface of the brain is now ex- 
 posed. The degree of congestion, and the existence of serum, pus, or 
 blood, beneath, within, or upon it, are now to be ascertained before the 
 brain is removed. The pia mater in old persons frequently loses its 
 transparency and becomes thick and white; this change is most marked 
 along the longitudinal fissure and large vessels. Marked and general 
 thickening of the pia mater is produced by chronic inflammation. Along 
 the longitudinal flssure, and sometimes at a considerable distance from 
 it, we usually find small elevated whitish nodules, which are the 
 Paccliionian bodies and are normal in the adult. 
 
 The amount of serum beneath the pia mater varies. A considerable 
 amount, especially in cachectic persons, may exist without brain disease. 
 Clear serum raising the pia mater and separating the convolutions of the 
 brain may be simply dropsical, or due to chronic meningitis. Turbid 
 and purulent serum, beneath and in the pia mater, are produced by acute 
 or chronic meningitis. The degree of flatness of the surface of the con- 
 volutions should be observed before removing the brain; for, when marked 
 it affords an important indication of pressure, from hemorrhage, inflam- 
 
P08T-M0ETEM EXAMINATIONS. 
 
 11 
 
 matory products, internal fluid effusions, and tumors. The pia mater 
 should be carefully examined for miliary tubercles. ; 
 
 The Brain. — After examining the convex surface of the brain, the 
 anterior lobes of the cerebrum are to be pulled gently backwards, the 
 nerves, vessels, and tentorium severed, and the 4ihedulla cut across as low 
 down as possible. The brain is now removed irom the cranium by pass- 
 ing the fingers of one hand down, beneath and behind the lobes of the 
 cerebellum, and drawing the brain out, supporting the convexity with the 
 other hand. 
 
 The adult brain in the male weighs on the average about 1,400 
 grms. (4:9|- oz.); that -of the female, about 155 grms. (5 oz.) less. The 
 average proportional weight of the brain to that of the body is about -^, 
 although in this, as in the absolute weight, there is considerable variation. 
 
 The exact situation of any lesion which is apparent externally, should 
 be described by its relation to the lobes, fissures, convolutions, and sulci. 
 
 Fig. 1. — Side View op the Human Brain, showing its Fissures and Convolutions. 
 
 The brain is first laid upon its convex surface, and the anterior, 
 middle, and posterior cerebral arteries, as well as the basilar and the caro- 
 tids, are to be examined for emboli, thrombi, atheroma, and aneurisms. 
 Extravasations of blood, tumors, and inflammatory lesions are now to be 
 looked for. The brain is next turned over on to its base. An incision is 
 made through the pia mater over the convex surface of the cerebrum. 
 The membrane is stripped up, and its adherence to the brain and its 
 thickness noted. 
 
 The halves of the cerebrum are then to be separated until the superior 
 
12 THE METHOD OF MAKING 
 
 surface of the corpus callosum is exposed. A longitudinal incision is 
 made through the janction of the corpus callosum and the cerebrum, and 
 downward into the ventricle. 
 
 The incision should be made carefully so as not to cut through the 
 ventricle into the ganglia below. The incision thus made through the 
 roof of the ventricle is prolonged backward and forward in the direction 
 of the cornua so as to expose the entire ventricle. A longitudinal inci- 
 sion is then made outward and backward into the hemisphere, from the 
 outer edge of the lateral ventricle, nearly to the pia mater. A second 
 incision is then made through this cut surface outward, and this is re- 
 peated until the hemisi^here is divided into a number of long prism- 
 shaped pieces, held together by the pia mater and a small portion of the 
 cortex. 
 
 The brain is now turned around so as to bring the other hemisphere 
 under the hand, and the operation is repeated on the other side. 
 
 The size, shape, and contents of the ventricles should be noticed, and 
 the thickness and appearance of the ependyma. 
 
 The fornix and the central portion of the corpus callosum are cut 
 across by passing the point of the knife through the foramen of Munro 
 and cutting upward. They are then drawn backward, one of the posterior 
 cornua of the fornix being severed and laid to one side. The velum 
 interpositum and the choroid plexus are now dissected up, the blood con- 
 tents and the general appearance noted, and the third ventricle examined. 
 N^ot infrequently small cysts of the clioroid are found, which seem to 
 have little or no pathological significance. 
 
 The fourth ventricle is now opened by a longitudinal incision through 
 the vermiform process. Bach hemisphere of the cerebellum is divided 
 first into two parts by an incision through the upper and inner convex 
 border, and then each segment is further divided by incisions in the same 
 direction. 
 
 Thin transverse sections are now made through the cerebral ganglia, 
 commencing in front. The ganglia are supported and the sections 
 caused to fall apart as they are cut, by carrying the fingers of one hand 
 under the brain, and gently lifting the ganglia at points just beneath 
 where the sections are made. It is important to observe the exact posi- 
 tion of any lesion which may be discovered in the cerebral ganglia, their 
 relations to the external and internal capsule, and to the caudate and 
 lenticular nucleus. 
 
 Finally the segments of the cerebrum and cerebellum are folded up 
 together into their original positions, the whole is turned over on to the 
 vertex, and thin sections are made through the medulla. Small clots in 
 the medulla should not be overlooked. 
 
 In case of the discovery of apoplectic clots, areas of softening, etc., 
 either in the hemispheres or in the basal ganglia, after their location and 
 
POST-MOETEM EXAMINATIONS. 13 
 
 extent is determined, they should be carefully searched for lesions of the 
 blood-vessels, minute aneurisms, areas of degeneration, and ruptures. 
 For this purpose it may be necessary to allow a stream of water to run 
 over the affected portion, so as to wash out the brain substance and ex- 
 pose the vessels. In some cases the blood-vessels are best exposed by 
 macerating the brain tissue at the seat of the lesion for some hours .in 
 water, and then washing out the brain substance under the faucet. 
 
 Tlie Base of the Graniuin. — We now return to the skull. The re- 
 maining sinuses of the dura mater should be opened, and this membrane 
 then entirely stripped from the bone. The bones at the base of the skull 
 are to be examined for fractures, inflammatory lesions, and tumors. In 
 cases of acute purulent meningitis, the temporal and frontal bones 
 should be carefully examined, as the inflammatory process is sometimes 
 transmitted from the internal ear, or mastoid cells, or frontal sinuses. 
 
 The eyes may be removed by breaking the roof of the orbit with a 
 hammer, removing the fragments of bone, and dissecting away bone and 
 muscles, so as to expose the optic nerve and posterior segment of the 
 eye. That portion of the globe which is not covered by conjunctiva can 
 now be cut away with a scissors, and removed witli the optic nerve. 
 
 Hardening and Preservation of the Tissues for Microscopical Examination. 
 ^For the study of tumors and inflammatory lesions of the bones of the skull and 
 ossifications of the dura mater and pia mater, the affected portions should be cut 
 into small pieces, decalcified with picric acid, and subsequently hai-dened in strong 
 alcohol. In the ordinary lesions of the dura mater, the tissues are best hardened 
 and preserved by stretching the diseased portions on a fiat piece of wood or cork 
 with pins, and placing them in MuUer's fluid." 
 
 The pia mater is so delicate, that if it be torn from the brain when quite fresh, 
 its tissues are apt to be injured. The portions of the pia mater which are to be 
 preserved should therefore be removed by cutting off slices of the brain substance 
 about t inch thick, with the zuembrane still attached, and placing the whole in 
 Miiller's fluid. After twenty-four hours the pia mater will have become sufficiently 
 hard to permit of its being stripped off without injury, and it is then stretched 
 on a flat cork with pins. The hardening is completed with MuUer's fluid and 
 alcohol, if sections are to be made. If it is to be studied in toto without sections, 
 after lying for ten days in Miiller's fluid it should be washed and be transferred 
 to, and preserved in a mixture of equal parts of glycerin, alcohol, and water. The 
 pia mater should not remain longer than twenty-four hours in Miiller's fluid be- 
 fore being stripped off; for after this time it usually becomes so flrmly attached to 
 the brain substance as to render its removal very difficult. 
 
 The ependyma should be sliced off with a sufficient quantity of undei-lying 
 brain substance to prevent its folding, and hardened in Miiller's fluid. Special 
 care should be exercised not to touch the surface of the ependyma, since the 
 epithelium is easily rubbed off. 
 
 The brain tissue in general and tumors are hardened in Miiller's fluid, the 
 pieces being cut quite small. Care should be exercised that the tissues are re- 
 
 ' For the details of the methods of hardening, decalcifying, staining, etc., 
 see the end of Part I. 
 
14 THE METHOD OF MAKING 
 
 moved from the MilUer's fluid, and placed in alcohol as soon as they become 
 hard; for after this they are apt to become brittle and difficult of manipulation. 
 
 Certain lesions, particularly the softenings of the brain, are best studied by 
 teasing, when fresh, inone-half-per-cent solution of sodium chloride, or in frozen 
 sections of the fresh tissue. (See chapter on the nervous system.) The blood-ves- 
 sels should be stretched on cork with pins, and hardened with Miiller's fluid and 
 alcohol. The eye and portion of the optic nerve, if removed, should be hardened 
 in MuUer's fluid. 
 
 THE SPINAL CORD. 
 
 The examination of the spinal cord may in many cases be omitted. 
 When it is necessary, it is usually most conveniently done after the re- 
 moval of the brain. 
 
 The body should be placed face downwards, with a block under the 
 thorax and the head hanging over the edge of the table. An incision 
 is made through the skin and muscles along the entire length of the spine, 
 and the soft parts dissected away on each side so as to expose the 
 laminae of the vertebral column. The laminee are. then divided close 
 within the articular processes, with the rachitome or with the saw and 
 cMsel. The spinous processes and laminae are then torn away together 
 with a stout hook, and the cord is thus exposed. 
 
 When the body has lain on the back, the membranes of the cord 
 may be found considerably congested without indicating the pre-existence 
 of any disease. If the body has lain for some time, especially in warm 
 weather, serous fluid may have accumulated within the membranes as 
 a result of post-mortem change. 
 
 The roots of the nerves are now to be cut across, and the cord re- 
 moved in its membranes, care being taken not to press it in any way. 
 It is the safest plan not to grasp the cord itself, but with a forceps to 
 seize the dura mater and thus lift it up at once; or the dura mater may 
 be slit open and the cord removed from it. If both are removed to- 
 gether, they are now laid on the table, and the dura mater laid open with 
 a scissors on the anterior and posterior surfaces over its entire length, and 
 searched for tumors, inflammatory lesions, etc. The finger should be 
 passed gently along the cord as it lies on the table so as to detect any 
 marked softening or sclerosis. It should now be held lightly over the 
 fingers, and smooth transverse incisions made with a very sharp knife, 
 about one inch apart through its entire substance. The cut surfaces 
 should be carefully examined for abnormal blood contents, hemorrhages, 
 inflammatory lesions, softening, scleroses, and pigmentations. Im- 
 portant lesion of the cord may be invisible to the naked eye, and hence, 
 if disease be suspected, the organ should be preserved for microscopical 
 examination. After removal of the cord, fractures and displacements of 
 the vertebrae are easily recognized. 
 
 Preservation of the cord and membranes.— The entire cord should %& sus- 
 
POST-MOETBM EXAMnSTATIONS. 15 
 
 pended in a long jar filled with Mfiller's fluid. If the dura mater has been re- 
 moved with the cord, the segments into which the latter has been divided are 
 held together and in position by the dura mater to which they remain attached 
 by the spinal nerve roots, and they should be left in this position until the hard- 
 ening is complete. The same care should be exercised as in the brain, not to 
 permit the cord to become brittle by remaining too long in the MuUer's fluid. 
 If the dura matter of the cord alone is to be preserved, it should be treated in the 
 manner suggested for the dura matter cerebralis. The pla mater spinalis is best 
 studied in sections through the entire cord, the membrane being left in situ. 
 
 THE THORAX AND ABDOMEN". 
 
 To examine these cavities, the body is replaced on its back, and a 
 single straight incision is made from the top of the sternum to the 
 pubes, passing to left of the umbilicus. For this purpose a lai-ge 
 knife should be used, held firmly in the whole hand, and the movement 
 should be mainly from the shoulder. The first incision should divide 
 everything down to the sternum and peritoneum. A short incision 
 should then be made through the peritoneum, just below the ensiform 
 cartilage. Into this opening two fingers of the left hand are introduced 
 and separated from one another, and the parietes being raised and the 
 sides of the opening being held apart by the fingers, the peritoneum is 
 divided to the pubes, care being taken to hold the knife horizontally 
 so as not to cut the intestines. The skin and muscles are then dissected 
 off from the thorax on both sides as far back as the false ribs. 
 
 This dissection should be made by long sweeps of the knife, which 
 should be made to cut with the full blade and not with the point only; 
 and if the skin and muscles be pulled strongly away from the chest with 
 the left hand, it may be done very rapidly and with a few strokes of the 
 knife. We notice here the amount of subcutaneous fat and the con- 
 dition of the muscles. In order better to expose the abdominal cavity, 
 the rectus abdominis muscles should be divided transversely beneath the 
 skin just above the pubes, and the abdominal flaps may then be turned 
 freely outward. 
 
 General inspection of the abdominal cavity. — We first notice the 
 position and general condition of the viscera. It is best at this stage of 
 the examination to note the condition of the vermiform appendix, and to 
 look over the peritoneal cavity for serum, inflammatory lesions, evi- 
 dences of perforation, and for the existence of invagination, incarceration, 
 and hernise of the intestines. A small quantity of reddish serum is fre- 
 quently found in the abdominal cavity, particularly in warm weather, as 
 the result of commencing decomposition. 
 
 It should be remarked here that a variety of striking changes in the 
 character and appearance of the internal organs are produced by putre- 
 faction; changes which are often mistakenly regarded as evidences of 
 disease, and much experience is required in judging of their significance 
 
16 THE METHOD OF MAKINO 
 
 correctly. These changes are in general, softening and discoloration, 
 both of which may occur as the result of disease. It may be said in 
 general that the post-mortem reddening or hypostases are most marked 
 in the more dependent parts of the organs. Post-mortem sof fening usually 
 affects entire organs, not being limited to a part, as is often the case in 
 disease. Gray or greenish-brown post-mortem discolorations are apt to 
 appear in those organs or parts of organs which lie in contact with the 
 intestinal canal. 
 
 The omentum should be found smoothly spread over the surface 
 of the small intestines, but it may be rolled up and displaced in a variety 
 of ways, or may be adherent at some point to the small intestines or the 
 abdominal wall. 
 
 The surface of the small intestines should be smooth and shining. 
 They may be greatly distended with gas, and thus so completely cover 
 the abdominal viscera that it becomes necessary to let out some of the 
 gas by a small puncture. Tlie transverse colon passes across the abdo- 
 domen through the upper part of the umbilical region. It may be lower 
 than the umbilicus or higher up against the liver and diaphragm, it may 
 be distended with gas or contracted. 
 
 The liver is situated in the right hypochondriac and epigastric re- 
 gions, filling the concavity of the diaphragm. Its upper border reaches, 
 in the linea mammilaris, to the fifth intercostal space; in the linea 
 axillaris, to the seventh intercostal space; close to the vertebral column 
 to the tenth intercostal space. At the median line the upper border of 
 the liver corresponds to the lower border of the heart. The left lobe ex- 
 tends about three inches to the left of the median line. The lower 
 border of the right lobe usually reaches to the free border of the ribs, 
 while the left lobe is visible for about an inch below the ensiform car- 
 tilage. In women the liver is usually lower than in men. 
 
 The position of the liver is affected by changes in the thoracic cavity 
 forcing it downward; by change in the abdominal cavity forcing it up- 
 ward; by constriction of the waist in tight lacing, forcing it either up- 
 ward or downward; by changes in the size of the organ itself. The liver 
 may not only be displaced downward, but dislocated, so that its convex 
 surface faces the abdominal wall, and its posterior edge is turned up- 
 ward against the diaphragm. 
 
 The stomach is situated in the left hypochondriac and epigastric 
 regions, extending also into the right hypochondrium; it lies in part 
 against the anterior wall of the abdomen, in part beneath the liver and 
 diaphragm, and above the transverse colon. Its anterior surface, which 
 is directed upward and forward, is in contact above with the diaphragm 
 and the under surface of the liver, and lower down with the abdominal 
 wall opposite to the epigastric region. Its posterior surface is turned 
 downward and backward, and rests on the transverse mesocolon, the pan- 
 
POST-MOETEM EXAMINATIONS. 17 
 
 creas, and the great vessels. To its lesser curvature or upper border are 
 attached the gastro-phrenic ligament and the gastro-hepatic omentum. 
 To the greater curvature or lower border is attached the gastro-colic 
 omentum. Its cardiac orifice communicates with the oesophagus, its 
 pyloric end with the duodenum. 
 
 When the stomach is distended, the greater curvature is elevated and 
 carried forward, the anterior surface is turned upward and the posterior 
 surface downward. When distended with food or gas, the organ is promi- 
 nent; when empty it may hardly be visible below the ribs; when the in- 
 testines are dilated it may be entirely covered by them. 
 
 Before opening the thorax, the hand should be passed up against the 
 under surface of the diaphragm on either side to determine its height. 
 According to Quain, the vault of the diaphragm rises in the dead body on 
 the right side to the level of the junction of the fifth rib and sternum, 
 on the left side as high as the sixth rib. Both the relative and the ab- 
 solute height of the diaphragm vary under a variety of pathological con- 
 ditions. 
 
 If the existence of air or gas in the pleural cavities be suspected, the 
 abdominal cavity should be filled with water and the diaphragm punc- 
 tured below the level of the fluid. If air be present it will escape in 
 bubbles through the water. 
 
 THE THORAX. 
 
 We now leave the abdominal viscera and proceed to the examination 
 of the thorax. With a costatome or a strong knife, the costal cartilages 
 are divided close to the ribs, the clavicles are disarticulated from the 
 sternum, and the latter removed, taking care not to wound the large 
 veins. We first examine the position of the heart and lungs. 
 
 The Heart. — The upper border of the heart is on a level with the 
 third costal cartilage, the lower border extends from 1.3 cm. (\ in.) below 
 the lower end of the sternum to the fifth left intercostal space. The 
 left boundary of the heart is situated to the left of the junction of the 
 fifth rib with its costal cartilage, aad behind or to the left of a vertical 
 line drawn downwards from the left nipple. The right boundary ex- 
 tends about 3.5 ctm. (1 in.) to the right of the right edge of the ster- 
 num. The portion of the heart uncovered by the lungs is of an irregu- 
 lar quadrangular shape. Its lateral diameter is from 3.8 ctm. to 11.1 ctm. 
 (1^4^ inches); its upper boundary varies from the level of the second 
 left costal cartilage to that of the fifth, but it is usually behind the thii'd 
 or fourth cartilage or fourth space. 
 
 The area of the heart which is found uncovered will, however, vary 
 much according to the degree to which the lungs collapse after opening 
 the chest. Any disease which diminishes the size of the lungs, or pleu- 
 ritic adhesions which retract or bind them down, may increase the area 
 2 
 
18 THE METHOD OF MAKING 
 
 of exposed heart. On the other hand, emphysema, pneumonia, or any 
 disease which increases the size of, or retains the air in the lungs, may 
 diminish the area of exposed heart. The exposed area varies also with 
 the size of the heart itself. 
 
 The pericardium is now opened by a slightly oblique incision on 
 its anterior surface. The existence of serous, fibrinous, or purulent exu- 
 dation, and of adhesions is to be noticed. A small quantity of clear 
 serum exists normally in the pericardial sac, and this serum may be 
 blood-stained from beginning decomposition. White thickenings of the 
 pericardium on the surface of the ventricle are often seen; they do not 
 indicate any important disease. 
 
 Now that the pericardial sac is open, the position of the heart can be 
 clearly seen. It lies obliquely in the chest, its long axis 9,t about an 
 angle of about 60 degrees with that of the thorax. The portion of the 
 heart which is first seen is the anterior surface of the right ventricle; up- 
 ward and to the right of this is the right auricle, which lies about | 
 on the right of the sternum and about \ behind it. Its upper border 
 usually corresponds to the plane of the middle of the anterior end of the 
 second intercostal space on the right side. Its size varies with the 
 amount of blood which it contains. The left auricle lies behind the root 
 of the pulmonary artery, so that only its appendix is visible. The mid- 
 dle of the auricle corresponds to the third costal cartilage. Of the left 
 ventricle only a narrow rim is seen, on the left side of the right ventricle. 
 The pulmonary valve is usually entirely or in part on the left side of the 
 sternum behind the second space, or third costal cartilage. 
 
 The aortic valve is usually at the level of the third cartilage or the 
 third space, and behind the left two-thirds or half of the sternum. The 
 mitral valve is oblique, the upper end to the left. It is on the level of the 
 third to the fourth cartilage near the middle of the sternum. The tri- 
 cuspid is oblique, its upper end to the left; the upper end is at the level 
 of the third cartilage, the third space, or the fourth cartilage. The valve 
 is opposite to the middle of the sternum. 
 
 The hand should now be passed over the arch of the aorta, to ascer- 
 tain whether or not an aneurism is present. The heart is then grasped 
 at the apex, raised out of the pericardium, tilted upward and removed 
 unopened by cutting through the vessels at its base. 
 
 To determine the sufficiency of the aortic and pulmonary valves, the 
 heart is held horizontally by both auricles, so as not to pull the valves 
 open, and water is poured into the aortic and pulmonary arteries, and 
 we observe how well the valves support the column of liquid. To ascer- 
 tain the sufficiency of the mitral and tricuspid valves, the auricles are 
 first laid open so as to expose the upper surfaces of the valves. A large 
 pipe is passed through the aorta or pulmonary artery beyond their valves, 
 and a small stream of water allowed to flow into the ventricles. The 
 
POST-MOETEM EXAMIKATIONS. 19 
 
 auriculo-ventricular valves will be swollen upward, and we can observ 
 their degree of sufficiency. The tricuspid valve is normally some\*hat 
 insufficient. The water tests, however carefully applied, are not very 
 reliable, since under the most favorable conditions the natural bearings 
 of the valves are not perfectly preserved. 
 
 To ascertain the size of the different valvular openings, we introduce 
 the fingers, held flat with their edges in contact, into each of the orifices, 
 and then measure the width of the fingers at the point where they fill 
 the orifice. In this way we find that, under normal conditions in the 
 adult, the aortic orifice measures about 2.5 ctm. (1 inch), the mitral valve 
 about 4.5 ctm. (1.8 in.), the pulmonary about 3.1 ctm. (1.3 in.), the 
 tricuspid about 5 ctm. (2 in.). 
 
 In order to examine the interior of the heart, we first make an inci- 
 sion through the anterior wall of the right ventricle, close to the septum, 
 and reaching to the apex of the ventricle; through this opening the 
 blade of the enterotome is passed into the pulmonary artery, and the 
 ventricle and artery laid open. With a little care, the incision may be 
 made to pass through one of the points of junction of the valves. 
 
 The auricles and ventricles may be empty, or may contain fluid blood, 
 or the so-called heart-clots. These heart-clots are of two kinds — those 
 which are formed some time before death, and those which are formed 
 during the last hours of life and after death. , The clots which are 
 formed some time before death are usually associated with organic dis- 
 ease of the heart, especially with dilatation of the ventricles. They are 
 firm, dry, and of whitish' color; they may soften or be infiltrated with 
 the salts of lime. They are free in the cavities of the heart, or entangled 
 in the trabecule or firmly adherent to the endocardium. They are com- 
 posed of coagulated fibrin, or, rarely, of sarcomatous tissue as a compli- 
 cation of sarcoma in other parts of the body. The clots which are 
 formed during the last hours of life and after death are red, yellow, or 
 white. They may be soft or succulent, or quite firm. They may be 
 free in the heart cavities, or be adherent to the trabeoulse, or extend 
 into the large vessels. They are usually most constant and of largest 
 size in the right auricle and ventricle. Such clots may be formed within 
 two hours after death. Clots of this character are a regular post-mortem 
 condition, and of no pathological significance. It is evident, however, 
 if the blood did coagulate in the heart within twenty-four hours before 
 death that this coagulum could not be distinguished from the ordinary 
 post-mortem clots. If it is supposed, therefore, that a person dies from 
 heart-clot developed a few hours before death, the proof of this must be 
 derived from the clinical symptoms, and not from the autopsy. 
 
 The condition of the pulmonary valves and of the endocardium and 
 the thickness and appearance of the walls of the ventricle are now noticed; 
 the left ventricle is opened by an incision through its anterior wall. 
 
20 THE METHOD OF MAKING 
 
 close to the septum, and examined in the same way. "We sometimes see 
 tlie endocardium of the upper part of the left ventricle thick and white 
 without the existence of valvular lesions or any clinical history of disease. 
 The endocardium and valves are often stained red, particularly in warm 
 weather, by imbibition of coloring matter of the blood get free by decom- 
 position. To complete the examination of the cavities, the enterotome 
 is passed into each auricle, carried down into the corresponding ventricle, 
 and an incision made along the outer border of both auricle and ventricle 
 to the apex of the latter. In this way the auriculo-ventricular valves are 
 completely exposed. 
 
 After removing the blood, the heart should be finally weighed. In 
 adults the normal average weight of the heart is in males about 300 grms. 
 (10 oz.), in females about 250 grms. (8 oz.); the relative weight to that of 
 the body is in males 1-158, in females 1-149. According to Bizot, the 
 thickness of the wall of the left ventricle is in males 11.2 mm. {j\ inch), 
 in females 8.1 mm. {-^-^ inch); of the right ventricle, in males 4.8 mm. 
 (^ inch), in females 3.2 mm. {^^ inch). Generally speaking, the size 
 of the heart corresponds to the size and the development of the indi- 
 vidual. In judging of an increase or decrease in its size, we must con- 
 sider the weight of the organ and the thickness of its walls. If the 
 person dies while the heart is contracted, the walls of the ventricles will 
 appear thicker, their cavities smaller than usual. If he die of some 
 exhausting disease, like typhoid fever, or if decomposition has com- 
 menced, the heart-walls will usually be flabby, and the cavities will 
 appear larger than usual. 
 
 Preservation of Specimens. — Parenchymatous and fatty degeneration of the 
 heart-muscle are best studied microscopically by teasing the fresh muscle in one- 
 half -per-oent salt solution, or by examining in the same solution fresh sections made 
 with the freezing microtome. For the study of interstitial changes, fatty infil- 
 tration, etc., small pieces of the heart-muscle should be hardened in MilUer's 
 fluid. The valves may be stretched on a flat cork with pins, laid for forty-eight 
 hours in a mixture of equal parts of one-sixth-per-oent chromic acid and alcohol, 
 and then transferred to strong alcohol. For the methods of detecting bac- 
 teria in ulcerative endocarditis, see section on bacteria staining. "When the 
 presence of bacteria is suspected, the specimen should be preserved in strong 
 alcohol. 
 
 The pleural cavities are next examined. The hand is passed into 
 each, and the existence of serous or fibrinous exudations or of old adhe- 
 sions ascertained. The method of detecting the presence of air has been, 
 given above. After the commencement of putrefaction, reddish serum 
 may accumulate in the j)leural cavities. This should not be mistaken 
 for the result of disease. 
 
 The Lungs. — Each lung is lifted up in turn, the vessels, etc., at 
 its base divided, and the organ removed. If the pleura is very adherent, 
 it is better to strip off the costal pleura with the lung. After inspecting 
 
POST-MOETEM EXAMINATIONS. 21 
 
 the external surface of the lung, observing its size, shape, color, and con- 
 sistency, we open the bronchi. For tliis purpose, we use scissors with 
 long, naiTow, blunt-pointed blades, one blade a little longer than the 
 other. The lung is held in the left hand with its base upward. We 
 :first open the large bronchi which run -on the inner side of the lower 
 lobe, afterward those of the upper lobe. Bach bronchus should be fol- 
 lowed to its smaller ramifications. 
 
 We should observe the contents of the bronchi and the appearance of 
 their walls. In the larger and medium-size bronchi the cartilages in 
 their walls do not form complete rings, but appear shining through the 
 mucous membrane like irregular white patches. This appearance should 
 not be mistaken for a pathological change. In bodies which have been 
 ■dead for some time, especially in cold weather, the bronchial mucous 
 membrane may be red and swollen as a post-mortem change. The con- 
 tents of the stomach are sonietimes forced after death into the jDharynx, 
 and thence find their way into the trachea and bronchi, giving them a 
 peculiar reddish and even gangrenous appearance. Bronchitis does not 
 always leave lesions which can be appreciated after death. 
 
 After the examination of the bronchi, the lung is turned over, the 
 Tessels, etc., at its root grasped with the left hand, and a long, deep 
 incision made from apex to base. We observe the appearance and 
 texture of the lungs, whether the air vesicles are dilated (emphysema- 
 tous), or filled with serum, blood, or inflammatory exudation. Fluid 
 •can be pressed out of the air vesicles without breaking down the lung 
 tissue. Solid inflammatory exudation, on the other hand, renders the 
 lung more resistant and easily broken down. Attention should be paid 
 to the oozing of purulent or other fluid from the smaller bronchi when 
 the lung is squeezed near the cut surface. It is the rule to find the 
 lower lobes much more congested than the upper. 
 
 Preservation of the Lungs and Bronchi. — If the lungs have been out, small 
 pieces from the affected portions of lung tissue or bronchi should be hardened in 
 JVIiiller's fluid, care being taken not to squeeze or handle them unnecessarily. It 
 is better, when the microscopical examination is more important than the maoro- 
 scopical, not to open the lungs at once, but to fill the air spaces with preservative 
 fluid by means of a funnel attached to a short rubber tube and canula, which is 
 tied into the main bronchus. In this way, not only are the minute structures pre- 
 served better, but the air vesicles are filled out and hardened in an approximately 
 natural condition. Care should be taken not to have too great a pressure from 
 the inflowing fluid, since then exudations might be displaced or the lung dis- 
 torted or ruptured. While the lung is being filled, it should be immersed in a 
 vessel of the same preservative fluid, in which it lies for twenty-fonr hours. It 
 is then cut into small pieces, and the hardening completed. A variety of harden- 
 ing agents may be used : Miiller's fluid, strong alcohol, or the mixture of equal parts 
 of one-sixth-per-cent solution of chromic acid and alcohol. For general purposes, 
 the latter fluid is perhaps the best. If, however, the lung is commencing to decay. 
 
22 
 
 THE METHOD OF MAKING- 
 
 strong alcohol will stop the process more quickly, and give as good results as are 
 possible under the circumstances. 
 
 It is often desirable, and particularly in cases in which the topography of 
 lesions is to be studied, as in acute miliary tuberculosis, acute and chronic 
 phthisis, infarctions, etc., to inject the blood-vessels with colored gelatin. The 
 lung should then be hardened in alftohol. 
 
 The Pharynx, Larynx, and (EsoiJhagus.—li these organs are to be 
 examined, which is not always necessary, the incision of the thorax is 
 prolonged to a point one inch below the chin. The soft parts are dis- 
 sected from the larynx, taking care not to cut the thyroid body, and an 
 incision is made through the floor of the mouth, following the internal 
 surface of the inferior maxilla. Through this incision the fingers are 
 introduced into the mouth, the tongue drawn down, the posterior wall 
 of the pharynx divided above the tonsils, and the pharynx and larynx 
 drawn out together. These organs are then dragged downwards, and 
 with the aid of the knife the trachea and oesophagus are removed entire, 
 the oesophagus being cut just above the stomach. If the contents of the 
 stomach are to be preserved, as in cases of suspected poisoning, a liga- 
 ture is put around the oesophagus just below the point at which it is to 
 be cut off. 
 
 With the enterotome the pharynx and oesophagus are now slit open 
 upon their posterior surfaces. The mucous membrane thus exposed is 
 examined for evidences of caustic poisons, of inflammation, tumors, stric- 
 tures, etc. The enterotome is next introduced into the larynx, and this 
 organ and the trachea laid ojien along the posterior wall. Here we look 
 for oedema of the aryteno-epiglottidean folds (oedema of tlie glottis), and 
 for evidences of catarrhal, croupous, ulcerative, and syphilitic inflamma- 
 tion, for tumors and lesions of the laryngeal cartilages. CEdema and red- 
 ness of the larynx may be produced by post-mortem changes, especially 
 in bodies which have been kept for several days in cold weather. A well- 
 marked oedema glottidis during life may leave no trace after death. 
 Putrefactive changes usually commence early in the larynx and trachea. 
 
 Preservation of the Larynx and Trachea, etc. — They are freed from superflu- 
 ous tissue and suspended entire by a thread in a large quantity of a mixture of 
 equal parts of J per cent chromic acid and alcohol. The mixture should be re- 
 newed at the end of twenty-four hours, and again on the third and sixth day; at 
 the end of ten days the specimen is washed and transferred to strong alcohol, 
 in which it is preserved. The oesophagus should be stretched on a flat coi'k with 
 pinH, and then treated in the same way. 
 
 THE ABDOMEN. 
 
 Returning now to the abdominal cavity, we first dissect off the omen- 
 tum. If tubercles of the peritoneum exist, they are best seen and 
 studied in the omentum. The colon is then raised and dissected free 
 to the ctecum on one side, and to the rectum on the other. The colon 
 
POST-MOBTEM EXAMnSTATIONS. 26 
 
 and small intestines are then drawn first to the right and then to the 
 left side so as to expose in turn the right and left kidneys. As each kid- 
 ney is brought into Tiew, an incision is made through the peritoneum 
 over the track of the ureter. The ureter is followed through its entire 
 length and its condition ascertained. 
 
 TJie kidneys are then removed, separating the peritoneum and fat 
 from them with the hand, and dividing the vessels with the knife. The 
 suprarenal capsules, which are attached to the upper end of each kidney, 
 are removed at the same time. The kidneys may be softened by putre- 
 faction, or the surface may have a greenish-gray color, caused by the 
 post-mortem action of putrefactive gases on the haemoglobin. 
 
 An incision is made through the capsule, along the convex border of 
 the kidney, and the membrane stripped off. We notice the degree of 
 adherence of the capsule to the kidney, and also the surface of the latter, 
 whether smooth or roughened, pale, congested, or mottled ; an incision 
 is made along the convex surface down to the pelvis, so that the organ is 
 divided into halves. We observe the relative thickness of the cortical 
 and pyramidal portions, as well as the size of the entire organ. To as- 
 certain the latter point, it is well to weigh each kidney ; the normal 
 weight is about from 140 grms. (4^ oz.) to 155 grms. (5 oz.). It is 
 necessary to remember, however, that in a kidney which is much 
 atrophied, there may be an increase of fat in the pelvis, which gives the 
 organ nearly its normal size and weight, while the kidney tissue proper 
 may have in great measure disappeared. 
 
 We now inspect the kidney tissue more closely, especially the cortical 
 portion. The pyramids consist largely of tubes running in nearly straight 
 lines from the apex to the base of each pyramid. These straight tubes 
 pass from the pyramids into the cortex in bundles, called medullary 
 rays, many of them retaining their straight course until they nearly 
 reach the surface of the kidney. These straight tubules send off branches 
 on all sides of the rays which become convoluted, form Henle's loofis, 
 and finally terminate in the glomeruli or Malpighian bodies. In this way 
 the cortex of the kidney, as seen in section, is divided into alternate 
 bands of straight tubes, convoluted tubes and glomeruli ; both sets of 
 bands being perpendicular to the surface of the kidney, and called respec- 
 tively medullary rays and labyrinths. About the convoluted tubules and 
 glomeruli is a rich venous plexus, and since after death the blood usually 
 remains in this plexus and in the glomeruli, the bands containing the 
 convoluted tubules, i. e., the labyrinths, usually appear red, while the 
 medullary rays are grayish-white. In a normal kidney, therefore, the 
 cortex should be regularly striped in narrow alternating red and whitish 
 bands. 
 
 If there be extensive congestion, the entire cortex is red. If the ejoi- 
 thelium of the tubules degenerates and fills them up, or if there are 
 
24 THE METHOD OF MAKING 
 
 considerable changes in the interstitial tissue, the regular bands are lost, 
 and the cortex is irregularly mottled. If the tubular epithelium becomes 
 filled with fat-globules, this is indicated by an opaque yellow color of the 
 affected parts; in many cases, therefore, the existence of kidney disease 
 can be recognized with the naked eye. 
 
 If waxy degeneration be present to a marked extent, it may be mani- 
 fest by a peculiar translucent appearance of the affected parts, but in 
 most cases it is necessary to apply reagents to demonstrate it satisfac- 
 torily. The cut surface of the kidney is washed with water to free it 
 from blood, and repeatedly brushed with an aqueous solution of iodine 
 (iodine 1 part, potassium iodide 3 parts, water 100 parts). The glomer- 
 uli and the blood-vessels are most frequently affected, and if so, they 
 will appear as mahogany-colored dots and lines on a yellow ground. 
 
 The pelvis should be examined for inflammatory lesions and calculi. 
 Sometimes a whitish fluid is seen in the pelvis, and can be squeezed from 
 the jDapillse; this is produced by a post-mortem desquamation of the epi- 
 thelium, but is liable to be mistaken for pus. 
 
 Preservation of the Kidney. — If the kidney be not opened, the blood-vessels 
 may be injected through the renal artery with Miiller's fluid, or with a mixture 
 of -g per cent aqueous solution of chromic acid 2 parts, alcohol 1 part. The organ 
 is immersed for twelve hours in the same fluid as that used for the injection, and 
 is then cut into small pieces, pyramidal in shape, so as to include a portion of the 
 cortex and medulla, and these are to remain for ten days in the same fluid, which 
 should be renewed once or twice. They are then soaked in water for an hour to 
 get rid of the chromic acid, and transferred to and kept in strong alcohol. If the 
 kidneys have been opened at the autopsy, they should be cut up and treated as 
 above, but of course without the injection. Parenchymatous degeneration of 
 the kidney is best studied in sections from the frozen fresh organ, or in frag- 
 ments teased in J per cent salt solution. Kidneys which are to be examined for 
 the presence of bacteria, should be cut into small pieces and placed at once in 
 strong alcohol, which should be changed once or twice, and in which they are 
 permanently preserved. 
 
 The Suprarenal Capsules are in the fretus of an ovoidal, in the adult 
 of a triangular shape. They are situated at the upper and inner border 
 of the kidney, to which they are loosely attached by connective tissue. 
 On the anterior surface is an irregular fissure, called the hilus, from 
 which the veins emerge. The size varies considerably, but in the adult 
 the average vertical diameter is from 3.2 ctm. {1\ in.) to 4.5 ctm. (If in.); 
 the transverse diameter about 3.2 ctm. (1^ in.), and they are from 4.3 
 mm. {\ in.) to 6.4 mm. (J in.) in thickness. They weigh in the adult 
 from about 4 grm. (1 3 ) to 8 grm. (2 3 ). They are composed of a cor- 
 tical and medullary portion, the cortex forming a yellowish shell around 
 the dark-red or brown medulla. They are inclosed in a connective tis- 
 sue capsule, from which fibrous processes extend inward, dividing the 
 gland into a series of irregular chambers. Those in the cortex are 
 mostly elongated, giving this portion a striated appearance, while those 
 
POST-MOETEM EXAMINATIONS. 25 
 
 in the medulla are polyhedral. It is in these spaces that the parenchyma 
 cells lie. The saprarenal capsules readily decompose; the inner layer of 
 the cortex may soften and break down, so that the outer zone forms a 
 sort of cyst filled with reddish-brown broken-down substance. Hyper- 
 trophy, tuberculosis, and cheesy degeneration, fatty degeneration, and 
 tumors are to be looked for. 
 
 Preservation. — The suprarenal capsules should be hardened in Miiller's fluid 
 or in sti'ong alcohol. 
 
 The Spleen. — This organ has, when removed from the body, the gene- 
 ral shape of a flattened ellipsoid, most curved on its external and posterior 
 surface. It is situated in an oblique position on the left side of the stom- 
 ach, and between its cardiac end and the diaphragm. The vessels are 
 given off from its inner surface, which is crossed by a more or less well- 
 marked vertical ridge. The point of emergence of the vessels is called 
 the hilus. Its long diameter extends from the seventh intercostal space 
 to the eleventh rib. Its upper portion is separated from the ribs by the 
 lungs; its lower portion by the diaphragm. Its usual length is 12.2 ctm. 
 (4f in.) to 14.1 ctm. (5^ in.); its breadth from 8.3 ctm. (SJ in.) to 10.2 
 ctm. (4 in.); its thickness from 3.2 ctm. (Ijin.) to 4.6 ctm. (If in.); its 
 average weight in the adult is about from 248 grm. (8 oz.) to 325 grm. 
 (10-J oz.). But its measurement and weight vary considerably within 
 the limits of health. It is in these respects the most variable organ in 
 the body. In old age the average weight gradually diminishes. 
 
 The spleen is enclosed in a fibrous capsule covered with peritoneum. 
 The parenchyma is formed of blood-vessels and fibrillar connective tissue, 
 and of a soft dark-red pulp, in which are embedded whitish spheroidal 
 or elongated bodies, the glomeruli or Malpighian bodies. In the normal 
 human spleen the glomeruli are hardly perceptible to the naked eye, but 
 sometimes they are very plain. Sometimes the fibrous stroma is very 
 apparent; sometimes not. 
 
 The size, consistence, and color of the organ vary a good deal with- 
 out any known cause. Decomposition softens it. Thickenings of the 
 capsule and abnormal adhesions are very common, and often occur with- 
 out any clinical history indicating disease. We should look for changes 
 in size, pigmentations, hyperplasia of the connective tissue, amyloid de- 
 generation, tubercles, and infarctions. 
 
 Not infrequently one or more spheroidal or flattened so-called acces- 
 sory spleens are found in the vicinity of the spleen; they vary in size 
 from that of a pea to that of a walnut. 
 
 Preservation. — In certain diseases of the pulp, leukaemia, leucocythemia, etc., 
 the tissue should be teased when fresh in one-half- per-oent salt solution. For 
 general purposes, small pieces of the organ are hardened in Miiller's fluid. 
 
 The Intestines. — The rectum is divided, the intestine seized with the 
 
26 THE METHOD OF MAKING 
 
 left hand, and being kept stretched, is separated from its attachments by- 
 repeated incisions through the mesentery close to the gut, until the duo- 
 denum is reached, where it is again cut ofE. The operation is more 
 cleanly if, before dividing the gut, ligatures are placed around it at either 
 end. The entire length of the gut is now laid open with the enterotome 
 along the mesenteric attachment, the mucous membrane is cleaned with 
 a stream of water, and then examined. 
 
 In cases of suspected poisoning, a ligature should be j)laced around 
 the rectal end of the gut and two around the duodenal end, and it is then 
 cut off below the former and between the latter ligatures. The gut is now 
 opened, and the contents emptied into a clean glass jar for delivery to- 
 the chemist, care being taken that they be not allowed to touch any- 
 thing but the inner surface of the jar. After washing the intestine in 
 pure fresh water and examining it, it should be placed entire in another 
 clean jar and sealed. 
 
 Cadaveric lividities are very common in the intestines, and are usu- 
 ally most marked in tlie dependent portions. They are apt to occur in 
 patches, but may be diffuse and very extensive. If the wall of the gut 
 be stretched, they are often seen to be discontinuous, owing to the pres- 
 sure of the blood from the. parts which are squeezed by folds. Small 
 patches of arborescent or diffuse red staining are often seen formed by 
 the imbibition from the vessels of decomposing htemoglobin. In the 
 more advanced stages of decomposition, the mucosa may be softened 
 and loosened. A dark i^urple or brownish discoloration of the entire 
 intestinal wall is frequently seen, either diffuse or in patches. Much 
 experience and careful observation are requisite in forming a correct judg- 
 ment regarding the significance of changes of color in the intestines. 
 Caution is necesssary in distinguishing normal digestive hypersemia from, 
 abnormal congestion. A very considerable congestion may exist without 
 disease. In cholera seasons- especially, observers are prone to call the 
 most moderate degree of congestion abnormal. 
 
 The lesions ordinarily to be looked for are catarrhal, croupous, and 
 ulcerative inflammations, perforations, hemorrhages, strictures, tumors, 
 amyloid degeneration, swelling, and ulceration of the solitary follicles 
 and Peyer's patches, and pigmentation. For the detection of amyloid de- 
 generation of the mucosa, this structure should be carefully washed and 
 brushed with a solution of iodine (see p. 24). 
 
 Preservation. — For the general purposes of microscopic study, portions of the 
 gut should be stretched on cork and hardened in chromic-acid mixture (one- 
 sixth-per-cent chr. acid and alcohol, equal parts), especial care being taken to 
 change the fluid frequently. For obvious reasons, the mucous membrane should 
 be handled as little as possible, for, in the majority of cases, decomposition and 
 softening has already set in at the time of the autopsy, and under the most favor- 
 able conditions, th,e epithelium is very easily rubbed off. If the wall of the intes- 
 tine is to be examined for bacteria, as in typhoid fever, cholera, etc., portions 
 
POST-MOETEM EXAMmATIONS. 2T 
 
 should be stretched and hardened entirely in strong alcohol. If decomposition bo 
 far advanced, strong alcohol is the best hardening agent in all cases. 
 
 The Stomach and Duodemim. — We now introduce theenterotome into 
 the duodenum, at its transverse portion, and open it on the convex border. 
 When the pylorus is reached, the incision is carried obliquely over to- 
 the greater curvature of the stomach, along ■which it is extended as far 
 as the oesophageal opening, and the organ examined in situ, or, if a more 
 careful examination of the stomach is called for, after ascertaining 
 whether or not the bile-duct is pervious (see below), the duodenum and 
 stomach may be removed together, and the stomach open'ed and exam- 
 ined on the table. (If poisoning be suspected, a ligature should have 
 been placed earlier in the examination [p. 26] around the lower end of 
 the oesophagus and the duodenum. The stomach and duodenum are 
 now removed together unopened. They are to be opened in a carefully 
 cleansed glass jar, and after an inspection of the mucous membrane and 
 the contents with the naked eye and a hand-lens, stomach, duodenum, 
 and contents are to be sealed in the jar for the chemist.) 
 
 We now look for the orifice of the bile-duct, which will be found 
 about the middle or the descending portion of the duodenum on its con- 
 cave border. Pressure on the gall-bladder or on the common duct will 
 cause the bile to flow into the intestine if the ducts are pervious. But a 
 sufficient degree of stoppage may exist in the ducts to give rise to marked 
 symptoms of disease without preventing the flow of bile under these con- 
 ditions, even with a moderate pressure. A long director is now passed 
 into the gall-duct, which is laid completely open; ulcerations, cicatrices, 
 gall-stones, inflammatory lesions, and tumors are looked for. At this 
 point, should there be any special reason for doing so, the portal vein, 
 ■which lies close behind the ductus choledochus, should be opened and ex- 
 amined for periphlebitis, phlebitis, and thrombosis. The mucous mem- 
 brane of the duodenum and stomach are now rinsed off and examined. 
 Acute inflammations from caustic poisons, chronic catarrhal inflamma- 
 tions, hemorrhages, ulcers, erosions, swelling of the solitary follicles, and 
 tumors are lesions most frequently seen. We sometimes find a diffuse 
 congestion of the stomach similar to that produced by irritant poisons, 
 as a result of doses of croton oil given just before death. 
 
 Preservation. — The same methods should be used as for the intestines (see- 
 above). Tumors should be cut into small pieces and hardened in Miiller's fluid. 
 
 The Liver. — To remove the liver, the diaphragm is first divided on 
 one side of the suspensory ligament as far back as the spine, the suspen- 
 sory ligament is then divided; then the right and left lobes being in turn 
 raised, the lateral ligg,ments are severed. Then seizing the left lobe, the 
 organ is dragged obliquely downward into the abdominal cavity, the re- 
 maining attachments being dissected away. The liver is first laid on its 
 superior surface, and the gall-bladder and its contents examined. The 
 
 r 
 \ 
 
28 THE METHOD OF MAKING 
 
 character of the gall is to be determined, and gall-stones, inflammatory 
 lesions, and tumors sought for. To determine the actual size of the 
 organ, it should be both measured and weighed. Its size varies greatly 
 in different healthy individuals, but in general it may be said that it 
 measures from 25 to 30 ctm. (10 to 12 in.) transversely; from 15.3 to 18 
 ctm. (6 to 7 in.) antoro-posteriorly, and about 9 ctm. (3^ in.) at its 
 thickest part; the ordinary bulk is about 229 to 253 c.c. (90 to 100 cu. 
 in.); its ordinary weight between 1,550 to 1,860 grm. (50 to 60 oz.). 
 In children, its weight relative to that of the body is greater than in 
 adults. The liver is increased in size and weight during digestion and 
 by congestion from any cause. 
 
 The surface of the liver is now examined, and it is then laid on its 
 lower surface and several deep incisions made from the convex surface down- 
 wards. The color and consistence of the liver tissue should be noticed, 
 also the distinctness with which the lobular outlines can be seen; whether 
 or not the centres of the lobules are congested or their peripheries lighter 
 in color than usual, the presence of tumors, tubercles, abscess, ecchino- 
 coccus, new connective tissue, and pigmentation. Suspected amyloid 
 degeneration should be tested for by the iodine solution (p. 24). 
 
 We often find the surface of the liver of a greenish or very dark-brown 
 color; less frequently the same color extends into the substance of the 
 organ. This discoloration, which is entirely post-mortem, is like the 
 similar discoloration of other internal organs, produced by the action of 
 the gases or putrefaction on the coloring matter of the blood. 
 
 Preservation. — For the study of parenchymatous degeneration, sections of the 
 fresh frozen tissue or small teased fragments should be examined in half-per-cent 
 salt solution. For general purposes, small pieces should be hardened in Miiller's 
 fluid. Tumors should be treated in the same way. In many cases of marked 
 cirrhosis, the topography of the lesion is best demonstrated by injecting the or- 
 gan with blue gelatin through the portal vein and then hardening in strong al- 
 cohol. 
 
 The Pancreas. — This organ, of a light yellowish-red color, is elongated, 
 irregularly prismatic in shape and flattened antero-posteriorly; the right 
 -end, called the head, is broader than the rest, and lies in the concavity 
 of the duodenum. Tlie remainder of the organ, the body and tail, are 
 usually tapering and lie transversly in the abdominal cavity, the tail 
 reaching to the spleen. Its size and weight vary considerably; its usual 
 length is from 15.3 to 20.3 ctm. (6 to 8 in.), its breadth about 3.8 ctm. 
 (1^ in.), its thickness about 1.3 to 2.5 ctm. {\ to 1 in.). Its weight is 
 usually from 70 to 108 grm. (2^ to 3^ oz.). The organ may be rounded 
 instead of flattened; the head and tail may be disproportionately large; 
 the tail may bo unusually long or may be divided or curved. The supe- 
 rior mesenteric artery and vein which pass behind the gland are usually 
 partly imbedded in it, but are sometimes completely inclosed. 
 
POST-MOETEM EXAMINATIONS. 29 
 
 A longitudinal incision should be made through the whole gland, 
 which may remain in situ, and its substance and duct should be searched 
 for calculi, tumors, malformations, and evidences of acute and chronic 
 inflammation and amyloid degeneration of the blood-vessels. The pan^ 
 creas is frequently of a dark-red color from post-mortem staining. 
 
 Preservation. — Portions of this organ or tumors may be hardened in the chro- 
 mic acid mixture. 
 
 THE GENITO-UKINAET ORGANS. 
 
 The Male Organs. — If the urine is to be examined, it may be drawn 
 off with a catheter; or a vertical incision may be made into the bladder, 
 just above the symphysis pubis, and some of the urine dipped out. The 
 cut end of the rectum should now be grasped with the left hand and 
 raised up, and this and the bladder, prostate gland, etc., dissected away 
 from the pelvis, the knife being carried close to the bone. The bladder 
 is now drawn backward and the loose tissue close under the symphysis 
 pubis cut. The body of the penis is then shoved backward within the skin 
 and dissected away from behind beneath the symphysis, and finally cut 
 off just behind the glans penis. The penis and bladder are now drawn 
 backward and upward and the pelvic organs removed together. Or the 
 penis may be removed by sawing away the bones above the pubic arch, and 
 then dissecting away the penis whose root is thus exposed. 
 
 The pelvic organs are then laid on the table, the bladder uppermost; 
 a long director is passed into the urethra which is opened on its upper 
 surface through its entire length and the bladder widely opened. In 
 the urethra the presence of strictures, diverticula, ulcers, inflammatory 
 lesions is to be noticed; in the bladder, inflammatory lesions, hyper- 
 trophies, congestion, and ecchymosis of the mucous membrane and 
 tumors. The organs are now turned over; the rectum opened and ex- 
 amined for varicose veins, hemorrhages, ulcers, strictures, and tumors. 
 The prostate gland is then cut into and the presence of calculi, inflam- 
 matory lesions, hypertrophies, and tumors sought for. Lastly the vesi- 
 culsB seminales are examined, in which, though rarely, we may find evi- 
 dences of tubei'cular inflammation and dilatation. 
 
 The Testicles may be removed when necessary, without cutting the 
 scrotum, by enlarging the inguinal canals from within, and crowding 
 the glands through them and cutting them off. Inflammatory lesions, 
 tuberculosis, abcesses, and tumors are the most frequent lesions. 
 
 Preservation. — The urethral canal and bladder may be pinned open and hard- 
 ened in the chromic acid mixture. The prostate, vesiculse seminales, testicles, 
 and tumors should be hardened in MllUer's fluid. 
 
 The Female Organs. — The position and general condition of the pel- 
 vic organs should first be determined by inspection. Abnormal adhe- 
 sions of the ovaries, broad ligament. Fallopian tubes and uterus, malpo- 
 
30 THE METHOD OF MAKING 
 
 sitions of the uterus, subserous tumors of the uterus and ovarian tumors, 
 are frequently observed. Hemorrhage into the posterior cul-de-sac is 
 sometimes found. The urine should be collected, if necessary, as above 
 directed; the organs should be dissected away laterally, as in the male, . 
 care being taken not to injure the ovaries and Fallopian tubes. The 
 bladder is then drawn strongly backward and upward, and dissected 
 away from the symphysis and the pubic arch, and the point of the knife 
 being carried forward and downward, the vagina is cut off in its lower 
 third, the rectum severed just above the anus, the remaining attachments 
 ■cut, and the pelvic organs taken out together. If it be necessary to 
 remove the external generative organs, after freeing the lateral surfaces 
 -of the internal organs and the bladder, the legs are widely sei^arated and 
 the vulva and anus circumscribed by a deep incision. The tissues close 
 beneath the pubic arch are now dissected away from below and the vulva 
 thrust back beneath the symphysis; it is now seized above the bone, and 
 together with the anus dissected away and removed with the other or- 
 gans. 
 
 The Bladder is first opened and examined. The vulva may now be 
 ■examined for hypertrophies, inflammatory lesions, ulcers, cicatrices, cysts, 
 and tumors. The vagina is opened along the anterior surface; its more 
 ■common lesions are inflammations, fistulse, ulcers, tumors, and rarely 
 cysts. 
 
 The Uterus. — Before opening this organ,. its size and shape should 
 be determined. The adult virgin uterus is a pear-shaped body, flattened 
 antero-posteriorly, the upper portion or body is directed upwards and 
 forwards; while the lower portion, the cervix, is directed downward and 
 backwards. It is covered anteriorly by peritoneum to a point a little 
 below the level of the os internum; posteriorly, to a point a little below 
 the level of its junction with the vagina. The peritoneal invest- 
 ment separates from the organ at the sides to form the broad ligaments. 
 The uterus is held in position by the broad and round ligaments and by 
 its attachments to the bladder and rectum and vagina. The upj)er end, 
 the fundus, does not extend above the level of the brim of the pelvis. 
 Its average length is about 7.6 cm. (3 in.); its breadth about 5.1 cm. 
 (2 in.); its thickness about 3.5 cm. (1 in.); its average weight is about 
 
 31 to 46 grm. (1 to 1^ oz.). During menstruation the uterus is slightly 
 enlarged, and the mucous membrane of the body becomes thicker, softer, 
 and its vessels engorged with blood; while its inner surface is more or less 
 thickly covered with blood and cell detritus. A description of the com- 
 plicated changes in the uterus which pregnancy entails may be found in 
 the works on obstetrics. After pregnancy, the uterus does not return to 
 its original size, but remains somewhat larger; the os is wider and fre- 
 ■quently fissured. 
 
 In the infant the uterus is small, the body flattened, the cervix dis- 
 
POST-MOETEM EXAMINATIONS. 31 
 
 proportionately large. During childhood the organ increases in size, but 
 the body remains small in proportion to the cervix. At puberty the 
 shape changes and the body becomes larger. We not infrequently find 
 in the mucous membrane of the lower part of the cervix, small trans- 
 parent spheroidal structures called ovula Nabothi; these are small reten- 
 tion cysts caused by the closure of the orifices of the mucous glands of 
 the part. The more common lesions observed in tlie uterus are malposi- 
 tions, malformations, lacerations, ulcerations of the cervix, acute and 
 chronic inflammation of the mucous membrane or muscularis or both, 
 thrombosis and inflammation of the veins and tumors. 
 
 The Ovaries are flattened, o.voidal bodies which are situated one on 
 each side and lying nearly horizontally at the back of the broad ligament 
 of the uterus. Their size is variable and they are usually largest in 
 the virgin state. Their average weight is from 3.9 to 6.5 grm. (3 to 53). 
 They measure about 3.8 ctm. (l^in.) in length, 1.9 ctm. (fin.) in breadth, 
 and nearly 1.3 ctm. (-J in.) in thickness. The sides of the ovary 
 and its posterior border are free; it is attached along the ante- 
 rior border; to its end is attached the ovarian ligament; to its outer ex- 
 tremity one of the fimbriae of the Fallopian tube. The ovary is covered 
 •on its free surface by cylindrical epithelium, and its surface is less glist- 
 ■ening than the general peritoneum. The surface of the ovary is smooth 
 in the young, but becomes rougher and depressed in spots as the process 
 ■of ovulation goes on. In adult females we usually find corpora lutea in 
 their various stages. We should seek for evidences of acute and chronic 
 inflammations, for tumors and cysts. 
 
 The Fallopian tubes, lying in the upper margin of the broad ligaments, 
 are between 7. 6 to 10 ctm. (3 to 4 in.) in length. They commence at the up- 
 per angles of the uterus as small perforated cords which become larger 
 farther outward, and bend backward and downward towards the ovary. 
 They terminate in an expanded fimbriated extremity about 2.5 ctm. (1 
 in.) beyond the ovary. They are covered by peritoneum, and the mu- 
 cous membrane lining them, continuous with that of the uterus, is 
 thrown into longitudinal folds. Malpositions by adhesions, closure, in- 
 flammations, and cysts are the more common lesions. The possibility of 
 tubal pregnancy should be borne in mind. 
 
 Preservation. — All of these organs and their tumors may be hardened in Miil- 
 ler's fluid. The vagina should be stretched flat on cork and the cavity of the 
 uterus laid wide open. Great care should be taken not to touch either the inter- 
 nal surface of the uterus or the external surfaces of the ovaries, since in both the 
 epithelium is very easily rubbed off. 
 
 Should decomposition have commenced in the mucous membrane of the ute- 
 rus (this usually occurs very early), it is better to place it at once in the chromic 
 acid mixture (p. 36) for twenty-four hours and then in strong alcohol. It is bet- 
 ter to suspend the ovaries by a thread in a jar of the preservative fluid, than to 
 let them lie on the bottom, since the epithelium is thus less liable to be rubbed off. 
 
32 THE METHOD OF MAKING 
 
 AUTOPSIES IN CASES OF SUSPECTED POISONIKG. 
 
 It is always best, in cases of suspected poisoning, to preserve for the 
 cliemist not only the stomach and intestine, but the entire liver and brain; 
 or if portions of these only can be saved, these should be carefully weighed, 
 as well as the entire organs, and the relative amount of tissue resei-ved care- 
 fully noted at the time. It is even well, particularly in cases in which the 
 administration of the readily diffusible poisons, such as arsenic, strychnia, 
 etc., is suspected, to preserve the whole of all of the internal organs, 
 together with a large piece of muscle and bone, since with large quanti- 
 ties of tissue the results of the chemical analysis depend less upon calcula- 
 tions and are hence more comprehensible to the average jury. In all 
 such cases jars should, if possible, be procured which have never been used 
 before, and these should be carefully washed and rinsed with distilled 
 water. They should have glass stoppers and be sealed at once and care- 
 fully labelled before leaving the hands of the operator. If they can be 
 delivered to the chemist without much delay, they should have no pre- 
 servative fluid added. If they are to be kept for a considerable time, 
 pending the action of a coroner's jury or for some other reason, a small 
 quantity of pure strong alcohol may be poured over them. In this case 
 the operator should be particular to reserve a quantity, at least a half a 
 pint, of the specimen of alcohol used, in a clean sealed and labelled bot- 
 tle so that this may be tested by the chemist and be proven to be free from 
 the poison. It is better in all cases, however, to avoid if possible the use of 
 alcohol. In all autopsies which may have medico-legal importance, full 
 notes should be taken by an assistant as the operation proceeds, carefully 
 read over immediately afterwards, and dated and kept by the operator for 
 future reference. The labelling and disposition of the jars should be re- 
 corded in the notes. 
 
 EXAMII^ATIOI^ OF THE BODIES OF I^EW- 
 BORI^ OHILDEEN. 
 
 In examining the bodies of new-born children, we may have to deter- 
 mine, besides the ordinary lesions of disease, the age of the child, whether 
 it was born alive, how long it has been dead, what was the cause of 
 death. 
 
 GENERAL INSPECTION". 
 
 The Size and Age. — Caspar' gives the following description of the 
 foetus during the different months of intra-uterine life. 
 
 At the fourthiueeh, the embryo is 8 to 13 mm. {-^-^ to -f-^ in.) long. The 
 cleft of the mouth and two points indicating the eyes can be recognized 
 
 ' Caspar: Handbook of Forensic Medicine. Revised German Edition by Li- 
 man, 1882, p, 865 et seq.: or Sydenham Society Translation. 
 
POST-MOETEM EXAMIJSTATIONS. 33 
 
 in the head. The extremities are represented by little wart-like projec- 
 tions. The heart can be distinguished, the liver is disproportionately 
 large. The umbilical vessels are not yet formed. The entire ovum has 
 about the size of a walnut. 
 
 At the eighth weeTc the embryo is3.3 to 4 ctm. (y'-j- to 1^^ in. ) long. The 
 head forms more than a third of the entire body, the mouth is very large; 
 the nose and lips can be distinguished, but not the external ear. The 
 hand is longer than the forearm; the fingers are formed, but joined to- 
 gethei', the toes look like little buds; the soles of the feet are turned in- 
 wards. The position of the anus is indicated by a point. The abdomen 
 is closed. All the viscera can be recognized. Centres of ossification are 
 formed in the apophysis of the first cervical vertebra, the humerus, ra- 
 dius, scapula, ribs, and cranial bones. There are rudimentary external 
 genitals, but the sex can hardly be distinguished. The ovum has about 
 the size of a hen's egg. 
 
 At tlie twelfth week, the placeuta is formed. Tlie embryo is 5 to 6.5 
 ctm. (2 to 3^ inches) long and weighs about 31 grm. The head is separated 
 from the thorax by a distinct neck. The eyes and mouth are closed. 
 The nails can be perceived on the fingers. The sex can be recognized. 
 The umbilical cord is inserted near the pubes; the muscles begin to be 
 recognizable. The thymus and supra-renal capsules are formed. The 
 cerebrum, cerebellum, medulla, and the cavities of the heart can be recog- 
 nized. The humerus is 1.7 mm. long; the radius 5.5 mm.; the ulna 
 6.6 mm.; the femur and tibia 4.4 to 6.6 mm.; the fibula 5.5 mm. The 
 ovum is as large as a goose's egg. 
 
 At the sixteeyith week, the embryo is 13 to 15 ctm. (5 to 6 in.) long, and 
 weighs 77 to 93 grm. (2-|-to3 oz.). The skin is of a rose-red color and has 
 considerable consistency. The formation of fat in the subcutaneous tis- 
 sue has begun. The scrotum and labia are formed. The face begins to 
 assume its characteristic appearance. There is whitish meconium in the 
 duodenum. The liver is not so disproportionately large and the gall- 
 bladder is formed; the anus is open. The length of the humerus, radius, 
 and ulna is 1.7 ctm.; the femur and tibia 8.8 to 11 ctm. The calcaneus 
 begins to ossify at the middle of the. fourth month. 
 
 At the tiventiethiveek, the embryo is 26 to 38 ctm. (10 to 11 in.) long; it 
 weighs from 325 to 320 grm. (7^'^ to 10 oz. ). The nails are quite percept- 
 ible; there is a thin down on the head. The head is still disproportion- 
 ately large, occupying about one-fourth of the body. There is as yet none of 
 the vernix caseosa. The secretion of bile has commenced and stains the me- 
 conium. The insertion of the umbilical cord is still further off from the 
 pubes. The liver, heart, and kidneys are large in proportion to the other 
 organs. The convolutions of the brain cannot bo recognized. The 
 humerus is 2. 8 to 3 ctm. long; theradius2.6 ctm.; the ulna 2.8 ctm.; the 
 3 
 
34 THE METHOD OF MAKING 
 
 femur, tibia, and fibula each 2.6 ctm. The astragahis and the upper 
 part of the sternurn begin to ossify. 
 
 From this time on, the length of the foetus forms an approximately 
 accurate basis for the estimation of its age. From this period till its 
 maturity, the length ofthefcutus, determined in centimetres, corresponds 
 to cibout \ of the numher of months of its age. Prom this time on, the 
 weight exhibits marked individual differences and is therefore a less re- 
 liable criterion of its age than is the length. 
 
 At the twenty fourth loeek, the embryo is 31 to 34 ctm. (12 to 13 in.) 
 long and weighs 750 to 875 grms. (24 to 28 oz.). The lanugo and vernix 
 caseosa are formed. The skin is of a dusky cinnabar-red color. The 
 meconium is darker. The scrotum is empty, small, and red; the labia 
 majora are prominent and held apart by the projecting clitoris. The 
 pupillary membrane is present and readily recognized. The length of 
 the humerus and radius is 3.5 ctm.; of the ulna, femur, tibia, and 
 fibula, each 3.7 ctm. 
 
 At the tiventy-eighth weeh, the embryo is 36.4 to 39 ctm. (14^ to 15 J in.) 
 long, and weighs 1,500 to 1,750 grms. (48 to 57 oz.). The hair is more abun- 
 dant and longer. The great fontanelle measures about 4 ctm. (14 in.) 
 in diameter and all of the fontanelles are readily perceived. The skin is 
 of a dirty reddish color and abundantly beset with the lanugo and vernix 
 caseosa. The large intestine contains much meconium. The humerus is 
 4.5 to 5 ctm. long; the radius 3.7 ctm.; the ulna 4ctm. ; the femur, tibia 
 and fibula each 4.2 to 4.6 ctm. 
 
 At the thirty-second tveeic, the embryo is 39 to 41.5 ctm. (15J to 16Jin.) 
 long, and weighs 1,500 to 2,500 grms. (48 to 81 oz.). The skin is lighter in 
 color; the pupillary membrane has disappeared. The testicles are in the 
 scrotum or the inguinal canal; the labia are still widely apart and the cli- 
 toris prominent. The nails reach nearly to the ends of the fingers. The 
 humerus is 5 to 5.2 ctm. long; the radius 4 to 4.3 ctm.; the ulna 4.8 to 5 
 ctm.; the femur 5.2 ctm.; the tibia and fibula each 4.8 to 5 ctm. The 
 last sacral vertebra begins to ossify. 
 
 At the thirty-sixth weelc, the embryo is 44.2 to 46 ctm. (17.4 to 18 in.) 
 long, and weighs about 3,000 grm. (97 oz.). The scrotum begins to be- 
 come wrinkled and the labia to close. The hair becomes more abun- 
 dant, while the lanugo begins to diminish in amount. 
 
 At the fortieth iveek,-the foetus is fully developed and the term of its 
 intra-uterine life accomplished. 
 
 The fresh corpse of a new-born child at term no longer resembles that 
 of the immature foetus. The skin is firm and pale, like that of an adult. 
 The lanugo has disappeared except on the shoulders. In the majority 
 of cases the hair on the head is 1.5 to 2 ctm. (| to f in.) long. The great 
 fontanelle is, in the average, 2 to 3 ctm. (yV ^ 1 tV i"-) long- As deter- 
 mined by an analysis of 661 cases, the average length is 50 ctm. (20 in.); the 
 
POST-MOETEM EXAMINATIONS. 35 
 
 •weight 3,356 grm. (105 oz.). The nails are hard and reach to the 
 tips of the fingers, but not to those of the toes. The cartilages of the 
 €ars and nose are hard. The labia are more nearly closed. An ossification 
 centre in the lower epiphysis of the femur should be sought for, as its 
 presence is one of the most reliable signs of the maturity of the foetus. 
 If it is absent, the foetus is, as a rule, not more than thirty-seven weeks 
 old; but in rare cases, it may be absent at term. A centre of ossification 
 1 mm. (.039 in.) in diameter, indicates an age of 37 to 38 weeks, if the 
 child was born dead or died soon after birth. Earely it is no larger than 
 this at term. A diameter, at birth, of 1.5 to 9 mm. (.058 to. 351 in.) indi- 
 cates an age of 40 weeks. A diameter of less than 9 mm. (.351 in.) indi- 
 cates, as a rule, that the child has lived some time after its birth; a less 
 diameter than 7 mm. (.273 in.), however, does not prove the contrary. 
 
 Twenty-four hours after the Mrth of the child, the skin is firmer and 
 paler. The umbilical cord is somewhat shriveled, although still soft and 
 bluish in color. Prom the second to the third day, the skin has a yel- 
 lowish tinge, and the cuticle sometimes appears cracked. The umbilical 
 cord is brown and dry. Prom the third to the fourth day, the skin is 
 yellower, and the cuticle is apt to separate from the skin. The umbili- 
 cal cord is of a brownish-red color, flattened, semi-transparent, and 
 twisted. The skin around its insertion is red and congested. 
 
 The head should be examined for the marks of injuries. Very com- 
 monly some portion of the scalp will be found swollen and infiltrated 
 with blood and serum. This may be the caput succedaneum formed dur- 
 ing delivery. The mouth and nose should be examined for the presence 
 of any foreign bodies which might have caused sufEocation. 
 
 The neck should be examined for marks of strangulation. The um- 
 bilical cord may be twisted around the child's neck and strangle it. The 
 mark left by the cord is usually continuous, broad, not excoriated, some- 
 times accompanied by ecchymoses in the skin. 
 
 The entire body should be examined for the presence of vernix case- 
 osa, blood, marks of injury, and the existence of putrefaction. It should 
 be remembered that putrefaction is apt to commence earlier in the bodies . 
 of young children than in those of adults. 
 
 The umbilical cord may be cut or torn. It usually separates by the 
 fifth day, sometimes not until the tenth. If the umbilicus is cicatrized 
 and healed, the child has probably lived for three weeks. A zone of 
 redness around the insertion of the cord may exist previous to birth. 
 Redness and swelling (which may disappear after death) with suppura- 
 tion can only be found in a child which has lived for several days. 
 The drying and mummification of the cord may take place as well in 
 dead as in living children. It is possible for a child to die by hfemor- 
 rhage from a cut or torn cord, either before or after it has breathed. 
 The extremities may exhibit fracture of the bones. These may oc- 
 
36 THE METHOD OF MAKING 
 
 cur during intra-uterine life, from injuries to tlie womau or from un- 
 known causes; or may be produced by violence in delivery, or by injuries 
 after birth. 
 
 INTERNAL EXA-MINATION. 
 
 The Head.— The fontanelles and sutures should first be examined as 
 to their size and for penetrating wounds. An incision should then be 
 made through the scalp across the vertex, and the flaps turned backwards 
 and forwards, as in the adult. With a small knife, the edges of the 
 bones should be separated from the membranous sutures and the dura 
 mater, beginning low down in the frontal and going back into the 
 lambdoidal suture on either side. The bones are then drawn outward 
 and cut through around the skull, with strong scissors. The brain is 
 removed and examined as in the adult.' 
 
 Bfiusions of blood — cephalhsematoma — may be formed soon after 
 birth, between the pericranium and bone, or, more rarely, between the 
 dura mater and bone. Clots are also found between the dura mater and 
 skull; between the dura and pia mater; more rarely, in the substance 
 of the brain, as the result of protracted or instrumental deliveries, or 
 of injuries after birth. 
 
 The cranial bones may be malformed, or exhibit the lesions of rickets 
 or caries, or be indented, fissured, or fractured. These latter lesions may 
 be produced during intra-uterine life by injuries to the mother, by un- 
 known causes, by difficult deliveries, or by direct violence after birth. 
 
 In cases of chronic internal hydrocephalus in young children in 
 which the ventricles are much dilated and the brain substance thinned 
 over the vertex, the brain is very apt to be torn in removal, and the amount 
 of dilatation thus becomes difficult of determination. It is, therefore, 
 better in such cases to place a pail of water beneath the head, or even 
 immerse the latter in it, and remove the brain in the water. In this way, 
 it floats after removal supported on all sides. It may now be opened in 
 the water and the extent of the lesion determined at once and parts 
 saved for microscopical examination. 
 
 If it be desired to preserve the brain for demonstration of the lesion, 
 or for a museum specimen, it should be transferred unopened to a large 
 jar containing a mixture of equal parts of alcohol and water. A portion 
 of the ventricular fluid should now be removed with a syringe provided 
 with a small canula and replaced by strong alcohol. This may be done 
 by puncturing the ventricles from below. The fluid in the jar, as well 
 as in the ventricles, should be changed in forty-eight hours and then 
 gradually increased in strength until the organ becomes hard. The 
 brain may then be cut transversely across, when the degree of dilatation 
 of the ventricles, etc., will be revealed. The brain, of course, shrinks 
 
 ' Or an incision through the bones with a fine saw may be made as in the adult. 
 
POST-MOETEM EXAMINATIONS. 37 
 
 considerably by this process, but the relative proportions are ap- 
 proximately preserved. 
 
 The brain is normally much softer and pinker than in the adult, the 
 pia more delicate; both may be much congested or anaemic without 
 known cause. The ventricles contain very little serum. Malforma- 
 tions, apoplexies, hydrocephalus, simple and tubercular inflammatory 
 lesions are to be looked for. 
 
 Spinal Cord. — Extravasations of blood between the membranes of 
 the cord may occur from the same causes as those in the brain. Spina 
 bifida is the most frequent malformation. 
 
 The Thorax and Abdomen. — These are opened as in the adult. The 
 peritoneal cavity contains a very little clear serum. A red fluid may be 
 produced by decomposition. The peritoneum is often the seat of intra- 
 uterine inflammation. 
 
 The Diaphragm. — In still-born infants its convexity reaches to the 
 fourth or fifth rib. After respiration, it reaches a point between the 
 fourth and seventh rib. Its position is, however, so variable that it is 
 ■of little diagnostic importance. 
 
 The Thorax. — The thymus gland, at this period very large, occupies 
 the upper portion of the anterior mediastinum, covering the trachea 
 ■and large vessels. Its average weight is about 15.5 grm. (^ oz.). It is 
 usually about 5 ctm. (2 in.) long, 3.8 ctm. (l| in.) wide at its lower part, 
 ■and about . 63 to . 85 ctm. (J to \ in. ) in thickness. It may be hypertrophied 
 ■and compress the large vessels, or be inflamed and suppurating. 
 
 The heart lies more nearly in the median line than in the adult. It 
 weighs from 46 to 108 grm. (1^ to 3 J oz. ). The ventricular walls are of nearly 
 ■equal thickness. The pericardium contains very little serum. A con- 
 siderable quantity of red fluid may accumulate here, as a result of decom- 
 position. There may be small extravasations of blood beneath the peri- 
 cardium in still-born children and in those born alive. Pericarditis, with 
 effusion of serum and fibrin, and endocarditis, with consequent changes 
 in the valves, may exist before birth. Malformations and malpositions 
 of the heart cavities and large vessels are not infrequent. The time of 
 ■closure of the foramen ovale and the ductus arteriosus varies yery widely 
 in different cases. 
 
 Tlie pleural cavities contain very little serum; but decomposition 
 may lead to the accumulation of a considerable quantity of red fluid. 
 Small extravasations of blood in the sub-pleural tissue may be found in 
 children which have died before birth and after protracted labors. In- 
 flammation, with exudation of serum, fibrin, and pus, may exist befoi'e 
 birth. 
 
 The lungs in a still-born child are small, do not cover the heart, are 
 situated in the upper and posterior portion of the thorax, are of a dark- 
 red color, and of firm, liver-like consistence, and do not crepitate. In 
 
38 THE METHOD OF MAKTNiG 
 
 a child born alive, and which has respired freely, thelungs fill the thoracic 
 cavity, but do not cover the heart as much as in the adult; they are of a 
 light-red or pink color, and crepitate on pressure. If respiration has 
 been incompletely performed, we find various intermediate conditions 
 between the foetal and inflated states. 
 
 If any doubt exists as to respiration having taken place, it is cus- 
 tomary to employ the hydrostatic test. This is done by placing the 
 lungs, first together, then separately, and afterwards cut into small pieces, 
 in water. It is commonly said that, if they sink, the child has not- 
 breathed; if they float, it has. This test is not, however, a certain one. 
 Taylor says regarding it: 
 
 1. That the hydrostatic test can only show whether a child has or has. 
 not breathed, not whether it was born alive or dead. 
 
 2. That the lungs of children who have lived after birth may sink in 
 water, owing to their not having received air, or to their being in a dis- 
 eased condition. 
 
 3. That a child may live for some time with the lungs only partly in- 
 flated. 
 
 4. That a child may live for fwenty-four hours, when no part of its 
 lungs has been penetrated by air. 
 
 5. The sinking of the lungs is no proof that a child has been born 
 dead. 
 
 6. That the lungs of children which have not breathed, and have- 
 been born dead may float in water from putrefaction or artificial in- 
 flation. 
 
 The lesions of inflammation, and vesicular and sub-pleural em- 
 physema may be found in the lungs of new-born Children. 
 
 'She pharynx should be opened and examined for foreign bodies. 
 
 The larynx and trachea should be examined for the lesions of inflam- 
 mation and for injuries to the cartilages. 
 
 The thyroid gland weighs about 12 grm. ( 3 iii.). It may be so en- 
 larged as to interfere with respiration. 
 
 Tlie Aidomen. — The Mdneys are lobulated and proportionately 
 larger than in the adult. There may be ecchymoses on their surface; in- 
 flammation; deposits of uric acid and urates in the tubules of the- 
 pyramids; cystic dilatation of the tubules, sometimes reaching an 
 enormous size. There may be absence or retarded development of one- 
 kidney. Malformations and malpositions of the kidneys are of frequent 
 occurrence. 
 
 The supra-renal capsules are large. They may be dilated into large- 
 cysts filled with blood. 
 
 The spleen is large and firm. It may be abnormally enlarged, and its 
 surface is sometimes covered with fresh inflammatory exudations. 
 
 The Intestines. — In the small intestines, inflammation, and swelling' 
 
POST-MOETEM EXAMI17ATI0NS. 39 
 
 and pigmentation of the solitary and agminated follicles are sometimes 
 found. The large intestine usually contains meconium, but this may be 
 CYacuated before or during bii'th. The sigmoid flexure is not as marked 
 as in the adult. 
 
 The formation of gas in the stomach and intestines does not usually 
 take place until respiration is established. If decomposition has com- 
 menced, however, gas may be formed as a part of the process. 
 
 The liver is of a dark-red color, is large, and contains much blood. Its 
 size diminishes after respiration is established. The size is so variable, 
 before and after respiration, that it gives little information as to the 
 age of the child. Large extravasations of blood are sometimes found 
 beneath the capsule of the liver, vs^ithout known cause. A variety of 
 pathological conditions, fatty and waxy degeneration, gummy tumors, 
 etc, , may be found. 
 
 The lladder may be full or empty both in still-born children and in 
 those which have breathed. Dilatation and hypertrophy may exist dur- 
 ng intra-uterine life. 
 
 Generative Organs. — The external generative organs in both males 
 and females are more prominent than in adults. The ovaries are high 
 up in the pelvis and large ; the cervix uteri is long; the body small and 
 lax, resting forward against the bladder. Phimosis in the male is the 
 normal condition. Malpositions and retarded development of the tes- 
 ticles should be noticed. It should be observed whether the anus is per- 
 forate. 
 
 The bones, in suspected cases, should be examined for the lesions of 
 inflammation, rickets, and syphilis. 
 
 Preservation. — The various foetal tissues may be preserved by the same 
 methods as are employed for those of the adult; but as they are very delicate 
 they should be handled with great care, and the preservative fluids changed with 
 sufficient frequency. 
 
40 GENERAL , MKTHODS OF PEESEEVIN& 
 
 GENERAL METHODS OF PEESERVIK"G 
 PATHOLOGICAL SPECIMENS AND PRE- 
 PARING THEM FOR STUDY. 
 
 It is not our purpose in this section to give a complete account of the 
 technical procedures required in the study of pathological specimens, 
 since the methods are for the most part identical with those employed in 
 the study of normal tissues, with which the student or practitioner is 
 presumably familiar before prosecuting pathological studies. We wish 
 simply to give a few brief hints as to the general methods which we have 
 found most useful. Additional details will be found in parts of the book 
 dealing with special tissues and organs. 
 
 The Study of Fresli Tissues.- — Although for the most part the con- 
 ditions for the minute study of tissues are more favorable after they have 
 been hardened in some preservative agent, it is yet in many cases very 
 important to examine them in the fresh condition. For this purpose 
 they may be teased apart in aone-half-per-cent solution of sodium chloride 
 and mounted and studied in the same. The same solution may be used 
 for studying semifluid substances, such as exudations from the mucous 
 membranes, pus cells, etc. These preparations are not suitable for per- 
 manent mounting, as they do not keep well. For staining the elements 
 of fresh tissues, particularly the nuclei, a one-per-cent solution of methyl 
 green or Bismark brown in a mixture of 2 pts. alcohol and 98 pts. 
 water may be used. 
 
 Thin sections of fresh tissues may be prepared by the use of some of 
 the forms of the freezing microtome. Thp freezing microtome devised 
 by Thoma and made by Jung, of Heidelberg, is simple, cheap, and effect- 
 ive. 
 
 Decalcifying. — Bones which are the seat of lesions, or calciBed tissues 
 must be freed from lime salts before thin sections can be made from them. 
 This is best accomplished by the use of a saturated aqueous solution of 
 picric acid. The bone or other tissue should be cut into small pieces, not 
 larger than a cubic centimetre, and suspended by a thread in a large 
 quantity of the fluid, which should have an excess of picric acid crystals 
 at the bottom, and should be frequently shaken. Considerable time is 
 required for decalcification by this method, but the results are better than 
 by any other. 
 
 If it be necessary to decalcify more rapidly, chromic acid may be used 
 at first and the process completed by nitric acid. The small pieces of 
 
PATHOLOGICAL SPECIMENS. 41 
 
 bone are suspended at first in a ^-per-cent aqueous solution of chromic 
 acid. After two or three days the strength of the solution is increased 
 to ^-per-cent and after three days to |-per-cent. After another week, 
 the fluid should be changed and 1 per cent of nitric acid should be added. 
 This fluid should be renewed every three days until the decalcification is 
 complete, which may be determined by passing a fine needle through the 
 specimen. The specimen should now be thoroughly soaked in water to 
 remove all traces of the acid, and after lying for a day or two in strong 
 alcohol is ready for embedding and section-cutting. 
 
 Hardening and Preservation. — In the majority of cases, pathological 
 specimens are best hardened first in MiiUer's fluid and the process com- 
 pleted by alcohol. Miiller's fluid is made by the following formula: 
 
 Potassium Bichromate 3 parts 
 
 Sulphate , , , . . . 1 " 
 
 Water 100 " 
 
 The specimens, which should be cut into small pieces, not more than one 
 or two cm. square, are placed in a large quantity of the fluid, at least 
 ten times the bulk of the specimen, and allowed to remain for two or 
 three weeks. The fluid should be changed after a couple of days and 
 again before the hardening is completed. Some specimens, such as brain 
 tissue, may require a longer time. In all cases, however, the hardening 
 process may be greatly hastened by keeping the fluid at a temperature of 
 about 35° C. The development of bacteria in the fluid may be pre- 
 vented by putting a small piece of gum camphor into it. In this way 
 tissues may be hardened in Miiller's fluid in from four to eight days. 
 After the specimens have acquired considerable consistency or have 
 been in the fluid for the proper time, they are removed from the fluid and 
 soaked for from twenty-four to forty-eight hours in water, which should 
 be frequently changed. They are then placed in equal parts of alcohol 
 and water for forty-eight hours, and then in strong alcohol, by means of 
 which the hardening is completed. 
 
 Chromic Acid Mixture. — For many purposes a very excellent harden- 
 ing may be obtained by using a mixture of \ per cent aqueous solution 
 of chromic acid 2 parts, and alcohol 1 part. This fluid, like all others, 
 should be frequently changed, and the hardening may be finally com- 
 pleted with alcohol. This is commonly spoken of simply as the chromic 
 acid mixture. 
 
 If the specimens are not in a good state of preservation, they will be 
 best preserved by putting them at once into strong alcohol, which may 
 be changed in two or three days. 
 
 Although the above is the routine method of hardening tissues, de- 
 partures from it are occasionally desirable in the preparation of different 
 organs or for the accomplishment of special ends. Thus, in some cases. 
 
42 GENEEAL METHODS OF PEESEEVING 
 
 as in the kidneys for example, the preservative fluids are brought into- 
 more direct and immediate contact witli the tissue elements if they are- 
 injected under low pressure directly into the blood-vessels. Or by means- 
 of an hypodermic syringe the fluids may be thrown directly into the in- 
 terstices of the tissue by thrusting the needle into them and slowly in- 
 jecting the preservative agent. This is called interstitial injection. 
 
 Osmic Acid is of great value for the hardening of small portions of 
 delicate tissues, since it serves to fix the elements in a nearly normal con- 
 dition and stains them of a brown or black color. It is generally used 
 inone-per-eent aqueous solution, the tissues being placed in it when quite 
 fresh and allowed to remain for twenty-four hours. They are now washed 
 in water and may be preserved in a mixture of equal parts of glycerin, 
 alcohol, and water. Such preparations are best adapted for teasing or 
 isolation by other methods than section cutting. If it is desired to make 
 sections of solid tissues preserved in osmic acid, the latter should be in- 
 troduced by interstitial injection, and the fragment immersed in the acid 
 for twenty-four hours, and then removed, washed and placed in strong 
 alcohol. Instead of using the one per cent osmic acid pure, very good 
 results are obtained by diluting it with an equal volume each of water 
 and strong alcohol. This is in many cases preferable, since the tissues 
 are not stained so dark by the acid, and are more readily preserved sub- 
 sequently in alcohol. 
 
 Pathological specimens which occur, or are isolated in the form of 
 membranes should be stretched with pins on a piece of wood or flat cork 
 before being immersed in the preservative fluids. 
 
 Minute formed elements, such as occur in exudations from the mucous 
 membranes ; in cyst fluids ; renal casts, etc., may be preserved by allow- 
 ing them to settle, decanting as much of the fluid as possible, and then 
 adding a considerable quantity of Muller's fluid, which after a few days 
 should be decanted and replaced by water. The latter should be renewed 
 by decantation several times, and finally the sediment may be preserved 
 in a mixture of equal parts of glycerin, water, and saturated aqueous 
 solution of picric acid. 
 
 Emiedding and Section Gutting. — Some dense tissues, after being 
 well hardened, are sufficiently solid to permit of thin sections being made 
 from them without further preparation, but in most cases very thin 
 sections cannot be prepared without filling the interstices of the tissue 
 with some embedding material which gives it greater consistency, and 
 holds the tissue elements firmly in their natural relations to one another 
 while the section is being made. Cacao butter, wax, paraffin, and vari- 
 ous other substances have been largely used for this purpose, and are 
 very useful ; but the more recently employed celloidin is by far the most 
 valuable material, and may be used in nearly all cases. 
 
 Celloidin, anon-explosive purified form of gun cotton, is best obtained 
 
PATHOLOGICAL SPECIMENS. 43 
 
 in the form of thin shavings/ since it is most easily dissolred in this 
 form. A strong solution is made in equal parts of sulphuric ether and 
 alcohol. The solution should have the consistency of thick molasses. 
 The specimen having been soaked for twenty-four hours in a mixture of 
 equal parts of alcohol and ether, is placed in the celloidin solution where it 
 remains until permeated by it. This will ordinarily occur, if the speci- 
 men be of moderate size, in from twelve to twenty-four hours. For this 
 preliminary soaking the celloidin solution may be alittle thinner than above 
 mentioned. If the specimen be small and requires but little support, it 
 may now be laid directly on the end of a small cork, and a few drops of 
 celloidin poured around.it. In most cases, however, it is better to make 
 a small paper box in which the specimen is placed in a proper position, 
 and the celloidin poured in around it so as to completely inclose it. In 
 either case, a considerable quantity of celloidin should be poured around 
 the specimen, since the celloidin shrinks considerably in hardening. If 
 sections are to be cut with the microtome, the paper box should be made 
 by winding a strip of filter paper around the end of a straight cork, 
 allowing it to project for a suflBcient distance beyond the end. The 
 paper is held in place by tying a thread around it. We have thus a cy- 
 lindrical box with a cork bottom which projects below it. It is better 
 to use filter paper than sized paper, because the hardening of the celloidin 
 takes place more readily through it. 
 
 After the specimen, either free on the end of the cork or in its box, 
 is surrounded by celloidin, it should be allowed to stand for a short time 
 exposed to the air, so that it may harden on the outside by the evapora- 
 tion of the ether. If the temperature be high, the too rapid evaporation 
 of the ether will cause bubbles to appear in the mass. This should be 
 avoided by covering the specimen with a bell-jar. After the celloidin mass 
 has acquired sufiBcient hardness on the outside to keep its shape, the 
 whole should be immersed in a mixture of equal parts of alcohol and 
 water, in which the celloidin will harden and acquire a sufficient con- 
 sistency for cutting in a few hours. "When this is accomplished, the 
 paper may be stripped off, and the specimen is ready for section cutting. 
 A little practice will teach the operator of what consistency to make the 
 celloidin solution, how long to expose to the air, etc. 
 
 After the sections have been cut, they may be stained in the usual 
 way (see below), and mounted in glycerin or balsam. If mounted in 
 balsam, the oil of cloves, which is ordinarily used for clearing up the 
 sections, will dissolve the celloidin. For some tissues this does no harm, 
 since they are firm enough to hold together even in thin sections, but in 
 handling friable and delicate tissues it is well to keep the celloidin in 
 
 ' It may be obtained from Messrs. Bachrachand Bro., cor. Eutaw and Lexing- 
 ton Streets, Baltimore, Md., or from Meyrowitz Bros., New York. 
 
44 GENEEAL METHODS OF PEESEEVING 
 
 place, mounting it with the specimen, with tlie study of which it does not 
 interfere. This may be accomplished by using the white oil of thyme 
 instead of oil of cloves for clearing. 
 
 The uncut portion of tissue may be preserved, embedded in celloidin, 
 by keeping it in eighty-per-cent alcohol. 
 
 Section Cutting may be done by the free hand with a razor ground 
 flat on the lower side, but better sections can be obtained by means of a 
 microtome. One of the most useful of these is Thoma's which is made 
 of three sizes, the intermediate or the larger one being the more useful. 
 These instruments are made by E. Jung, Heidelberg, and may be obtained 
 of the Prang Educational Co., 7 Park street, Boston, Mass., or of 
 Meyrowitz Bros., cor. Fourth avenue and 23d street, E"ew York. 
 
 Metliods of Staining. — Sections of hardened tissues may be stained 
 for microscopical study in a variety of ways, but for routine work the 
 double staining with hematoxyUn and eosin is most generally useful and 
 applicable to nearly all cases. 
 
 The solution of hematoxylin is prepared as follows: To make 600 c.c. 
 of the solution, take.400 c.c. saturated solution of ammonia alum, and 
 add to this 4 grm. crystallized hematoxylin (Merck's) dissolved in 25 c.c. 
 strong alcohol. This is exposed to the light in an unstoppered bottle 
 for three or four days, when the color will gradually change from a dirty 
 red to a deep bluish purple color. The solution is now filtered and 100 
 c.c. each of glycerin and Hasting's wood naphtha are added.- After 
 standing for a day or two, the solution is filtered, allowed to stand for 
 another day and again filtered, and this is repeated until a sediment no 
 longer forms in the fluid. 
 
 The solution is now ready for staining, and should be considerably 
 diluted with water as it is used, the best results being obtained by dilut- 
 •ing the fluid with from ten to twenty times its bulk, of water. The 
 sections are placed in the fluid and allowed to remain until they have 
 acquired a distinct purple color, which persists after rinsing in water. 
 They are now placed for a moment in a dilute alcoholic solution of eosin, 
 and then mounted in glycerin which has been colored lightly with an 
 alcoholic solution of eosin. In this way the nuclei of the cells will be 
 stained of a purple color; while the cell bodies, and to a certain extent the 
 intercellular substance, will be colored a light rose-red. 
 
 If specimens are to be mounted in Canada balsam, they are stained 
 with hematoxylin as before, and the eosin staining is done by tinging 
 with eosin the alcohol with which the final dehydration of the specimen 
 is accomplished. 
 
 Methods of Preserving Specimens for Gross Demonstration and for 
 Museiims. — When specimens of diseased tissues or organs are to be pre- 
 served entire for exhibition in jars in a museum, it suffices in most cases, 
 after removing superfluous parts and making the requisite dissection, to 
 
PATHOLOGICAL 8PECIMBNS. 45 
 
 suspend them in proper position in jars containing thirty per cent alco- 
 hol. The alcohol should be changed as often is it becomes discolored by 
 blood, and the specimens may be finally preserved in forty per cent alco- 
 hol. It is desirable that specimens which are to be examined without 
 removal from the jars should be placed in proper position before the 
 alcohol is added, since when they are once hardened it is usually difficult 
 to place them in good positions again ; but this may be in most cases 
 deferred for a day or two, until a part of the blood is soaked out of them 
 by the first dilute alcohol. 
 
 Cysts, such as ecchinococcus cysts, small embryos in their membranes, 
 cystic kidneys, etc., may be preserved in a nearly natural condition by 
 placing them in a five-per-cent aqueous solution of chloral hydrate, and 
 after a week replacing this by a ten-per-cent solution of the same, in 
 which they may be permanently preserved. 
 
 If it be desired to preserve the natural color of specimens, this may be 
 partially done by placing them in Wickersheimer's fluid, one of the for- 
 mula for which is as follows: 
 
 Arsenious acid. 
 Sodium chloride. 
 
 For injecting. 
 16 grms. 
 80 " 
 
 For immersing. 
 12 grms. 
 60 " 
 
 Potassium sulphate. 
 
 200 " 
 
 150 " 
 
 Potassium nitrate. 
 
 25 " 
 
 18 " 
 
 Potassium carbonate. 
 
 20 " 
 
 15 " 
 
 G-lycerin, 
 
 Wood-naphtha, 
 
 Water, 
 
 4 litres. 
 
 a a 
 
 10 " 
 
 4 litres. 
 10 " 
 
 The fluid may be used for injecting the vessels or for soaking the tissues, 
 or both; the object being to bring the fluid into as direct contact with 
 the tissues as possible. The attempt to preserve the natural appearance 
 of specimens by this method is never entirely successful, but it is useful 
 in many cases, particularly when it is desired to keep specimens for a 
 few days for demonstration. 
 
 We would most urgently commend to the reader the importance of 
 putting pathological specimens which are to be hardened and subse- 
 quently examined microscopically, at the earliest possible moment into 
 the preservative fluids, which should always be abundant. And further- 
 more, when specimens are large, it is Tery desirable to cut them open, so 
 that the fluids may come into direct contact with the tissues. It should 
 be borne in mind that immediately after death or the removal of parts from 
 the body, especially in warm weather, changes commence in the tissues 
 and progress very rapidly, so that in some cases a few hours or even a 
 few moments delay, "will not only render subsequent microscopical exam- 
 inations difficult and unsatisfactory, but may lead to serious errors. As 
 
46 PEESEETING PATHOLOGICAL SPECIMENS. 
 
 above stated, Miiller's fluid or alcohol are the most generally useful 
 agents. Carbolic acid, glycerin, and usually chloral, should be avoided, 
 and the not uncommon practice of wrapping a specimen in a cloth soaked 
 in alcohol or carbolic acid, and permitting it to remain in this for hours 
 or days, is of no use whatever in preserving specimens of which microsco- 
 pical examinations are to be made. Almost equally useless is the too 
 common practice of placing a specimen in a bottle which it nearly fills, 
 and pouring a little preservative fluid around it. Not only should the 
 proper fluid be used, but it should be abundant, and the specimen so 
 prepared and arranged that it may come into direct contact with it. 
 
PART II. 
 
 MORBID CHANGES IIsT THE CIEOULATIOIvr 
 OF THE BLOOD. 
 
 CHAI^GES 11^ THE COMPOSITIOI^ OF THE 
 
 BLOOD. 
 
 DEGEI^^ERATIOI^S. 
 AI^IMAL PAEASITES Al^D BACTERIA. 
 
 Il^FLAMMATIOE". 
 
 TUMORS. 
 
MOEBID CHANGES 11^ THE CIEOULATION 
 OF THE BLOOD. 
 
 HTPERiEMiA and Anemia. — -There is an important series of changes 
 in the character of the circulation during life, which may, when death 
 ensues, either alter considerably in appearance or disappear altogether. 
 Among the more important of these changes are hyper cemia — excess of 
 blood in a part; and anmmia — deficiency of blood in a part. These con- 
 ditions and the causes which lead to them will not be described in detail 
 in this book, which has chiefly to do with alterations of the tissue which 
 persist and may be studied after death. Tissues which have been the 
 seat of a temporary, and sometimes of a prolonged hypersemia, may show 
 to the naked eye nothing abnormal after death, or they may look redder 
 than normal, tliey may be CBdematons, and more blood than usual may 
 flow from them when incised. On microscopical examination, the blood- 
 vessels may be normal in appearance, or more or less distended with 
 blood. Long-continued hypersemia may lead to htemorrhage and transu- 
 dation, to an hypertrophy of tissue, or to an atrophy of tissue through 
 pressure, or even to death of tissue. 
 
 The paleness which is characteristic of ancemic tissues may not be 
 evident after death. Ansemia may lead to no recognizable microscopical 
 changes. On the other hand, if long-continued, it may induce atrophy 
 and fatty degeneration, and, if excessive, may lead to death of tissue. 
 
 HiEMOKRHAGE AN"D TEANSLDATION. 
 
 Hmmorrhage is an escape of blood from the heart or vessels. It may 
 occur from a rupture of the walls of tlie vessels, and is then called 
 hsemorrhage by rhexis. The rupture may be occasioned by injury, by 
 some disease of the walls of the vessels which renders them too weak to 
 resist the blood pressure from within, or it may occur from the blood 
 pressure in the thin and incompletely developed walls of new-formed ves- 
 sels in granulation tissue, tumors, etc. 
 
 Under other conditions, without recognizable changes in the walls of 
 the vessels, all the elements of the blood mav become extravasated by 
 4 
 
50 MOEBID CHAJ^GES m THE 
 
 passing without rapture through the walls of the vessels. This is called 
 haamorrhage by diapedesis. These hemorrhages are usually small, but 
 may be very extensive. They usually occur in the smaller veins and 
 capillaries, the cells and fluids of the blood passing out through the 
 cement substance between the endothelial cells. Although no marked 
 morphological changes have as yet been detected which explain this 
 extravasation, it is probable that some change in the nutrition of the 
 walls does occur which renders them more permeable. Haemorrhage by 
 diapedesis is apt to occur as a result of venous congestion, or when the 
 flow of blood in the smaller vessels has been suspended for some time; 
 or it may result from the action of some poison, or from an injury not 
 leading to rupture ; or it may occur in incompletely developed blood; 
 vessels, in tumors and other new-formed tissues. 
 
 In the extravasation of blood by diapedesis, the white blood-cells may 
 pass through the walls of the vessels, partly at least in virtue of their 
 amceboid movements; the red cells, on the other hand, having no power 
 of spontaneous movement, are, according to Arnold, carried passively 
 through the walls by minute currents of fluid which, under the changed 
 condition, stream in increased force and volume through the endothelial 
 cement substance into the lymph spaces outside. 
 
 The altered condition of the blood-vessels leading to haemorrhage may 
 be local or general, and in the latter case it may either be congenital, as 
 in some cases of the hsemorrhagic diathesis, or it may be the result of 
 some general disease, as scurvy, purpura, etc. The presence of bacteria 
 in the vessels, as in malignant endocarditis, and in haemophilia neona- 
 torum, is believed in some cases to produce changes in the walls of the 
 vessels leading to extravasation. 
 
 Very smull hemorrhages are called petechim or ecchymoses. A com- 
 plete infiltration of a circumscribed portion of tissue with blood is called 
 a hcBinorrliacjic infarction. A collection of blood in a tumor-like mass is 
 called a hcematoma. 
 
 Tlie extravasated blood in the tissues usually soon coagulates, although 
 exceptionally it remains fluid for a long time. A certain number of the 
 white blood-cells may wander into adjacent lymph-vessels, or they may 
 remain entangled with the red cells in the meshes of the fibrin. The 
 fluid is usually soon absorbed ; the fibrin and a portion of the white 
 blood-cells disintegrate and are absorbed. The red blood-cells soon give up 
 their hfemoglobin, which decomposes, and may be carried away or be de- 
 posited either in cells or in the intercellular substance at or near the seat 
 of the hsemorrhage, either in the form of yellow or brown granules or as 
 crystals of haematoidin. Sometimes all trace of extravasations of blood 
 in the tissues disappears, but frequently their seat is indicated for a 
 long time by a greater or less amount of pigment, or by new-formed con- 
 nective tissue. Occasionally the blood-mass, in a more or less degene- 
 
OIECULATION OF THE BLOOD. 51 
 
 rated condition, becomes encapsulated by connective tissue forming a 
 cyst. 
 
 Transudation is the passage through the walls of the blood-vessels 
 into the lymph-spaces outside, of fluid from the blood, with little or no 
 admixture of its cellular elements. This occurs constantly, to a certain 
 extent, under normal conditions, and forms the commencement of the 
 lymph circulation. But when the amount of fluid passing through the 
 walls of the blood-vessels is increased, or its outflow into the larger lymph 
 trunks is hindered so that it accumulates in undue quantity in the inter- 
 stices and lymph channels of the tissues, the condition is pathological, 
 and is called transudation. An accumulation of transuded fluid in the 
 interstices of the tissues is called cedema; in the serous cavities, dropsy. 
 Its occurrence is usually dependent upon some hindrance to the venous 
 circulation or upon some change in the condition of the blood, which 
 may become more watery, or lead to alterations in the walls of the blood- 
 vessels. A simple interference to the outflow of lymph does not usually 
 alone suflBce to induce transudation, although it may favor its occurrence. 
 Tl:e transuded fluid is usually transparent and colorless or yellowish ; it 
 contains the same salts as the blood plasma, but less albumen. It may 
 contain fat, mucin, urea, biliary acids, coloring matter of the bile ; fibrino- 
 gen is usually present in variable quantity, and rarely fibrin. It may 
 contain endothelial cells from the lymph spaces, and a variable number 
 of red and white blood-cells. The amount of fluid which may accumulate 
 in the tissues varies greatly, depending upon whether they are loose or 
 dense in texture. The fibres and cells of loose tissues may be crowded 
 widely apart, the cells are apt to be more granular than normal, and may 
 be atrophied. Transudations occurring in inflammation usually contain 
 a considerable number of white blood-cells and more or less fibrin, and 
 differ in this from the non-inflammatory transudations; but there is no 
 sharp distinction in some cases between them. The inflammatory transu- 
 dations are often called exudations. 
 
 THROMBOSIS AlfD EMBOLISM. 
 
 Thrombosis. — Thrombosis is a coagulation of blood in the heart or 
 vessels during life. The coagulum is called a thrombus. Thrombi may 
 lie against the wall of a vessel, only partially filling tlie lumen, and are 
 then called ^jamte^ thrombi ; or they may entirely fill the vessel, and 
 are then called an obliterating thrombi. 
 
 Thrombi may occur as the result of an injury to the wall of a vessel, 
 or may follow its compression or dilatation; they may result from some 
 alteration of the wall of the vessel by disease, or by the retardation of 
 the circulation. So long as the endothelial linings of the vessels are 
 intact, simple retardation of the circulation does not usually alone suffice 
 to induce coagulation; but changes in the endothelium from a great 
 
52 MOEBm CHANGES IN THE 
 
 variety of causes, such as inflammation, degeneration, atheroma, calcifi- 
 cation, and the presence of tumors and foreign bodies, favor its occur- 
 rence. 
 
 Thrombi may be composed of fibrin and of red and white blood-cells, 
 intermingled in about the same proportion as in an ordinary extravascu- 
 lar blood-clot. These are called red thrombi, and usually occur from 
 some sudden stoppage of the circulation. Other thrombi, usually such 
 as form while the blood is in motion, may consist almost entirely of 
 white blood-cells with a little fibrin; these are called white thrombi. 
 Red thrombi, when decolorized by changes in the blood-pigment, may 
 somewhat resemble genuine white thrombi. Mixed thrombi are usually 
 lamellated, and contain varying iDroportions of fibrin and red and white 
 blood-cells. 
 
 The changes which occur in the thrombus after its formation may be 
 either in the direction of degeneration or organization. In some cases 
 they seem to undergo a simple shrinkage and decolorization, and 
 to become infiltrated with salts of lime, forming the so-C2iMed. phleboUths 
 or: vein-stones ; in other cases, they may soften and disintegrate. Cer- 
 tain thrombi contain bacteria or other infectious material, and on soften- 
 ing of the thrombus, these may be carried into the circulation, produc- 
 ing very disastrous results. Finally, the thrombus may be replaced by a 
 new formation of vascular connective-tissue, itself disappearing as the 
 new tissue is formed. This is called organization of the thrombus, but 
 in reality the new connective tissue is produced, in large measure at 
 least, not from the cells of the thrombus itself, but from the cells of the 
 walls of the affected vessel, from whose vasa-vasorum the new blood-ves- 
 sels of the thrombus also arise. It is possible, however, that the white 
 blood-cells of the thrombus may contribute somewhat to the formation of 
 the new tissue. In this way the vessel may be completely and permanently 
 occluded, or more rarely, a channel may be re-established through the 
 new connective-tissue mass. 
 
 Thrombi in veins may lead to hypersemia and oedema; in arteries, to 
 an anaemia whose significance will vary greatly, depending upon the sit- 
 uation of the occluded vessel. 
 
 Emiolism. — This is the stoppage of a blood-vessel by the arrest in its 
 lumen of some material carried along in the circulating blood. The sub- 
 stance causing the stoppage is called an embolus. This may be composed 
 of a great variety of substances. The most common emboli are de- 
 tached portions of thrombi, and these may have all the variety of struc- 
 ture which thrombi present. Masses of bacteria or other parasites, frag- 
 ments of the heart valves and of tumors, droplets of fat from the medulla 
 of fractured bones, masses of pigment, bubbles of air, etc., may form 
 emboli. Embolism is, in a majority of cases, confined to the arteries 
 and to the branches of the portal vein. 
 
CIEOtTLiTION OF THE BLOOD. 53 
 
 The primary effect of the stoppage of an arterial trunk, is of course, 
 to largely deprive the region of the body to which its branches are dis- 
 tributed of its normal supply of blood. If the branches of the occluded 
 artery form anastomoses with other arteries beyond the point of stop- 
 page, a collateral circulation may be established, and the embolus do no 
 harm. If, however, the occluded vessel be a so-called termitial artery, that 
 is, one whose branches do not form anastomoses with other arteries, the 
 result of the embolism is quite different. "When a terminal artery is oc- 
 cluded by an embolus, the tissue of the affected region usually dies, and 
 there may be an extravasation of blood by diapedesis, leading to the 
 formation of a dark-red solidified area called an hwmorrhagic infarction.' 
 The area of infarction corresponds to the region supplied with blood by 
 the occluded vessel, and is usually more pr less wedge-shaped. 
 
 After a time, the infarction becomes decolorized; inflammatory 
 changes may occur in its periphery, the blood and involved tissues may 
 undergo degeneration and be absorbed, and finally the seat of the infarc- 
 tion may be indicated only by a mass of cicatricial tissue, which fre- 
 quently contains more or less pigment. 
 
 In another class of cases, instead of an extravasation of blood in the 
 affected region, the tissue is simply deprived of nourishment and under- 
 goes necrosis. The affected area is then usually light in color, and is 
 called a zvhite infarction. Inflammatoi-y changes may occur in its peri- 
 phery, and a new connective-tissue capsule form around it, and the 
 dead mass may thus persist for some time, or be gradually absorbed and 
 replaced by cicatricial tissue. The scope of this book does not permit us 
 to consider the somewhat complicated and often obscure reasons why in 
 one case we have hsemorrhagic, in another white infarction, as a result of 
 embolus. 
 
 If the embolic material consists of or contains infectious substances, 
 such as some forms of bacteria, in addition to the mechanical effects of 
 simple emboli, we may have gangrene, suppuration, and formation of 
 
 ' "When an embolus lodges in a terminal artery, and the circulation in the ter- 
 ritory supplied by its branches ceases, the pressure from tlie side of the artery is 
 reduced to zero; but, on the other hand, according to Cohnheim, the venous pres- 
 sure now makes itself felt in a backward direction, and the capillaries and small 
 veins in the affected region become crowded with blood. This blood is stagnant, 
 however, and the walls of the small vessels being deprived of their usual nour- 
 ishment, undergo, it is believed, degenerative changes, which favor the occur- 
 rence of extensive diapedesis. Thus, in the hEcmorrhagic infarction, not only the 
 blood-vessels, but the extravascular tissues also are crowded with stagnant blood. 
 The researches of Litten make it seem probable that, in most cases, the back 
 pressure in the region of infarction comes, not from the veins, or not from them 
 alone, but from adjacent arterial twigs, which communicate with the capillaries 
 of the affected region. 
 
54 MOEBIU CHABTGES IN THE CIECULATIOIT OF THE BLOOD. 
 
 abscesses, ebc, as the result of the local action of the infectious mate- 
 rial, even though this may be present in very small amount. 
 
 The organs in wliich embolic infarctions most frequently occur are 
 the spleen, kidney, brain, lungs; less frequently the retina, liver, and 
 small intestines. Hemorrhagic infarctions are not liable to occur 
 in the liver from emboli in the branches of the portal vein, on account 
 of the blood-supply which may come to the affected region through the 
 branches of the hepatic artery. On the other hand, embolic abscesses 
 from infectious emboli are of not infrequent occurrence here. Hsemor- 
 rhagio infarctions may occur exceptionally in regions not furnished with 
 terminal arteries, as in the small intestines. 
 
CHAI^GES 11^ THE OOMPOSITIOI^ OF THE 
 
 BLOOD. 
 
 Only tlie more common morphological alterations of the blood will 
 he considered here, and particularly such as may be appreciable after 
 death. 
 
 The coagulnhility of the Mood and the characters of the resulting clot 
 vary widely, depending partly upon the composition of the blood and 
 partly upon the conditions under which the coagulation occurs. There 
 may be very little coagulation of the blood in death from the ex- 
 clusion of air from the lungs, or from diseases and accidents which in 
 ■any way interfere with the aeration of the blood, and permit the accu- 
 mulation of carbonic acid within it. Thus, in death from strangulation 
 ■or drowning, many chronic diseases, scurvy, and under many conditions 
 which we do not understand, the blood may remain fluid, or nearly so, 
 After death. On the other hand, in a variety of acute inflammatory dis- 
 ■eases, such as rheumatism, pneumonia, etc., very voluminous clots may 
 be formed, although this is by no means constantly the case. The fact 
 that large clots form after death is not conclusive evidence that an un- 
 due amount of fibrin-forming elements were present in the blood, nor 
 does the absence of marked coagulation prove a diminution in tlie blood 
 of fibrin-forming elements. 
 
 The blood may be very thick from the removal of its fluid constitu- 
 ents, in diseases associated with excessive serous discharges from the in- 
 testines. This is especially marked in some cases of cholera, and is called 
 ■anliydrmmia. On the other hand, the blood may contain a large amount 
 of water in proportion to its solid ingredients — albumin and blgod-cells. 
 This is called hydrcemia, and occurs in a variety of diseases of the heart, 
 kidneys, liver, and lungs. In ansemia, etc., the blood looks more or less 
 watery. 
 
 There may be a diminution in the number of the red blood-cells and 
 in their haemoglobin content, as well as changes in their sliape. This 
 may be seen in various forms of anrnmia. The red blqod-cells may be 
 unduly pale from a decrease in the amount of hemoglobin. Varying 
 numbers of spheroidal or irregular shaped bodies, smaller than the red 
 
56 MOEBID CHAITGES IN THE 
 
 blood-cells but having the same color, may be found, particularly in 
 marked cases of jiernicions anaemia. These are called mi'c?-oc?/^«s and may 
 be ill-developed red blood-cells or red blood-cells in a degenerated con- 
 dition. The number of red blood-cells in extreme cases of ansemia may 
 be diminished to ^V of ^^''^ normal or to about 500,000 in the cubic milli- 
 metre. Under these conditions the white blood-cells may remain in nor- 
 mal proportion or they may be increased in number. Fatty degenera- 
 tion of the heart and blood-vessels, liver, kidney, etc., and capillary 
 hsemorrhages and a change of the yellow into red marrow are frequent 
 accompaniments of excessive anasmia. This latter change is largely due 
 to the disappearance of the fat. Nucleated red blood-cells are also ob- 
 served in the red marrow. 
 
 Leucocytosifi signifies a temporary increase in the number of white- 
 blood-cells, and this is usually of moderate amount. It occurs in a 
 variety of acute inflammatory diseases, in profuse suppuration in any 
 part of the body, often in connection with cancerous growths, tuber- 
 culosis, etc., and may, as above stated, be associated with anaemia. 
 
 LeuJccemia (Leucocythcemia). — This disease is characterized by a 
 persistent, progressive, and often enormous increase in the number of 
 the white blood-cells. The blood is pale in well-marked cases, but not 
 watery, and the number of white blood-cells may in extreme cases equal 
 or even exceed that of the red. There are sometimes nucleated cells in 
 the blood, of irregular shape and larger than the leucocytes, and others 
 which are smaller. The origin of these cells is not yet certain, the leu- 
 cocytes are frequently in a condition of fatty degeneration. There may 
 be a decrease in the number of red blood-cells in leucocythEemia. There 
 are marked changes in the liver, spleen, and lymph glands, as well as in 
 the bone marrow, in leuksemia; the degree of involvement of the different 
 organs varying in diilerent cases (see leulcmmia, in section devoted to- 
 general diseases). 
 
 Most of the above-mentioned changes in the morphological characters 
 of the blood are better studied during life than after death, since the re- 
 distribution of its elements, owing to the clotting and the efllects of 
 gi-avity, render the obtaining of a pure sample very difficult or impossible,, 
 and the results of examination only in a very general way reliable. 
 
 Melaifcemia. — In this condition, the blood contains larger and smaller 
 irregular-shaped particles or masses of brown or black pigment. This 
 condition is most frequently the result of intermittent and remittent 
 fever, particularly the severer forms. It may be accompanied by ansemia 
 and leucocytosis. It does not occur in all cases of the above-named afEec- 
 tions. It may be transient in character. The pigment may be free, or 
 more usually is fticlosed in leucocytes. Under the same conditions, pig- 
 ment may be deposited in the liver, spleen, lymph glands, bone-marrow, 
 and blood-vessels. Owing to the deposit of pigment in the organs, they 
 
OOMPOSITIOK OF THE BLUOD. 5T 
 
 may assume a gray or slate color. The pigment is supposed to originate 
 in the decomposition of the hemoglobin. 
 
 Pigment which has been taken into the lungs from the air, such as 
 coal-dust, etc., may find its way into the blood either before or after de- 
 position in the bronchial or other lymph glands, and may be afterwards 
 deposited in the spleen and liver. 
 
 Foreign Bodies in the Blood. 
 
 Various bodies which do not belong there, aside from those above 
 mentioned, may find access to the vessels, and mingle with the blood. 
 Pus-cells may get into the blood from the opening of an abscess into the 
 vessel, or from some inflammatory change in its walls. Desquamated 
 endothelial cells from the vessel-walls, either in a condition of fatty de- 
 generation or in various stages of proliferation, may be mingled with the 
 normal blood elements; also tumor cells of various kinds, fragments of 
 disintegrating thrombi, portions of heart valves, etc. Crystals of biliru- 
 bin have been found in the blood in icterus. 
 
 Fat, in a moderate amount, is a normal ingredient of the blood dur- 
 ing digestion and in lactation. Under pathological conditions it may 
 occur in larger and smaller droplets. LijJcemia occurs as a result of 
 deficient oxidation, in diabetes, in drunkards, and in some cases of 
 dyspncea from various causes. The droplets are small and liable to escape 
 observation. 
 
 In many cases of injury, particularly in crushing fractures of the 
 bone, the fat of the marrow finds its way into the blood, and it may col- 
 lect in large drops in the vessels of the lungs, forming the so-called fat 
 emboli, or it may pass the lungs, and form emboli in other parts, as 
 the brain, kidneys, etc. The fat may be absorbed from the vessels, hav- 
 ing produced little or no disturbance; or in some cases it may produce 
 serious results by the stoppage of a large series of vessels in the lungs, 
 brain, or other parts of the body.' The fat may be best seen by cutting 
 sections of the fresh tissues with the freezing microtome and staining 
 them at once for twenty-four hours with one-per-cent acpeous solution of 
 osmic acid. They may then be mounted in glycerin. 
 
 Air in the Blood, as the result of an opening in the veins, is of occa- 
 sional occurrence. If the amount of air be small, it appears to be readily 
 absorbed, and does little or no harm. If, on the other hand, a large 
 quantity is admitted to the veins at once, it collects in the right side of 
 the heart from which the contractions of the organs are unable to force 
 it in any considerable quantity, and the supply of blood being thus cut 
 off from the lungs, death very quickly ensues. It is especially from 
 
 ' Consult for resume of this subject, with good bibliography, article by Park 
 on Fat Embolism.— New York Med. Jour., Aug. 16th, 1884. 
 
58 MOEBID CHANGES IN THE COMPOSITION OF THE BLOOD. 
 
 wounds of the veins of the neck and thorax that the accident is most 
 apt to occur. But it may be due to the introduction of air into the 
 uterine veins in intra-uterine injection, or in the removal of tumors.' 
 
 The occurrence of animal and vegetable parasites is considered more in 
 detail in parts of this book devoted to these organisms. It will suffice to 
 mention here that the more important of the animal parasites of the blood 
 are: the Filar ia sanguinis Iwminis; the Distoma licematoiium, and the 
 embryos of trichina and ecliinococcus which are of occasional, and usually 
 temporary occurrence. 
 
 Among the bacteria may be mentioned the anthrax iacillus, the 
 spirochwte Obermeyeri, the bacillus of typhoid fever, and various less 
 well-defined forms, chiefly micrococci, which occur in septicaemia and 
 other acute infectious diseases.^ 
 
 ' Consult: Couty, Etudes exp. sur rentree de Fair dans les veines, Paris, 1875, 
 for experiments and older literature; also later article by Couty, Arch. dePhj^sioI. 
 nor. et path., 2d ser., T. 4, p. 429, 1877. More recent consideration of the subject 
 in Archiv ftir klin. Medicin, Bd. 31, p. 441, 1883, by Jiirgensen. 
 
 ^ For literature and detailed consideration of morphological and other altera- 
 tions of the blood, consult Cohnheim, Vorlesungen tiber allgemeine Pathologie, 
 Bd. I., 8dEd., or Orth, Lehrbuch der speciellen pathologischen Anatomie, or 
 Birch-Hirschfeld, Lehrbuch der pathologischen Anatomie. 3d Ed., Bd. II. For 
 methods of blood examination for clinical purposes, consult Bizzozero, Hand- 
 buch der klinischen Mikroscopie, translation into German by Lustig and Bern- 
 heimer. 
 
 For method of blood-counting, apparatus, etc., consult Thoma and Lyon, Ueber 
 die Methode der Blutkorperzahlung, Virchow's Arch., Bd. 84, p. 131,1881. For 
 alterations in size under various diseased conditions consult article by Gram in 
 Fortschritte der Medicin, Bd. II., No. 3, Jan. 15th, 1884, which contains consid- 
 erable literature. 
 
DEGENERATITE CHANGES 11^ THE TISSUES. 
 
 Necrosis. — TSTecrosis is the death of acircamscribed portion of tissue. 
 It may be the result of insufficient nutrition from the cutting off of the 
 blood supply; or it may depend upon the action of destructive chemical 
 agents, extreme degrees of temperature, certain materials produced by 
 the life processes of some forms of bacteria; or it may be due to mechani- 
 cal injury. The appearances which dead tissues present under the mi- 
 croscope vary greatly. In some cases we have a simple and gradual dis- 
 integration and softening of the tissue, resulting in a mass of degenerated 
 cells and cell detritus, with more or less fluid and various chemical sub- 
 stances resulting from decomposition. The softening of the brain in 
 embolism is an example of simple necrotic softening. In some cases 
 the dead tissues simply gradually dry and shrivel and become hard and 
 dark-colored. 
 
 In another class of cases the dead tissuesare permeated by fluids, which 
 may be dark-red in color from the solution of coloring matter from the 
 blood, and contain bacteria which induce putrefaction with the produc- 
 tion of gases and various new chemical substances. The tissues become 
 swollen and granular and disintegrate; and finally the whole may form a 
 mass of irregular granules with fat droplets, various forms of crystals, 
 shreds of the more resistant kinds of tissue, and bacteria. 
 
 Coagulation necrosis. — If the supply of blood is shut off from a por- 
 tion of tissue which is surrounded by, or continuous with other tissue 
 in which the blood continues to circulate, there results a death and trans- 
 formation of a peculiar character. The composition of the cells of the 
 tissue is altered so that the cell bodies are shining and translucent, di- 
 minished in size, sometimes altered in shape, and the nuclei of the cells 
 disappear. This condition is often succeeded by cheesy degeneration. 
 The white infarctions of the spleen and kidneys, the areas of coagulation 
 necrosis in phthisis, and the epithelial cells in croupous inflammation of 
 the mucous membranes are the most common examples of this lesion. 
 
 If, for example in the spleen, one of the small arteries is plugged by 
 an embolus, a corresponding portion of the spleen becomes anaemic and 
 
60 DEGEMEEATIVE CHAIv^GES IN THE TISSUES. 
 
 appears as a white, wedge-shaped mass, sharply defined from the sur- 
 rounding splenic tissue. If sucli a white infarction has existed but a 
 short time, there is hardly any difference between the appearance of its 
 anatomical elements and those of the surrounding spleen, except that 
 they are differently affected by staining fluids. If the infarction is older, 
 the cells are small and shiny and their nuclei cannot be seen. 
 
 In croupous inflammations of mucous membranes covered by pave- 
 ment epithelium, the epithelial cells become shiny, the nuclei disappear, 
 and the shape of the cells is changed so that a number of them together 
 look like a net-work of coagulated fibrin. 
 
 Cheesy degeneration is the second stage, or the necrobiotic result of an 
 originally hyperplastic growth-process, and the cheesy substance is 
 nothing but the dead remains of broken-down tissue. In this necrobio- 
 sis both the newly-formed and the old parts die; the circulation stops, . 
 and the vessels disappear; the cells degenerate, partly by an incomplete 
 fatty metamorphoses, partly by a shrinkage from the loss of water. 
 Thus is formed the totally anaemic, dry, dense, and almost amorphous 
 mass (Virchow). 
 
 Parenchymatous Degeneratiooi (Cloudy swelling). — In this condi- 
 tion the cells of tissues and organs are swollen and filled with small albu- 
 minous granules which may be so abundant as to entirely conceal the 
 original cell structure. The granules disappear on treatment with acetic 
 acid, and are insoluble in ether. This degeneration may be present in 
 the parenchyma cells of any inflamed organ, but is most marked and 
 frequent in the liver, kidney, heart-muscle, and mucous membrane of 
 the gastro-intestinal canal. It may occur in infectious or severe febrile 
 diseases, after severe burns, and in poisoning with arsenic, phosphorus, or 
 mineral acids. The cells in a condition of parenchymatous degeneration 
 may regain their normal condition, or become fatty, or disintegrate. In 
 such organs as the liver, kidney, and heart, the gross appearances are often 
 very characteristic; the tissue is swollen and has a less translucent and 
 more dull and grayish look than under normal conditions. 
 
 The microscopical study of this lesion is best done in sections of the fresh 
 tissue made with the freezing microtome or in teased fresh tissue, in one-half- 
 per-cent salt solution. 
 
 Fatty Degeneration. — This is the conversion of the protoplasm of 
 cells into fat, which accumulates in the cell body. The fat is usually 
 present in the cell in very small particles or droplets, but these may 
 coalesce to form large drops. The protoplasm may even be almost 
 entirely replaced by the fat. 
 
 Fatty Infiltration of cells is a common occurrence under normal as 
 Avell as pathological conditions, but in this case the fat is believed to 
 originate outside of the cells and simply accumulate in them, causing a 
 passive atrophy of the protoplasm. In this way fatty infiltration is 
 
DEGENEEATIVE CHANGES IN THE TISSUES. 61 
 
 believed to differ essentially from fatty degeneration, but in many cases 
 a definite distinction between the two is impossible with our present 
 knowledge of the chemistry of cell life. In general the fat droplets are 
 larger in fatty infiltration than in fatty degeneration, yet to this there 
 are many exceptions. Fat granules and droplets are recognized in 
 cells by their strong refraction, by their solubility in alcohol and ether, 
 and their insolubility in acetic acid, and by the black color which they 
 assume when the fresh tissue is treated with osmic acid. Not infrequently 
 feathery clusters of delicate fat crystals occur within the cells. Patty 
 degenerated cells may break down and form an oily detritus, in which, 
 especially when much moisture is present, cholesterin crystals may be 
 formed by decomposition of the fat. 
 
 To the naked eye, organs in a condition of marked fatty degeneration 
 . are usually larger and softer than normal, have a grayish yellow color, or 
 are mottled with yellowish streaks or patches, and the normal markings 
 of cut surfaces are more or less obscured. 
 
 Fatty degeneration may be due to local or general disturbances of 
 nutrition, from a great variety of causes; disturbances which either 
 •directly affect the life processes of the cells themselves, or which produce 
 alterations in their nutritive supply. In addition to its local occurrence, 
 as a result of local disturbances of circulation, in the vicinity of inflam- 
 mations or in tumors, etc., it is apt to occur in the liver, heart-muscle, 
 and kidney in chronic exhausting diseases and in conditions and diseases 
 to which profound anaemia is incident, or as the result of the action of 
 certain poisons such as phosphorus and arsenic. Fatty degeneration is 
 as a rule, a more serious lesion than fatty infiltration. 
 
 Tissues in a condition of fatty degeneration or infiltration may be studied by 
 teasing, or cutting tlie fresh tissue with the freezing microtome and examining 
 unstained, or lightly stained with eosin, in one-half -per-oent salt solution. Or they 
 may be placed when fresh for twenty-four hours in one-per-cent solution of osmic 
 acid and then studied either after teasing or in sections, in glycerin. A prelimi- 
 nary hardening in Mtiller's fluid and afterwards in alcohol gives moderately good 
 results if the lesion is extensive. But it should be remembered that in tissues 
 which have been soaked in alcohol the fat is no longer present, its former seat 
 being indicated by clear spaces which are filled with the mounting medium. The 
 fat crystals, however, often persist after prolonged soaking in alcohol. 
 
 Amyloid Degeneration (Waxy or lardaceous degeneration). — This 
 is a process by which the basement substance of various forms of con- 
 nective tissue, and especially the walls of the blood-vessels, become swollen 
 arid thickened by their conversion into a translucent, firm, glassy, color- 
 less material, albuminous in character. This albuminous material may 
 be present in the tissues in such small amount as to be recognizable only 
 under the microscope, or it may be so abundant as to give a very char- 
 acteristic appearance to the tissue. Parts in which the lesion is marked 
 are usually larger and contain less blood and feel harder than normal 
 
62 DEGENEEATIVE CHANGES IN THE TISSUES. 
 
 and have a peculiar dull shining and translucent appearance which varies 
 in character, depending upon the extent and distribution of the degen- 
 erated areas and upon its association with other lesions, such as fatty 
 degeneration. It most frequently occurs in the smaller arteries and 
 capillaries whose lumen becomes encroached upon by the thickening of 
 the walls which the process involves. It is the media and intermedi- 
 ary layers of the intima which are earliest and most extensively affected. 
 The change also often occurs in the interstitial connective tissue and 
 membrane proprise of organs and in reticular connective tissue. It is 
 both asserted and denied that it may affect the parenchyma cells of organs. 
 We have not been able to find unmistakable evidence of its occurrence in 
 parenchyma cells. These, however, frequently undergo atrophy as the 
 result of pressure from the swollen degenerated tissue. 
 
 It is not yet known whether amyloid degeneration is due to a direct, 
 transformation of the tissue, or is an infiltration of the tissue by some 
 abnormal material formed elsewhere and brought to it, or derived from 
 the blood. 
 
 Amyloid degeneration occurs most frequently and abundantly in the 
 liver, spleen, kidneys, intestinal canal, and lymph glands ; but it may 
 occur, usually to a less marked degree, in other parts of the body ; in 
 the larger blood-vessels, in the interstitial tissue of the heart and mucous 
 membranes of the air passages, and in the generative organs. It may 
 occur locally, or appear in various parts of the body at once. It may 
 exist without any known cause, but it most frequently occurs in con- 
 nection with severe wasting diseases, particularly in those involving 
 chronic suppuration and ulceration, especially of the bones. It frequently 
 occurs in tuberculosis, syphilis, in the cachectic condition induced by 
 malignant tumors and is occasionally seen 'in severe malarial infection, 
 dysentery, and leuktemia. 
 
 For microscopical examination, the tissue, either fresh or after preservation, 
 should be cut into thin sections, and these deeply stained with one-per-cent aqueous 
 solution of methyl violet; the sections are washed in water and mounted in gly- 
 cerin. The differentiation between the amyloid and other parts is more distinct 
 if, after staining, the specimen be dipped for an instant in HCl and alcohol 1— 
 100, and then carefully rinsed, before niounting in glycerin. The degenerated 
 areas are thus stained rose red, while the normal tissue elements have a bluish 
 violet color. In some cases, for reasons which we do not know, the amyloid 
 substance does not show a well-marked reaction with methyl violet. Other ani- 
 lin dyes also differentiate amyloid substance from normal tissues. On treating 
 sections of amyloid tissue with solution of iodine, the degenerated parts acquire 
 a mahogany color. If they are then treated with sulphuric acid, the degenerated 
 portions acquire a greenish or blue color; but the latter reaction is not very re- 
 liable. 
 
 Corpora Amylacea are small spheroidal homogeneous or lamellated 
 bodies which assume a bluish color on treatment with solution of iodine 
 
DEGENEEATIVE OHAJSTGES IN THE TISSUES. 63 
 
 or iodine and sulphuric acid. They are frequently found in the acini 
 of the prostate gland, sometimes in large numbers; in the ependyma 
 of the ventricles of the brain, and in areas of sclerosis of the brain and 
 cord; also in extravasations of blood and in various other situations. They 
 may occur under normal as well as pathological conditions, and are ap- 
 parently of little importance. They seem to have nothing to do with 
 amyl6id degeneration, although they somewhat resemble its products. 
 Some of the tube-casts of the kidney resemble in many respects the cor- 
 pora amylacea. 
 
 Mucoid Degeneration may occur in cells or in intercellular substance. 
 When occurring in cells, it consists, under pathological as under normal 
 conditions, of the transformation of the protoplasm into a translucent 
 semi-fluid material, occupying more space than the unaltered proto- 
 plasm, and hence causing a swelling of the cells. This new-formed 
 material contains mucin in solution, which is precipitated by acetic acid. 
 It occurs under a variety of conditions, sometimes as a morbid increase 
 of a normal function of cells, as in many catarrhs, sometimes as an en- 
 tirely abnormal transformation. The cells may be entirely destroyed by 
 the accumulation of the mucoid material within them. 
 
 In certain cases, as in many tumors, in cartilage, bone, and other tissues, 
 the intercellular substance undergoes conversion into mucin-containing 
 material, losing almost entirely its original structure. The cells in 
 such cases may be affected only secondarily by the pressure which the 
 new-formed material exerts upon them. 
 
 Colloid Degeneration is very closely allied, both in chemical and mor- 
 phological characters, to mucoid degeneration, and in many cases there 
 is no definite microscopical distinction between them. But colloid 
 material is firmer and more consistent than mucous, does not yield a pre- 
 cipitate on addition of acetic acid, and its formation is usually confined 
 to cells; not involving intercellular substance, except by an atrophy 
 which its accumulation sometimes induces. The cells may contain 
 larger and smaller droplets of colloid material, or it may nearly or entirely 
 replace the protoplasm, and accumulate to such an extent as to cause 
 rupture and destruction of the cell. In this way, and by the atrophy of 
 intercellular substance which its accomulation causes, cysts may be 
 formed containing colloid material and cell detritus. Colloid degeneration 
 is of frequent occurrence in certain tumors and in the thyroid gland, and 
 occurs occasionally in other places. 
 
 Hyalin Degeneration is the transformation of tissues into a transparent 
 glassy substance, much resembling amyloid in its morphological charac- 
 ters; but it does not give the micro-chemical reactions of amyloid, and 
 appears under different conditions. Hyalin substance is quite resistant 
 to the action of acids, and stains readily with eosin. It occurs especially 
 in the walls of the smaller blood-vessels in various parts of the body, in 
 
64 BEGENEEATIVE CHANGES EST THE TISSUp:S. 
 
 Toluntaiy muscle fibres, and is said to sometimes involve interstitial tis- 
 sue. It has been described as occurring in the brain, lymph glands, and 
 ovaries ; in the tubules of the kidney, in the walls of aneurisms, in 
 muscle fibres, in the lesions of diphtheritis, tuberculosis, and syphilis, in 
 the hyaloid membrane and vessels of the eye, and elsewhere. It is some- 
 times called vitreous or fibrinous, and also waxy degeneration. It seems 
 to be, in some ways, allied to coagulation necrosis, but its exact signifi- 
 cance and relations to other forms of degeneration and the conditions of 
 its occurrence are not yet known. 
 
 In Calcareous Degeneration there is a deposition, either in cells or in 
 the intercellular substance, of larger and smaller granules composed 
 chiefly of phosphate and carbonate of calcium. These particles, when 
 abundant, give hardness, brittleness, and a whitish appearance to the af- 
 fected tissue. Under the microscope, they appear dark by transmitted, 
 white and glistening by reflected light. The addition of strong acids 
 causes their solution, usually with the formation of bubbles of carbonic 
 acid gas, whose evolution may be observed under the microscope. Tis- 
 sues may be nearly completely permeated with the salts, or the latter may 
 be scattered in patches through them. Sometimes large lamellated concre- 
 tions are formed in tissues, usually at the seat of some old inflammatory 
 process. Calcification usually occurs in parts of tissues which are dead, 
 or are in a condition of reduced vitality, as a result of some antecedent 
 morbid process, usually of an inflammatory nature. Among the most 
 common and important examples of calcareous degenerations may be 
 mentioned those which occur in the valves of the heart and walls of the 
 blood-vessels. 
 
 Pigmentation. — The pigment which is present in the body under ab- 
 normal conditions may be formed in the body or may be introduced into 
 it from without. It may be deposited in the cells or in the intercellular 
 substance, and is sometimes visible to the naked eye and sometimes not. 
 The pigment occurring in the body may be in the form of yellow, brown, 
 black, or reddish granules, or in crystalline form. In the majority of 
 cases, the pigment is f6rmed by the decomposition of hasmogiobin from 
 extravasated masses of red blood-cells. Parts which have been the seat 
 of long-continued hypersemia may have a diffuse grayish appearance from 
 the alterations of the haemoglobin inured blood-cells which have es- 
 caped from the vessels by diapedesis. Pigment may be formed in the 
 blood-vessels in severe cases of malarial infection, and circulate in the 
 blood. In another class of cases, various forms of cells seem to be ac- 
 tively concerned in elaborating pigment; this is exemplified in the true 
 melanotic tumors, and the process has its iihysiological prototypie in the 
 formation of pigment in the choroid, skin, and some connective tissues. 
 Pigmentation of tissue from the bile occurs under a variety of condi- 
 tions, and may be the result of the deposition of granules or crystals. 
 
DEGENEEA.TIVE CHAJSfGES IN THE TISSUES. 65 
 
 A difEuse staining also frequently occurs from the bile without the for- 
 mation of solid particles. 
 
 In many cases, the mode of formation of pigment is not at all under- 
 stood. In tissues which are normally somewhat colored, the color may 
 greatly deepen by a simple atrophy of the tissue without the new forma- 
 tion of pigment, as in simple atrophy of the heart-muscle and in atro- 
 phied fat. 
 
 As examples of pigment introduced into the body from without, we 
 may mention the de[)osition of minute particles of silver from the in- 
 ternal use of silver nitrate; the coloring of the skin and lymph glands 
 from tattooing; and especially, the pigmentation of the lungs and bronchial 
 glands from the inhalation of coal and other dust, which is universally 
 present under the conditions which-modern civilization imposes.' 
 
 ' For the literature on the subjects treated of in this chapter see the extensive 
 bibliography in Recklinghausen's Handbuoh der AUgemeinen Pathologle, which 
 constitutes parts 2 and 3 of Billroth and Luecke's Deutsche Chirurgie, 1883. 
 
PAEASITES. 
 
 The scope of tliis work permits us to do little more than enumerate and 
 give a very brief description of some of the more important forms of ani- 
 mal parasites found in man. Among the vegetable parasites, however, the 
 bacteria are at the jDresent time assuming such an important place in the 
 consideration of the etiology of certain diseases that they justly claim 
 a somewhat extended notice. 
 
 ANIMAL PARASITES. 
 PEOTOZOA. 
 
 Among the unicellular organisms several genera and species occur in 
 the human body, bat none are of great pathological significance. A spe- 
 cies of amceha has been found a few times in large numbers in the intes- 
 tinal contents in dysentery. Amoeba has also been found in the mouth. 
 The so-called psorospermim — minute oval structures about .035 mm. 
 long, with a thick capsule and coarsely granular contents — which are of 
 very frequent occurrence in the liver of the rabbit, forming a part of the 
 contents of yellowish, irregular-shaped cysts, have been found three or 
 four times in the liver of man. Another smaller form occurring in the 
 intestinal epithelium of dogs, cats, and rabbits, has been found in two 
 cases in a similar situation in man. 
 
 Among the itifusoria we find in man representatives of several genera. 
 The more common of these are Oercomonas intestinalis, a pear-shaped 
 flagellate structure about 0.012 mm. long, making, when alive, rapid 
 movements. It has been found iu the evacuations of persons suffering 
 from cholera, typhoid fever, and diarrhosa. Trichomonas vaginalis has 
 an oval or pear-shaped body, about 0.01 mm. long, on which are a few 
 cilia, and at the end two or three flagellje, somewhat longer than the 
 body. They are of very frequent occurrence in acid vaginal exudations 
 in catarrhal vaginitis. The possibility of mistaking the T. vaginalis for 
 human spermatozoa should be borne in mind in medico-legal examina- 
 tions, although to an observer familiar with either structure such a mis- 
 take could hardly occur. 
 
PARASITES. 6T 
 
 Some forms of ciliated infusoria have been found in large numbers 
 in the intestines in typhoid fever, jDarticularly in the north of Europe. 
 Most of the above-mentioned parasitic protozoa are apparently of little 
 significance and simply accompany, not cause, the lesions with which 
 they are occasionally associated. 
 
 WORMS. 
 
 Trematoda {Flulces). — These worms are small, flat,, tongue-shaped 
 ■or leaf-like creatures, with an intestine, and discoidal structures on the 
 under surface, by means of whicli they attach themselves. There are 
 several genera and species found in man. The most common genus is 
 Distoma. Of the^e, D. hepatictivi is of most frequent occurrence. It is 
 about 30 mm. long, and usually occurs in the gall-ducts and gall-bladder. 
 The embryos are attached generally to water-plants, from eating of 
 which the infection is believed to occur. D. lancenlatum is more slender, 
 pointed at the ends, 8 to 10 mm. long, and has been found a few times 
 in the gall-bladder. D. sinense is a slender worm about 15 mm. long, 
 and has been found in the bile in considerable numbers, jDarticularly in 
 the Chinese. D. limmatoMum is a more nearly cylindrical worm ; the 
 sexes are distinct ; the male from 13 to 14 mm. long, the female 16 to 
 18 mm. long, and occurs especially in Egyjotians in the portal and other 
 abdominal veins. 
 
 Cestoda {Tafe Worms). — These important worms consist, in the 
 mature state, of more or less rectangular or elongated segments, each one 
 of which represents a single individual, arranged in alinear series to form 
 a colony, at one end of whicli, called the head, is a variously formed 
 structure for the attachment of the colony to its host. The neck and 
 head are called the scolex, while the segments are called proglotiides 
 (Fig. 3). These worms have neither mouth nor alimentary canal. They 
 are hermaphrodites, the sexes being united in the proglottides. The head 
 and neck (scolex) may exist as an immature form in various tissues 
 and organs where they are encysted, and are often called cysticercus. 
 
 Tmnia solium is of frequent occurrence in man. It may be several 
 metres in length, and may be coiled up or stretched out in the small in- 
 testines. The head, about the size of a pin's head, has a projecting 
 proboscis or rostellum, around which are arranged a double row 
 of horny hooklets. Below these are four sucking discs at the sides of 
 the head. The booklets of the anterior row are larger than those in the 
 posterior row, and are from 0.16 to 0.18 mm. long. The proglottides, 
 when fully developed, are from 10 to 13 mm. long, and from 5 to 6 mm. 
 wide, but those nearest the head are much shorter and imm.ature. The 
 eggs of T. solium are ovoidal structures, about 0.03 mm. in diameter. 
 The embryo of this worm is most commonly seen in the muscles of the 
 pig as an encysted scolex, commonly called a "measle." It occasionally 
 
68 
 
 PARASITES. 
 
 occurs in man in the muscles, brain, eye, etc., and is called cysticercus 
 cellulosm. It is usually about the size of a pea, but may be as large as a 
 pigeon's egg, and surrounded by a connective-tissue capsule. 
 
 Infection with the worm occurs in the human subject from the in- 
 gestion of insufiBciently cooked " measly " pork, or in the case of cysti- 
 cercus cellulosEe, from the ingestion of the eggs, which may, in a variety 
 of wavs in uncleanly persons, get into the food. 
 
 Tmnia mediocanellata {T. saginata Leuckakt).— The head of this 
 species is somewhat cuboidal without either rostcllum or booklets, but 
 with four sucking discs. The segments are generally broader and 
 
 Fig. 
 
 Fia. 3. 
 
 Ftg. 2.— Head of Taenia solium, x 40. 
 
 Fig. 3.— Head and Pkoglottidbs op T.fflNiA mediocanellata. 
 
 A, Head, X 15. 
 
 B, Mature Proglottid showing generative apparatus, nat. size.' 
 
 C, Head and small fragments of Immature Proglottides showing gradual tapering of the neck^ 
 nat. size. 
 
 shorter than in T. solium and the worm is usually larger. In the em- 
 bryonal form the scolex occurs as the Cysticercus TcenicB mediocanellatm 
 in the form of small cysts in the muscles of cattle, from the eating of' 
 which in the uncooked condition the infection occurs. This is the most 
 common tape-worm in the United States. 
 
 TcBiiia echinococcus. — This worm in the mature condition forms a 
 short small colony inhabiting the intestine of the dog. The head is about 
 0.3 mm. in diameter and has a double row of booklets around the rostellum. 
 The proglottides are three or four in number, the last being the larger. 
 
PAEASITES. 
 
 69 
 
 The entire colony is not more than 4 to 5 mm. in length. The signi- 
 ficance of this parasite in human pathology depends upon the cysts 
 called hydatids which it forms, in the immature or cysticercus stage, in 
 various parts of the body. When the eggs of the mature worm get into 
 the intestinal canal of man, they undergo partial development and find 
 their way into the tisssues and organs, most frequently into the liver. 
 
 Fig. 4.— CuTiouLA of EcHiNococons Cyst, X 250. 
 
 Here cysts are formed which become encapsulated by a connective-tissue 
 membrane produced by the inflammatory reaction of the organ. 
 The cyst-wall of the parasite is formed of two layers — an outer finely 
 lamellated layer called the cuticula, and an inner granular layer con- 
 taining muscle-fibres and blo'od-vessels, called i\\B parencliymatous layer. 
 Inside of the primary cyst, secondary cysts sometimes form, called daugh- 
 ter cysts, and within the latter tertiary cysts, called granddaughter 
 cysts, may develop. On the inner surface of the cysts, either pri- 
 mary, secondary, or tertiary, the scolices or heads of the immature 
 
 Fia 6 —Scolices of Taenia ECHiNoooccns X 60 
 In one the rostellum is projected, in tlie others it is withdrawn. 
 
 worm are formed. These develop in the walls of the pediculated vesicles 
 called brood capsules. The walls of these vesicles have a lamellated 
 cuticula and a parenchymatous layer similar to those of the primary cysts. 
 The scolices, of which there may be several in each brood capsule. 
 
■70 PARASITES. 
 
 are similar to the heads of the mature tape-worm. They are about 
 0.3 mm. in diameter, having a rostellum surrounded by a double 
 row of booklets and four sucking discs. At the posterior end of the 
 scolex is a pedicle by which it is originally attached to the wall of the 
 brood capsule. Little lamellated concretions of lime salts are often present 
 in the scolex. The anterior portion of the scolex, the rostellum, booklets, 
 and suckers, are often invaginated in the posterior portion. The scolices 
 may be free inside of the brood capsules, or, owing to the rupture of the 
 latter, they may be free in the cavity of the primary cysts. They may 
 die and degenerate, forming a granular mass in which the booklets may 
 be embedded, or the booklets may be free in the brood capsules or in the- 
 primary cysts. Sterile cysts are often found, that is, those in which 
 
 Fig. 6. — Hooklkts from Scolex of Tjsnia echinococcqs, X 750. 
 
 neither brood capsules nor scolices are developed. The cysts contain, in 
 addition to the scolices, a clear gelatinous fluid. This fluid may become 
 turbid by admixture with disintegrated scolices or fragments of the 
 parenchymatous layer, or it may contain fatty detritus, cholesterin crys- 
 tals, and particles of lime salts. The fluid may be partially absorbed, 
 leaving a thick grumous material within the cysts, which may become- 
 calcified or converted into a stony mass. When the scolices are not found 
 entire, the diagnosis may be made by the discovery of the separate 
 booklets, or fragments of the characteristically lamellated cyst-walls. 
 The connective-tissue walls of the primary cysts may become fatty or 
 cheesy or calcified. 
 
 Sometimes the secondary vesicles project outwards instead of inwards,, 
 forming a series of cysts outside of the primary one. This variety of 
 development is sometimes seen in man, but is more common in the do- 
 mestic animals. It is called echino coccus scolecipariens or exogena. 
 
 Another variety of echinococcus, called E. muUilocnlaris, is almost al- 
 ways found in the liver, and appears to be the result of incomplete and 
 disturbed development of the embryos or cysts. It consists of a congeries- 
 of irregular, usually small cysts, surrounded by broad and narrow bands 
 of connective tissue, and sometimes containing gelatinous fluid and 
 scolices or booklets ; but the latter structures are commonly absent or 
 
PAEASITES. 71 
 
 difficult of detection. The whole is often surrounded by a dense con- 
 nective-tissue capsule which may be calcified. The entire mass often 
 presents an alveolar structure, and was formerly regarded as a tumor — 
 alveolar cancer. The diagnosis may be established by the' discovery of 
 the booklets or scolices, or fragments of the lamellated cuticula. 
 
 There are four or five other species of taenia occurring rarely in man. 
 
 T. nana. — This species occurs in the form of small colonies about 
 15 mm. iu length. The rostellum is surrounded by a single row of' 
 booklets. It has been seen once in large numbers by Bilharz in the 
 duodenum of a child which died of meningitis in Cairo. 
 
 T. flavopunctata, a species about which little is known, is reported 
 twice in America, as occurring in the intestine of young children. 
 
 T. madagascariensis, also little known and rare, has been seen in two 
 children in Madagascar. 
 
 T. cucumeriiia. — This species occurs in colonies about 20 cfcm. long. 
 The head is very small and spheroidal, and has four rows of booklets. 
 It is frequent in the small intestines of dogs or cats. It occurs occasionally 
 in man. Its scolex inhabits the dog louse, and infection may occur in 
 man by the transference of the lice or the embryos of the parasite to the 
 mouth, as the result of the filthy habit of kissing dogs and cats, or per- 
 mitting the face to be licked by them. 
 
 Bothriocephalus latus. — This the largest of the human tape-worms, 
 has very broad quadrangular proglottides.^ The head is ovoidal and 
 about 3 mm. long and 1 mm. broad. It has no proper sucking discs and 
 no booklets ; but by long grooves on either side of the head, the animal 
 attaches itself to its host. The neck is long and filiform. It occurs 
 most frequently in Europe, particularly in the northern provinces. The 
 eggs undergo partial development in water, and are taken up by the pike 
 and eel-pout, and perhaps by other fresh- water fish, from the ingestion of 
 whose flesh in an imperfectly cooked condition the human infection 
 occurs. Two other species of Bothriocephalus have been described as of 
 rare occurrence in man: B. cordatus in Greenland and Iceland, and B. 
 cristatus. 
 
 Nbmatoda {Round- Worms). — These worms are in general cylindrical, 
 elongated, usually pointed at the ends, and sometimes filiform. The 
 surface is sometimes smooth, sometimes irregularly beset with hairs and 
 papillae, or possesses longitudinal elevated striae or transverse rings ; but 
 the body is not segmented. There is a mouth at the anterior portion, 
 and a ventral anus near the posterior end. The intestine is straight. 
 The sexes are in most forms distinct, the male being in general smaller 
 than the female. 
 
 Ascaris lumbricoides. — This is one of the most common of the human 
 intestinal parasites, and is of particularly frequent occurrence in children. 
 It is of a light brownish or reddish color. The female is from 30 to 40 
 
72 PARASITES. 
 
 Gtm. long, and from 5 to 6 mm. thick. The male is somewhat more than 
 half as large. Both sexes are pointed at the ends, the posterior end of the 
 male being curved into a spined hook. The eggs, from 0.05 to 0.06 mm. in 
 diameter, are surrounded by an albuminous envelope, and are quite re- 
 sistant to destructive agencies. The mode of development and life his- 
 tory of these parasites are not very well understood. Their usual seat, in 
 man, is the small intestine, but they may wander into the stomach, and 
 exceptionally get into the mouth, nose, bronchi, gall passages, peritoneal 
 cavity, etc. They may be single in the gut or present in great numbers. 
 
 Two other species of Ascaris have been found in man. A. tnariiima 
 was found in the vomit of a child in Greenland, in an immature condi- 
 tion. A. mystax, a tolerably common form in cats and dogs, has been 
 found a few times in man. It is smaller than A. lunibricoides. 
 
 Oxyuris vermicularis (Thread-worm or Pin-worm). — This species is 
 very small; the female has a pointed tail, and is about 1 ctm. long. The 
 posterior end of the male, which is about 4 mm. long, is blunt, and after 
 death somewhat curled. The eggs are produced in great numbers, are 
 oval, and about 0.053 mm.' long. This parasite is very common in chil- 
 dren, and may be present in large numbers in the colon. They may in 
 the female enter the vagina and uterus. This worm is only known to 
 infest the human subject, and infection doubtless occurs by the ingestion 
 of the eggs, which are widely distributed in a variety of ways on many 
 objects, fruits, etc. 
 
 Strongylus gigas. — This is a slender red worm, the female being 
 sometimes 1 metre long and over 1 ctm. in diameter. It has been found 
 several times in the pelvis of the kidney in man. It is more common in 
 the wolf, fox, horse, seal, and some other animals. Strongylus longeva- 
 ginatus. The female is about 2.5 ctm. long, the male, as usual, shorter. 
 It is of a yellowish-white color, and has been found once in the lung of a 
 boy in Germany. 
 
 Dochmiiis duodenalis. — The female is from 1 to 2 ctm. long, the male 
 about 1 ctm. long. The body of the male is dilated anteriorly and curved 
 backwards. Its mouth is furnished with a chitinous capsule, and 
 chitinous claws and teeth. It is found in the small intestine of man in 
 Italy, Switzerland, Egypt, and Brazil. The head is burrowed into the 
 mucous membrane of the host, and the animal is nourished by the blood 
 which it sucks out, and which is usually seen in its intestine. An 
 ecchymosis is produced at the point of attachment or even severe hsemor- 
 rhage, and marked anseniia may be the result of tlie presence of largo 
 numbers of the parasites. 
 
 Trichocephalus dispar (Whip-worm). — The males and females are 
 of nearly equal size, 4 to 5 ctm. long. A little less than one-half of the 
 body (the posterior portion) is about 1 mm. thick, and in the male is 
 rolled into a flattened spiral, but in the female is but slightly bent. The 
 
PAEASITBS. 
 
 73 
 
 anterior part of the body is very slender, and is embedded in the mucous 
 membrane of the host. The eggs are elongated, oval-shaped, about 
 O.05 mm. long, and about one-half as wide, with a thick brown capsule. 
 This parasite is very common in some countries ; it dwells in the csecum 
 in small or large numbers. It is usually of little pathological significance, 
 commonly producing no symptoms. Its developmental history is not 
 well known. 
 
 Trichina spiralis. — The female of this most dangerous and common 
 parasite is in the mature condition about 3 mm. long ; the male from 
 1 to 1.5 mm. long ; they are filiform in shape and white in color. The 
 young are born in the form of tiny worms about 0.01 mm. in length, 
 and somewhat similar to the adult in shape. Infection occurs in man 
 from the ingestion of insufficiently cooked pork. The muscle of the 
 diseased pig contains the embryos of the parasite in an encysted condi- 
 tion. In the stomach the capsule of the worm is dissolved, and the 
 embryos ai-e set free. They very rapidly mature, increasing ia size, 
 and the females give birth in the small intestine to very large num- 
 bers of young. It is estimated that a single female may give birth 
 to from 1,300 to 1,500 young. These find their way through the 
 mucous membrane and wall of the gut into various parts of the body. 
 
 
 r^n 
 
 w^p^ywii /Si^ 
 
 Fig. T.— Trichina Encysted in Muscle. 
 In one capsule the parasite is dead and its remains calcified. 
 
 The exact course which they take in getting out of the gut is not fully 
 established, probably they traverse the tissues in different ways. At any 
 rate, they find their way to the voluntary striated muscle tissue, which 
 they penetrate, and enter the, muscle fibres. Here they cause a disinte- 
 gration of the contractile substance, and coil themselves inside of the sar- 
 ■colemma. In this situation they become encapsulated by material in 
 part furnished by themselves, in part by means of the inflammatory re- 
 action which their presence induces in the connective tissue of the mus- 
 cle. The worms are surrounded inside the capsule by granular material. 
 
T4 PAEASITES. 
 
 The capsule after a time becomes partially calcified, and in this condition 
 may be readily seen by the naked eye as a tiny white speck. In this 
 encysted state they may remain inactive but living, for an indefinite, often 
 for a very long time. Most frequently the cysts contain but one embryo, 
 but they may contain from two to four. The embryo may die and its 
 remains become calcified. 
 
 The same course of events transpires when the muscle trichinae are 
 eaten by the pig or a variety of other animals. 
 
 The embryos in the muscle are killed by a temperature of 55° 0. 
 
 The embryos may mature, and a new generation be born within from 
 five to eight days after the ingestion of the diseased meat. 
 
 As the result of the presence of these parasites in the body, if the 
 invasion be severe, acute catarrhal enteritis, with diarrhoea and vomit- 
 ing, high fever, and severe pains are apt to occur. Oedema of the face 
 and of other parts of the body, broncho-pneumonia, and fatty degene- 
 ration of the liver, may be found at the post-mortem examination of 
 cases which have succumbed to the disease. The encapsulated embryos 
 may be found in enormous numbers in various voluntary muscles of the 
 body, but they are most apt to be found, when not very abundant, in 
 the muscles of the neck and larynx, in the intercostals, and the diaphragm.. 
 They tend to collect towards the tendinous extremities of the muscles. 
 Trichinae also occur in the rat, cat, mouse, and other animals.' 
 
 Fllaria medinensis (Guinea worm). — This is a thread-like worm; the 
 female, which is alone known, being sometimes as much as 80 ctm. long 
 and from 0.5 to 1.7 mm. thick. It is common in the east, and inhabits 
 the subcutaneous connective tissue, in which it often gives rise to abscesses 
 
 ' For the examination of muscles for the detection of the presence of the para- 
 site, small pieces are snipped out witli the scissors, and squeezed into a thin sheet 
 between the slide and a thick cover-glass, and examined with a. low power. A 
 considerable number of bits of muscle should be examined, particularly from the 
 above-mentioned favorite situations, before excluding them in a suspected 
 case, because they are sometimes present in small numbers. A thorough search 
 is of especial importance in the examination of pork, since, owing to the enormous 
 fertility of the parasites, even a moderate number may give rise to a severe infec- 
 tion. 
 
 For the minute examination of the parasite, bits of muscle should be hardened 
 in Milller's fluid and alcohol, and decalcified if necessary, and after embedding in 
 celloidin, thin sections out and stained double with hsematoxylin and eosin, and 
 mounted in balsam. Bits of muscle may be also teased, the embryos picked out 
 with a needle, and the cysts either broken open under a lens with the needle, or 
 squeezed under the cover-glass. The embryo worm thus set free may be mounted 
 in a mixture of equal parts of glycerin and picric acid The adult forms, which 
 may be obtained by feeding rabbits with uncooked trichinous muscle, and exam- 
 ining after the proper interval, may be hardened in MtiUer's fluid, and mounted 
 in a mixture of equal parts of picric acid and glycerin, or in the same mixture 
 which has been lightly tinged with eosin. 
 
PARASITES. 75 
 
 and ulcers. The embryos live for a time free in fresh water, and are 
 then taken up by a species of fresh-water crustacean, in whose body they 
 undergo farther development, and by the ingestion of which the infec- 
 tion of the human subject occurs. 
 
 Filaria sajiguinis hominis. — The embryo of this parasite, which in- 
 habits the blood of men, especially in Brazil, Egypt, and some parts of 
 the Orient, and occasionally occurs in this country, is about 0.35 mm. 
 
 Fig. 8.— Filaria Sanguinis Hominis, x 200. 
 
 From a case in the New York Hospital. The specimen was prepared and loaned to the writer 
 by Dr. Frank Ferguson. 
 
 long, rounded anteriorly, and pointed at the tail. It has about the dia- 
 meter of a red blood-cell. It occurs, sometimes in great numbers, in 
 the blood during the night-time, being as a rule absent during the day. 
 It may occur in the urine in connection with chyluria and hsematuria. 
 The mature female is from 8 to 10 ctm. long, and has been found in- 
 habiting the lymph-vessels of man, particularly in the scrotum and lower 
 extremities. Owing to the obstructions which it causes in the lymph- 
 circulation and to the local irritation which its presence induces, it some- 
 times gives rise to lymphangiectasis, cedema, abscesses, and perhaps ele- 
 phantiasis. One of the embryonic stages of development is believed to 
 transpire in the body of a species of nocturnal mosquito. Through the 
 bodies of the dead mosquitos, which are liable to fall into the drinking- 
 water, it is believed that the spread of the parasite may occur. 
 
 There are several other species of filaria occasionally found in man 
 which it is not necessary to enumerate here. 
 
 Rhabdonema strongyloides. — A small filiform worm from 1 to 3 mm. in 
 length is found, often in enormous numbers, in the intestines, biliary 
 and pancreatic ducts of man in Cochin China, giving rise to endemic 
 chronic diarrhoea. It has been thought that there are at least two spe- 
 cies, which have been described under the generic name Aguillula, but 
 recent researches by Leuckart have led him to believe them to be dif- 
 ferent developmental stages of the same form, for which he suggests the 
 above name. 
 
 The scope of this work does not permit us to enter into the subject 
 of external parasites, which will be found described in treatises on dis- 
 eases of the skin, or in the general works on parasites referred to below. 
 
 Modes of Study and Preparation of the Internal Parasites. — Hhe proto- 
 zoa may be studied in the living condition in one-half-per-cent solution 
 of sodium chloride. They may be killed and preserved by allowing a 
 
Y6 
 
 PAEASITES. 
 
 drop of one-per-cent osmic acid to run under the cover-glass, and re- 
 placing this after a few hours by glycerin lightly tinged with eosin. The 
 smaller and embryonic forms of the various kinds of parasitic worms may 
 be hardened best under the cover-glass with Muller's fluid or osmic acid, 
 and these may be, when the hardening is completed, replaced by dilute, 
 and this by strong alcohol, and the latter finally replaced by eosin-gly- 
 cerin, in which the specimens are permanently preserved; or they may 
 be stained lightly by tinging the alcohol with eosin, and then cleared up 
 by oil of cloves, and finally mounted in balsam. 
 
 It is necessary, however, for detailed study of the larger parasites, 
 to make thin longitudinal and transverse sections from different parts of 
 the body. This can be readily donp even in very small forms by imbed- 
 ding the animal — after careful hardening in osmic acid or in Miiller's 
 fluid, and afterwards in alcohol — in celloidin, and using the microtome. 
 The sections may be stained double with hsematoxylin and eosin and 
 mounted in balsam. 
 
 The general arrangement of the generative organs in the proglottides 
 of tape woi-ms maybe well seen by staining in eosin or eosin-glycerin after 
 moderate hardening in dilute alcohol, and then squeezing the segment 
 between two glass slides. 
 
 Bibliography. — Especially to be recommended for detailed descriptions of hu- 
 man parasites, together with practical suggestions for their study, is the small 
 work of Braun, " Die thierisohen Parasiten desTVIenschen," 1883, which contains 
 also the more important bibliography. 
 
 The more extended classical works of Cobbold, " Entozoa of Men and Ani- 
 mals," 1879, and Kiiohenmeister and Zilrn, " Die Parasiten des Menschen," 2d Ed., 
 should be consulted, and both contain valuable bibliography. Various forms of 
 external parasites of men and animals are fully described and illustrated in the 
 -work of Megnin, " Les Parasites et les Maladies parasitaires chez I'horame," etc., 
 1880. The plates of Stein, illustrating the Oestoda, 1883, are carefully executed. 
 In the ''Report on Trichinae and Trichinosis," in 1880, by Glazier, Surgeon in the 
 Marine Hospital Service, will be found an illustrated account of the natural his- 
 tory of this parasite, history of the disease, etc., and a section on its occurrence 
 in the United States. 
 
 PARASITIC FUNGI. 
 
 These lowly vegetable organisms which are of not infrequent occur- 
 rence on and in the human body, both in health and disease, embrace 
 the structures commonly known as moulds and yeasts. Of these, the 
 moulds are of the greatest importance, and these present varying degrees 
 •of significance. The scope of this work does not permit us to describe 
 •either the natural history of the group or the different forms. For this 
 we refer to works on skin disease and on vegetable parasites. 
 
 We may simply mention as the more common and important the 
 Acliorion SchonleiniioY favus fungus; the Trichophyton tonsurans or ring- 
 
PARASITES. Y7 
 
 ■vvorm fungus; the Microsporon furfur or the fungus of pityriasis versi- 
 color. A form of Aspergillus is of occasional occurrence in the external 
 meatus of the ear, and on the membrana tympani. The peculiar white 
 pellicle often seen ou the mucous membrane of the mouth and pliarynx, 
 sometimes in adults who are the victims of exhausting diseases, but more 
 often in young children {thrush) is associated with the fungus Oidium 
 albicans {Sacoharomyces albicans). 
 
 Actinomycosis (Eay fungus). This fungus grows in radiate masses 
 especially in the jaws of cattle, but is of occasional occurrence in man. 
 The fungous mass may form a large tumor in the jaw, by its own growth and 
 by the formation of granulation tissue, which is apt to slough and spread 
 so that not only may the tissues of the tongue, pharynx, larynx, etc.. be 
 involved, but nodules of similar character may form in the gastro-intes- 
 testinal canal, lungs, skin, etc. These nodules were formerly considered 
 to be some form of sarcoma. The fungus forms little yellow masses as 
 large as a millet seed or smaller, which are scattered through the new- 
 formed granulation tissue or mingled with the pus, giving the growths 
 a very characteristic appearance. It is the peculiar radiate grouping of 
 the filaments of the growth which gave rise to the name ' ray fungus.' 
 The disease is propagated from one animal to another by inoculation or 
 by contact of the growth with a wound or an abrasion of the mucous 
 membrane.' 
 
 BACTERIA. 
 
 Morphology and Physiology. — Bacteria are minute vegetable organ- 
 isms of the lowest and simplest form. They are widely distributed in 
 the air, water, and surface soil, and are particularly abundant among the 
 habitations of men, or wherever animal and vegetable substances are 
 undergoing decay. They are also invariably present in greater or less 
 numbers in the mouth, nose, lungs, and gastro-intestinal canal of men 
 and animals. The largest of them are too small to be seen with the 
 naked eye, and the smallest require for their recognition the most perfect 
 and powerful of our microscopic aids. They have various shapes: 
 spheroidal, rod-like, filiform, or spiral. They are simple cells, multi- 
 plying, when the conditions are favorable, with extraordinary rapidity, 
 by transverse division, or by the formation of spores which develop into 
 the adult forms. They are very resistant to the action of dilute 
 acids and alkalies, and are believed to possess a membrane inclosing the 
 protoplasm, which may appear homogeneous or granular. 
 
 They lie sometimes singly, sometimes in pairs or chains, and some- 
 times in masses embedded in a transparent gelatinous substance, and are 
 
 ' For general consideration of the fungi and their relations to disease, ci)nsult 
 Fliigge, '"Fermente und Mikroparasiten, Handbuch der Hygiene und der Ge- 
 werbe-Krankheiten." Pettenkofer und v. Ziemssen, 1883. 
 
T8 PARASITES. 
 
 then called zobglma colonies. Some are capable of pei'forming rapid 
 movements, others not, and the same form may be at one time mobile, 
 and at another immobile. Some of them have a cilium at the ends by 
 means of whose vibrations they may perform active progressive move- 
 ments. 
 
 They require for their nourishment'nitrogen and the hydrocarbons, 
 oxygen is necessary for the proliferation and activities of some forms, and 
 for others not. 
 
 They are active only in the presence of moisture, but when this and 
 other conditions favoring their activities fail, they do not necessarily die, 
 but some forms may remain, either as spores or as fully developed 
 organisms, for long periods wholly dry and inert, but capable of resuming 
 their activity whenever they are again restored to favorable conditions. 
 
 Some are and some are not very sensitive to changes of temperature. 
 At a temperature below + 5° C. they are incapable of activity or prolifera- 
 tion, but some forms are not killed by a temperature of —111° 0. As the 
 temperature is raised, their activities increase up to a certain point. It may 
 be said in general that they are most active at about the temperature of 
 the body, although species differ considerably in this respect. In fluids, 
 many bacteria are killed by a temperature of 80° C. and all are killed by 
 a temperature of 100° C, if this be long enough continued. When dry 
 they resist much higher temperatures than when moist. The spores are 
 as a rule more resistant to high temperatures than the bacteria them- 
 selves; some having been exposed, dry, to a temperature of 140° 0. with- 
 out destruction of life. Fluids containing the spores of bacteria which 
 resist very high temperatures, may be sterilized by boiling for a short 
 time, then being allowed to stand at ordinary temperatures for several 
 hours, and then again boiling; this process being repeated several 
 times. In this way, although the spores themselves are not killed by 
 the heat, the bacteria into which they develop during the intervals are 
 killed, so that finally the medium is entirely freed from both livingspores 
 and adult bacteria. 
 
 As a result of their growth and activities, certain materials are pro- 
 duced in the nutrient media, which, when sufficiently concentrated, may 
 bring their activities to a stand-still. Putrefaction and putrefactive pro- 
 ducts are always dependent upon their presence and activity. In the 
 same nutrient medium one form of bacteria, for whose growth the soil is 
 more favorable, may interfere with or even destroy another, by its own 
 excessive growth. 
 
 Certain disinfecting agents, when brought into contact with bacteria, 
 are capable of greatly reducing their activities, or destroying them al- 
 together; but different forms differ greatly in their power of resisting 
 the action of these agents. The spores of certain bacteria are exceedingly 
 resistant, much more so than the bacteria themselves, to the action of disin- 
 
PAEASITES. 79 
 
 fecting agents. Among these disinfectants may be mentioned carbolic 
 acid, sulphurous acid, solutions of chlorine, iodine, and bromine, and 
 especially solutions of corrosive sublimate, which is very inimical to the 
 life of some bacteria and their spores even in very dilute solutions 
 (1 : 1000-1 : 5000), or less. 
 
 Glassification of Bacteria. — These organisms are so small and so dif- 
 ficult to obtain for experimentatiou in a pure, unmixed condition, and 
 their systematic study is of so recent a date, that much uncertainty 
 still exists as to the life history of the different forms. It is even not 
 yet 'absolutely established whether or not the different forms of bacteria 
 belong in all cases to different and distinct species. The theory is ad- 
 vanced by some observers that, standing, as they do, very low in the 
 ■scale of living beings, they are capable of being so influenced by 
 their environment as to undergo such marked morphological and phy- 
 •siological alterations as to insure a mutability of species, so that a single 
 form is capable of changing from one species into another. "While this 
 possibility must be recognized, the most careful researches tend to con- 
 firm the belief that species are distinct and practically permanent. 
 
 The most useful classification of the bacteria and the one generally 
 adopted is that of Cohn, by which all forms are brought into four main 
 groups, depending upon their shape. 
 
 I. Sphero-bacteria. — Spheroidal-celled bacteria. 
 
 II. Micro-iacteria. — Short-rod-celled bacteria. 
 
 III. Desmo-lacteria. — Filiform-celled bacteria. 
 
 IV. Spiro-bacteria. — Spiral-celled bacteria. 
 
 This classification is provisional, and doubtless, in the light of future 
 research, will be essentially modified; but it is at present almost indis- 
 pensable for purposes of study. 
 
 I. Bpliero-iacteria. — The most common and important genus of tViis 
 group of bacteria is Micrococcus, of which there are many species. Some 
 of these are capable of producing coloring- materials of various kinds in 
 the nutrient media and are called chromogenous micrococci; others in- 
 duce different forms of fermentation — zymogenous micrococci; still others 
 occurring in the body in connection with various diseases are called 
 patliogenous micrococci. The cells of most of the species of micrococci 
 are very small, having, for the most jDart, a diameter of less than 1 ^ 
 (0.001 mm.); but some forms are considerably larger. They occur either 
 singly or joined together in pairs — diplococciis; in longer or shorter 
 beaded chains, or in zoogloea masses. They are believed never to exhibit 
 spontaneous movements, although liable to show the Brownian move- 
 ment. The species differ from one another in size, sometimes slightly 
 in shape, in mode of grouping, in refractile power, and in their phy- 
 siological activities. 
 
 Among the chromogenous micrococci may be mentioned the Micro- 
 
80 PARASITES. 
 
 COCCUS 2^1'odigiosus which produces a deep-red color in its nutrient me- 
 dium, and which is supposed to have given rise to the alleged miracle of the 
 bleeding host, and which sometimes occurs, in a very destructive way, 
 on bread. Micrococcus luteus forms yellow droplets upon the surface of 
 the nutrient medium. Both may be readily cultivated for experimenta- 
 tion on the surface of boiled and sterilized potatoes (see below, methods- 
 of studying bacteria). 
 
 V * * 
 
 r\f 
 
 Fig. 9.— Sphero-bactebia (Genus Mioboooooos). 
 
 1. Micrococci from Ulcerative Endocarditis, a, single; 6, zooglcea. 
 
 2. Micrococci Cultivated from Laboratory Dust, o, in pairs (diplococcus form); b, in tetrads,* 
 c, in chains (sometimes designated as Streptococcus). 
 
 Specimens stained with f uchsin, X 700. 
 
 Among the zymogenous micrococci may be mentioned M. urece, 
 which frequently occurs in urine, inducing ammoniacal fermentation. 
 Other species are found in fermenting wine and in a great variety .of 
 putrefying substances. 
 
 The so-called pathogenous micrococci belong, as a rule, among the 
 minuter forms, and moriDhological distinctions between the species are as 
 yet, for the most part, wanting. 
 
 Micrococci have been found at the seat of lesion or in various parts of 
 the body in diphtheria, erysipelas, ulcerative endocarditis, syphilis, 
 cerebrospinal meningitis, lobar pneumonia, osteo-myclitis, and infec- 
 tive periostitis and syphilis. Their occuri'ence and' significance will be 
 considered in the descriptions of the lesions of these diseases in the sec- 
 tion of this book devoted to Special Pathology. 
 
 In the exudation of gonorrhoea, large micrococci, mostly in the form 
 of diplococciis, are found, sometimes in the cells, sometimes free (see lesions 
 of the urethra). In pymmia s^di puerperal fever, micrococci have been 
 found in various parts of the body, sometimes in the blood-vessels, some- 
 times in the tissues, and frequently in abscesses and necrotic areas. They 
 are assumed by some observers to be the cause of these diseases, but this is 
 not yet proven. Inoculation of material containing the micrococci from 
 the bodies of pyasmic persons may produce the same or a similar disease 
 in healthy animals.' 
 
 Micrococci have also been described as occurring in scarlatina, typhus 
 and typhoid fever, measles, lupus, pyelitis, acute yellow atrophy of the 
 
 ' ConsultKoch : " Traumatic Infective Diseases " ; and Rosenbach : " Mikro-Or- 
 ganismen bei den Wund-Infections-Krankheiten," 1884. 
 
PAEASITES. 81 
 
 liver, small-pox, hemophilia neonatorum, and in other diseases; but no 
 definite proof has yet been furnished that they stand in a causative rela- 
 tion to them. They frequently occur in connection with the process of 
 suppuratioji; but their influence upon the process, if any, has not yet 
 been definitely determined. 
 
 Another genus of sphero-bacteria is Sarcma, which embraces several 
 species. Among these is the 8. veniriculi, consisting of large cells 
 usually grouped in clusters of four to sixteen. They are found in 
 the stomach, both in health and disease, but are not proven to stand in 
 a causative relation to the diseased conditions in which they occur. 
 
 II. Micro-iacteria (rod bacteria). — This group is represented by a 
 single genus — Bacterium, from which is derived the general name ap- 
 plied to this whole class of organisms. They have the form of short rods 
 or cylinders and are sometimes elliptical. The cells usually appear in 
 pairs or in rows of four, but seldom form longer chains. They not in- 
 frequently form zoogloea colonies. They are capable of active spontaneous 
 movements. The different species may be grouped into chromogenous, 
 zymogenous, and pathogenous bacteria. Among the chromogenous 
 species may be mentioned Bacterium synxanthwn, which is found in the 
 so-called yellow milk, and the B. mruginosicm, which sometimes gives a 
 greenish-blue color to pus. 
 
 The most common representative of the zymogenous species is Bac- 
 teriuvi termo. This is the most common and wide-spread of all the 
 bacteria and is found usually in active proliferation wherever putre- 
 faction is going on, although the part which it plays is not definitely 
 known. It is usually associated with other bacteria. Its cells ai-e short 
 
 / 
 
 '/.v 
 
 1 
 
 Fig. 10.— Micro-bacteria (Genus Bacterium). 
 1, Bacterium termo. 2, Bacterium lineola. 
 Specimen stained with fuchsin, X 600. 
 
 cylinders usually from 1 to 2 /« in length. It performs tremulous pro- 
 gressive movements, sometimes turning on its axis and jerking about in 
 a most fantastic manner. Cilia are described as projecting from its 
 ends and causing its movements. Frequently associated with B. termo, 
 and very common in stagnant water and jDutrid infusions is a larger, 
 but quite similar species — B. lineola. 
 
 The species of Bacterium supposed, with much reason, to be pathogen- 
 ous in character are very few in number and mostly confined to the dis- 
 eases of animals. One species is found in, and supposed, as the result of 
 6 
 
82 PAEASITES. 
 
 careful experiments, to be the cause of septicsemia in rabbits. Another 
 is believed to be the cause of the so-called chicken cholera. Some forms 
 of Bacterium have been described as occurring in loiar pneumonia, 
 septicaemia, and jyy^T'Onephritis, but of their significance here we have 
 little definite knowledge. 
 
 III. Desmo-bacteria — filamentous bacteria. — The members of this 
 group consist of elongated or filiform cells, which are sometimes joined to- 
 gether at the ends, forming longer and shorter chains. They often occur in 
 dense masses, and rarely in the form of zoogloea colonies. In shape there is 
 no sharp distinction between the desmo- and the micro-bacteria, as there 
 seem to be intermediate forms. They frequently proliferate by the for- 
 mation of spores within the cells, and may exhibit spontaneous move- 
 ments. There are zymogenous and chromogenous species, and others 
 belong to the most important of the pathogenous bacteria. The most 
 important genus is Bacillus. 
 
 Zymogenous iacilli. — Of these the most common species is B. sul- 
 tilis, usually formed of long, delicate, thread-like chains of cells. These 
 are ciliated at the ends, and may perform very marked pendulous pro- 
 gressive movements, often bending and turning on their axes. This is 
 one of the bacteria requiring oxygen for its development. Its spores are 
 very abundant in the air, in dust, and on the surfaces of the greatest 
 variety of objects. When growing, it forms a light yellow pellicle on the 
 surface of its nutrient medium. It is readily obtained for experimenta- 
 tion- from the dust of hay or from hay infusions. Another common form, 
 similar in appearance to the last, is Bacillus hiityricus, which induces 
 butyric fermentation in a great variety of organic substances. 
 
 Among several species of pigment-forming bacilli may be mentioned 
 the Bacillus syncyanum, which is found with other bacteria in the so- 
 called blue milk. 
 
 Patlwgenous Iacilli. — Bacillus anthracis. — Its cells have the form 
 of filaments from 5 to 20 /^ long) and about 1 pt broad, which may be 
 
 !>■— 
 
 y—^- 
 
 Fig. 11.— Desmo-bacteria (Genus Bacillus). 
 Bacillus anthracis, from spleen of mouse inoculated with the bacillus. Specimen stained with 
 methylen blue, X 600. 
 
 straight or curved; they are not rounded at the ends, and often hang to- 
 gether in chains. They proliferate by transverse division and by the 
 formation of spores. Spontaneous movements have not been observed 
 
PAJJASITES. 83 
 
 in them. They are constantly found in the body in splenic fever (malig- 
 nant pustule), usually in large numbers in the spleen and in the capillary 
 blood-vessels, especially in the lungs, liver, kidneys, and intestine. They 
 are readily cultivated outside of the body, and when thus purified, their 
 inoculation into a number of different animals produces the disease, and 
 in the blood of the diseased animals multitudes of the bacilli are found, 
 showing their proliferation in the blood-vessels and elsewhere. They are 
 of especial interest and importance, because we know more of their life- 
 history than of almost any other of the bacteria, and because it was this 
 bacterium which was first absolutely demonstrated to be the cause, and 
 the only cause, of a well-defined disease in man. 
 
 Bacillus tuberculosis — B. Kochii. — -This species was first definitely 
 identified by Dr. Eobert Koch in 1883. It is very short and slender, 
 and apparently of the utmost importance in connection with tuberculosis. 
 Its characters and significance will be considered under tuberculosis in the 
 section on the general diseases. 
 
 Bacillus leprcB. — This is in many respects similar to the B. tubercu- 
 losis, and is supposed by some observers to cause the lesions of lej)rosy, 
 under which heading it is considered. 
 
 Bacillus malaricB. — For a brief consideration of this, the alleged cause 
 of malai-ial fever, see section on Malarial Fever. 
 
 Bacilli have been found in the lesions of glanders, which are believed 
 to cause the disease. They are somewhat smaller than B. tuberculosis. 
 
 Bacilli, believed by many observers to be constantly present and the 
 probable cause of the diseases in typhoid fever and cholera, will be 
 considered under the lesions of these diseases. 
 
 Bacilli of septicmmia of mice. — Dr. Koch has described a small bacil- 
 ■ lus — 0.8 to 1 /f long — occurring sometimes in pairs, sometimes in chains, 
 which are found as spores or as developed bacteria in a great variety of 
 putrefying fluids. They may be readily cultivated on gelatin, and the 
 inoculation of the purified organisms or of the putrefying fluids into house 
 mice, produces symptoms characteristic of septicsemia. The bacilli may 
 be found in great numbers in the leucocytes, in the subcutaneous tissue 
 about the seat of inoculation, and very generally in the blood-vessels. 
 The animals may die, or if they survive exhibit a marked immunity from 
 the characteristic effects of subsequent inoculations. Field mice are 
 not affected by inoculation with these bacilli, and rabbits usually but 
 slightly. 
 
 Bacilli of malignant oedema of mice, guinea-pigs, and ralbits. — These 
 are from 3. to 3.5 /t long, rounded at the ends, and more slender than 
 the B. anthracis, which they somewhat resemble. They frequently 
 occur in pairs, and may exhibit spontaneous movements. They occur 
 in cultivated soil, in hay, putrefying fluids, and elsewhere. When intro- 
 duced into the subcutaneous tissue of the above-named animals, they 
 
84 
 
 PAEASITES. 
 
 proliferate and produce a wide-spread oedema about the seat of inocula- 
 tion. In the clear reddish oedematous fluid multitudes of the bacilli 
 may be found. After death they may be found in the blood, in the 
 juices of internal organs, or upon serous surfaces. It is very difBcult to 
 cultivate them outside of the body. 
 
 Leptothrix. — There exist under almost all conditions in the mouth 
 and about the junction of the teeth and gums, single or in larger or 
 smaller masses, long, slender, filiform bacilli, usually without transverse 
 divisions, which have received the general name Leptothrix buccalis. 
 There are some reasons for supposing that they may be concerned in ca- 
 ries of the teeth, in connection with which they are often found. But 
 beyond this fairly well-founded conjecture, we have no reason to suspect 
 them to be of any pathogenic significance. They are frequently entan- 
 
 FiG. 12, — Leptothrix Buccalis with MicRococcrs Colonies from the Mouth of a Healthy 
 Person. Stained with gentian violet, X 600. 
 
 gled among scattered or larger and smaller masses of micrococci. Lep- 
 tothrix is a general name only, and we do not know whether it represents 
 a single genus or species, or whether it is made up of undeveveloped 
 forms of some variety of bacillus. 
 
 IV. Spiro-iacteiHa — s'piral-ceWed bacteria. — The spirals of these cells 
 may be close or open, few in number or numerous; some of them are 
 ciliated at the ends. One of the common genera of these bacteria is 
 SpiiriUum: S. o-icgula occurs in swamp water, on the surfaces of the teeth, 
 and in fseces. It is thick, has open spirals, and occurs in chains or inter- 
 lacing masses. Other species, among which may be mentioned S. ser- 
 pens, occur in stagnant water and in putrefying fluids. 
 
 Fia. 13.— Spiro-bacteria (Genus Spirillum). 
 Spirillum serpens. From putrefying hay infusion stained with fuchsin, x 600. 
 
 Another important genus of spiro-bacteria is Spirochwte, whose cells 
 are in general larger and more flexible than those of spirillum, with more 
 closely set spirals. 
 
 Spirocluete denticola is found in the mucous membrane of the mouth 
 
PAEASITES. 85 
 
 and on the teeth mixed with Leptothrix, and also in carious teeth. It is 
 usually about 10 to 20 /* long, and pointed at the ends. iS. pUcatitis 
 is about 110 to 225 ja long, very slender, with many spirals, and blunt 
 €nds. It moves with great rapidity, and is frequently found in summer, 
 in swamp water and in eavetroiighs. 
 
 The most important member of this group of bacteria is Spirochmte 
 Oiermeieri, because there is little doubt that this species stands in a cau- 
 sative relation to relapsing fever. The cells are quite similar in appear- 
 ance to those of Spirochsete denticola, but somewhat longer and thicker, 
 with compressed spirals. It performs rapid undulating movements. It 
 is constantly found in the blood in greater or less numbers during the 
 attacks of relapsing fever, but is absent in the intervals. The inocula- 
 tion of the blood of relapsing fever patients which contains the bacteria, 
 into monkeys, induces the disease, with the appearance of the bacteria 
 in their blood. They have not as yet been obtained in a pure condition 
 by cultivation outside of the body. 
 
 It should always be borne in mind, in examining tissues taken from 
 the dead body, that various forms of bacteria commence to proliferate in 
 the fluids and tissues very soon after death, and may develop in extra- 
 ordinary numbers in a very short time. 
 
 The Relations of Bacteria to Disease. — Bacteria of various forms may 
 occur on the surface of the skin and mucous membranes, and in the 
 lungs, exerting no apparent influence whatever, so far as we can judge by 
 morphological appearances, upon the surrounding parts. They may occur 
 on the surface of wounds, ulcers, etc., without the production of any 
 evident changes; they sometimes lie within cells which appear otherwise 
 perfectly normal. On the other hand, the cells and tissues in their 
 vicinity may show very marked alterations, which are presumably due to 
 their influence. The cells may be swollen, their nuclei may break down 
 ■or disappear, and the protoplasm may be converted into a mass of shining 
 or coarsely granular particles, or may completely disintegrate. The inter- 
 cellular substance near the bacteria may also soften and disintegrate. In 
 a word, the tissue in their immediate vicinity is often found in a condi- 
 tion of necrosis of one kind or another. The walls of blood-vessels near 
 which they lie may die, and the blood which they carry may form 
 thrombi. The bacteria may themselves enter the vessels and proliferate 
 in the blood; they may be swept away as emboli to remote parts of the 
 body, and establisla new foci of bacterial proliferation and tissue necrosis. 
 Some forms, instead of causing the immediate death of the tissue, appear 
 to incite inflammatory changes about themselves. These may be simple, 
 -and similar to those produced by the presence of any irritating foreign 
 body, or, it would seem that the bacteria may determine, in some way as 
 yet unknown to us, very peculiar and characteristic inflammatory 
 ■changes, which may result in the formation of new tissues of various 
 
86 
 
 PARASITES. 
 
 kinds. Some forms of bacteria find in the blood, others in the lymph- 
 spaces and vessels, the conditions most favorable for their proliferation. 
 
 It will be seen from what has now been said of the bacteria, that in 
 different parts of the system in health, and in a- large number of diseased 
 conditions, various forms of bacteria occur; but it is quite evident that 
 the significance which we must attach to their mere presence varies 
 greatly. In a large number of cases, especially when on parts exposed to 
 the air or in the gastro-intestinal canal, they are evidently of no more 
 importance than so much inorganic dust. When, however, special forms 
 of bacteria are found to occur uniformly in connection with well-defined 
 
 Fig. 14. — Colonies of Micrococci in the Blood-Vessels op the Kidney Forming a 
 
 Small Abscess. 
 Around the dilated and partially necrotic blood-vessel, in which the micrococci lie, is an area, 
 of necrotic tissue and small cell infiltration. From a case of pyaemia, X 700 and reduced. 
 
 diseases, or in their lesions, the conjecture is certainly justified that they 
 may have something to do with their production. Yet in all such cases 
 we have to consider the possibility that it is the diseased state or the 
 character of the lesion, produced perhaps by other causes, which affords 
 conditions suitable for bacterial growth; and that they may consequently 
 occur in considerable numbers; while in the absence of these conditions 
 they would be unable to develop. Even the constant occurrence in the 
 body, ill certain diseases, of bacteria which evidently produce well- 
 
PAEASITES. 87 
 
 marked local effects, either inflammatory or degenerative, does not abso- 
 lutely prove their causative relation to the disease, although it renders 
 it to a certain degree probable. In order to absolutely prove the bacterial 
 origin of an infectious disease, we must not only be able to demonstrate 
 the constant presence in the body at some time of a special form of 
 bacteria, but we must obtain them in an absolutely pure condition, un- 
 mixed with any other living thing, or with any chemical substance not 
 belonging to them, and by the introduction of the purified organisms into 
 a healthy animal, be able to produce the disease, in some definite form. 
 When all this is done, and not before, can we assert with absolute cer- 
 tainty the causative relation between a given form of bacteria and any 
 special infectious disease. But the fulfilment of these strict require- 
 ments is very difScult in many cases, and in some, apparently, almost if 
 not quite impossible, for we must remember, in the first place, that the 
 lower animals, upon which alone, for the most part, inoculation experi- 
 ments are practicable, are apparently hot subject to certain impor- 
 tant diseases of men; and second, that they present among themselves 
 the most marked difEerences in the degree and manner in which they are 
 affected by the inoculation of pathogenic bacteria. Desirable as is the 
 complete fulfilment of the above requirements in every case, it must 
 be admitted that a reasonable certainty regarding the bacterial origin of 
 a given disease may be arrived at without positive results from the inoc- 
 ulation of the bacteria associated with its lesions. 
 
 It is furthermore very important to remember in this connection that 
 the conceptions expressed by the terms pathogenic and infectious are not 
 identical. For a given species of bacteria may be capable of producing 
 lesions in the body or causing a well-defined disease, in other words may 
 be pathogenic, without necessarily being capable of transmitting the dis- 
 ease by direct inoculation. 
 
 To cite the example adduced by Koch in illustration of this point. 
 "Assuming intermittent fever to be a bacterial disease, which indeed re- 
 quires further proof, it would furnish an excellent example of a micro- 
 organism which is pathogenic, but not infectious." 
 
 The discussion of the probabilities of the bacterial origin of certain 
 classes of disease, and the long series of phenomena exhibited by them, 
 which the bacterial theory very satisfactorily explains, does not fall 
 within the scope of this book. 
 
 The complete demonstration which certainty requires has as yet been 
 furnished in but a very small number of cases. In a considerable number 
 of other cases, although the complete cycle of proof has not yet been es- 
 tablished, enough has been (^one in the way of study and experimentation 
 to render it altogether probable that certain forms of bacteria are the 
 cause of the diseases. 
 
 Splenic fever has been proven to be caused, and caused alone, by the 
 
00 PAEASITES. 
 
 Bacillus anthracis. The exhaustive researches of Koch on the Bacillus 
 tuberculosis have covered all the i^oints, so far as we can see at present, 
 which a rigid logical demonstration requires, and judging from them 
 alone, tuberculosis must be regarded as a bacterial disease. These experi- 
 ments are recent, however, and, as an intelligent conservatism should al- 
 ways require, must be confirmed at the hands of other equally conscien- 
 tious and expert observers. All the more important researches on the 
 Bacillus tuberculosis, since the announcement of its discovery, seem in the 
 main to confirm Dr. Koch's observations and conclusions, but none have 
 as yet covered the entire ground. 
 
 All the known facts point towards the Spirochsete Obermeieri as the 
 producer of relapsing fever, and its significance in this respect is generally 
 accepted, although the full cycle of proof has not yet been completed by 
 its cultivation and isolation outside of the body. The proof of the bac- 
 terial origin of erysipelas must also be considered complete, if the investi- 
 gations of Fehleisen and others shall receive the support of confirmatory 
 research. The same may be said of diphtheria, typhoid fever, and chol- 
 era. However probable the alleged causative connection between any 
 of the scores of other diseases in association with which bacteria have 
 been more or less constantly found, it has at the present time (1884), 
 in the writer's opinion, not yet been fully demonstrated. 
 
 Methods of Studying Bacteria. — ^The simplest mode of studying bac- 
 teria is to examine them either in the fluids in which they lie, or in thin 
 sections of the tissues mounted in one-half-per-cent salt solution, and for the 
 study of many of the phenomena of life this method is important. The 
 tissue and other elements, however, with which they are often associated, 
 greatly interfere wi th the study of the bacteria, and many forms are so small 
 as to be scarcely recognizable in the natural condition. We may partially 
 overcome the interference of tissue elements in preparations, by the use of 
 acetic acid, or an aqueous solution of caustic potash (1 to 10), which ren- 
 der the tissues more transj)arent, while but little affecting the bacteria. 
 The latter may be often differentiated in this way from albuminous 
 granules, fat-droplets, etc. 
 
 By far the most important aid, however, is derived from the use of 
 staining agents. Most of the bacteria are stained more or less readily by 
 one or more of the anilin dyes. The ease witli which they are colored 
 varies considerably in different species and with the different dyes. The 
 tissue elements, and a variety of other materials with which the bacteria 
 may be associated, also stain more or less readily at the same time; but 
 most of these part with their color more readily than do the bacteria, on 
 heing treated with alcohol or dilute acids. AVe are thus enabled to ob- 
 tain a differentiation in color between bacteria and other structures. 
 The bacteria, moreover, differ among themselves, in respect to the tena- 
 city with which they hold their stain in the presence of decolorizing 
 
PARASITES. 89 
 
 agents; and upon this fact is based one of the important methods of dis- 
 tinguishing between different species. 
 
 The anilin dyes consist, in the main, of two great groups; the acid and 
 the basic. The acid dyes are those in which the coloring principle acts 
 as the acid. This is not necessarily a free acid, nor does the dye neces- 
 sarily have an acid reaction, but it may be, and in the common commer- 
 cial dyes usually is, combined with some base forming a salt. The basic 
 anilin dyes, which are almost exclusively used for staining nuclei and 
 bacteria, usually come in commerce in the form of salts in combination 
 with some acid, such as acetic or hydrochloric. The common commer- 
 cial fuchsin, for example, is an hydrochlorid of rosanilin. 
 
 Among the anilin dyes more commonly employed for bacteria stain- 
 ing may be mentioned fuchsin, gentian violet, methylen blue, and Bis- 
 mark brown. These are conveniently employed in one-per-cent aqueous 
 solution with about -^V alcohol, to prevent formation of fungi. Some 
 bacteria require special methods for their differentiation, for example, 
 the Bacillus tuberculosis (see Tuberculosis in section on General Diseases). 
 The following methods are well adapted for general use. 
 
 To Stain Bacteria in Fluids. — A small drop of the fluid is placed on 
 a cover-glass, and a second cover-glass pressed close down upon it, 
 so as to spread it into a very thin layer. The glasses are then slid apart, 
 and the fluid dried on to the cover. This may be done by grasping the 
 cover with forceps and passing it, specimen side up, two or three times, 
 quickly through the flame of an alcohol lamp or Bunsen-bnrner. The fluid 
 is to be well dried, but not burned. This drying not only fixes the contents 
 of the fluid firmly on to the glass, so that it will not easily soak off, but it 
 renders insoluble any albuminous materials which may be mixed with the 
 bacteria, and which might otherwise interfere with subsequent examina- 
 tions, by forming granular precipitates. The cover-glass, with its adhe- 
 rent specimen, is now placed in contact with the staining fluid. If a short 
 exposure only is required, a few drops of the stain may be placed directly 
 upon the inverted cover; or, if a longer exposure is required, it is best to 
 float the specimen on the surface of the fluid, in a small disli. The time 
 of exposure required for staining varies considerably in different species 
 •of bacteria, but in general, from flve to thirty minutes will suffice, al- 
 though a longer time usually does no harm. The staining is hastened 
 by gently warming the fluid — not above 40 to 50° 0. The specimen is 
 now washed with distilled water and may be mounted iu glycerin; 
 or better, carefully dried over the lamp, and mounted directly in Canada 
 balsam. It is well to use balsam which has not been softened with 
 chloroform, since the latter extracts the color from some bacteria. It is 
 well, when other materials, besides the bacteria, are present in the fluid, 
 and may be also stained, to extract the color from them, by rinsing the 
 
90 PAEASITES. 
 
 specimen with alcohol or with water to which a few drops of acetic acid 
 have been added (5 to 10 drops to 100 c.c.)- 
 
 To Stain Bacteria in Tissues. — The tissues should be well hardened 
 in alcohol. Thin sections are placed in the coloring solutions where they 
 may remain from one to ten hours. Gentle warming (40 to 50° C.) will 
 hasten the staining. The entire tissue, as well as the bacteria, is in this 
 way deeply colored. The sections are rinsed with distilled water, and 
 then placed in alcohol. This, with varying degrees of rapidity, with 
 different stains and tissues, gradually extracts the color from the tissue, 
 most slowly from the nuclei. The time required and the exact degree of 
 decolorization to be sought for, must be learned by experience in different 
 cases. Sometimes five, sometimes thirty minutes are required. It is 
 often necessary, and the decolorizing of the tissue is thereby hastened, to 
 add a few drops of acetic acid to the alcohol. When acetic acid is used, 
 it should be finally thoroughly washed out by alcohol. The specimens are 
 now cleared up by oil of cloves, and mounted in balsam. Oil of cloves 
 removes the color from some forms of bacteria, and in this case, zylol or 
 oil of bergamot should be substituted for it. 
 
 In specimens prepared in the above way, the nuclei of cells usually 
 retain to some extent a color similar to that of the bacteria, but their size 
 and shape serve for the differentiation. A very useful method of differen- 
 tiating the stained bacteria from tissue elements in many, although appar- 
 ently not in all cases, is that devised by G-ram.' Sections of tissues to be 
 stained must be preserved in absolute alcohol. They are then stained 
 for from one to three minutes (the tubercle bacillus requires from twelve 
 to twenty-four hours) in anilin-gentian violet solution. This is prepared 
 by adding to a filtered saturated aqueous solution of anilin oil a con- 
 centrated alcoholic solution of gentian violet, until a precipitate forms: 
 then filter. This must be freshly filtered each time before using, and 
 should be frequently freshly prepared. From the staining solution the 
 sections are transferred directly to a solution of iodine in potassium 
 iodide and water (I 1.0— KI 2.0— H^O 300.0). In this they remain 
 from one to three minutes, a p)recipitate forming in the solution, and 
 the sections becoming of a dark reddish or slate color. The sections are 
 now transferred to absolute alcohol which should' be changed, and in- 
 this they become almost completely decolorized. They may now be 
 cleared up in oil of cloves and mounted in balsam. 
 
 Certain coloring materials, such as eosin and carmin, have the power 
 of replacing the color in the nuclei, and not in the bacteria, if applied 
 after the anilin staining; and in this way we may get a double staining, 
 which leaves the nuclei of one color and the bacteria of another. For 
 this purpose the anilin staining may be done in the usual way, with 
 
 " Gram: Fortschritte der Medicin, Bd. 2, No. 6, March 15th, 1884. 
 
PAEA8ITES. 91 
 
 some dark-colored dye, such as gentian violet, and after sufficient de- 
 colorization in alcohol or alcohol and acetic acid, the sections are washed 
 in water, and laid for from one-half an hour to an hour in picro-carmin 
 solution. They are then dehydrated with alcohol, passed through oil of 
 cloves, and mounted in balsam. The nuclei are thus stained red, while 
 the bacteria are bluish in color. 
 
 For the recognition and study of bacteria, especially of the, minuter 
 forms, the best optical apparatus is requisite. Good dry lenses will an- 
 swer in many cases; but for finer work, homogeneous immersion lenses 
 (at least ^^) must be employed. 
 
 A special mode of illumination is also in many cases requisite, such as 
 may be obtained by the use of the Abbe condensor. The structural out- 
 lines which the tissue elements present, in many cases greatly interfere 
 with the observation of the color by which the stained bacteria are rec- 
 ognized. This interference is considerably reduced-, by mounting the 
 specimens in balsam; but usually not sufficiently so for the study of the 
 minuter forms. The Abbe condensor is a combination of lenses, placed 
 close beneath the object, by means of which, owing to the direction in 
 which the rays of light are brought upon the object, structural outlines 
 are made to nearly entirely disappear, and in this way the stained objects, 
 the bacteria, stand out much more distinctly than would otherwise be 
 the case, against the nearly homogeneous background. 
 
 Artificial Cultivation of Bacteria. — For the complete investigation of 
 the different forms of bacteria, particularly in their relations to disease, 
 we must study their life-history, and the effects of their inoculation 
 into healthy animals. It has long been known that bacteria could be 
 cultivated in a variety of artificially compounded, so-called nutrient 
 media or soils. Fluids were formerly used for this purpose, but it is very 
 difficult, if not impossible, to cultivate a single species through several 
 generations in fluid media, without an admixture with other forms, or to 
 detect such contaminations when they occur. Moreover, the inevitable 
 mechanical disturbances of the fluid prevent, for the most part, the 
 formation of gross characteristic appearances in the masses of growing 
 bacteria. Dr. Eobert Koch introduced a technical improvement of in- 
 estimable value, in suggesting and formulating the details of using solid 
 media for the cultivation of bacteria. Among these may be mentioned, 
 sterilized boiled potatoes, and gelatinized infusions of various natural or 
 artificially compounded substances, sterilized by heat. Different species 
 of bacteria often require different nutrient media, and some require dif- 
 ferent temperatures for their most flourishing growth. They usually 
 grow on the surface of the nutrient media in sharply circumscribed 
 masses, and different species may grow side by side in the same recep- 
 tacle for considerable periods, without in the slightest degree interfering 
 with one another, or tending to mix. The mode of growth and general 
 
92 
 
 PAEASITES. 
 
 appearances of the proliferating bacterial masses on the solid medium 
 often present very characteristic differences between different forms, and 
 thus not only furnish valuable means of identifying species, but renders 
 possible an early detection of contamination from chance admixture of 
 species. A given species of bacteria may be cultivated through a series 
 of generations by transferring, with proper precautions, a minute portion 
 from a growing colony to a fresh surface of sterilized soil. After culti- 
 vation through several generations, the species may be presumed, and by 
 microscopical examinations proved to be entirely pure, and the effects, if 
 any, produced by its inoculation into healthy animals, to be due to it 
 alone. 
 
 Tlie preparation and use of culture suhstances. — There are many cul- 
 ture media, some of which are best suited for one, some for another, spe- 
 cies of bacteria. Those most commonly used are boiled potatoes, gela- 
 tinized bouillon, and the so-called gelatinized blood-serum. 
 
 The cut surfaces of sterilized toiled potatoes furnish an excellent me- 
 dium for the cultivation of a variety of common atmospheric and some 
 pathogenic bacteria. The potato is first scrubbed clean with water, and all 
 defects on the surface carefully scraped out. It is then washed with a 
 solution of corrosive sublimate 1-1000 to whicli a few drops of HCl are 
 added, in which it should lie for a couple of hours. It is then exposed 
 to a current of live steam for half an hour. The steaming is done in an 
 apparatus called a steam sterilizer.' The steamed potatoes are now taken 
 out (the hands of the operator being carefully washed with sublimate so- 
 lution), and cut into slices with knives whicli have immediately before 
 been heated to redness and cooled. The slices whose surfaces are only 
 to be touched by the sterilized knife-blade, are quickly placed on a plate 
 on which moistened blotting pajDcr is spread, and covered by a bell jar. 
 The plate, bell-jar, and paper should have been disinfected with sublimate 
 solution. The slices may now be kept for some time to see whether they 
 are completely sterilized, or whether bacteria from the air have fallen on 
 them during the manipulations. A simple exposure for a short time to 
 
 ' This consists of a tube 12 ctm. in diameter and about one metre long, at the 
 upper end of which is a conical cover with one opening in the top for tlie escape 
 of steam and one for a thermometer. Tlie substance to be sterilized may be sus- 
 pended in the tube, in a bucket made of wire gauze, by a wire or cord passing 
 up througli the hole in the cover. This whole upright tube is fastened on to the 
 middle of a cover which is to be fitted tightly over any pot or can in which water 
 may be vigorously boiled. An iron pot eight inches in diameter answers very 
 well. The upright tube may be made of tin and should be covered with thick felt 
 or some non-conducting material. On boiling water in the pot, the live steam 
 passes up through the chamber, and any object therein placed can thus be much 
 nrore effectually and thoroughly exposed to the temperature of boiling water 
 than if placed in the water itself. Other forms of sterilizers answer the same 
 purpose. 
 
PAEA SITES. 93 
 
 the air of an inhabited room will usually suffice for the deposition on the 
 sterilized surface of a number of different forms of bacteria, which will 
 rapidly multiply and produce circumscribed masses or colonies of varying 
 color and appearance. If it be desired to study any of these under the 
 microscope, the cover should be cautiously raised, and a small portion 
 removed with a looped platinum wire, fused into a glass rod, which im- 
 mediately beforehand is sterilized by heating to redness. The removed 
 portion may be studied fresh in salt solution, or spread on a cover glass 
 and stained in the usual way. If it be desired to cultivate the separate 
 forms, minute portions may be transferred with the sterilized wire to 
 fresh sterilized potato slices, on which they are planted in a series of 
 lines. Thus a given species may be grown through several generations. 
 Contamination will usually show itself in some change of color or mode 
 of growth of the colonies on the nutrient surface, and may readily be 
 detected by the microscope. 
 
 Less easy to prepare, but of much more general value, is the sterilized 
 gelatiJi louillon. Lean beef is cut into small pieces and pounded in a mor- 
 tar, then mixed with an equal weight of water, and allowed to stand 
 eight to ten hours in a cool place. The watery extract is now squeezed 
 through the cloth and boiled until a clear fluid separates from the coag- 
 ulate. It is now again filtered through cloth and dilated to the original 
 volume with water. To this is added one per cent pepton siccum, one- 
 half per cent sodium chloride, from four to five per cent gelatin. In warm 
 weather more gelatin will be required, sometimes as much as ten per cent. 
 The gelatin may be soaked in the cold in a portion of the beef extract 
 and when it has become softened it may be mixed with the rest, and warmed 
 until the whole is fluid. The acidity of this mixture is neutralized by a 
 suSicient quantity of a saturated aqueous solution of basic sodium phos- 
 phate. It is now filtered warm through sterilized flannel into a sterilized 
 flask, and the neck of the latter stopped with a sterilized cotton plug at least 
 three ctm. long. The filtering of the warm gelatin is facilitated by using 
 a double funnel between the walls of which hob water is allowed to flow. 
 The flasks, cotton plugs, filter, test- tubes, and pipettes to be subsequently 
 used are sterilized by heating in a dry oven for at least an hour to a tem- 
 perature of at least 150° C. The gelatin is now steamed for an hour in 
 the sterilizer or boiled for an hour in water. It is then drawn off by a 
 sterilized pipette into a number of sterilized test-tubes, each of which is 
 filled about ^ full and immediately plugged with sterilized cotton. The 
 contents of the tubes are now allowed to cool and stand for twenty-four 
 hours. They are then steamed again for an hour and set away to cool. 
 Although all developed bacteria are killed by this process, the spores are 
 sometimes so resistant that they will still develop and then may be killed 
 by again boiling and allowing to stand as before. The development 
 of the spores becomes evident by the appearance of opacities upon or 
 
94 PAEASITES. 
 
 within the clear amber-colored gelatin. If the operations have been 
 carefully performed, very few of the tubes will usually show any change, 
 although kept at temperatures suitable for bacterial development. When 
 no more appear, or when those tubes in which a development of spores 
 occurred have been re-sterilized, the tubes are ready for inoculations or 
 may be kept for an indefinite time without exhibiting the slightest 
 change. When the gelatin is permitted to cool for the last time, the 
 tubes should be slightly inclined so as to furnish a larger surface for cul- 
 tivations. The gelatin should not be heated of tener than necessary, and 
 not too long, since it may then lose its power of solidifying. It is well 
 to keep the tubes in a moist chamber to prevent the drying of the surface 
 of the gelatin. 
 
 For inoculation, the cotton plug should be carefully removed, the 
 tube being held horizontally, and the material introduced on the sterilized 
 wire, as in planting bacteria on jootatoes, and the cotton quickly replaced. 
 The wire to which the inoculating material adheres may be rubbed over 
 the surface or stuck into the gelatin for a short distance. 
 
 Gelatinized Mood serum is best adapted for the cultivation of the 
 Bacillus tuberculosis, and is well suited for many other forms. Blood of 
 cattle or sheep is drawn directly into a sterilized iiask, and allowed to 
 coagulate in perfect quiet in a cool place. The serum is transferred with 
 a sterilized pipette to a series of sterilized test-tubes, which are imme- 
 diately plugged with sterilized cotton. These tubes are kept heated an 
 ■hour each day for six successive days to a temperature of 58° C. In this 
 way, it is possible in most cases to completely sterilize the serum. The 
 tubes are now heated to 65° 0. and kept at this temperature in an in- 
 clined position, so as to get a large culture surface, until the contents 
 become stiff. It has now a yellowish, transparent, or opalescent appear- 
 ance, and should be kept for several days at about 35° 0. to see whether 
 it contains any spores capable of development. Those tubes which show 
 no change are ready for inoculation with tuberculous or other materials. 
 
 A number of other materials may be used for solidifying the culture 
 media, among the most generally useful of which are a form of sea-weed 
 known as Agar-Agar and the so-called Japanese isinglass.' The cultures 
 may be conducted in tubes as above described, or when it is desired to 
 study the mode of growth under the microscope, the gelatin may be 
 poured in thin layers on glass slides, which are preserved for inoculation 
 under bell jars, the air of which is kept moist. The temperature at 
 which the ordinary bacteria grow most readily is from 20°-25° 0., and 
 
 ' One per cent of the Agar-Agar may be substituted for the gelatin, and pos- 
 sesses the advantage of not losing its power of solidifying by repeated heating. 
 The Japanese isinglass remains solid at higher temperatures than gelatin, and 
 may be used in 1 to 3 per cent solution. 
 
PAEASITES. 95 
 
 for the maintenance of this temperature they may be kept in a water 
 oven. 
 
 The most scrupulous care is required in sterilizing the nutrient media 
 and the utensils and instruments used, and the greatest caution should be 
 exercised in transferring the bacteria from one receptacle to another to 
 prevent contamination. A large experience in this sort of manipulation 
 is necessary before reliable results can be obtained in original investiga- 
 tion, since the slightest error or carelessness in manipulation or failure 
 to observe the occurrence of contamination are liable to entirely vitiate 
 the results of long series of experiments. It is only by an extended pre- 
 liminary training in the cultivation of some of the more characteristic 
 and easily recognizable forms, under a variety of conditions, in a perfectly 
 pure state, through a series of generations, that one can be assured of 
 his capacity to carry on researches in this most difficult and intricate 
 field. 
 
 The methods of inoculation of animals with pure cultures and the 
 precautions to be observed must be sought in more extended treatises on 
 this subject. 
 
 Bibliography. — The most useful work for general purposes is that by Fliigge 
 on "Fei-ments and Microparasites " in the " Haudbuch der Hygiene und der 
 Oewerbekrankheiten," by Pettenkofer andZierassen, ErsterTheil, 3. Abtheilung, 
 1. Heft, in which will be found an excellent bibliography. Most valuable 
 also are the publications of Koch, among which especially to be noted are 
 ■"Wundinfeotionskrankheiten,-' Leipzig, 1878;" English translation, "Traumatic 
 Infective Diseases," Sydenham Soc, 1880; and " Mittheilung a. d. k. Gesund- 
 Iheitsamte," Berlin, 1881, Vol. I. Among the general works in English the trans- 
 lation of Ziegler's " Pathological Anatomy," by MaoAlister gives the most useful 
 series of references. The work of Sternberg and Magnin on " Bacteria " contains 
 a valuable bibliography and general description of various forms of bacteria, 
 with micro-photographs, modes of staining, etc. 
 
 The voluminous recent literature may be found for the most part in the 
 ■" Index Medicus " for the past few years. 
 
IITFLAMMATIOI"^. 
 
 A Tery considerable number of the lesions which we find in the 
 human body are the results of the various morbid processes which we 
 group together under the name of inflammation. Not only are there 
 different kinds of inflammation, but there are also different tissues which 
 are inflamed and different causes of the inflammatory process. So it 
 happens that the inflammatory lesions yary in their character, their 
 degree, and their anatomy. 
 
 It is convenient to consider separately the phenomena and lesions of 
 inflammation as they are presented to us in connective tissue, in the 
 mucous membranes, and in the viscera. 
 
 I. INFLAMMATION OF CONNECTIVE TISSUE. 
 
 Connective tissue forms a large and important part of the whole body, 
 and is distributed everywhere through it. The tendons, ligaments, 
 membranes, and fascise; the walls of the blood-vessels, the stroma of the 
 viscera, and the frame-work of the mucous membranes all are composed 
 of connective tissue. 
 
 Wherever it exists, connective tissue is composed of a basement sub- 
 stance and of cells, and imbedded in it are blood-vessels, lymphatics, and 
 nerves. 
 
 "When connective tissue becomes inflamed, there follow certain 
 changes in the blood-vessels, the lymphatics, the cells, and the basement 
 substance, and new materials make their appearance, called inflammatory 
 products. The predominance of one or other of these new morbid con- 
 ditions gives a certain character to the particular inflammation, so that 
 we may properly distinguish the following varieties: 
 
 1. Cellular inflammation. 
 
 3. Inflammation, with the production of serum, fibrin, and pus. 
 
 3. Abscesses. 
 
 4. Inflammation, with the production of serum, fibrin, pus, and 
 new connettive tissue. 
 
 5. The formation of granulation tissue. 
 
 6. The formation of new connective tissue. 
 
INFLAMMATION. 
 
 97 
 
 7. Tubercular inflammation. 
 
 8. Syphilitic inflammation. 
 
 1. Cellular Inflammation. 
 
 In this form of inflammation, serum, fibrin, and pus are absent. The 
 circulation of the blood in the inflamed part is but little altered, and the 
 inflammatory lesion is confined to the cells. That the changes in the 
 cells require some change in the nutritive material which they receive 
 from the blood-vessels seems evident, but this is not attended by any 
 marked vascular lesions visible after death. It is probable that such an 
 inflammation, of which the only lesion is a growth and multiplication 
 of connective-tissue cells, may take place in various parts of the body, 
 but the only regions in which we can speak of it with certainty are the 
 serous membranes. Many young connective-tissue cells cannot be dis- 
 tinguished from emigrated white blood-cells, but the endothelial cells 
 can. 
 
 This form of inflammation does not seem to be an early stage of other 
 forms, but is an individual process. It occurs both as an acute and a 
 chronic condition, and is observed in the pia mater, the peritoneum, and 
 the pleura. 
 
 Fig. 15.— Omentum op a Dog. Cellular Peritonitis on the 4th Day, X 500 and reduced. 
 
 In the acute form, the flat connective-tissue cells (endothelium) of 
 the affected membrane are increased in size, and quantities of new cells 
 somewhat resembling them are produced. At the same time the blood- 
 vessels are moderately congested. There is very little swelling or redness 
 7 
 
98 
 
 INFLAMMATION. 
 
 of the inflamed tissue, the changes to the naked eye are slight; and yet 
 this apparently trivial lesion produces marked clinical symptoms and 
 often death. 
 
 In the chronic form, the inflammatory process may stop short at the 
 production of new flat cells, or the cells may become aggregated together 
 into delicate membranes, which cover the surfaces of the inflamed parts 
 or form adhesions. 
 
 2. Inflammation with the production of serum, fibrin, and pus. 
 
 This form of inflammation is in strong contrast with the preceding. 
 The connective tissue and its cells remain comparatively passive, while 
 the blood-vessels and the blood are the active agents. We are able not 
 only to observe the results of this form of inflammation after death, but 
 also to witness the different stages of the process during life. 
 
 The transparent connective-tissue membranes of some of the lower 
 
 ,FiG. 16. — Emigration of White Blood-cells in inflamed Bladder of Frog, X 500 and reduced. 
 
 animals can be studied under the microscope while inflammatory changes 
 are going on. In this way we have learned that there is first a dilatation 
 of the arteries, veins, and capillaries, and an increased rapidity of the cir- 
 culation of the blood. Then the blood-current becomes slower, white 
 blood-cells accumulate in the small veins and capillaries, and adhere to 
 their walls. Then the white cells, changing their shape, find their way 
 between the endothelial cells of the vessels, through their walls, and ap- 
 pear on the outside of the vessels in the tissue (Fig. 16). This process is 
 called emigration. Red blood-cells in smaller numbers may also pass 
 
INFLAMMATION. 99 
 
 tlirougli the walls of the capillaries and veins, and this is called diapedesis. 
 At the same time the plasma of the blood transudes through the walls of 
 the vessels and infiltrates the tissues as serum; while by the union of 
 substances contained in the blood plasma and in the white cells fibrin is 
 formed. 
 
 Ill this simple manner are elaborated the inflammatory products — 
 pus, serum, and fibrin, which are sometimes called exudations. The 
 pus-cells are emigated white blood-cells; the serum is part of the plasma 
 of the blood; the fibrin is produced by a union of the fibrinogen in solu- 
 tion in the blood plasma with substances contained in the white blood- 
 cells, and appears coagulated in the form of granules, amori:)hous masses, 
 or a reticulum. 
 
 In order that these inflammatory products may be formed, it is evi- 
 dently necessary that the blood should continue to circulate through the 
 vessels of the inflamed tissue. 
 
 Different examples of this form of inflammation give different 
 amounts of inflammatory products, and also different relative proportions 
 of serum, fibrin, and pus ; wliile extravasated red blood-cells may also be 
 intermingled with them. 
 
 The inflammatory products may accumulate wherever there are cavi- 
 ties to receive them, in the interstices of connective tissue, on the sur- 
 faces of the serous membranes, and in the serous cavities. 
 
 The ordinary course of such an inflammation may be modified: 
 
 {a) The congestion may be extreme, the blood may cease to circulate 
 in the vessels, and in this way a considerable area of tissue may die with- 
 out the production of any considerable amount of serum, fibrin, or pus. 
 
 (5) The inflammation may be of a very intense type; the production 
 of inflammatory products, especially of flbrin, very large ; there may be 
 stasis in some of the vessels. As the combined result of the stasis, and 
 the pressure of the inflammatory products, there is necrosis of small por- 
 tions of tissue. 
 
 (c) The congestion is so great that the blood ceases to circulate in 
 some of the vessels of the inflamed part, while it continues to do so in 
 others. There is at the same time a large production of pus-cells, and a 
 necrosis and breaking down of tissue. In this way are formed 
 
 3. Abscesses. 
 Abscesses are collections of pus contained in cavities. The cavities 
 are formed by the destruction of tissue. The pus is a fluid composed of 
 serum, pus globules, and fragments of necrotic tissue. According to 
 the relative quantity of these three substances, the character of the pus 
 will vary. Whether all the pus-cells are emigrated white blood-cells, or 
 whether some of them are derived from connective-tissue cells cannot be 
 certainly determined. Pus contained in a cavity seems to act as an ir- 
 
100 
 
 INFLAMMATION. 
 
 ritant to the siu-rounding tissues, and sets up in them inflammation of a. 
 more or less severe type. In this way the abscess often becomes larger 
 and extends in different directions. In most abscesses bacteria of 
 various kinds are found in the pus. 
 
 4. Inflammation with the production of serum, fibrin, pus, and 
 new connective tissue. 
 
 In this form of inflammation, both the blood-vessels and the connect- 
 ive-tissue cells take an active part. From the blood-vessels come the 
 serum, fibrin, and pus. Prom the connective-tissue cells and from the 
 emigrated white blood-cells are produced new cells, which are at first 
 small and of indiflierent type, but later assume the characteristic shape 
 of the cells of the new tissue. As the inflammation subsides, the serum, 
 fibrin, and pus, and some of the new connective-tissue cells are absorbed 
 after degenerative processes. The rest of the new connective-tissue cells 
 2:0 on to the formation of new connective-tissue with cells and basement 
 substance, so that the result of the whole process is the formation of per- 
 manent new connective tissue, or of granulation tissue. 
 
 5. Granulation Tissue. 
 This name is employed to designate a peculiar form of new tissue, 
 which is developed from connective tissue, or from emigrated white 
 
 Fig. 17.— Gbanhlation Tissue from Wound 01? Skin, x 500 and reduced. 
 
 blood-cells, in the course of acute and chronic inflammations, and after 
 the destruction of tissue by wounds or necrotic processes. 
 
 Granulation tissue (Pig. ] 7) is composed of cells, a basement sub- 
 stance, and blood-vessels. 
 
 The cells are numerous and often close together. Some resemble 
 
INFLAMMATION. 
 
 101 
 
 white blood-cells ; some are small, polyhedral cells with a large nucleus; 
 some are larger, polyhedral cells resembling epithelial cells; some are 
 fusiform or branched. 
 
 The basement substance is at first scanty and homogeneous, or 
 finely granular. As the granulation tissue grows older, it becomes more 
 abundant, denser, and fibrillated. 
 
 The blood-vessels are very numerous and at first thin-walled. They 
 are formed from the original blood-vessels of the connective tissue by the 
 ■outgrowth of solid sprouts of protoplasm which afterwards become chan- 
 nelled, so that tlie blood passes into them, and changed so as to form a 
 wall of endothelial cells (Pig. 18). 
 
 Frn. IS. Fie. 19. 
 
 Fig. 18.— Developing Blood-vessels in new-pormed Tissue, x 500 and reduced. 
 Fig. 19. — Cicatricial Tissue, X 500 and reduced. 
 
 The surface of sach granulation tissue is dry, or coated with serum, 
 pus, or fibrin. 
 
 It may remain in the condition of granulation tissue for an indefinite 
 length of time, or it may be gradually changed into cicatricial connective 
 tissue. In the latter case, the basement substance increases and becomes 
 dense, the cells disappear, the new blood-vessels are obliterated, and 
 there results a dense, contracted area of connective tissue (Fig. 19). 
 
 Such granulation tissue is the ordinary result of wounds of all kinds, 
 and is the medium by which they are repaired. 
 
 Any destruction of tissue is followed in the same way by the forma- 
 tion of this new tissue, so that the floors and walls of ulcers and abscesses 
 may be formed of granulation tissue. 
 
 Acute and chronic inflammation of connective tissue are often at- 
 tended with an abundant cell growth and the splitting up of the base- 
 ment substance, so that here, too, granulation tissue is formed. 
 
-[Q2 INFLAMMATION. 
 
 6. Inflammation with the prodvction of connective tissue. 
 This form of inflammation is of a chronic type. It runs a slow course, 
 and the formation of new tissue is gradual. There is no production of 
 serum fibrin, or pus. The inflammatory product is new connective tis- 
 sue—both cells and basement substance. The cells may be numerous, 
 and the new tissue approach the type of granulation tissue; or the base- 
 ment substance may be formed in large quantity, so that the new tissue 
 
 is firm. • , ^ „ 
 
 7. Tubercular Inflammation. 
 
 This form of inflammation is characterized by the formation of an 
 inflammatory product called tubercle tissue, a tissue nearly related to 
 
 Fig 20— Tubercle Tissue from Acute Phthisis X loOO and leduced 
 
 granulation tissue. It is composed of a basement substance and cells. 
 The basement substance is very delicate and transparent, or denser and 
 more opaque, according to the duration of the inflammatory process. In 
 the basement substance are round and oval nuclei, the oval nuclei being- 
 particularly transparent and delicate. 
 
 The basement substance is arranged so as to form a reticulum con- 
 taining spaces, and in each space is a polygonal nucleated cell. The large 
 multinuclear masses of protoplasm, called giant-cells, are often present 
 and seem either to form part of the basement substance, or to be in the 
 shape of circumscribed cells. 
 
INFLAMMATION. 
 
 103 
 
 Tubercle tissue is arranged in the form of little spheroidal masses — 
 tubercle granula, or of a diffase tissue — tubercle tissue. 
 
 Tubercular inflammation is regularly accompanied by other inflam- 
 matoi-y processes with the formation of pus, fibrin, connective-tissue 
 cells, and granulation tissue. 
 
 Wherever tubercle tissue is produced, there is a change in the small 
 blood-vessels. In some there is an obliterating endarteritis, in others a 
 growth of the endothelial cells. There is also hardly any formation of 
 new vessels in the tubercle tissue, so that it is apt soon to degenerate. 
 
 The little bodies called miliary tubercles may be formed of tuber- 
 
 ^f 1. 
 
 
 Fig. 21.— a Tubercle Granulum from the Pleura, X 850 and reduced. 
 The giant-cells form part of the basement substance. 
 
 cle tissue alone, or mixed with inflammatory products, or of granulation 
 tissue mixed with other inflammatory products. 
 
 In most forms of tubercle tissue, especially when in the state of 
 active formation or of cheesy degeneration, we find the Bacillus tubercu- 
 losis of Koch in greater or less numbers. It is also found in the miliary 
 tubercles which are not composed of typical tubercle tissue. (See Tuber- 
 culosis.) 
 
 8. Syphilitic Inflammation. 
 
 The poison of syphilis gives rise to a variety of inflammations aSect- 
 
INFL AMM ATION . 
 
 ■^ 
 't"?^ 
 
 
 ^^ji- a 
 
 <^J 
 
 u 
 
 ^-«r**'lf^' '.. '^5/_v:j3^ 
 
 
 
 
 
 
 ■■ 3 
 
 4i^ 
 
 
 
 If ^ -/r^'ij^ 
 
 Fig. 23.— a Tdeebcle Geanuldm from a Lymphatic Gland, X 850 and reduced. 
 The giaut-oells are enclosed by the basement substance. 
 
 
 
 
 • ■^^ 
 
 
 
 - n 
 
 > t 
 
 
 .*T' *• 
 
 '^> 
 
 #c 
 
 i 
 
 ^^"■'i 
 '^t* 
 
 N* 
 
 ^ 
 
 # 
 
 • > 
 
 Fig. S3.— a Tubercle Granulcm and diffuse Tubercle Tissue from Cbrokio Phthisis, 
 
 X 850 and reduced. 
 
INFLAMMATION. 105 
 
 • 
 
 ing difEerent parts of the body. Only one of the inflammatory processes, 
 howeyer, can be fairly said to present characteristic structural features — 
 the one which results in the production of the gummy tumor. From the 
 circumscribed character of this inflammatory product and the size which 
 it often reaches, it is frequently described among the tumors, but it is 
 really only a result of inflammation. 
 
 Syphilitic inflammation has been observed in many difEerent parts of 
 the body. Wherever connective tissue exists, either in the form of mem- 
 branes, as the stroma of viscera, as the frame-work of mucous mem- 
 branes and the skin, or as the periosteum of bones, it is liable to this 
 form of inflammation. 
 
 The inflammatory process may be acute, or slow and chronic. The 
 inflamed part becomes swollen, and in the acute form congested. There 
 is a production of ^ small round cells and of a basement substance. The 
 cells are fragile and imperfectly formed, the basement substance is of 
 soft, gelatinous character. These inflammatory products are usually 
 formed within a circumscribed area, so as to make a sort of tumor — the 
 gummy tumor. 
 
 The inflammatory |)roduct may remain in this condition of cells and 
 gelatinous basement substance for some time, and then be absorbed and 
 disappear, or it may undergo further changes. 
 
 Most frequently it undergoes cheesy degeneration, and then is sur- 
 rounded by a zone of granulation tissue and fibrous tissue. Or it may 
 be changed into fibrous tissue, or it may suppurate, and form abscesses. 
 
 In a recent gummy tumor of the periosteum, this membrane is split 
 uj) into layers. At the centre of the gumma the connective tissue is infil- 
 trated with cells and fibrin, all in the condition of coagulation necrosis. 
 The periphery of the gumma is' infiltrated with cells, and the arteries are 
 changed. Their walls are thickened, and the endothelial cells are 
 increased in size and numbers. 
 
 Bacteria have been repeatedly found in the characteristic lesions of 
 syphilis by several observers, among whom may be mentioned Klebs.,' 
 Birch-Hirschfeld,' Aufrecht,' Barduzzi," Morison.' While some of these 
 observers describe the bacteria as small rods, the later researches of 
 Birch-Hirschfeld, and those of Aufrecht, Barduzzi, and others, go to 
 show that they are micrococci which are often arranged in pairs or in 
 short chains and which may readily be mistaken for rods. That these 
 
 'Klebs, Arohiv f. exp. Path., Bd. x., pp. 161-221, 1879. 
 
 =i Biroh-Hh-schfeld, Centralblatt f. Med. Wiss., 1882, Aug. 19th, p. 582, and 
 Nov. 4th, p. 785. 
 
 8 Aufrecht, Centrbl. f. Med. Wiss., 1881, p. 228. 
 
 ^Barduzzi, Gazz. degliospitali, 1884, No. 13, Review in Centrbl. f. Klin. Med., 
 1884, No. 12. 
 
 'Morison, Maryland Med. Jour., Jan. Isfc, 1883. 
 
106 rSTFLAMMATION. 
 
 bacteria stand in a causative relation to the disease has not yet been 
 proven. 
 
 II. INFLAMMATION OF MUCOUS MEMBRANES. 
 
 Mucous membranes are composed of a layer of epithelium, a connec- 
 tive-tissue framework, and of glands. The epithelium is of the cylindri- 
 cal, or ciliated, or polygonal variety, according to the particular mucous 
 membrane. The connective-tissue' framework supports the epithelial 
 layer, and is itself provided with blood-vessels, lymphatics, and nerves. 
 The glands are of the tubular and racemose character; they are embedded 
 in the connective-tissue framework; their function is to produce mucus. 
 During health, mucus of normal quantity and quality is constantly pro- 
 duced by the glands or epithelium of the surface. The epithelial layer 
 is in a constant condition of growth of the deeper cells, and desquamation 
 of the superficial ones. 
 
 Mucous membranes may be affected by catarrhal, croupous, purulent, 
 tubercular, and syphilitic inflammation. 
 
 1. Catarrhal Inflammation. 
 
 (a) Acute catarrhal inflammation. — This form of inflammation is 
 much better marked during life than after death. During life the le- 
 sions are evident, but they are of such a character that after death they 
 can often no longer be recognized. 
 
 The first evident result of the inflammatory process is congestion, and 
 swelling of the affected membrane; the congestion and the swelling, 
 and the preponderance of venous congestion, varying with the intensity 
 of the inflammation. In the worst cases the congestion is so extreme 
 that the blood ceases to circulate, and the part becomes gangrenous. At 
 first, the function of the mucous glands is suspended so that the surface 
 of the inflamed membrane is unnaturally dry; later these glands produce 
 mucus in increased quantity and of altered quality, which coats the in- 
 flamed membrane or runs off from its surface. 
 
 The superficial layers of epithelium desquamate more rapidly than in 
 health, while in the deeper layers new cells are produced in increased 
 numbers. 
 
 The congestion of the vessels is attended with the emigration of only 
 a moderate number of white blood-cells, which infiltrate the connective 
 tissue or reach the surface, and are mixed with the mucus and desqua- 
 mated epithelium. 
 
 Eed blood-cells may escape in considerable numbers either by diape- 
 desis or by rupture of vessels, so that fluid blood is discharged from the 
 free surface of the membrane. In mucous membranes provided with 
 lympathic glands, these glands may become swollen, they may soften and 
 break down and thus form small, round ulcers. 
 
INFLAMMATION. lOT 
 
 (b) Chronic Gatarrlial Inflammation. — This form of inflammation 
 is regularly attended with structural changes which are evident after 
 death. But yet these changes are not always in proportion to the symp- 
 toms observed during life. The excessive production of mucus and pus 
 which exists during life is not necessarily attended with marked changes 
 in the mucous glands or blood-vessels. 
 
 The layer of epithelium often becomes irregular, thinned in some 
 places and thickened in others. The cells are deformed in various ways. 
 
 The blood-vessels may be increased in number, dilated and distended 
 with blood; the inflamed membrane is then of a red or purple color. Or 
 the blood-vessels are small, contain but little blood, and the membrane is 
 pale. Or there may be an irregular deposit of pigment so that the mem- 
 brane is of a blackish color. 
 
 The connective-tissue framework may be atrophied or hypertrophied. 
 When it is atrophied the entire membrane is thinned. The hypertrophy 
 maybe diffuse with thickening of the entire membrane; or circumscribed 
 with the formation of j)olypoid growths. 
 
 The secretion of the mucous glands may be increased, altered in 
 character and mixed with pus; or it may be diminished. 
 
 The glands themselves maybe atrophied and obliterated; or they may 
 be dilated so as to form cysts; or they may be hypertrophied. Some- 
 times the circumscribed hypertrophies of the stroma are associated with 
 hypertrophy of one or more glands, and then the polypoid outgrowths 
 will be composed partly of glands. 
 
 If the inflamed membrane has lymphatic glands embedded in its wall, 
 ulcers are often formed by the swelling and breaking down of these 
 glands. 
 
 2. Purulent Inflammation. 
 
 This form of inflammation resembles acute catarrhal inflammation in 
 some respects. There is the same congestion and swelling of the mucous 
 
 Fig. 24.— Pus Cells fkom Purulent Inflammation of Bronchial Mucous Membkane, X 1200 and 
 
 reduced. 
 
 membrane, the same increased production of mucus, the same desqua- 
 mation of the superficial and growth of the deep epithelial cells. But 
 all these changes are much more intense in purulent inflammation than 
 in catarrhal. The characteristic difference, howeveiv between the two 
 
108 
 
 nSTFLAMMATION. 
 
 forms of inflammation is that in jourulent inflammation there is a large 
 emigration of white blood-cells from the congested vessels. These cells 
 do not infiltrate the mncons mem.brane to any great extent, but for the 
 most part find their way to its surface and there are mixed with the 
 mncns. 
 
 3. Croupoits Inflammation. 
 
 There is a very great convenience in having some name to designate 
 that form of inflammation of mucous membrane which is characterized 
 by the production of pus and fibrin, without any reference to the cause 
 which produces the inflammation. The term 'croupous inflammation' 
 is not a good one, but it will answer the purpose if we use it as an arbi- 
 trary name to designate a definite anatomical lesion confined to the mu- 
 cous membranes. The term ' diphtheritic inflammation ' is also used to 
 express the same lesion. But this word is more objectionable, as it im- 
 plies that the process is related to the general disease, diphtheria. In 
 diphtheria the characteristic lesion is a croupous inflammation, but this 
 
 -ia? -- 
 
 Fig. 35.— Croupous Inflammation of Trachea, X 500 and reduced. 
 In this case there is purulent infiltration of the mucosa and submucosa and of portions of the 
 mucous glands, a. False membrane, b, Portion of intact epithelium, u, Infiltration of the mu- 
 cosa with fibrin, d, Portion of mucous gland infiltrated with pus. 
 
 inflammation does not differ anatomically from the croupous inflamma- 
 tion due to other causes. 
 
 In croupous inflammation the Avhole thickness of the mucous mem- 
 brane is congested and swollen. The production of mucus is arrested. 
 The white blood-cells emigrate, and the plasma exudes from the vessels. 
 In this way are produced pus and fibrin which infiltrate the interstices 
 of the connective-tissue framework, and make their appearance on the 
 
INFLAMMATION. 109 
 
 surface of the inflamed membrane as a false membrane. In some cases 
 the superficial layers of the epithelium undergo coagulation necrosis, the 
 cells are changed in their shape and appearance, so that they look like a 
 network of coagulated fibrin. 
 
 In some cases the congestion of the vessels and the pressure of the in- 
 flammatory products are sufficient to cut off the vascular supply of por- 
 tions of the inflamed mucous membrane, and so cause their death. This 
 death is followed by sloughing, and in this way ulcers are formed. 
 
 The whole inflammatory process is, therefore, one in which the blood- 
 vessels take the most active part, but which is complicated by the ten- 
 dency to superficial and deep necrosis. 
 
 The intensity of the process, the quantity of fibrin and pus, the de- 
 gree and depth of the infiltration of the connective-tissue framework, 
 and the extent of the necrosis, vary in the different cases. 
 
 The false membrane which coats the surface of the inflamed mucous 
 membrane is composed either of fibrin and pus alone, or of necrotic 
 epithelium alone; or both of these are present in varying proportion. 
 Bacteria of different varieties are also often infiltrated in the false mem- 
 brane or lie upon its surfrce. 
 
 4. Tuliercular Inflammation. 
 
 Tubercular inflammation is developed in two different ways, which 
 may exist separately or be combined. 
 
 (a) Tubercle granula are formed in the connective-tissue framework 
 of the mucous membrane close beneath the epithelium. Bound cells of 
 indifferent type infiltrate the connective tissue around the tubercle, and 
 a diffused catarrhal inflammation is developed. The tubercle granula 
 may become cheesy and soften; the epithelium and tissue over them 
 then become necrotic and slough away, and in this way ulcers are 
 formed. 
 
 In the intestines the tubercle granula are usually formed in the 
 solitary or agminated glands instead of in the connective tissue. 
 
 {b) A diffuse catarrhal inflarflmation of a peculiar type is developed. 
 There is an increased production of mucus, desquamation and prolifera- 
 tion of the epithelium, and an infiltration of the connective-tissue frame- 
 work with round cells and tubercle granula. There is a marked tendency 
 to cheesy degeneration, not only of the tubercle, but also of the other in- 
 flammatory products and of the tissue of the mucous membrane. So we 
 find the inflamed membrane coated with cheesy matter, and itself thick- 
 ened, cheesy^ and ragged. 
 
 5. Sypliilitic Inflammation. 
 
 In the mucous membranes the only characteristic syphilitic inflam- 
 matory lesion is the 'Mucous Patch,' or 'Condyloma.' 
 
-^-^Q INFLAMMATION. 
 
 A mucons patch is at first a circumscribed flattened swelling, formed 
 by the growth of imperfect granulation tissue in the connective-tissue 
 framework beneath the epithelium. Later this granulation tissue dies 
 and degenerates, the epithelium over it becomes loosened and detached, 
 and in this way ulcers are formed. The process may be still further 
 complicated by the development of a suppurative inflammation of the 
 surrounding connective tissue. 
 
 III. INFLAMMATION OF THE VISCERA. 
 
 Every viscus is composed of a connective-tissue stroma, in which are 
 blood-vessels, nerves and lymphatics, and of cells. These cells are the 
 characteristic anatomical constituents of each viscus by which its pro- 
 per functions are effected. Such cells, therefore, besides living, have to 
 perform functions, and any morbid process affects not only their vitality, 
 but their capacity for performing their proper functions. So we find 
 that the importance of inflammation of the viscera is principally on ac- 
 count of the consequent derangement of their functions. 
 
 We can distinguish : 
 
 1. PareticJiymatous InflcmiDiaiion. 
 
 In this form of inflammation the lesions are confined to the charac- 
 teristic cells of the viscus. The stroma and the vessels take no active 
 share in the process. 
 
 The cells are first swollen, then the substance which forms the cell 
 body is changed and becomes granular, then it is infiltrated with coarse 
 granules and small fat-globules, and finally it breaks down into an 
 amorphous granular mass. 
 
 Such changes seem identical with other changes which are simply 
 degenerative; but yet they are often developed in the viscera in such a 
 way as to deserve the name of an acute inflammation. 
 
 2. Interstitial In-fiainmation. 
 
 This is an inflammation of the stroma of the viscera, and is of the 
 same characters as have been already described in speaking of connective 
 tissue. 
 
 There may be a congestion of the blood-vessels and an emigration of 
 white blood-cells with exudation of plasma, so that the inflamed stroma 
 is infiltrated with serum, fibrin, and pus in different proportions. 
 
 The emigration of white blood-cells may be associated with necrosis 
 and liquefaction of portions of tissue, and so abscesses are formed. Or 
 the inflammation may be of a chronic character with the production of 
 new connective tissue, both basement substance and cells. 
 
 In all cases the inflammation is confined to the stroma, and the cells 
 of the viscus only undergo degenerative or necrotic changes. 
 
INFLAMMATION. HI 
 
 3. Diffuse Inflammation. 
 
 "We may employ this term to designate those inflammations of the 
 yiscera, in which there are active changes both in the stroma and in the 
 parenchyma cells. Such an inflammation may run either an acute or a 
 chronic course. 
 
 In the stroma there may he an inflltration with serum and pus, and a 
 new growth of connective-tissue cells with or without a growth of base- 
 ment substance. 
 
 In the cells there are changes of the same character as those which 
 occur in parenchymatous inflammation. Besides this, the cells become 
 degenerated, deformed, and displaced in various ways. 
 
 Both tubercular and syphilitic inflammations are developed in the 
 viscera, but no satisfactory general description of them can be given. 
 They must be described as they occur in each particular yiscus. 
 
TUMOES. 
 
 SECTION I. GENERAL CHARACTERS. 
 
 Tumors are composed of the same types of tissue as those normally 
 existing in the body, and from the hitter they are derived by a prolifera- 
 tion of pre-existing cells. The tissues of tumors may be similar to those 
 of the part in which they grow, when they are called hoviologous; or they 
 may be dissimilar, and are then called heterologous. Tumors are not 
 only analogous to the normal tissues of the body in structure, but their 
 life history transpires under the same general laws of nutrition, growth, 
 reproduction, etc. With this important difference, however, that while 
 the normal tissues, serving as they do a definite purpose in the organism, 
 are closely limited in their growth and minute chai'acters by physical 
 and other conditions which determine the uniform development and cor- 
 relation of various parts; the tissues of tumors exhibit a certain lawless- 
 ness in growth, structure, and life history, which gives them a distinctive 
 character while not removing them from the physiological types. Thus 
 in the Chondromata,' the tissue, while distinctly cartilaginous in type, 
 presents itself not only in places where it does not belong, but may 
 show a tendency to the develojjment of fibres in one part of its base- 
 ment substance, while another may be distinctly hyaline or another soft 
 and almost gelatinous. The cells also are apt to exhibit great lack of 
 uniformity in size, shape, and grouping. The lawlessness in tumor tis- 
 sues is shown in their tendency, under certain conditions, to change from 
 one form into another, as from fibrous tissue into bone. 
 
 Tumors are supplied with blood-vessels which grow into them from 
 adjacent healtliy parts, just as they do into granulation tissue, so that 
 they may finally possess a more or less independent vascular system of 
 arteries, capillaries, and veins. They are furnished with lymph-vessels 
 and some of them with nerves. The cell division by which tumors grow 
 exhibits the same minute phenomena as does cell division in normal 
 tissues. Tumor tissues are subject to the same degenerative changes as 
 
 ' Tumors are designated by the termination oma (plural omata). 
 
TIJMOES. 113 
 
 other tissues; they may become fatty or calcified, ulcerated, gangrenous, 
 pigmented, etc. By necrotic changes a tumor may be largely destroyed, 
 but complete obliteration rarely occurs in this way. They are liable to 
 undergo the ordinary inflammatory changes, granulation tissue may form 
 in them, and abscesses and cicatrices. 
 
 The rapidity of growth of tumors varies greatly; some grow very 
 dowly indeed, and may change but imperceptibly in size and appearance 
 for years, while others, on the other hand, grow so fast that they do not 
 acquire solidity, and their elements remain in an incompletely developed 
 •condition, and are thus more liable to destructive changes than normal 
 tissues are. In healthy tissues the blood-vessels are supported by sur- 
 rounding elements, which aid them in sustaining the blood-pressure from 
 within. In rapidly growing tumors this external support is often lacking, 
 and as the walls of the blood-vessels are themselves badly formed, the 
 result is that the walls are apt to become pouched or aneurismal, and 
 they often burst, giving rise to larger- or smaller interstitial hemorrhages. 
 
 Tumors have various shapes: nodular, tuberous, fungoid, polypoid, pa- 
 pillary, dendritic, etc. 
 
 Tumors may occur singly or in greater or less numbers in the same or 
 in different parts of the body. If they are multiple, they may have oc- 
 curred simultaneously or at different times, as independent structure. 
 Or, multiple tumors may occur as the result of the dissemination in the 
 body from a primary tumor, of cells which form a starting-point for new 
 tumors. Many tumors are sharply circumscribed, may be even encapsu- 
 lated, and influence surrounding parts only by the pressure which they 
 €xert upon them. In this way tJiey may cause disi^lacement, atrophy, or 
 necrosis; they may by pressure on neighboring vessels cause oedema, 
 thrombosis, etc.; they may in the same way cause dislocation, and caries 
 of bones. 
 
 Tumors may grow largely by increase of elements within them, thus 
 simply expanding; this is called central groivth. They may grow in part 
 or largely at the surface — peripheral growth. In this case the growth may 
 be a direct continuous enlargement of the mass at or near the periphery, 
 or it may be by the formation of secondary nodules near the priniiiry 
 growth, which, gradually enlarging, finally coalesce with the latter, form- 
 ing a part of the nodular tumor. This mode of enlargement is called 
 discontinuous peripheral groivth, and is due to the dissemination of cells 
 from the mother tumor into the adjacent tissue, through the blood or 
 lymph channels, and their proliferation at the points of lodgment. This 
 dissemination may occur by the agency of blood or lymph currents or by 
 the amoeboid movements of the cells. 
 
 It is not yet certain whether the new-cells which are produced in 
 tumors are altogether the result of the proliferation of the primary tumor 
 cells, or whether the ordinary tissue cells of the part, connective-tissue 
 8 
 
J 14 TUMORS. 
 
 cells, white blood-cells, etc., may undergo transfoi-mation and prolifera- 
 tion 'under the influence of the characteristic cells of the tumor. It is 
 not unlikely that both modes of increase occur, although the former is 
 probably the more common and important. Some tumors increase by 
 an infiltration of surrounding tissues, whose elements they gradually re- 
 place. In certain tumors the old tissue of the part in which they grow 
 may remain with its vessels, and form a sort of matrix whose interstices 
 are infiltrated with the new tumor-tissue. The irritation of the tumor 
 may induce infliimmatory new formation of tissue of the old matrix 
 about or within the tumor. 
 
 But all tumors are not limited to that part or region of the body in 
 which they first occur. Sooner or later, secondary nodules resembling the 
 first m:iv be found in the most distant parts of the body; sometimes 
 singly, sometimes in great numbers. These may grow like the parent 
 tumor, and themselves form foci for new disseminations. 
 
 This dissemination of tumors is one of the most important elements of 
 malignancy, and is called metastasis, the secondary tumors being called me- 
 tastatic tumors. This occurs by the transportation of tumor-cells through 
 the blood or lymph channels. Since the tumor itself may be filled with 
 new and badly formed blood and lymph-vessels, and its structures be in 
 close contact with the vessels of the tissue in which it grows, the cells of 
 the primary tumor may, by ulceration through, or by atrophy of the 
 walls, readily find their way into the lumen of the vessels, and be swept 
 away by currents as emboli, and finding lodgment, proliferate and grow, 
 forming secondary tumors; or the jirolif oration may occur in the vascu- 
 lar endothelium itself, when the formation of emboli is easy to under- 
 stand. When carried through the lymph-vessels, the tumor-cells may 
 for some time be kept from the larger channels, and from general dis- 
 semination by lodgment in the lymph glands, where they may establish 
 independent tumors. The parts of the body in which metastatic tumors 
 are most apt to form, depend, of course, upon the situation of the 
 primary tumor and the distribution of the vascular channels through 
 which dissemination occurs. 
 
 The tumors in which metastasis is most apt to occur are, as a rule, 
 those which grow rapidly, are vascular and succulent, and contain many 
 cells. 
 
 Not less variable than the size, mode of growth, and structure of tu- 
 mors is their significance in the organism. Surgeons have in the past, 
 and to a certain extent still do classify tumors, for practical purposes, as 
 malignant and benign, and for a long time malignant tumors and can- 
 cer were synonymous terms. Now we know that other tumors as well 
 as cancers are malignant, and furthermore, contrary to the former 
 belief, that malignancy does not depend upon any specific agent in the 
 tumor. If we mean by a malignant tumor one which may cause death 
 
TUMORS. 115 
 
 any tumor may be malignant if growing in the right place. Thus a 
 simple fat tumor, by pressing on the trachea, may cause suffocation, and 
 any tumor may secondarily cause death by hemorrhage or septicasmia. 
 The rpal signs of malignancy in a tumor are: 1. Invasion of adjacent tis- 
 sues by eccentric or peripheral growth. 2. The tendency to local recur- 
 rence after removal. 3. The formation of metastases. 4. A tendency 
 to interfere with the nutrition and general well-being of the body, which 
 may give rise to a condition known as cachexia. The modes of inva- 
 sion of surrounding tissues and the formation of metastases have been 
 considered above. The tendency to local recurrence after removal is 
 probably in most, if not all cases, due to the incomplete removal of the 
 peripheral infiltrating cells. These may be very few in number and lack- 
 ing in characteristic structural features, but are none the less endowed 
 with the capacity of proliferation and development into a new and simi- 
 lar tumor at or near the seat of the extirpated one. The infiltrating 
 peripheral cells may remain dormant for a long time after an operation, 
 or may immediately commence to grow. The mere fact that a second 
 tumor develops in the place of one removed does not imply malignancy, 
 since it may result from the same mechanical cause which produced the 
 first, as in the case of certain carcinomata of the lip induced by the 
 mechanical irritation of a pipe. 
 
 The drain upon the system by the rapid growth of a tumor, together 
 with the absorption from it into the body of deleterious putrefactive 
 materials, from sloughing, ulceration, and degeneration, may give rise to 
 fever and well-marked septicaemia. Or they may induce feebleness, anae- 
 mia, and that general impairment of the nutritive functions of the body 
 known as cachexia. This condition is frequently rendered worse by the 
 mental status of the patient in the presence of such a traditional object 
 of alarm. 
 
 It should be remembered, however, that so long as they are localized 
 and have not undergone degenerative changes, even the most malignant 
 tumors do not usually give rise to a cachexia, .since the drain upon the 
 nutritive powers of the system by their simple growth is not under or- 
 dinary conditions very considerable. When the system is deteriorated 
 by the absorption of septic materials from tissue-degeneration, however, 
 this may become a vei-y important factor. 
 
 This condition of cachexia, so evidently secondary to the growth and 
 degeneration of the tumor, was formerly termed a dyscrasia or diathesis, 
 and was supposed to precede and induce the growth of malignant tumors, 
 particularly cancers. 
 
 It is further to be noted that the fragments of tumors which have 
 found access to the veins may act as simple emboli and produce immedi- 
 ate death or simple metastatic abscesses. 
 
116 TTJMOES. 
 
 The Cause of Tumors. 
 
 In regard to the causation of tumors, our actual knowledge is still 
 very meagre. In a certain number of cases, mechanical influences are 
 undoubtedly sufiicient inciting causes. In other instances, heredity is an 
 important factor. But to both of these influences too much importance 
 has been attributed in former times. The most recent, and to a certain 
 extent plausible hypothesis, and one which most satisfactorily accounts 
 for the occurrence and character of many tumors, is that of Cohnheim, 
 called the hypothesis of the embryonal origin of tumors. This is to the 
 effect that all true tumors are due to faulty embryonal development; that 
 certain embryonal cells of various kinds in the course of the development 
 of the body are superfluous, or become displaced, or do not undergo the 
 normal changes, and remain ready, when the conditions shall become fa- 
 vorable in later life, from whatever reason, to commence growing with 
 all the potencies of embryonic and lowly organized cells in the midst of 
 the mature tissues. Not being restrained, however, by the regulating 
 influences which determine the nature and relative extent of growth in 
 normal development, they go on to the production of tumors, which 
 represent, though in atypical form, the various tissues which the strayed 
 or unused cells were destined normally to produce. 
 
 The evident hereditary character of many tumors, the congenital nature 
 and early development of others, their atypical structure in general, and 
 the tendency of many forms to occur in situations in which, during the 
 development of the embryo, considerable complexity exists, as well as 
 their heterologous occun-euce and their frequent primary multiplicity; 
 all of these characters of tumors seem to favor Oohnheim's hypothesis. 
 On the other hand, the theory leaves unexplained the sudden growth of 
 the alleged gea-ms which have long remained dormant, and lacks as yet 
 the absolute demonstration of a morphological basis, since no one has 
 seen the strayed or delayed embryonic cells. These may, of course, be 
 very small and difficult of demonstration, and this, according to Cohn- 
 heim, fully explains the lack of a definite histological basis to his hy- 
 pothesis. It should be remembered furthermore that, under ordinary 
 conditions in the body, certain cells which are destined to replace others 
 which have fulfilled their destinies, as in the skin, possess to a greater or 
 less degree the characters of embryonal cells, and that, while in the strug- 
 gle for existence the growth of these cells may be held in check, as by 
 conditions of pressure, nutritive supply, etc., if these conditions be al- 
 tered, these cell may undergo proliferative changes as significant as those 
 of the alleged belated germs of Oonheim. Such a changed condition of 
 affairs has been shown by Thiersch to occur frequently in the skin in old 
 age, and to explain in large measure the occurrence of certain epithe- 
 lial tumors. It should be remembered that this hypothesis was offered 
 
TUMOES. 117 
 
 by Conheim only as a suggestion to facilitate research, and tliat he ex- 
 pressly warned his confreres against attaching a premature importance 
 to the possibility to which he called attention. Thus, while the hypoth- 
 esis of the embryonal origin of tumors is most fascinating, and for cer- 
 tain forms quite satisfactory, we may well demand a more definite basis 
 of fact before accepting it as of universal application. 
 
 It was formerly supposed, when the doctrine of the specific nature of 
 tumors prevailed, that the cells of malignant tumors, jsarticularly of can- 
 cer, had a characteristic structure and appearance, and that by the exami- 
 nation of single or of a few separated cells the nature of the tumor could 
 be determined. From the above considerations, it will be evident, as all 
 tumor cells have their prototypes in the normal body, that therefore there 
 is nothing pathognomonic in the appearances "of single cells. It is by 
 a study of the general structure, and the topography of tumors, as well as 
 of the characters of the individual cells, that we are enabled to determine 
 their nature. And even then we must often bring to our aid the clinical 
 history and gross appearances of the growth before we can arrive at a 
 definite conclusion. We may, indeed, sometimes, aided by the clinical 
 history or gross appearances, be able, by the microscopical examination of 
 scrapings from a tumor or of fluids from an internal cavity in which it is 
 growing, to form a reasonable conjecture regarding its nature. 
 
 As a rule, the peripheral portions of the more rapidly growing tumors 
 are best adapted for microscopical examination, because here secondary 
 degenerative changes are less likely to have occurred than in' the central 
 parts. 
 
 Classification of Tumors. — The fact that tumors are composed of 
 structures which resemble the various types of tissue found in the normal 
 body suggests the guiding principle'in their classification. If we wish to 
 arrange in groups the difEerent kinds of tumors found in the body, we 
 have only to recall the varieties of tissue which normally exist there, and 
 their grouping, and upon the classification of the physiological types to 
 construct the classification of tumors. It should be remembered that 
 the usual separation of the normal tissues into groups is useful rather 
 because it facilitates their study than because it expresses absolute and 
 fundamental distinctions, and the same may be said of all the classifica- 
 tions of tumors. In both, an increase of our knowledge concerning their 
 structure and genesis will doubtless lead to a more accurate grouping; 
 but for the present such an arrangement as the following will be found 
 of .practical value for the purposes of studying tumors. 
 
 /. Tumors Composed of Tissues of the Type of those Forming the 
 Connective Tissue Group. (Histioid or Connective-Tissue Tumors.) 
 
 Physiological Type. Tumors. 
 
 1. Fibrillar connective tissue. 1. Fibroma. 
 
 3. Mucous tissue. 3. Myxoma. 
 
118 TUMOES. 
 
 3. Kmbiyonal connective tissue. 3. Sarcoma. 
 
 4. Endothelial cells. 4. Endothelioma. 
 
 5. Fat tissue. 5- Lipoma. 
 
 6. Cartilage. 6. Chondroma. 
 7 Bone. '''• Osteoma. 
 
 8. Neuroglia. 8. Glioma. 
 
 //. Tumors Composed of Tissues of the Type of Muscle Tissue.— Kjomai^. 
 
 Physiological Type. Tumors. 
 
 1. Smooth muscle tissue. 1. Leiomyoma. 
 
 3. Striated muscle tissue. 2. Ehabdomyoma. 
 
 III. Tumors Composed of Nerve Tissue.Semomiita.. 
 
 Physiological Type. Tumors. 
 
 1. Nerve tissue. 1- Neuroma. 
 
 IV. Tumors Composed of Vascular Tissue. — Aiigioraata. 
 
 Physiological Type. Tumors. 
 
 1. Blood-vessels. 1. Angioma. 
 
 2. Lymph-vessels. 2. Lymphangioma. 
 
 V. Tumors in which the Predominant or Characteristic Elements are 
 
 Epithelial Cells. 
 
 Physiological Type. Tumors. 
 
 1. Glands. 1. Adenoma. 
 
 3. "Various forms of epithelial cells 2. Carcinoma. 
 
 and associated tissues. 
 
 VI. Tumors Formed by Various Combinations of the above 
 Types. — Mixed Tumors. 
 
 Aside from the above well-marked classes, we may mention here for 
 the sake of completeness : 
 
 (a) Complex Congenital Tumors, — Teratoma. — These are congenital 
 tumors which frequently contain a great number of different forms of 
 tisssue, such as various forms of fibrillar connective tissue, cartilage, bone, 
 teeth, hair, skin, muscle, and glands. They are most frequently found at 
 the lower end of the spine, about the head and neck, or in the generative 
 organs. Some of them probably arise by an inclusion of portions of 
 another foetus. These are called teratoid tumors or teratomata. Among 
 them are sometimes classed other and simpler congenital formations, 
 such as dermoid cysts, congenital angiomata, and the so-called pigmented 
 moles. 
 
 (b) Cysts. — These structures, for the sake of convenience, are usually 
 classed among the true tumors, although in general characters, struc- 
 ture, and genesis, they are entirely different. products. They are usually 
 divided into two classes: 
 
TUMOES. 119 
 
 I. Cysts which develop in pre-existing cavities. 
 
 II. Gysts which originate independentlij as the result of pathological 
 changes. 
 
 I. Cysts which develop in pre-existing cavities. 
 
 1. Retention Gysts. — These are chiefly formed by the accumulation 
 in glands or their excretory ducts of the more or less altered secretion of 
 the gland. They usually occur as the result of some hindrance to the 
 normal discharge, as from inflammatory contractions, pressure, etc. The 
 ■contents of such cysts are usually mucous, sebaceous, serous, or of a 
 mixed character. Their walls are the more or less altered walls of the 
 original structure. To this class belong comedones, milium, atheroma, 
 chalazion, ranula, the ovula ISTabothi, milk cysts, and certain serous cysts 
 of the ovaries. Fallopian tubes, gall-ducts, and uriniferous tubules. 
 
 2. Exudation Cysts. — These arise usually, though not always, as the 
 result of a chronic inflammatory process in lymph-spaces or serous sacs, 
 and among them are to be classed the so-called ganglia, hydrocele, etc. 
 ■Certain of the so-called hematoceles, in which blood is extravasated into 
 closed cavities, form a variety of the cysts of this group. 
 
 II. Cysts which originate independently as the result of pathological 
 changes. 
 
 1. Cysts formed hy the softening and disintegration of tissue. — Such 
 cysts may at first be small and have very meagre contents, and no well- 
 deflned wall. A wall may finally be present either as an entirely new- 
 formed structure, or the more or less modified capsule of the organ in 
 which they occur may partly or entirely form the wall. The contents of 
 such cysts are usually the more or less altered detritus of the tissue by 
 whose disintegration they are formed. Such cysts are very apt to occur 
 within true tumors, particularly those which are succulent and of rapid 
 growth, since these, as above stated, are very liable to degeneration. Old 
 abscesses may change into well-defined cysts of this kind. 
 
 2. Cysts formed around Foreign Bodies. — The inflammatory reaction 
 induced by the presence of foreign bodies of various kinds, parasites, 
 masses of extravasated blood, etc., frequently result in the formation of 
 well-defined encapsulated cysts. 
 
 3. Cysts formed by a new growth of tissue in whose spaces various 
 Mnds of fluid accumulate. — These spaces may or may not be lined with 
 epithelium, and have something of the glandular character. Such forms 
 are exemplified in some of the compound ovarian cysts — the so-called 
 ovarian cystomata. 
 
 4. Congenital Cysts. — -These are of various forms, and their mode of 
 origin is in most cases but imperfectly understood. The so-called der- 
 moid cysts of the subcutaneous tissue and ovary are marked examples of 
 this class. Certain congenital cysts of the kidney and other internal 
 organs are conveniently grouped in this class, although it is quite proba- 
 
120 TUMOES. 
 
 ble that some of them at least originate during foetal life in one or other of 
 the above-described ways, and hence are not essentially different in 
 ■nature from some of the cysts of other classes. 
 
 There are certain enlargements of the lymph-glands or nodes which 
 are in reality hyperplasias, sometimes inflammatory in character, and 
 sometimes not, and which are often grouped among the tumors as 
 ly7npliomata. They are not, strictly speaking, true tumors, and will be 
 considered under the lesions of the lymph nodes. 
 
 In the same group are often classed the enlargements of the lymph- 
 glands in leukgemia and in other general diseases, which will be treated 
 in another part of this book. Another group of tumors, sometimes called 
 lymphomata, are in reality sarcomata, and these will be described under 
 the latter heading. 
 
 There is also a group of nodular new formations, the so-called Infec- 
 tive Granulomata, which are sometimes classed among the tumors. 
 These are found in tuberculosis, leprosy, syphilis, lupus, glanders, and 
 actino-mycosis. They seem, however, to be more closely allied to inflam- 
 matory new formations than to true tumors, and as our knowledge regard- 
 ing them increases, seem more and more to be dependent upon the irrita- 
 tion caused by the presence of vegetable parasites. (See section devoted 
 to General Diseases.) 
 
 Nomenclature of Complex Tumors. — The simple occurrence of more 
 than one kind of tissue in a tumor does not make it a complex or mixed 
 tumor. It is only when a special kind of tissue occurs in safficient quan- 
 tity to be of definite significance, or is of such a nature as to render its 
 presence, in any amount, of importance, that we recognize its presence 
 in the name. The name of mixed tumors is usually formed by joining 
 the names of the tissues to be recognized. Thus a combination of fibro- 
 ma and sarcoma is called fibro-sarcoma; the general rule of construction 
 being that the name of the more important tissue shall serve as the 
 substantive which that of the loss important one qualifies. It should be 
 remembered, however, that the more important tissue is not always the 
 one which is present in greatest amount. Thus, owing to the great 
 clinical significance of carcinomatous tissue, a very large fibroma with 
 a small quantity of cancer tissue intermingled, would be a fibro-carci- 
 noma and not a carcino-fibroma. 
 
 Preservation.— In general, tumors, like all tissues for microscopical study, 
 should be cut into small pieces before immersing them in the preservative fluids, 
 and the .sooner they can be placed in tliese after removal, the better will be the pre- 
 servation. In some cases much ma}' be learned from large sections of tumors to- 
 gether with their surrounding tissues. In this case the proper part of the tumor 
 must be preserved whole, and is best hardened in strong alcohol. For the ordi- 
 nary routine hardening of tumors, Miiller's fluid is probably the best agent; the 
 hardening being completed in the usual way with strong alcohol (see p. 41). In 
 
TUMORS. 12 L 
 
 many oases an interstitial injection of one-per-cent aqueous solution of osmic acid, 
 or a mixture of this with equal parts of alcohol and water, and subsequent immer- 
 sion in alcohol, secures a very perfect perservation of the cells. 
 
 When it is desired to study the living cells of tumors — and much may bo 
 learned in this way — fragments should be teased in one-half -per-cent salt solution 
 and examined on a warm stage. 
 
 SECTION II.— SPECIAL FORMS OF TUMORS. 
 BIBEOMA. 
 
 The fibromata are composed of fibrillar connective tissue, which, as in 
 the physiological type, is sometimes dense and firm, Fibroma durum, and 
 sometimes loose in texture and soft. Fibroma molle. They are usually 
 sharply circumscribed and are frequently encapsulated, but they may be 
 difEuse, and merge imperceptibly into the surronnding tissue. Some 
 fibromata consist almost entirely of intercellular substance, containing 
 
 Fig. 26.— Fieeoma of Abdominal Wall. 
 This is one of the denser varieties; some of the bands of connective-tissue fibres are cut trans- 
 versely, others longitudinally. X BOO and reduced. 
 
 but few flattened or spindle-shaped cells; others contain very many 
 variously shaped cells. The denser varieties usually contain but few 
 blood-vessels, although they are occasionally quite vascular. Many of the 
 softer varieties are very vascular. Nerves also are occasionally seen. The 
 course and arrangement of the fibres in these tumors is usually quite 
 irregular, often crossing and interlacing in a most complex manner. The 
 fibromata are usually of slow growth, but exceptionally they grow very 
 rapidly. They are benign tumors, but by pressure on important organs, 
 by ulceration, or by changing into other varieties of tissue, they may be- 
 come of serious import. Pare fibromata do not form metastases, but 
 they are often multiple, and when so are frequently congenital. They 
 may, like most tumors, exhibit local recurrence when not fully removed. 
 They are frequently very small and insignificant, but on the other hand, 
 may grow to an enormous size. 
 
 They are quite frequently combined with other kinds of tissue to form 
 complex tumors. The looser softer varieties not infrequently become 
 
122 
 
 TUMOES. 
 
 oedematons, when they may closely resemble myxomata. They are liable 
 to calcification, and to fatty and mucous degeneration. By metaplasia 
 they may partially change to form flbro-chondroma, fibro-lipoma, fibro- 
 sarcoma, or fibro-osteoma. The latter transformation frequently occurs 
 when they form in the periosteum. Developing as they do in the con- 
 nective tissue, they occur in the most various parts of the body : in the 
 skin and subcutaneous tissue ; in intermuscular tissue and fasciee ; in 
 periosteum; in the nerve-sheatlis and intrafascicular connective tissue; 
 in the dura mater, the interstitial tissue of organs and in the mucous 
 membranes. Many of the so-called polypi of the mucous membranes; 
 some psammomata; certain forms of warts and common papillomata, are 
 forms of fibroma. 
 
 Occasionally in the ducts of glands, fibrous polypi grow to an enormous 
 extent, their epithelial covering keeping pace, in growth, with their devel- 
 opment until they form very large, irregular, loose-textured tumors, which 
 often finally ulcerate. Such forms are seen in the mammary gland, where 
 they are frequently mistaken for carcinomata. They are called Intra- 
 canalicular Fibromata. It is often difficult to distinguish between 
 genuine fibromata and inflammatory connective-tissue hyperj^lasia, such 
 as elephantiasis, and perhaps the fuller knowledge of the future will show 
 that the distinctions are not as definite as we are now disposed to believe. 
 
 MYXOMA. 
 
 Mucous tissue is essentially an embryonic tissue, for in the normal 
 adult it is present 'only in a very imperfect and atypical form in the vit- 
 
 
 Fig. 27.— Myxoma of SuBOUTANEons Tissue of Back, X 600 and reduced one-half, 
 
 reous of the eye, and perhaps exceptionally in small amount about the 
 heart, kidneys, and medulla of bone. 
 
TUMORS. 123 
 
 The myxomata are thus essentially embryonic-tissue tumors. These 
 tumors consist, in their most typical forms, of a homogeneous or finely 
 fibrillated, soft gelatinous basement substance, in which are embedded a 
 variable number of spheroidal, fusiform, branching, and often anastomos- 
 ing cells. They may contain few or many blood-vessels and nerves. By 
 the addition of acetic acid mucin may be precipitated from the basement 
 substance. The very soft forms which contain comparatively few cells 
 and much translucent basement substance, are called Myxoma gelatino sum 
 or M. molle. The presence of many cells renders them more consistent 
 and gives them a whiter and more opaque appearance ; such forms are 
 called M. meduUare. 
 
 Pure myxomata are not very common. The myxomata are very apt 
 to be combined with fibrillar connective tissue as fibro-myxo7na; or with 
 fat tissue — lipo-inyxoma; and they very frequently become sarcomatous, 
 or take part in the formation of very complex tumors. They may be 
 diffuse or encapsulated with fibrillar connective tissue; they are fre- 
 quently very large, and may be multiple. Owing to the character of the 
 basement substance, the blood-vessels not infrequently rupture, giving 
 rise to larger or smaller hemorrhages within the tumor, or to the forma- 
 tion of cysts. The cells are liable to undergo fatty degeneration. 
 
 
 
 \\ 
 
 
 riQ. 28.— Myxoma growing into Abdominal Cavitt, x 450. 
 Some of the cells show accumulation of fat in the bodies. 
 
 Composed as they are of a type of tissue from which fat-tissue is de- 
 veloped in the embryo, the relations of these tumors to fat-tissue are very 
 intimate. They are most frequently developed in, and probably directly 
 from fat-tissue, and are very often combined with it as lipo-my- 
 xoma. They are also found in the subcutaneous, submucous, and sub- 
 serous tissue, in the marrow and periosteum; in the brain and cord; m 
 the sheaths and intrafascicular tissue of peripheral nerves; in intermuscular 
 septa, and in the interstitial tissue of glands, such as the mamma and 
 parotid. The myxomata are in general benign; yet they are very prone, 
 especially the lipomatous forms, to local recurrence. They sometimes, 
 grow very rapidly, and sometimes, though very rarely, form metastases. 
 
224 TUMOES. 
 
 In the not infrequent combination witli sarcoma, they may exhibit the 
 most marked malignancy. Many of the polypi of mucous membranes 
 are myxomata, and to this class of growths belong the so-called hydatid 
 moles which sometimes develo]) in the villi of the chorion. 
 
 CEdematous, loose, and cellular forms of fibrillar connective tissue so 
 closely resemble some of the forms of mucous tissue that certain ob- 
 servers consider them as identical. So prone are many tumors to under- 
 go mucous degeneration, and so frequent are the combinations of the 
 myxomata with other forms of tumors that it is often difficult, some- 
 times impossible, to say whether the mucous tissue in a given composite 
 tumor is primary or secondary. 
 
 SARCOMA. 
 
 These tumors are formed on the type of connective tissue, but they 
 are, as a rule, largely composed of cells; the basement substance, though 
 a constant and important factor, being much less conspicuous than in 
 adult connective tissue. They more closely resemble, in general, the de- 
 veloping connective tissue of the embryo, or the granulation tissue of 
 inflammation. They are therefore conveniently described as present- 
 ing the type of embryonal tissue. The prominent and characteristic 
 cells of the sarcomata are most varied in size and shape. They may be 
 fusiform or spindle-shaped, spheroidal, branched; they may be multi- 
 nuclear and very large, or they may be very small and spheroidal, re- 
 sembling leucocytes. The fibrillar basement substance may be present 
 in such small quantity as to entirely escape a superficial observation, 
 covered as it may be by the abundant cells; or it may be so abundant as 
 to give the tumor the general appearance of a fibroma. It may be in- 
 timately intermingled with the cells in fascicles, or it may bo in large 
 open-meshed networks, giving to the tumor an alveolar appearance. 
 The cells, however, always stand in an intimate relationship to the base- 
 ment substance which they sometimes reveal by fibrillar processes con- 
 tinuous with it. Blood-vessels also form a constant and important 
 structural element in these tumors, being in some of them so predomi- 
 nating a factor that they give structural outline and general character to 
 the growth. They, too, as in the normal connective tissue, are in- 
 timately associated with the basement substance and with the tumor- 
 cells. 
 
 A single form of cells is often so predominant as to furnish a suitable 
 name for the tumor, but in many cases the cell-form varies greatly in 
 the same growth. It may be said in general that there is a tendency to 
 reproduce in these tumors some of the special characteristics of the tis- 
 sues in which they originate. Thus, sarcomata of the bones are apt to 
 be osteo-sarcomata; those of pigmented tissue, like the choroid, are apt 
 to be pigmented sarcomata. It will be more convenient for our present 
 
TDMOES. 
 
 125 
 
 purpose to briefly describe the more common forms one after another, 
 than to attempt any systematic classification of them, 
 
 It should be remembered, however, that the various forms are not 
 sharply specific in character, but are apt to merge into one another and 
 to intermingle in various ways. 
 
 Sarcomata are most frequently found in the skin, subcutaneous tis- 
 sue, facise, subserous connective tissue, the marrow or periosteum, and in 
 the choroid. They may also occur, though more rarely, in the dura 
 mater; brain and cord; lymph nodes; in the adventitia of blood-vessels 
 and in nerve-sheaths; in submucous tissue; in the uterus, and in the 
 kidney. In the liver and lungs and heart they may occur by metas- 
 tasis. 
 
 They are more apt to occur at an early period in life than later. The 
 cellular character, the rapid growth, the vascularity and succulence of 
 many forms; the marked tendency to local recurrence, and the formation 
 of metastases, stamp the sarcomata as malignant tumors. But in this 
 they vary greatly; while some of the forms belong in every sense to the 
 most malignant of tumors, others grow slowly, are very dense, and may 
 remain localized and harmless for years. Their tendencies in this respect 
 will be mentioned under the special forms. 
 
 Intimately related as they are to the blood-vessels, metastasis is more 
 apt to occur through the blood than through the lymph channels, and j 
 consequently adjacent lymph-glands are much less apt to be involved 
 than in some other forms of tumor, notably the carcinomata. 
 
 Fig. 29. — Large Spindle-celled Sarcoma of Humerus, 
 
 Spindle- celled Sarcoma. — The cells in these tumors may be large — 
 large spindle-celled S.j or they may be small — small spindle-celled S. 
 They may consist largely of cells, or may contain so much intercellular 
 fibrous tissue as to be appropriately called fibrosarcoma. The cells 
 are frequently arranged in fascicles which surround the blood-vessels, 
 and these fascicles may cross and interlace. These tumors are, as a rule, 
 denser and firmer and less malignant than other forms of sarcoma, but 
 
126 
 
 TUMOES. 
 
 to this there are many exceptions. They may be encapsulated or in- 
 filtrating. To this class belongthe growths formerly described as fibro- 
 
 
 Fie. 
 
 —Small Spindle-celled Sarcoma of Forearm, x 500. 
 
 plastic tnmorsj and recurrent fibroids. They frequently occur in the 
 periosteum, subcutaneous tissue in muscle, in the uterus, and in yari- 
 ous glands; notably in the mamma, testicle, thyroid, etc. These forms 
 are among the most frequent of the sarcomata. 
 
 Round-celled Sarcoma.- — Of these there are two classes — 1, small 
 round-celled sarcomata and large round-celled sarcomata. 
 
 1. The small round-celled sarcomata consist of cells of about the size 
 and appearance of lymph-cells, and may have much or little intercellular 
 substance, which may be irregularly disposed or arranged in large meshes 
 resembling alveoli. In many cases so small is the quantity of inter- 
 cellular substance that it is difficult of detection without special modes 
 of preparation. These tumors are apt to contain many blood-vessels and 
 
 FiQ. 31.— Small Round-celled Sarcoma of Liver, x 400. 
 
 be very soft and succulent. Their growth is sometimes rapid and they 
 are often very malignant. 
 
TUMOES. 
 
 127 
 
 They most frequently occur in the connective tissn.e of the muscles 
 and fascise, in bone, and in lymph-nodes [lymphosarcoma). They also 
 occur in the internal organs, not infrequently in the brain, associated with 
 glioma as glio-sarcoma. 
 
 3. In the large routid-celled sarcomata the cells vary in size, but are 
 ^^sually very much larger than in the last variety. Their nuclei are usu- 
 
 Fio. 32.— Large Eound-oelled Sarcoma of Leg, x 350. 
 
 ally large and contain prominent nucleoli. They, too, are often very vas- 
 cular, and contaia a variable quantity of basement suostance. They are 
 occasionally alveolar in character. They are as a rule less soft and 
 malignant than the small-celled varieties. 
 
 The round-celled sarcomata were formerly supposed, on account of 
 their macroscopical and clinical resemblance to some of the soft forms of 
 carcinoma, to belong to these tumors and were called medullary cancers. 
 
 Melano- Sarcoma. — These tumors consist most frequently of spindle- 
 cells of various sizes, although cells of other shapes frequently occur in 
 them. They are characterized by the presence in the cells, and less fre- 
 
 Fig. 33.— Melano-sarcoma from Submaxillary Kegion, X 500 and reduced one-half. 
 
 queutly in the intercellular substance, of larger and smaller particles of 
 brown or black pigment. The pigment is usually quite irregularly dis- 
 tributed in patches or streaks, and is located chiefly in the cell-body. 
 
128 
 
 TUMOES. 
 
 They arise most frequently in the skin and in the choroid. Pigmented 
 moles of the skin often form their starting-points. They belong to the 
 most malignant of tumors. They very readily form metastatic tumors 
 in various parts of the body, which are, like the parent tumor, pig- 
 mented. 
 
 Various forms of tumors may contain brownish pigment deposited in 
 them, by the degeneration of the hemoglobin from extravasated blood; 
 these should not be mistaken for melanotic sarcomata. 
 
 Myeloid or Giant-celled Sarcoma. — Tumors of this class are usually 
 formed chiefly of spheroidal or fusiform cells of variable size, but their 
 characteristic feature is the presence of larger and smaller multinuclear 
 cells, called giant-cells. These are closely intermingled with the other 
 cells, and may be very abundant or very few in number. Giant-cells 
 
 Fig. 34.— Giant-celled Sarcoma of Bone (Tibia), x 600. 
 
 may occasionally occur in other tumors, but are most abundant and 
 characteristic in these. They are chiefly formed in connection with 
 bone, and may commence in the marrow or in the periosteum. They 
 are sometimes very soft and vascular, and subject to interstitial hemor- 
 rhages. Some of these vascular sarcomata were formerly classed together 
 with other kinds of vascular tumors as fungus hematodes. Somerf the 
 forms of epulis are giant-celled sarcomata. 
 
 When these tumors originate in the marrow of the long bones, which 
 IS a favorite place for them, they are apt to cause resorption of the bone, 
 and although the tumor may be for along time inclosed by a shell of new- 
 formed bone, which enlarges with the enlarging tumor, it usually sooner 
 
TUMORS. 
 
 129 
 
 or later, breaks through this and infiltrates adjacent tissues. They are 
 liable to form metastases and frequently grow to a very great size. The 
 periosteal forms are apt to be firmer in texture, and are prone to the de- 
 velopment of irregular masses of new bone within them, thus forming 
 one of the varieties of osteo-sarcoma. 
 
 Osteosarcoma. — These are spindle or round celled tumors, usually, 
 but not always, connected with bone, in which irregular masses of bone 
 tissue are present. The bone is usually of irregular atypical structure; 
 the regular lamellation and typical Haversian canals being usually ab- 
 sent. They may form metastases which present similar characters. 
 
 Calcification, which should be distinguished from ossification, may 
 occur in various forms of sarcoma. 
 
 Angio-Sarcoma. — In many of the sarcomata in various parts of the 
 body, the blood-vessels form so prominent and important a feature as to 
 give special character to the growth, not alone by their size and general 
 prominence, but sometimes by the peculiar arrangement which their 
 
 Fie. 35.— Angio-Sabcoma of Livbb. 
 The thin-walled blood-vessels around which the tumor-cells are formed are dilated in places. 
 
 presence gives to the cells. While in most of the sarcomata the blood- 
 vessels have a very important influence in determining the topography 
 of the tumor, in most of the denser, and in many of the softer varieties, 
 this influence is not easily traced. In many forms, however, particularly 
 those which are soft and very cellular, the cells are closely grouped 
 around the vessels as if they were developed in their adventitias, and had 
 formed close sheaths around them. The masses of cells thus formed, 
 with a blood-vessel for a centre, may be closely packed together in long 
 strings with more or less frequent anastomoses (Fig. 35), or they may be 
 
130 
 
 TUMOES. 
 
 arranged in rounded groups giving to the tumor an alveolar appear- 
 ance. 
 
 In other cases, the blood-vessels may appear as characteristic factors 
 simply on account of their size or relative abundance. 
 
 Sometimes the walls of the blood-vessels and the adjacent tissues, in 
 these as in other forms of tumors, undergo a peculiar hyaline degenera- 
 tion, giving to the whole or to parts of the tumor a more or less gelatin- 
 ous appearance. Sach tumors are not very common, and are frequently 
 grouped in an ill-defined class called cylindroma. 
 
 Alveolar Sarcoma. — Sometimes, as above stated, the basement sub- 
 stance of the sarcomata, particularly in some of the round-celled varieties, 
 is quite abundant and arranged in a wide-meshed net, in the meshes of 
 which the cells lie. These spaces are called alveoli, and this variety of 
 structure has acquired importance from the general resemblance which 
 these tumors have to the well-defined and characteristic alveolar struc- 
 ture which many of the carcinomata exhibit. It is true that occasionally 
 the resemblance is very close indeed, but usually the sarcomata present a 
 more or less intimate relation between the cells and basement substance. 
 The cells usually do not simply lie in the cavities, but are often attached 
 to the intercellular substance, which not seldom sends finer trabeoulae 
 into the alveoli between the cells. Sometimes a careful shaking of sec- 
 tions in water is necessary to reveal the characters of the reticulum. 
 
 Fig. 36.— Myxo-Sarcoma of Pharynx, x SOO and reduced. 
 
 The cells, moreover, are usually, though not always, distinctive in char- 
 acter. This form of tumor is, in some cases at least, determined, as above 
 stated, by the new-formation and peculiar arrangement of the blood- 
 vessels. Tumors of this kind are not common, but may occur in the skin 
 lymph-nodes, bones, and pia-mater. They are usually very malignant. 
 
TUM0E8. 
 
 131 
 
 In addition to the above more or less well-defined forms of sarcoma, 
 there exist various modifications which have received special names. 
 Thus sarcomata in which cysts form, either by the softening of tissue by 
 degeneration, or by the dilatation of gland-ducts by pressure, or by the 
 new-formation of tissue in gland-ducts or alveoli which dilate with the 
 growth of the tumor, have received the name of cysto-sarcomata. 
 
 Mucous degeneration is frequent in the various forms of sarcoma. 
 A combination of myxoma and sarcoma — myxo-sarcoma — is common (see 
 Fig. 36). 
 
 Combinations of sarcoma with fat-tissue, Upo-sarcomaj with glandular 
 
 
 ^ — 
 Fig. 37.— Adeko-Saecoma of Pabotid, X 600 and reduced. 
 
 structures, adeno-sarcoma; with cartilage, cliondro-sarcmna; with muscle 
 tissue, myosarcoma; and with various other tissues, are of frequent oc- 
 currence. Some forms of 2^sammoma or "brain sand" found chiefly in 
 the dura-mater are fibro-sarcomQ.ta which have undergone calcification, 
 the lime being deposited in lamellated masses of various shapes within 
 them. 
 
 Some of the soft papillomata and warts, and occasionally the polypi 
 of the mucous membranes, belong to the type of sarcoma or myxo- 
 sarcoma. 
 
 The so-called chloromata, which have been found in a variety of 
 places in the body, but are rare, are apparently forms of sarcoma. Chlo- 
 roma is characterized by a greenish color the nature of which is not 
 known. 
 
 Sometimes in various forms of sarcoma, as in other tumors, the endo- 
 thelial cells lining the lymph-spaces appear to proliferate, giving rise to 
 a variety of rounded, elongated, or reticular structures, which somewhat 
 resemble a typical gland formation. Such tumors are sometimes called 
 adenoid sarcomata, but they require more careful and extended study 
 
132 TUMOES. 
 
 before they can be definitely classified. Some of them belong to the 
 tumors of the next class. 
 
 ENDOTHELIOMA. 
 
 Under the name of endotheliomata are grouped a number of tumors 
 which on the one hand are closely related to the sarcomata in genesis, 
 and in some cases in appearance, while on the other hand some of them 
 so closely resemble some forms of carcinoma as to be difficult of distinc- 
 tion from them. The endotheliomata originate in that form of connec- 
 tive-tissue cells called endothelium, and seem to develop by a prolifera- 
 tion of these. Sometimes the cells of the endotheliomata resemble 
 closely the normal endothelium; sometimes, however, they differ con- 
 siderably from them, being occasionally very large, often thick and 
 irregular in shape, and even nearly cylindrical or cuboid al. They are 
 asssociated with a more or less abundant vascular stroma which may be 
 alveolar in formation. In this case, as in alveolar sarcoma, it may often 
 be seen that the cells have an intimate relationship to the trabecule of 
 
 1^ i\ 
 
 X 
 
 ^^**^ 
 
 
 Fig. 38,— Endothelioma of Dura Mater, x 300. 
 
 the stroma. Sometimes the cells of the endotheliomata are packed 
 together in dense concentric masses, which may have a glistening 
 appearance, and such tumors are sometimes called cliolesteatomata. 
 Although, for the most part, the jieculiar glistening appearance of these 
 tumors is due to the closely packed thin cells which compose them, they 
 not infrequently contain crystals of cholestearin, sometimes in large 
 quantities, which may share in producing their characteristic appear- 
 ance. But the cholestearin may be absent or present in small amount. 
 
 The endotheliomata may occur of considerable size and be nodular, 
 or they may be multiple, numerous small tumors being scattered over 
 the surface of the jjart in which they grow; they may even form a 
 thicker or thinner pellicle over surfaces, or cause adhesions between 
 
TUMOES. 133 
 
 adjacent organs. They may form metastases. They occur in the dura 
 mater and pia mater, in the pleura and peritoneum, and have been 
 described in the lymph-nodes, ovary, liver, brain, and testicle.' 
 
 LIPOMA. 
 
 LipOmata are tumors formed of fat-tissue. The fat-tissue occurs in 
 lobules and is similar to normal fat, except that the cells and lobules are 
 usually larger. There may be little connective tissue in the tumors, 
 when they are very soft, almost fluctuating — lipoma molle — or there may 
 be so much as to give the tumor considerable ^vmness—fibro-lipoma. 
 They may be in part transformed into mucous tissue — myxo-lipoma. 
 Cartilage not infrequently develops in them, or they may undergo par- 
 tial calcification. 
 
 Occasionally the blood-vessels are very abundant and dilated — lipoma 
 telangiectoides. They are usually sharply circumscribed, but may infil- 
 trate surrounding tissues. They are not infrequently pediculated. They 
 sometimes grow to enormous size, and may ulcerate. 
 
 They are usually isolated, but may be multiple. They are the most 
 common of tumors, occurring usually in the subcutaneous or other 
 fat-tissue. They may occur in the mucous membrane of the gastro- 
 intestinal canal, in the peritoneum, more rarely in the dura mater, 
 kidney, liver, and lungs. They are benign tumors, not forming metasta- 
 ses, but they may be deleterious by ulceration or gangrene, and when not 
 fully removed may exhibit local recurrence. 
 
 CHONDROMA. 
 
 These tumors, composed of either of the physiological forms of carti- 
 lage, are usually hard, but sometimes quite soft. The cells do not pre- 
 sent the same uniformity in size, shape, number, and relative position 
 that they do in normal cartilage. Sometimes they are very large, 
 spheroidal, and grouped in masses, and again small and far ajjart. They 
 are frequently fusiform or branching. Fibrillar connective tissue in vary- 
 ing quantity is usually present in the chondromata, either as a capsule or 
 running in bands between the nodules of cartilage, or passing in fascicles 
 into them (Pig. 19). The cartilage may change to mucous tissue, forming 
 
 ' This class of tumors is unsatisfactory, for, as will be seen, we have no very- 
 definite morphological characteristics which cover all cases, and their relations 
 to other tumors are so close that we often need to know the seat of the growth 
 and something of its genesis before we can arrive even at a measurably definite 
 determination of it, and even then we may fail. This indefinite state of affairs 
 arises from the fact that we do not yet know enough about the normal relation- 
 ships between endothelial and other connective-tissue cells; and, furthermore, 
 we do not yet know exactly to what extent the progeny of one class of cells 
 may grow to resemble or become identical with those of another class. 
 
134 TUMOES. 
 
 myxo-cliondroma (Fig. 40); the cells may undergo fatty degeneration or 
 they may calcify or ossify. Choudromata frequently form a part of 
 mixed and complex tumors. 
 
 ^r'J^-ti 
 
 if£^!ii 
 
 '^!w^^ 
 
 
 [^J '" i 
 
 
 I f 
 
 :/ 
 
 Yio. 39. Chondroma of Subcutaneous Connective Tissue, x 500 and reduced. 
 
 They may form in connection with bone or cartilage, and are often 
 traceable to irregularities in fcEtal development. Or they may occur in 
 soft parts where cartilage is not normally present, as in tlie parotid, tes- 
 ticle, mamma, and ovaries, where they are apt to be mixed with other 
 tissues; or in subcutaneous connective tissue and fascise. 
 
 
 Fig. 40.— Myxo-Chondroma of Cervical Region, x 500 and i educed. 
 
 They are in general benign tumors, but metastases sometimes occur, 
 most frequently in the Umgs, sometimes in the heart. 
 
 Small hyperplastic growths on the surfaces of cartilage are called 
 ecclwndrose's . 
 
 OSTEOMA. 
 
 The formation of bone in the body in abnormal places occurs quite 
 frequently and under a great variety of conditions. It is on this account 
 
TUMORS. 135 
 
 not easy to define the term osteoma, and it is frequently diflBcnlt to 
 determine whether or not a given mass of new-formed bone is an osteoma 
 or not. Bone tissue often occurs in tumors of tlie connective-tissue 
 group as a secondary or complicating structure — osteo-fibroma, osteo- 
 chondroma, osteosarcoma, etc. It may occur in muscles as a result of 
 certain exercises, or as a result of a peculiar inflammatory process (see 
 lesions of the muscles), or it may occur in connection with chronic in- 
 flammation in a variety of tissues. A circumscribed mass of abnormal 
 bone, not of inflammatory origin, may be called an osteoma. Small 
 masses of new-formed bone of various shape, projecting from a bony 
 surface and frequently of inflammatory origin, are usually called osteo- 
 phytes. Bony tumors projecting from the surface of bones are frequently 
 called exostoses. 
 
 An osteoma may be loose in texture, consisting of bone tissue similar 
 to cancellous tissue, or it may be denser, resembling compact bone tissue, 
 or it may be very hard and dense like ivory, so-called ivory exostoses. 
 The difference between these forms lies chiefly in the varying number 
 ■and size of the vascular and medullary spaces which they contain. 
 
 Osteomata may develop in connection with the bone or periosteum, 
 which is most frequently the case, or independently of bone, in soft parts. 
 New-formed bone has been found in the soft parts of the body, in the 
 brain substance, dura mater and pia mater, in the pleura, diaphragm, 
 and pericardium; in the skin, choroid, air passages, lungs and penis, and 
 in other places. To what extent some of these bone formations may have 
 been due to inflammatory action it is not possible to say, and it is quite 
 probable that the fuller knowledge of the future may show relationships 
 between the development of certain tumors and some forms of chronic 
 inflammation which we do not now recognize. 
 
 The growth of the osteomata is, as a rule, slow. They are benign 
 tumors, and are not infrequently multiple. 
 
 GLIOMA. 
 
 The gliomata are developed in connection with the characteristic con- 
 nective-tissue frame-work of nerve-tissue, the neuroglia, which in structure 
 many, though usually not all of its cells closely resemble. Small cells 
 with inconspicuous bodies and numerous delicate branching processes are 
 most characteristic; but in connection with these there is usually a greater 
 or less number of small spheroidal cells with proportionally large nuclei. 
 It is usually necessary to shake sections in water or carefully tease frag- 
 ments of the tumor in order to see the characteristic neuroglia or so-called 
 'spider' cells (Pig. 41). These tumors may contain very numerous and 
 frequently dilated thin-walled blood-vessels. They may be very soft or 
 moderately hard; and especially when occurring in the substance of the 
 
136 TITMOES. 
 
 brain, are frequently not sharply outlined against the adjacent normal 
 tissue. They usually occur singly, and are comparatively slow in growth. 
 They are very apt to be complicated with other tumor-tissue forming 
 glioma-myxoma, glio-sarcoma, etc. Owing to the abundance of thin- walled 
 blood-vessels and the softness of the growth, they are liable to interstitial 
 hemorrhages, and may then, when occurring in the brain, readily be mis- 
 taken for ordinary apoplectic clots. They are liable to fatty degenera- 
 
 FiG. 41.— Neuroglia or 'Spider' Cells, from Glioma op Brain. Teased. X 500. 
 
 tion. They usually occur in the brain, spinal cord, and in the optic and 
 other cerebral nerves. The so-called giiomata of the retina are usually 
 small spheroidal-celled sarcomata. 
 
 Pure giiomata are benign tumors, though in their most common com- 
 bination with sarcoma they may be very malignant. Their usual situa- 
 tion, however, is such as to make them almost always significant, 
 although technically they are benign tumors. 
 
 MYOMA. 
 
 Tumors composed of muscular tissue are of two kinds, following the 
 two physiological types of muscle-tissue, the non-striated and the 
 striated. 
 
 I. Myoma leio cellular eov Leiomyoma. — The characteristic elements of 
 these tumors are fusiform, smooth muscle-fibres, with elongated or rod- 
 shaped nuclei. These are packed closely together, frequently interlacing 
 and running in various directions, and are intermingled with a variable 
 quantity of more or less vascular fibrillar connective-tissue (Fig. 43). 
 When, as is not infrequently the case, the connective-tissue elements are 
 present in large amount, the tumor is called fibro-myoma. It is not always 
 easy in sections to distinguisli between these tumors and certain cellular 
 fibromata, but the characteristic shape of the isolated cells and their nuclei, 
 together with their uniformity in size, will usually sufiBce. These tumors 
 are frequently infiltrated with lime salts, and owing to their density and 
 
TUMOES. 
 
 137 
 
 lack of blood-vessels they not infrequently degenerate, forming cysts or 
 becoming gangrenous. They may occur single or multiple, are usually 
 of slow growth, may be large or small, and are benign. They may occur 
 wherever smooth muscle-tissue exists. They are most frequently found 
 in the uterus, where they are often multiple. They may occur in the 
 wall of the gastro-intestinal canal, and have been seen in the bladder and 
 in the skin of the nipple and scrotum. The so-called hypertrophies of 
 the prostate, so frequent in advanced life, are usually leiomyomata of the 
 interstitial muscle-tissue of that gland. 
 
 Fig. 42.— Mymoma of Uterus. (Leiomyoma.) X 350. 
 
 II. Myoma striocellulare or Rhaidomyovia. — In these rare tumors 
 striated muscle-fibres are the characteristic elements. They very rarely 
 compose a great part of the tumor, but are intermingled with other ele- 
 ments, fibrillar connective tissue, spindle-shaped and spheroidal cells of 
 various forms, which often appear to be incompletely developed muscle- 
 cells. They are not infrequently associated with sarcomatous tissue. 
 Blood-vessels and sometimes nerves are also present. The- muscle-fibres 
 difier, as a rule, from normal striated muscle-fibres in their arrangement, 
 which is usually quite irregular, and also in size, being in general smaller 
 than normal fibres, although varying greatly. The sarcolemma is either 
 absent or incompletely developed. These tumors are usually small or of 
 moderate size, and are supposed to originate from inclusions of cells 
 destined to form muscle-tissue in places where they do not belong. 
 
 In the heart and certain other muscular parts, small circumscribed 
 masses of striated muscle-tissue have been described, and are sometimes 
 called Jiomologoics rhabdomyomata. But genuine heterologous rhabdo- 
 myomata are, in almost all cases thus far recorded, confined to the genito- 
 urinary organs, kidney, ovary, and testicles. The writer (T.M.P.) has 
 described an exceptional case of rhabdomyoma occurring in the parotid 
 gland. These tumors, when not associated with other and malignant 
 tumors, are benign, and are of much greater theoretical than practical 
 interest. 
 
138 TUMOES. 
 
 NEUROMA. 
 
 A true neuroma is a tumor containing new-formed nerve-tissue. Such 
 tumors are comparatively rare. Tumors developed in the connective 
 tissue of nerves and composed usually of fibrous or mucous tissue are 
 common, and are frequently called neuromata, but they should be called 
 fibromata or myxomata, etc., of the nerves or false neuromata. The true 
 neuromata are of two kinds, ganglionic or cellular neuromata and fibrillar 
 neuromata, depending upon the character of nerve-tissue which they con- 
 tain. The ganglionic neuromata are found associated with other struc- 
 tures in certain of the teratomata in the ovaries, testicles, and in the sacral 
 region; they also occur in the gray matter of the brain. 
 
 The fibrillar neuromata are, according to Virchow, of two kinds, mye- 
 linic and ainyelinic, depending upon whether the nerve-fibres which they 
 contain are medullated or not. The neuroma rnyelinicum is the more 
 common and the best understood. The medullated nerve-fibres in these 
 tumors are associated with fibrillar connective tissue, and are usually 
 curled and intertwined in a most intricate manner. They occur either 
 single or multiple on the peripheral nerves. They may occur in consid- 
 erable numbers as nodular tumors on the branches of a single nerve- 
 trunk, or they may form an irregular, diffuse, nodulated enlargement of 
 the nerve-branches, jjlexiform neuroma. These neuromata may or may 
 not be painful. They not infrequently form at the cut ends of the 
 nerves in amputation stumps. They are benign tumors, never forming 
 metastases. 
 
 The false neuromata are myxomata, or fibromata, or sometimes myxo- 
 sarcomata of the nerve-sheaths or intrafascicular connective tissue, and 
 may occur singly or multiple. In the latter case they may affect the 
 branches of ar single nerve trunk or they may be found on nearly all the 
 cerebro-spinal peripheral nerves. The writer (T.M.P.) has described a 
 case in which over eleven hundred and eighty-two distinct tumors were 
 found distributed over nearly all the peripheral nerves of the body (see 
 lesions of the peripheral nerves). The nerve-fibres in these tumors may 
 be crowded apart by the new growth and considerably atrophied; or, in 
 cases in which the tumor is composed of soft tissue, as in myxoma or the 
 soft fibroma, they may pass through or around the tumor entirely un- 
 changed. The multiple false neuromata are in many cases congenital. 
 
 ANGIOMA. 
 
 Angiomata are tumors consisting in large part or entirely of new- 
 formed blood-vessels or blood-cavities. In many tumors of various kinds, 
 the new-formed or the old blood-vessels may be very abundant or prom- 
 inent by reason of their dilatations; the blood-vessels of otherwise normal 
 tissues may also be largely dilated, thus simulating vascular tumors. 
 
TUMOES. 
 
 139 
 
 These are, however, not true angiomata, although sometimes reckoned 
 among them, and in many cases closely allied to then. Such are the so- 
 called arterial varix, or cirsoid aneurisms, and hemorrhoids. True 
 angiomata are of two kinds: 
 
 I. Those formed largely of capillary blood-vessels with either thin or 
 thickened walls, embedded in a more or less abundant connective-tissue 
 
 Fig. 43.— Angioma Telangiectoides (Vascular Nsevus) from skin over scapula of child. 
 
 stroma. These are called simple angiomata or angioma telangiectoides. 
 The walls of the vessels in these tumors are frequently dilated or pouched, 
 and usually form a tangle of curled and intertwined vessels. They occur 
 most frequently in the skin or subcutaneous tissues, usually about the 
 
 Fig. 44.— Angioma Cavernosa op Liver. 
 
 face, and may project above the general surface or be on a level with it. 
 Such are the so-called vascxilar nmvi or straiuberry marks, which are usu- 
 ally congenitah They are sometimes sharply circumscribed, and some- 
 
140 TUMORS. 
 
 times merge imperceptibly into the surrounding skin. They sometimes 
 occur in the mucous membranes, in the mamma, bones, and brain. They 
 are benign tumors, never forming metastases, but may be associated witii 
 sarcomata. 
 
 II. The second form of angioma, called angioma cavernosa, consists 
 largely of a series of intercommunicating irregular-shaped larger and 
 smaller blood-spaces lined with endothelium, and surrounded by a variable 
 quantity of fibrillar connective tissue, which may contain smooth muscle- 
 cells (Fig. 44). They resemble the erectile tissue of the corpora cavernosa of 
 the penis and clitoris. They are apparently formed by a dilatation of old 
 and new-formed capillaries and veins. They are sometimes erectile, and 
 sometimes pulsating and are not infrequently multiple. They may be 
 seated in the skin and subcutaneous tissue, forming the so-called project- 
 ing nsevi or in internal organs. They are often found in the liver and 
 less frequently in bone, the brain, spleen, uterus, kidney, intestines, 
 bladder, and muscles. They are usually of little significance, though 
 they may give rise to hemorrhages. 
 
 LYMPHANGIOMA. 
 
 These tumors consist of dilated lymph-channels, which either preserve 
 approximately the general shape of the original lymph-vessels, or are dis- 
 tinctly cavernous in character or even cystic. They probably originate in 
 part in new-formed, in part in old lymph-channels. A strict distinction 
 between tumors formed by a dilatation of preformed and new-formed 
 lymph-channels is not possible, owing to the very primitive character of 
 some of the ultimate lymph-spaces, and our lack of knowledge of their 
 exact relations to adjacent parts. 
 
 In the lymphangiomata there may be much or little connective tissue 
 between the dilated channels, which are usually filled with a translucent 
 or milky fluid resembling, and probably identical with the normal lymph. 
 These tumors are usually congenital, but are sometimes acquired. They 
 usually occur in the skin as soft, sometimes considerably, sometimes but 
 slightly elevated tumors, and may occur in the tongue— some forms of 
 so-called macroglossia. They are benign tumors, but may rupture, giving 
 rise to a serious lymphorrhoaa. 
 
 TUMORS IN WHICH EPITHELIAL CELLS ARE PREDOMINANT OR CHARAC- 
 TERISTIC ELEMENTS.— EPITHELIAL TUMORS. 
 
 I. Adenoma. 
 
 II. Carcinoma. 
 
 General Considerations. — While the tumors thus far described in de- 
 tail are formed on the type of tissues which originate in the so-called 
 middle embryonic layer or mesoblast; the epithelial tumors are charac- 
 terized by elements which originate either in the external or internal 
 
TUMOES. 141 
 
 layer, the epiblast or hypoblast. We have accordingly two series of cri- 
 teria by which to describe and identify them; first, morphological, and 
 second, histogenetic criteria. 
 
 While in the main, in the normal body, the general distinctions be- 
 tween epithelial and other tissues are fairly well marked, there are still 
 particular cases, especially those in which epithelial tissues are in jn-ocess 
 of physiological growth or rejuvenation, in which the distinctions are 
 quite ill defined. When we remember the rapid growth of many tumors, 
 the tendency to incomplete formation of their cells, their diverse seats, and 
 the various complicating conditions under which they originate and de- 
 velop, it does not seem strange that the exact limitations of this class of 
 tumors are not easy to fix, nor that they seem sometimes to merge into 
 one another and into tumor-tissues belonging to other classes. If epi- 
 thelial cells under all circumstances had a definite and characteristic 
 structure, or if, on the other hand, we could always know whether a 
 given cell-group originated in epithelium or not, the matter of distin- 
 guishing between tumors of this and other classes would be simple and 
 6asy enough. As it is, in some cases both morphological and histogenetic 
 criteria fail us, and the clinical history and gross appearance are not 
 characteristic. Such cases, which are indeed rare, but which do some- 
 times occur, suggest to us the possibility that the desirability of accurate 
 classification has led us into seeking distinctions which Nature herself 
 has not sharply drawn. While these difiQculties in special cases must be 
 acknowledged, the distinctions are in the main definite enough, and very 
 useful both for clinical and scientific purposes. 
 
 Epithelial tumors always contain, in addition to the more or less 
 characteristic cellular elements, a connective-tissue stroma, which gives 
 them support and carries the vessels. This stroma may be sparse or 
 abundant, may contain few or many cells, is sometimes arranged in ir- 
 regular fascicles or bands, and very frequently forms the walls of well- 
 defined variously shaped spaces or cavities called alveoli, in which the 
 epithelial cells lie. The epithelial cells, in most cases, lie along the walls 
 of the alveoli without an intimate connection with them, as is the case in 
 the alveolar sarcomata. They are, moreover, packed together without 
 more intercellular substance than the usual cementing material common 
 to epithelial cell masses. In this lack of fibrillar intercellular substance 
 within the alveoli, and in the loose relationship between the cells and the 
 alveolar walls, lie in many cases the chief morphological distinctions 
 between certain carcinomata and alveolar sarcomata. 
 
 In certain of the epithelial tumors, there is a reproduction of typical 
 gland-tissue of various kinds, depending upon the seat and conditions of 
 growth of the tumor. Such tumors are called adenomata. A simple 
 hypertrophy of a gland or an increase in its size by excessive growth of 
 its interstitial tissue do not constitute an adenoma. There must be an 
 
142 
 
 TUMOES. 
 
 actual new formation of typical gland-tissue. This is not always or fre- 
 quently of exactly the same character as the gland-tissue in which it 
 originates, and always exhibits a certain lack of conformity to the type, 
 in structure and mode of growth. The alveoli and ducts usually have a 
 lumen and sometimes a membrana propria, but the cells may differ in 
 shape from one another and from those of the gland from which they 
 spring. 
 
 Epithelial tumors in which there is no conformity to a glandular 
 type, but a lawless growth of various kinds of more or less typical epi- 
 thelial cells in the meshes of an old or new formed connective-tissue 
 stroma, are called carcinomata. 
 
 It will readily be seen that there must be a border region between the 
 adenomata and carcinomata where conformity to the glandular type 
 merges into the lawlessness of growth characteristic of carcinomata. In 
 this border region, a certain degree of individual bias must be permitted 
 in assigning a name to the new growth. In some cases a sharp distinc- 
 tion cannot be made, or the tumor may share in the characteristics of 
 both, and then we very properly make use of the term adeno-carcinoma 
 or carcino-adenoma. 
 
 I. ADENOMA. 
 
 The structure of the cellular elements of these tumors and their 
 arrangement into acini and ducts vary even more than do those of the nor- 
 
 FiG. 45.— Adenoma of Mamma, x 100, 
 
 mal glands whose types they follow. The acini usually possess a more 
 or less well-defined lumen and membrana propria. The adenomata 
 
TUMOES. 
 
 143 
 
 sometimes merge into the surrounding tissue, or are continuous with the 
 gland-tissue in which they originate; sometimes they are distinct in out- 
 line, and encapsulated. The interstitial tissue is sometimes abundant, 
 sometimes sparse, and may contain few or many cells. The irregulari- 
 ties of their growth often lead to the stoppage of the lumina of their 
 ducts and the formation of cysts. They may undergo mucous meta- 
 morphosis, and may become sarcomatous. 
 
 Adenomata occur in the mamma, ovary, liver, kidney, thyroid, sali- 
 vary, and lachrymal glands; in the mucous membrane of the nose, 
 pharnyx, stomach, intestine, and uterus, and occasionally in the seba- 
 ceous and sweat glands of the skin. The so-called multilocular cysto- 
 mata of the ovary are among the most important of the adenomata. 
 There are numerous papillary and polypoid growths, in gland-ducts 
 and on mucous membranes, in which there is an actual new forma- 
 tion of gland epithelium, but this is usually secondary to a primary 
 growth beneath the epithelial layer, of some other tissue, such as fibrous 
 or mucous tissue, and the new growth of gland epithelium simply keeps 
 pace with the growth of the latter, to which it serves as an investment. 
 Such growths are sometimes classed among the adenomata, but do not, 
 strictly speaking, belong there. 
 
 The adenomata are in general benign tumors, being slow of growth 
 and localized, but there are very important exceptions. Some of the 
 adenomata of the stomach and intestines belong to the most malignant 
 
 Fig. 46.— Adenoma of Stomach (a form which is on the horder-line of carcinoma). X 300 
 
 and reduced. 
 
 of tumors in rapidity of local extension, in the formation of metastases, 
 and the development of cachexia. Certain of the adenomata of the 
 
144 TITMOES. 
 
 mamma and thyroid are also very malignant. It should be remarked, 
 however, that, as a rule, the malignant adenomata are those which, in 
 structure, lie close ujDon the border-line between tumors of this class and 
 carcinomata, and by such observers as incline to lay more stress ujDon 
 clinical than morphological distinctions, they are usually classed among 
 the latter. 
 
 CAKCINOMA. 
 
 These tumors are composed, as above stated, of a connective-tissue 
 stroma, forming more or less well-defined communicating -spaces or alve- 
 oli, in which lie variously shaped epithelial cells, arranged in an atypical 
 manner. The stroma, containing few or many cells, may be, especially 
 in the advancing portions of the tumor, comjoosed largely of the old con- 
 nective tissue of the part. It may, however, be entirely new formed. 
 The cells which lie in the spaces or alveoli bear sometimes a very close, 
 sometimes but a very general resemblance to epithelium. 
 
 It was formerly believed that new epithelium might be formed, both 
 from old epithelial cells and from the connective-tissue cells, and possi- 
 bly from white blood-cells, and among many observers this belief still 
 exists, and has never been disproved. Still, within the last twenty years, 
 the opinion that new epithelial colls in tumors arise exclusively from old 
 epithelium has found general acceptance, and for very good reasons. 
 No one has actually seen an epithelial cell originate under the microscope, 
 and until this can be done, our beliefs must rest upon indirect observa- 
 tions. In the first place, all the epithelial structures in the embryo ori- 
 ginate in connection with the epiblast or hypoblast, that is, in the layers 
 which are largely characterized by the presence of epithelium. In re- 
 generation, after an injury in the adult, a study of the successive phases 
 of the process shows that new epithelium is always formed in continu- 
 ity with the old, and apparently by a proliferation of old epithelial cells. 
 Epithelial tumors are almost exclusively found in parts normally contain- 
 ing epithelium, and frequently the new growth can be distinctly seen to 
 be continuous with the old cells. 
 
 The occurrence of primary epithelial tumoi's in parts of the body in 
 which epithelium does not normally occur, as in bone and the lymph nodes, 
 has been recorded, but these may have been metastatic tumors, in which 
 the primary tumor was small and overlooked, or they may have been 
 displaced embryonic germs which, according to Cohnheim's hypothesis, 
 would explain their heterologous occurrence. These possibilities of er- 
 ror should be taken into the account in the apparently exceptional cases, 
 and it is to be remarked that these are becoming less and less as our 
 knowledge increases and our technical facilities for research improve. 
 
 A considerable number of the tumors formerly described as heterol- 
 ogous primary carcinomata are now known to be formed by proliferation 
 
TUMOES. 
 
 145 
 
 of endothelium, and hence to belong to another class, although closely 
 resembling the carcinomata in structure. 
 
 A great practical difficulty in the description, and to beginners, in the 
 recognition of the carcinomata and their varieties, lies in the great diver- 
 sity in shape which their cells present. It should be always borne in 
 mind that the shape of cells depends in part upon their inherited 
 tendencies in growth which we cannot see under the microscope, but to 
 a greater degree upon the varying conditions of nutriment and pressure 
 to which they are exposed during life. In the normal body, these condi- 
 tions conform to a certain standard, so that cells of a given kind at a 
 given stage of development are approximately similar. 
 
 In tumors, however, the lawlessness and lack of fixed conditions in 
 growth is such that we may have many young and atypical so-called in- 
 
 FiG 47. — Cancer-cells Infiltrating the Tissue in the Vicinity of a Tumor. From Carcinoma 
 
 Mammee. X 460. 
 
 different forms of cells; while even the adult forms may depart widely 
 from normal shapes. Thus, in cylindrical-celled carcinomata, there are 
 many fully developed cells which are never cylindrical; there are many 
 others not fully developed which are quite indifferent in form, looking 
 just like many other young cells, cells which are not, but which are des- 
 tined to become epithelium. Finally, we have the cells produced by 
 ordinary inflammatory processes about and within the tumor, which acts 
 like an irritating foreign body. Thus it is that there is no characteris- . 
 tic cancer-cell, as was formerly supposed. Some of them are typical and 
 10 
 
146 
 
 TUMORS. 
 
 some not, and the more typical ones may look just like normal epithelial 
 cells, and the atypical ones Just like simple inflammatory cells, or young 
 connective-tissue cells, or white blood-cells. It is always in the topog- 
 raphy, together with the general characters of the cells and the situation 
 of the growth, that we must seek for the evidences of its nature. 
 
 The carcinomata are very prone to local extension, the advancing 
 tumor-cells in the periphery making their way through the lymph-spaces 
 and'forming new foci (Fig. 47). Metastasis is of frequent occurrence in 
 some forms, and takes place chiefly, though not exclusively, through the 
 
 Fig. 48. — Metastatic CARCiNoMA.—Masses of Cancer-cells growing in the Lymph-vessels of the 
 Pleura. The Primary Tumor was in the Liver. X lEO and reduced. 
 
 lympli-vessels, frequently involving adjacent or remote lymph-nodes. 
 The secondary tumors are in the main similar in general structure to 
 the primary foci, but may vary from them in vascularity and the abund- 
 ance of the stroma, or in the shape of the cells. The carcinomata' are, 
 as a rule, malignant tumors, but the difEerent forms vary much in this 
 respect. They are liable to fatty, colloid, mucous, and amyloid degene- 
 ration, and are especially prone to ulceration, to hemorrhage, and simple 
 inflammation. They may become partially calcified, and are not infre- 
 quently combined with other forms of tissue in the mixed tumors. 
 
 They are more frequent in middle and old age than in the young, 
 but they may occnr at any age. 
 
 Forms of Carcinoma. — In certain cases of carcinoma which occur in 
 the skin and in some mucous membranes, the cells j)resent the structure 
 and general characters of the epithelium of the part in which they occur, 
 and since here the tendency of the cells as they approach the surface is 
 to become flattened or squamous, these tumors are called squamous or flat- 
 celled carcinomata, or simply HJjnthelioinata. 
 
 In another class of tumors such as frequently occur in the gastro- 
 
TUMOES. 
 
 147 
 
 intestinal canal and uterus, the cells are more or less cylindrical in shape, 
 forming a palisade-like lining to the irregular alveoli ; such tumors are 
 called Gylindrical- Celled Oarcinomata, although here again many of the 
 cells are not cylindrical at all, but may have a great variety of forms. 
 
 There is a third and very common form of tumor in which the epi- 
 thelial cells have no constant characteristic shape, but vary as much as do 
 the cell-forms in the various glands of the body. Such tumors are conve- 
 niently classed together as gland-celled carcinoma or carcinoma simplex. 
 
 In addition to these forms, there are several others which depend for 
 their characteristics upon various metamorphoses or degenerations, or 
 upon the preponderance of one or other of the anatomical constituents of 
 the growth. It will be most convenient to give a brief description of 
 these various kinds, one after another, with the understanding that they 
 are not absolute specific forms, but are simply varieties which it is con- 
 venient to recognize for clinical as well as anatomical purposes. 
 
 Flat-celled Carcinoma or Epithelioma. — These tumors occur in the 
 skin and in the mucous membranes which are covered with squamous 
 epithelium. The cells present all of the various forms which normally 
 
 Fig. 49. — Epithelioma of Neck. 
 Shows epithelial pearls, spined cells, and reticular masses of Tariously shaped epithelial cells. 
 X about 400 and reduced. 
 
 exist in these parts; the cuboidal and polyhedral cellsof the rete Malpighii 
 as well as the more superficial flattened forms (Fig. 49). Frequently the 
 spined cells or so-called " prickle" cells " are largely reproduced. Having 
 to a certain extent the same life history as the cells in which they 
 
148 
 
 TUMOES. 
 
 originate, many of tlie tumor-cells become dry, thin, and horny, like the 
 epidermis cells, as they grow older, and since their growth and changes 
 often occur within the old lymph-spaces of the affected tissue, or in the 
 new-formed alveoli, the cells are sometimes packed together in spheroidal 
 concentric masses called " epithelial pearls," which may sometimes be seen 
 
 Fig. 50. — Epithelioma of Axillary Lymph-Gland. 
 K^This metastatic tumor was secondary to a larg^e epithelioma of tlie baclc of tlie hand, Fig. 51. 
 Tile small cells with darker nuclei are the cells of the Ijmph-gland. X 300. 
 
 wi th the naked eye upon or near the surface of the growth (Fig. 50). The 
 new cell masses may be large or small, may be separated by much or little 
 
 
 Fig. 51.— Epithelioma of Back of Hand. 
 The flat tumor occupied nearly the entire back of the hand, and was ulcerating at the centre. 
 The figure shows the edge of the tumor and a portion of, the ulcer. The papillae of the skin over 
 the edge of the growth are hypertrophied, and the tissue about it infiltrated with small spheroidal 
 cells. X 15 and reduced. 
 
TUMORS. 
 
 149 
 
 
 u Small Epithelioma op the Side of the Nose, X f 
 
150 
 
 TUMOES. 
 
 stroma; often form reticular masses, and may infiltrate the tissues deeply 
 or remain near the surface ; or may project abofe the surface forming 
 wart-like or papillary growths. These tumors frequently ulcerate on the 
 surface. 
 
 They are most apt to occur in the skin, especially in those parts in 
 which it becomes continuous with mucous membranes — lips, external 
 nasal openings, eyelids, labia, and glans penis; and are frequent in the 
 mouth, oesophagus, vagina, and about the cervix uteri. 
 
 There are also carcinomata of the skin composed of cuboidal cells 
 arranged in tubules or masses, which do not follow the type of the 
 epithelium of the skin, but rather that of the sweat-glands or sebaceous 
 glands. These tumors are found most frequently on the nose and eye- 
 lids (Figs. 52 and 53). 
 
 Epitheliomata are apt to recur if not thoroughly removed, and may 
 form metastases, but in general they are the least malignant of the carci- 
 nomata. The prognosis is in most cases good if there is early and com- 
 plete removal. 
 
 Cylindrical-celled Carcinoma. — These tumors, closely allied to sonre 
 
 Fig. 64.— Carcinoma MAMMiE (Scirrhus Variety). X 400 and reduced. 
 
 forms of adenoma, occur in the stomach, intestines, and uterus. The cells 
 may be only in part cylindrical, the remainder having various shapes, and 
 all being loosely or closely packed in larger or smaller alveoli. They may 
 have much or little stroma. They merge imperceptibly into the next class: 
 Gland-celled Carcinoma, or Carcinoma simplex. — These, which are 
 by far the most frequent of the carcinomata of internal parts, are charac- 
 terized by the alveolar structure and by the absence of any special charac- 
 teristic shape in the cells, which maybe spheroidal, polyhedral, fusiform. 
 
TUMORS. 
 
 151 
 
 or euboidal. They may or may not i-esemble the epithelium of the gland 
 in which they originate. They are usually nodular tumors, and may be 
 hard or soft. If the stroma is abundant and dense, and preponderates 
 over the cellular elements, the tumor is usually hard, and is called scirrhus 
 or fibro-carcinoma (Fig. 54). If, on the other hand, the cellular elements 
 largely preponderate, the tumor is usually soft, and if it do not contain 
 too many blood-vessels, may have a general resemblance to brain-tissue, 
 
 Fig. 55. — Medullary Carcinoma of Stomach (Carcinoma MoUe). 
 
 and is then called e7icej)haloid or medullary cancer ; or better. Carcinoma 
 molle (Fig. 55). These are among the most malignant of the cancers. The 
 intercellular tissue may become so abundant as to nearly obliterate the 
 cellular elements, but it is doubtful if carcinoma ever undergoes sponta- 
 neous cure in this way. These tumors may be hard in one portion and 
 soft in another. They may contain vei'y many blood-vessels, C.telangiec- 
 toicles. They occur,as primary tumors in the mamma, livei', thyroid, sali- 
 vary, and prostate glands, in the pancreas, kidney, testicle, and ovary. 
 
 Colloid Carcitiotna. — The cells of certain cancers, especially of the 
 gastro-intestinal canal, may suffer a more or less complete infiltration 
 with a translucent material somewhat resembling gelatin, and called 
 colloid, whose nature is not well understood. Sometimes this infiltration 
 is only partial, when the protoplasm of the cells may be more or less 
 encroached upon by the translucent droplets of the colloid material ; but 
 in other cases over large areas the cells are partially or entirely destroyed, 
 
152 
 
 TUJrOES. 
 
 and replaced by the new materia], so that the alveoli of the tumor are 
 distended by it, and their walls appear very distinct in the midst of the 
 colloid substance (Fig. 56). In such cases the alveolar structure of the 
 tumor is sometimes very evident to the naked eye, and these tumors are 
 therefore often called alveolar carcinoma. Sometimes only a part of the 
 tumor is affected in this way. 
 
 Fig. 66.— Colloid Carcinoma of Eeotum. 
 
 Carcinoma myxomatodes. — The cellular elements of earcinomata may 
 suffer mucous softening, and thus larger and smaller cysts containing a 
 mucous fluid are sometimes formed. To this form of metamorphosed 
 
 Fig. 37.— Carcinoma Myxomatodes of Mamma. 
 
 tumor the above name is sometimes applied, but it more properlv belongs 
 to cancers in which the stroma is composed of mucous tissue (Fio'. 57). Such 
 
TinviOES. 153 
 
 tumors are most frequently found in the gastro-intestinal canal and 
 mamma. 
 
 Melano-carcinoma. — Tumors of this class are rare, and are character- 
 ized by the presence of a variable quantity of black or brown pigment 
 particles either in the stroma or the cells. They are usually soft and 
 malignant, and most frequently occur in the skin.' 
 
 ' Bibliography. — The most extensive and important work on tumors, contain- 
 ing avast store of information, is that of Rudolph Virchow, " D.e krankhaften Ge- 
 schwiilste." It is not completed and is somewhat old, but is still invaluable as a 
 work of reference. The section on tumors in v. Pitha and Billroth's work on sur- 
 gery (" Handbuoh der AUgemeinen u. speciellen Chirurgie "), which comprises the 
 first section of the second volume, by Dr. Liicke, is very complete. A valuable 
 bibliography and digest of recent observations on tumors will be found in the 
 last edition (1882) of Birch-Hirschfeld's work on Pathological Anatomy (" Lehr- 
 buch der Pathologischen Anatomic "), vol. i. 
 
PART III. 
 
 MOEBID ANATOMY- OF THE OEG-AI^S. 
 
THE NERVOUS SYSTEM. 
 
 THE MEMBRANES OP THE BRAIN. 
 The Dura Mater. 
 
 The dura mater is a dense connective-tissue membrane, which serves 
 the double purpose of a periosteum for the inner surface of the cranial 
 bones, and of an investing membrane for the brain. It is itself but 
 poorly supplie'd with blood-vessels, but it contains the large venous si- 
 nuses which carry the blood from the brain. Lesions of the dura mater, 
 therefore, are apt to be associated with lesions of the cranial bones, of the 
 pia mater, or of the venous sinuses. 
 
 In young children the dura mater adheres closely to the inner surface 
 of the cranial bones, in adults it is more readily detached, and in old 
 persons it is again more adherent. Low grades of chronic inflammation 
 of the external layers of the dura mater also render it more adherent to 
 the bones. 
 
 Hemorrhages. — We find extravasations of blood between the dura 
 mater and the cranial bones, in the substance of the membrane, and be- 
 tween the dura mater and the pia mater. 
 
 The hemorrhages in the substance of the dura mater are small and of 
 little consequence. 
 
 The hemorrhages between the dura mater and the pia mater occur 
 with chronic pacchymeningitis, or are derived from the vessels of the pia 
 mater. 
 
 The hemorrhages between the dura mater and the cranial bones are pro- 
 duced by blows and injuries of the head. They are often of considerable 
 size, separate the membrane from the bones, and may compress the brain. 
 They are often associated with laceration of the brain, and hemorrhages 
 between the dura mater and pia mater. 
 
 The pressure on the head of the infant in labor may produce, in addi- 
 tion to the extravasations of blood between the bones and the peri- 
 cranium, additional extravasation between the bones and the dura mater. 
 
 Thrombosis of the venous sinuses is not uncommon. Any inflamma- 
 
158 THE NEEVOtJS SYSTJ:M. 
 
 tion of the dura mater is liable to produce it; injuries and inflammations 
 of the brain and pia mater, of the cranial bones, of the middle ear, and 
 of the scalp, may also produce thrombosis. The changes in the blood 
 produced by the exhausting and infectious diseases may produce throm- 
 bosis of the venous sinuses as they do of the reins in other parts of the 
 body. There are also rare cases in which such a thrombosis is developed 
 without discoverable cause in persons previously healtliy, and produces 
 marked symptoms and death. 
 
 Some of these thrombi are firm, of white or red color, and apparently 
 produce no secondary lesions. 
 
 Others are of firm consistence, but they jDroduce softening with small 
 hemorrhages of portions of the brain. In these cases the thrombus ex- 
 tends from the venous sinus into one of its veins, and the portion of 
 brain belonging to this vein is softened and hemorrhagic. Such a soften- 
 ing of the brain is often attended with inflammation of the pia mater. 
 
 In other cases, the thrombi are soft and puriform, fragments of them 
 become detached and lodge as infectious emboli in the arteries in difier- 
 ent parts of the body. 
 
 Inflammation of the dura mater is called pacchy meningitis, and this 
 may involve the external layers of the membrane, 2JCicchymeningitis ex- 
 terna, or the interna] layers, pacchy menitigiiis interna. It may further- 
 more be either acute or chronic. The tissues of the substance of the 
 dura mater participate to a greater or less degree in these changes, but 
 the chief lesions are upon the surfaces. 
 
 Acute pacchy meningitis externa is usually secondary to injuries or 
 diseases of the cranial bones; thus fractures of the skull, either depressed 
 or not, ostitis, caries, suppurative inflammation of the internal and mid- 
 dle ear and mastoid cells may produce it. The dura mater is usually 
 congested, thickened, and softened, and may present small ecchymoses. 
 The inflammation is usually suppurative, and pus may accumulate be- 
 tween the membrane and the bone, or in the substance of the membrane. 
 The areas of inflammation are not usually extensive. It sometimes in- 
 duces thrombosis of the venous sinuses, and sometimes gangrene of the 
 dura mater occurs. The inflammation may extend to the inner surface 
 of the dura mater, to the pia mater and brain, or it may remain localized 
 and undergo resolution. 
 
 Acute pacchijmeningitis interna may be secondary to inflammation of 
 the external surface, or it may occur as a complication in pyaemia, puer- 
 peral fever, chronic difEuse nephritis, in the exanthemata and erysipelas, 
 or idiopathically. There is a general or circumscribed production of 
 fibrin and pus, so that the internal surface of the membrane is lined with 
 a layer of soft, yellow exudation. 
 
 Simple chronic pacchymeningitis consists in the formation of new 
 connective tissue in the dura mater, by which it becomes thicker, and in 
 
THE JSTEEVOUS SYSTEM. 
 
 159 
 
 many cases abnormally adherent to the bones of the skull. This thicken- 
 ing may be general or circumscribed, and may involve the entire thick- 
 ness of the membrane. Not infrequently, when the external layers are 
 especially involved, firm adhesions to the slcuU occur, with ossification of 
 the outer layers, so that shreds of the membrane containing little masses 
 of bone (osteophytes) remain sticking to the skull when the membrane 
 is stripped off. 
 
 There is an important form of chronic inflammation of the internal 
 layer of the dura mater, called pacchymeningitis interna hcemorrhagica 
 characterized by the formation of layers of new delicate connective tis- 
 sue with numerous very thin-walled blood-vessels from which the blood 
 is prone to escape. The membrane may at first appear as a delicate 
 fibrinous pellicle, with small red spots scattered through it, or it 'may 
 look like a simple reddish or brown staining of the inner surface of the 
 
 Fig. 58.— Chronic Pacchymeningitis Interna H^imorrhagica, X 100. 
 
 dura mater. Microscopical examination shows this membrane to consist of 
 numerous blood-vessels, mostly capillaries with very thin walls, which may 
 be distended or pouched, and which have grown out from the vessek of 
 the dura mater (Fig. 58). Between the vessels is a homogeneous or slightly 
 differentiated basement substance, containing a variable number of sphe- 
 roidal, fusiform, or branching cells. Red blood -cells in variable quantity, 
 and blood pigment in various forms, frequently enclosed in the new cells 
 
160 THE NEEYOTJS SYSTEM. 
 
 and small calcareous concretions (brain-sand) (Fig. 59) also lie in the inter- 
 vascular spaces. In more advanced stages the new membrane may become 
 greatly thickened, its outermost layers being changed into dense fibrous 
 tissue with obliteration of the vessels; while the more recently formed layers 
 are similar in structure to those at first developed. Considerable blood 
 usually escapes from the vessels of the new membrane by diapedesis, in 
 all stages of its formation, and the vessels are also very liable to rupture, 
 giving rise to extensive hemorrhages either into the substance of the 
 membrane, or between it and the pia mater. Sometimes masses of new 
 
 Fie. 69.— Brain-Sand from Paoohtmeningitis Intekna, X about 350. 
 
 tissue and blood, from a half an inch to an inch or more in thickness, are 
 in this way formed, greatly compressing the brain. These new mem- 
 branes are most frequently formed over the convexity of the brain, but 
 may extend over nearly the entire surface of the dura mater. Sometimes, 
 when old, the entire membrane, densely pigmented and firm, lies loosely 
 beneath the dura mater without compressing tlie brain or giving any 
 clinical indication of its presence. The membrane may induce chronic 
 clianges in the pia mater, with or without accompanying changes in the 
 cortical portion of the brain. 
 
 Earely, serum accumulates between the layers of the new membrane, 
 and in this way cysts of large size may be formed. In rare cases, diffuse 
 suppuration of the entire new membrane occurs. 
 
 The slighter degrees of this form of inflammation may occasion no 
 symptoms during life. They are not infrequently found in persons 
 suffering from various chronic brain lesions and from chronic alcoholism, 
 but they may occur unassociated with complicating lesions. The more 
 advanced forms of the lesion are frequently found in idiots, epileptics, 
 etc. 
 
 Tubercular paccJiymeningiiis may occur secondarily to that forin of 
 inflammation in the pia mater or the bones; or as a part of general 
 miliary tuberculosis. The tubercles may be situated on either surface of 
 the membrane or in its substance, and may be single or aggregated, form- 
 ing large masses. 
 
 SypMlitic 2}acchy meningitis manifests itself by the formation of 
 so-called gammy tumors either upon the external or internal sur- 
 face of the dura mater. These tumors may be single or multiple, and 
 
THE NERVOUS SYSTEM. 161 
 
 vary greatly in size. They may be accompanied by simple inflammatory 
 changes in the dura mater in their vicinity. They may undergo suppu- 
 ration with the formation of abscess, the inflammation may extend to 
 the pia mater, inducing simple or syphilitic meningitis and adhesions 
 between the dura mater and pia mater. The gnmmata may, on the 
 other hand, when occurring on the outer surface of the membrane, cause 
 absorption and perforation of the bones of the skull. 
 
 Tumors. — The most common tumors of the dura mater are sarcomata 
 and of these the spindle-celled forms are of more, the round and poly- 
 hedral celled of less frequent occurrence. They may grow from either 
 surface of the membrane. Some of the round and polyhedral ceHed 
 forms are soft and very vascular, and are apt to involve the neighboring 
 pia mater and brain-tissue, or the bones of the skull, which they may 
 perforate. They sometimes project through the opening in the skull 
 in fungous bleeding masses. 
 
 Psammomata are small globular tumors, often multiple and pedicu- 
 lated, growing from the inner surface of the dura mater. They are 
 usually composed of tissue sarcomatous in charactai', and contain 
 variously shaped calcareous concretions similar in appearance to the so- 
 called brain-sand. 
 
 Endotheliomata. — These tumors may grow inward or outward, causing 
 pressure on the brain or absorption and i')erforation of the bones; they 
 often attain considerable size. Some of these tumors somewhat resemble 
 certain forms of epitheliomata, and have often been described as primary 
 carcinomata. 
 
 Fibromata and Lipomata occur rarely in the dura mater and are of 
 small size. 
 
 Small Gliondromata are sometimes found connected with the dura 
 mater at the base of the brain. 
 
 Osteomata. — In addition to the formation of osteophytes in chronic 
 external pacchymeningitis, plates, and, more rarely, globalar masses of 
 bone may be formed in the dura mater, unconnected with the bones of 
 the skull. They are most frequently found in the falx cerebri, but may 
 occur elsewhere. Tiio new bone may be dense or loose in texture, and 
 usually produces no symptoms. 
 
 THE PIA MATER. 
 
 The external surface of the brain is invested by a connective-tissue 
 membrane which covers the convolutions, dips down into the sulci, and 
 extends into the ventricles. This membrane is abundantly supplied with 
 blood-vessels, and from it numerous vessels extend into the brain, so that 
 any disturbance in the circulation of the blood in the pia mater involves 
 a disturbance in the circulatioq of the blood in the brain also. 
 
 The connective tissue which makes up the pia mater is arranged in a. 
 11 
 
162 THE NEEVOUS SYSTEM. 
 
 series of membranes and fibres reinforced by elastic tissue, so arranged 
 as to form a spongy membrane containing numerous cavities, more or 
 less filled with fluid. These cavities are continuous with the perivascular 
 spaces which surround the vessels that pass from the pia mater into the 
 brain. 
 
 The outer layers of the pia mater are the most compact, and are 
 covered on their outer surface by a continuous layer of endothelial cells. 
 This external layer of the pia mater is often described as a separate 
 membrane called the 'arachnoid,' but it is really only part of the pia. 
 
 The deeper layers of the pia contain the blood-vessels. The mem- 
 branes and fibres which compose the pia muter are partly coated with 
 cells which have irregular and delicate cell- bodies, and large distinct 
 nuclei.- 
 
 In all inflammations of the pia mater the inflammatory products reg- 
 ularly collect in the spaces within it. 
 
 Along the borders of the longitudinal fissure and, more rarely, on the 
 under surface of the brain, are a number of small, white, firm, irregular 
 bodies — the Pacchionian bodies. They vary in their size, their number, 
 and in the extent of the surface of the hemispheres covered by them. 
 They may perforate the dura mater, or, more rarely, tlie wall of the lon- 
 gitudinal sinus, and may produce erosions of the skull-bones. They are 
 composed of fibrous tissue and may undergo fatty or calcareous degenera- 
 tion. As they are so commonly found and are not known to be of any 
 pathological significance, they may almost be regarded as normal struc- 
 tures; at any rate, we do not know what causes them or their variations 
 in size and number. 
 
 The pia mater is frequently thickened, opaque, and white, either in 
 diffuse patches or, more commonly, along the course of the vessels. In 
 other cases, single or multiple small white spots, of the size of a pin's 
 head or smaller, may be seen in the membrane, not appreciably elevated 
 above the surface, but due to localized thickening. These slight opaci- 
 ties of the pia mater are commonly believed to be dependent upon re- 
 peated congestions of the membrane or upon chronic meningitis, but 
 there is no evidence that this is always the case. They are most fre- 
 quently found in old persons, but may exist at any age, and do not 
 necessarily indicate the pre-existence of disease, although similar appear- 
 ances are common in the chronic insane and in drunkards. 
 
 The amount of blood contained in the vessels of the pia mater after 
 death varies greatly, and is by no means a reliable indication of the 
 amount present during life. In general anemia, the vessels of the pia 
 mater may contain little blood, but, on the other hand, they sometimes 
 seem to contain a relatively larger amount than other parts of the body. 
 In oedema of the brain and pia mater, the vessels of the latter may con- 
 tain but a small amount of blood. 
 
THE NERVOUS SYSTEM. 163 
 
 The pia mater may be hypercBinic in early stages of meningitis, after 
 death from delirium tremens, or following epileptic convulsions, from 
 various infectious diseases, certain poisons, the presence of tumors or 
 exudations pressing on the veins, as well as from general and local dis- 
 eases of the circulatory apparatus. But whether they are overfilled or 
 comparatively empty after death seems to depend upon the position in 
 which the body has lain; upon the time which has elapsed between 
 death and the examination, upon the rapidity with which the blood co- 
 agulates, and upon conditions entirely unknown to us. 
 
 CEdema. — The amount of serum beneath the pia mater and infiltrat- 
 ing its tissue is very variable in amount. It may accumulate as a result 
 of atrophy of the brain substance or of venous hypersemia, and sometimes 
 is, and sometimes is not, accompanied by oedema of tlie brain substance. 
 It may be difEuse or localized. It is not infrequent to find in hospital 
 patients sufEering from chronic nephritis, cardiac or pulmonaj-y disease, 
 or chronic alcoholism, a very considerable amount of serum in this situ- 
 ation, and yet the patient has been free from cerebral symptoms. In 
 other cases again, this same serous effusion affords the only explanation 
 of grave cerebral symptoms. It is necessary to be very careful in judging 
 of the importance of this accumulation of fluid. 
 
 It should always be borne in mind that an accumulation of fluid b* 
 neath and in the meshes of the pia mater may occur as a result of post- 
 mortem changes. 
 
 Hemorrhage. — This may occur either into the space between the dura 
 mater and pia mater — intermeningeal liemorrhage — or in the meshes of 
 the pia or between the latter and the brain. It may be due to injury, to rup- 
 ture of aneurisms, or otherwise diseased blood-vessels, to thromboses of 
 the venous sinuses, or to causes which we are unable to ascertain. 
 Hemorrhages, without known cause, not infrequently occur in the sub- 
 stance of the'pia mater in young children, but in adults they are apt to 
 be the result of injury. Multiple ecchymoses, however, in the substance 
 of the pia mater sometimes occur in infectious diseases and also in, acute 
 inflammation of the pia mater. Hemorrhages in the brain substance 
 may lead to the accumulation of blood beneath or in the meshes of the 
 pia mater. Intermeningeal hemorrhage in infants as a result of injury 
 during birth is not uncommon. Small, and sometimes considerable, ex- 
 travasations of blood may occur from diapedesis, and sometimes as a re- 
 sult of chronic congestion, degenerated blood pigment collects along the 
 walls of the vessels. The extravasated blood in meningeal hemorrhage, 
 if small in quantity, may be largely absorbed, leaving a greater or smaller 
 accumulation of pigment at the seat of the hemorrhage, and such pig- 
 mentations may last for a long time. 
 
 Inflammaiion of the pia mater is called lepto-meningitis, or simply 
 
164 
 
 THE NEEVOUS SYSTEM. 
 
 meningitis. We distinguish acute, chronic, tubercular, and syphilitic 
 
 meningitis. 
 
 Acute meningitis occurs most frequently as the characteristic lesion of 
 epidemic cerebro-spinal meningitis; it is a not very infrequent compli- 
 cation of pneumonia, Bright's disease, typhus and typhoid fever, and 
 the exanthemata; it is secondary to injuries and inflammation of the cra- 
 nial bones, of the dura mater, and of the middle ear, and it is sometimes 
 an idiopathic lesion. 
 
 In any ease of acute meningitis, the inflammation is apt to extend 
 downwards and involve the pia mater of the cord. It may also involve 
 the ependyma of the ventricles, and cause the distention of these cavi- 
 ties with serum. This latter condition belongs especially young chil- 
 dren. 
 
 There are two anatomical varieties of -acute meningitis, which give, 
 however, exactly the same clinical symptoms. 
 
 Fig. 60. — Cellular Meningitis, x 850 and reduced. 
 
 (1) Acute cellular meningitis. — The pia mater is somewhat congested, 
 its surface is dry ansl lustreless, and it is somewhat opaque. These 
 changes in the gross appearance of the membrane are not marked, and 
 are easily overlooked, but the minute changes are more decided. There 
 is an abundant production of cells somewhat resembling the cells which 
 
THE NERVOUS SYSTEM. 
 
 165 
 
 coat the surfaces of the membranes and fibres which make up the pia 
 mater. This cell-growth is general, involving the pia mater over most 
 of the surface of the brain. The inflammation, then, is one which re- 
 sults in the production, not of fibrin, serum, or pus, but of new con- 
 nective-tissue cells. This form of meningitis is of frequent occurrence, 
 and is attended with the ordinary clinical symptoms of acute meningitis. 
 (2) Smple acute meningitis of the exudative form is characterized by 
 the accumulation, chiefly in the meshes of the pia mater and along the 
 walls of the blood-vessels, of variable quantities of serum, fibrin, and 
 pus. Sometimes one, sometimes another of these exudations prepon- 
 derates, giving rise to serous, fibrinous, or purulent forms of the inflam- 
 mation. The absolute quantities, too, of the exudations vary greatly. In 
 somecases death maybe caused with so slight aformation of exudation that, 
 to the naked eye, the pia mater may look quite normal, or perhaps only 
 moderately hypersemic or oedematous; the microscope, however, in these 
 ■cases, will reveal pus-cells in small numbers^ and sometimes flakes of 
 fibrin in the meshes and along the walls of the vessels. In other cases, 
 turbid serum in the meshes of the membrane is all that can be seen, and 
 the microscope shows the turbidity to be due to pus-cells or a small 
 amount of fibrin. Again, either with or without marked oedema of the 
 pia mater, yellowish stripes are seen along the sides of the veins, some- 
 
 J ~%a«( ^P^^fLL_ n ^ , I 'Hi , &^^^ 
 
 -^ i^-fp-^ Jif^T" -^ -^ \ \\1 / 'hi '^ J?^ 
 
 \u '^^ ^ I ' ' 
 
 Fio. 61.- -Acute Purdlent Meninc3itis, X 24, 
 a, Convolutions of cerebrum; 6, pia mater heavily infiltrated witii pus; c, blood-vessels enter- 
 ing brain from pia, and surrounded by a zone of pus cells; d, congested blood-vessels of pia mater; 
 *, smaller blood-vessels of pia, around which pus cells are collected in dense masses. 
 
 times appearing like faint turbid streaks, and at others, dense, opaque, 
 thick, and wide, and almost concealing the vessels. These are due to the 
 accumulation of pus-cells and fibrin in large quantities along the vessel, 
 and they are best seen and most abundant around the larger veins which 
 run along over the sulci. In still other cases, the infiltration with pus 
 
166 
 
 THE NEEVOUS SYSTEM. 
 
 and fibrin is so dense, and thick, and general that the brain-tissne, con- 
 volutions, and most of the vessels of the pia mater themselves are con- 
 cealed by it. This is usually of a greenish-yellow color, and is sometimes 
 so thick as to form a sort of cast of the brain -surface at the seat of the 
 lesion (Fig. 61). Sometimes extravasated red blood-cells are mingled with 
 the other exudations as the result of diapedesis. Microscopical examina- 
 tion shows numerous white blood-cells sticking in the walls of the veins 
 and cajiillaries, or the vessels may be blocked with them. It is evident 
 that a large part of the pus-cells originate by emigration. The connec- 
 tive-tissue cells of the pia mater may be detached from their places or 
 degenerated. In some cases there are considerable accumulations of pus 
 between the pia mater and the brain-substance and along the vessels which 
 enter the latter. More rarely pus is found upon the free surface of the 
 membrane. The brain-substance may be compressed by the accumulated 
 exudation, so that the convolutions are flattened. Tlie cortical portion 
 of the brain may be simply infiltrated with serum — osdematous — or it 
 may undergo degenerative changes, or it may be the seat of punctate 
 
 Fig. 62.-FATTY Degeneration of Cells along Blood-vessels of Pia Mater after Exudative 
 
 Meningitis, x 300 and reduced. 
 
 From the pia mater of a child 5 years old. 
 
 hemorrhages. Not infrequently the inflammation extends to the ven- 
 tricles, which may contain purulent serum, and to the pia mater of the 
 cord. This form of inflammation is most frequent on the convexity of 
 the brain, bat may extend, or even be confined to the base. It may be 
 localized, but frequently extends widely over the surfaces of the hemi- 
 spheres. 
 
THE NEEVOUS SYSTEM. 
 
 167 
 
 When recovery from acute exudative meningitis occurs, there may be 
 fatty degeneration of the cells which have accumulated in the pia mater, 
 particularly along the vessels (Fig. 62), and this may produce white patches 
 in the membrane and threads along the blood-vessels, which resemble the 
 appearance of an accumulation of exudation in the acute stage. Fatty 
 degeneration of the blood-vessels and cells of the pia mater may also oc- 
 cur without acute inflammatory changes. 
 
 Sometimes in children and young adults, the inflammatory changes 
 in the ventricles persist for days and weeks after the subsidence of the 
 inflamniE^tlon of the pia mater. 
 
 Chronic meningitis. — Either the pia mater at the base of the brain 
 alone may be inflamed (basilar meningitis), or the pia mater over the 
 convexity alone, or the entire pia mater, or circumscribed patches of the 
 membrane. The j^ia mater is thickened and opaque, the thickening 
 being sometimes very considerable. There is a formation of new con- 
 nective tissue and a production of pus, fibrin, and serum; the relative 
 quantity of these inflammatory products vary in different cases. Firm 
 and sometimes extensive adhesions may be formed between the dura 
 mater and the pia mater. Not infrequently the cortical portions of the 
 brain participate in the morbid process, and we find infiltration of small 
 spheroidal cells around the blood-vessels, thickening of the walls of the 
 vessels, and degenerative changes and atrophy of the nerve-tissue. New 
 connective tissue may also form in the brain-substance, which may become 
 closely adherent to the pia mater. The ventricles of the brain also may 
 contain an increased amount of serum, and may be dilated, and the epen- 
 dyma may be thickened and roughened. This form of inflammation may 
 be the result of injury or disease of the cranial bones, or secondary to 
 
 chronic pacchymeningitis, or to inflammation of the brain-substance. 
 It may occur in the vicinity of tumors of the brain or meninges. It 
 may be a complication of chronic diffuse nephritis or the result of chronic 
 alcoholic poisoning. It may occur in marked form in the general para- 
 lysis of the insane. 
 
 Tuiercular meningitis. — This is especially characterized by the for- 
 mation in the pia mater of miliary tubercles, associated with more or 
 less well-marked exudative inflammation. It may occur in adults and 
 
168 
 
 THE NERVOUS SYSTEM. 
 
 in children, but is more common in the latter. The dura mater may be 
 unchanged, or its inner surface may be besprinkled with miliary tuber- 
 cles. The pia mater may or may not be congested; it may look dry on 
 the surface or it may be CEdematous. Usually the brain seems to fill 
 the cerebral cavity to an unusual degree, and the convolutions are flat- 
 tened. If the pia mater be cedematous, the serum may be clear or tur- 
 bid with pus and fibrin. The membrane may present any of the general 
 appearances of exudative meningitis. But always in addition to these, and 
 sometimes without them, miliary tubercles, either widely scattered or in 
 great numbers, may be seen, usually more abundant over the sulci than 
 elsewhere. They are usually more abundant at the base of the brain 
 than on the convexity, and are frequently confined to the base. Some 
 of the tubercles are so small as to be scarcely visible or entirely invisible 
 
 FiQ. 64.— A Miliary Tubercle of the Pia Matf.r, x 8S0 and reduced. 
 Composed of a simple aggregation of cells. 
 
 to the naked eye, others are as large as a pin's head or larger. They are 
 usually most abundant along the blood-vessels, but may occur elsewhere. 
 They may be formed in the membranous prolongations of the pia mater 
 which dip into the sulci, around the vessels which enter the brain-sub- 
 stance, in the choroid plexus and ependyma of the ventricles, and may 
 exist in the spinal cord. 
 
 The miliary tubercles do not all have the same structure. Some of 
 
THE NEEVOUS SYSTEM. 
 
 169 
 
 them are simply small aggregations of round cells within the perivascular 
 sheaths of the smaller arteries. Others are composed of small masses of 
 polyhedral and round cells without any basement substance between 
 
 
 •?i-<,. *■ 
 
 Fie/ 65.— A Miliary Tudbrole, X ITO and reduced. 
 Formed of tubercle tissue and situated around a small artery, which is the seat ot endarteritis. 
 
 them, and without any relation to the blood-vessels. Many others have 
 the ordinary structure of tubercle tissue, basement substance, polyhedral 
 cells, and giant cells. These tubercles are usually situated around or near 
 a blood-vessel, and this blood-vessel is apt to be at the same time the seat 
 of an obliterating endarteritis. This form of tubercle is also prone to 
 cheesy degeneration (see Fig. 63.) 
 
 In children the ventricles are usually more or less distended by an 
 accumulation of transparent or turbid serum, and the walls of the ventri- 
 cles may be studded with miliary tubercles (see Figs. 66 and 67). In 
 
 Fig. 66.-MILIARY Tubekoles of the Ependyma of the Lateral yENTRioLES, X TO and reduced. 
 
 adults the ventricles are less frequently involved. The brain-tissue around 
 the ventricles is often softened. The central canal of the spinal cord may 
 also be dilated. It is the dilatation of the ventricles which causes the 
 flattening of the convolutions, and the flattening is usually in direct pro- 
 
170 
 
 THE JSTEEVOUS SYSTEM. 
 
 portion to the amount of accumulated fluid. Miliary tubercles in the 
 choroid of the eye are present in a considerable proportion of cases. 
 
 The cortex of the brain may be hypersemic, and punctate haemorrha- 
 ges may be present in the cortex and in the pia mater. 
 
 In almost all cases of tubercular meningitis, there is tubercular inflam- 
 mation in other parts of the body. 
 
 In adults, as in children, while the tubercular inflammation is always 
 
 
 
 .StiV 
 
 Fi(j. G7. — A Miliary Tubercle of the Ependyma of the Lateral Ventricle, more highly 
 magnified, X 500 and reduced. 
 
 present, the accompanying simple inflammation may be very slight or 
 extensive, and the degree to wliich it develops does not seem to depend 
 upon the abundance of the miliary tubercles. Owing to the freqency 
 of the dilatation of the ventricles with serum in children, the disease is 
 often called acuie hydrocephalus. 
 
 In both children and adults, the tubercular inflammation may produce 
 
THE NERVOUS SYSTEM. ITl 
 
 large masses of tubercular tissue, which undergo cheesy degeneration, in 
 the pia mater and the brain tissue. 
 
 Syphilitic Meningitis. — In this form of inflammation, which is 
 usually circumscribed, there is a development of gummy tumors of varia- 
 ble size, frequently associated with simple inflammation of the membrane, 
 either with the formation of serum fibrin and pus, or with the develop- 
 ment of new connective tissue and the consequent thickening of the 
 membrane. The gummata may form in the pia mater covering the 
 convexity, or at the base of the brain. They may grow outwards 
 involving the dura mater, or inwards enci'oaching upon or involv- 
 ing the brain-tissue. Although usually circumscribed, the syphilitic 
 inflammation may occur as a difEuse thickening of the membrane. The 
 syphilitic nodules, including the gummata and new-formed connective 
 tissue are often very small, but m'ay be as large as a hen's egg. 
 
 Tumors. — Aside from the Pacchionian bodies, which are sometimes so 
 large as to simulate tumors, the most common forms of primary tumors 
 are sarcomata and endotheliomata (cholesteatomata). Small fibromata, 
 lipomata, angiomata, and mgxomata occnr, but are rare. Lymphangio- 
 inatoiis cysis sometimes occur in the pia mater, and various forms of 
 carcinoma may occur as secondary tumors. The pia mater is frequently 
 involved in tumors growing from the dura mater or the brain substance. 
 
 Variously shaped pigment ceZfe not infrequently occur in the pia mater, 
 either scattered or sometimes in considerable masses ; they seem to have 
 little pathological significance. Not infrequently thin plates of new- 
 formed bo?ie are found in the pia mater, associated with a thickening of 
 the membrane. 
 
 Parasites. — Oysticercus has been observed in the pia mater. 
 
 THE VENTRICLES OF THE BRAIN. 
 THE EPEKDYMA AND CHOROID PLEXUS. 
 
 As the lymph-spaces of the pia mater and the ventricles of the brain 
 are in communication, it might be supposed that they would share alike 
 in the accumulation of fluids. This, however, is not the case. The 
 membranes of the brain may be highly CBdematous, while the ventricles 
 contain about the normal quantity of fluid ; or, on the other hand, the 
 ventricles may be widely dilated and the pia mater unusually dry. Many 
 of these varying conditions may be understood by remembering that the 
 skull and spinal canal form a closed cavity, and that accumulations of 
 fluid in one part must be at the expense of some material occupying other 
 parts, either blood, serum, or brain-tissue. It is not always easy to see, 
 however, exactly how the compensation occurs. 
 
 There may be an unusual amount of fluid in the ventricles of the 
 brain as a result of post-mortem change ; in connection with senile or 
 
172 THE NEEVOUS SYSTEM. 
 
 other atrophy of the brain; or in the general vascular changes which lead 
 to oedema of the brain; in connection with inflammation of the menin- 
 ges, or of the ependyma; or under conditions which we do not under- 
 stand, as in some cases of congenital and acquired hydrocephalus. 
 Accumulations of fluid in the ventricles are often called internal hydro- 
 cepMlus, to distinguish them from accumulations in the meninges— 
 external hydrocephalus. 
 
 Acute inflammation of the Ependyma {Acute Ependymitis). — In this 
 condition, which may occur by itself, but is usually assofciated with 
 inflammation of other parts of the brain, the ependyma is congested, 
 the vessels are more prominent than usual, and are often tortuous. The 
 ependyma and the adjacent brain-tissue may be thickened and infiltrated 
 with pus-cells, and the surface of the ependyma covered with fibrin and 
 pus in variable quantity. The cavity of the ventricles may contain 
 purulent serum. Small hemorrhages may also be present in the tissue 
 of the ependyma. This, as well as other forms of inflammation, is more 
 common in the lateral ventricles than in the others, but not infrequently 
 involves the fourth ventricle. The choroid plexus may participate in 
 the inflammatory changes of the ependyma. Tubercular inflammation 
 of the ependyma is, as above-mentioned, a not infrequent accompaniment 
 of tubercular meningitis. 
 
 Chronic Inflammation of the Ependyma {Chronic Ependymitis). — 
 This lesion, which is much more common than simple acute inflamma- 
 tion of the ependyma, occurs under a variety of conditions, and its 
 nature and causation are in general very obscure. The ependyma 
 is thicker, whiter, and more opaque than normal, so that the ves- 
 sels may be nearly or quite invisible. The thickening may occur 
 in patches or diffusely, and the surfacg of the ependyma may be 
 smooth, or roughened and granular. On microscopical examination the 
 surface of the ependyma may be covered with the usual epithelium, but 
 the new connective tissue which forms beneath it often raises it up in 
 places, causing the roughness of the surface. The new tissue is usually 
 rather loose in texture and may contain many small spheroidal cells, but 
 it may be dense in texture and contain few cells. The brain-tissue 
 beneath the thickened ependyma may be softened or infiltrated with cells. 
 The sides of the ventricles may be grown together in places by the adhe- 
 sion of the thickened and roughened ependyma. The ventricles usually 
 contain more serum than normal, and sometimes this accumulation is so 
 great as to cause an enormous dilatation of them. While these are in 
 general the prominent lesions in chronic inflammation of the ependyma, 
 the cases vary greatly in the degree to whicli these changes are developed. 
 
 The accumulation of fluid, and the dilatation of the ventricles being 
 the most marked feature in all this class of lesions, they are often called 
 chronic hydrocephalus, and indeed in many cases we have no evidence 
 
THE NEEVOUS SYSTEM. 
 
 1Y3 
 
 that the change in the ependyma is an important or even an actual 
 primary factor. 
 
 We may, for convenience of study, consider three classes of cases of 
 chronic hydrocephiilns: first, congenital hydrocephalus in young chil- 
 dren; second, secondary hydrocephalus in children and adults; third, 
 primary hydrocephalus in adults. 
 
 1. Conyenitnl Hydroceplialus. — The lesion may be in an advanced 
 stage at the time of birth, or it may be scarcely evident or but 
 moderately developed. It may progress rapidly, and cause the early 
 death of the child, or it may develop gradually or come to a stand-still. 
 In the more marked forms of the disease, the ventricles are widely dilated 
 and filled with serum, which is usually transparent. Not only the lateral 
 ventricles, but also the third and fifth may be involved, the fourth is less 
 apt to participate in the lesion, although it is sometimes dilated, as well 
 as the central canal of the cord. 
 
 The distention, especially of the lateral ventricles, may be so great 
 that the brain-tissue over the vertex is crowded up into a thin layer be- 
 neath the dura mater, or it may be entirely destroyed. When the dilatation 
 of the ventricles is considerable, the convolutions are fl.attened (see Fig. 68), 
 
 Fig. 68.— Congenital HYDttocEPHALUS— Child, half natural size, 
 a, a, Dilated lateral ventricles; 6, cornua unequally dilated; c, third ventricle; c(, middle com- 
 missure. 
 
 and may be almost entirely obliterated. The skull-bones may be thin and 
 bulging over the forehead and vertex; the fontanelles and sutures widely 
 open. The ependyma in these cases is usually thick and rough, but it may 
 be softened, and the blood-vessels may be dilated. The basal portions of 
 the brain may be flattened, but are usually much less affected than the 
 upper portions. The brain-tissue is usually soft and anaemic. 
 
 2. Secondary Hydroceplialus. — This may occur in children and adults, 
 and may be a result of epidemic cerebro-spinal meningitis, or of acute 
 meningitis, or of chronic meningitis. It sometimes occurs in chronic 
 
17i THE NERVOrS SYSTEM. 
 
 alcoholic poisoning, and in general paralysis of tlie insane. The amount 
 of dilatation of the ventricles varies greatly in these cases, but it is never 
 so great as in congenital hydrocephalus, and is not accompanied by the 
 changes in the shape of the skull whicii form so prominent a feature in 
 the latter disease, since the bones are firmer and the sutures united. In 
 this form of chronic hydrocephalus, the changes in the ependyma above 
 described are usually more or less well marked, and they may be associ- 
 ated with the production of fibrin and pus. 
 
 3. Primary HyArocBplialus in Adults. — The conditions leading to 
 this form of lesion are not understood. It is apt to occur in persons over 
 thirty years of age. Sometimes one, sometimes both lateral ventricles 
 are dilated. The dilatation is usually moderate, sometimes very slight, 
 and never as great as in congenital hydrocephalus. The ventricles usually 
 contain transparent serum, and the ependyma is thickened and rough- 
 ened. In some cases it will be the only lesion found to account for the 
 death of the patient. 
 
 Tumors. — The new formation of connective tissue in the ependyma, 
 although usually diffuse, may be circumscribed and form small projecting 
 connective-tissue nodules, which may be reckoned among the fibromata. 
 Small fibromata are sometimes detached from the walls of the ventricles 
 and lie free in the cavity. Small lijiomata, angiomata, and also sar- 
 comata occur rarely. Clionclromata and angiomata may occur in the 
 choroid plexus, and the latter are sometimes as large as a hen's egg. The 
 choroid plexus is not infrequently the seat of transparent cysts usually of 
 small size; they may contain a clear fluid or colloid material, or droplets 
 of fat or calcareous particles. A small dermoid cyst containing hairs has 
 been described. These cysts have no special pathological significance. 
 
 Primary carcinomata are sometimes found in the ventricles. 
 
 The calcareous bodies called Irain-sand^ occur frequently in the 
 choroid plexus (see Pig. 59), and corpora amylacea may occur here and 
 beneath the ependyma. 
 
 Cysticercus and ecchinococcus cysts are sometimes found free in the 
 fluid of the ventricles. 
 
 PINEAL fiLAND AND PITUITARY BODY. 
 
 Pineal gland. — The lesions of this structure are not very common 
 or important. It may participate in inflammatory changes involving 
 neighboring structures. It may become hypertrophied and dense, and 
 has thus attained the size of a walnut. Small cysts may form in it, and 
 of very frequent occurrence is a considerable increase in the amount of 
 
 ' The little hard masses called brain-sand consist of aggregations of small par- 
 ticles of carbonate and phosphate of lime, with a very small amount of phosphate 
 of ammoma and magnesia. With these there is more or less organic matter. 
 
THE NEEVOrs SYSTEM. 175 
 
 brain-sand which is usually found there in moderate quantity under normal 
 conditions. 
 
 Tlie Pituitary Body. — This body may share in inflammatory changes 
 occurring in its vicinity, or may be the seat of tubercular and syphilitic 
 inflammation. The most important of the tumors which may originate 
 in this structure are adenomata, usually cystic in character; these may 
 be as large as a hen's egg. Carcinomata and sarcomata may occur, form- 
 ing tumors of considerable size. Small lipomata and a teratoma have 
 been described. 
 
 THE BRAIN. 
 
 THEOSIBOSIS AKD EMBOLISM. 
 
 In studying the occurrence and effects of thrombosis and embolism 
 in the brain, certain peculiarities of the circulation should be borne in 
 mind. The arteries of the brain areSn part terminal arteries (see p. 53), in 
 part such as have anastomoses among their branches. Thus the arteries 
 which are distributed to the cortical regions form abundant anastomoses 
 in the pia mater and are very small when they enter the brain, while 
 those which are distributed to the basal region, and which supply the 
 basal ganglia, are larger and do not, beyond the circle of Willis, form 
 anastomoses with one another. Thus it is that occlusions of the arteries 
 supplying the basal ganglia are of much more serious import, aside from 
 the importance of the parts involved, than those passing to the cortex. 
 
 Thrombi may form in the arteries as a result of any degenerative or in- 
 flammatory process in the wall of the vessel leading to a roughening or 
 death of its intima, or from pressure upon the vessel from without, or 
 they may occur in vessels in whose walls we can detect no 25rimary lesion. 
 The most common causes are atheroma or simple endarteritis. Thrombi 
 may also form around an embolus which does not entirely occlude the 
 vessel. 
 
 Emboli of the cerebral arteries most commonly arise from acute or 
 chronic endocarditis or cardiac thrombi; they may arise from aneurisms 
 or atheroma of the aorta, from the carotid or vertebral arteries or from 
 the pulmonary veins. The materials constituting emboli vary greatly, 
 depending on their mode of origin (see p. 52). The effects on the brain- 
 tissue of emboli and thrombi of the arteries are essentially the same in 
 their main features. In some cases, however, in which large emboli, 
 usually from endocarditis, suddenly block up a large vessel, the indi'- 
 vidual may die almost instantly without other apparent lesion than the 
 stoppage of the vessel. 
 
 In general the first effect of the occlusion of an artery is to deprive 
 the region to which it is distributed of blood. In arteries whose branches 
 anastomose, as in the cortex of the brain, the affected area is soon supplied 
 with blood by the establishment of a collateral circulation. In terminal 
 
1T6 
 
 THE NERVOUS SYSTEM. 
 
 arteries, on the other hand, the blocking of the vessel is followed, as a 
 rule, by degenerative changes and softening, in the brain-tissue. The 
 appearances which these degenerated areas present vary greatly, depending 
 upon the stage of the degeneration and the amount of blood which may 
 be extravasated. Dense infiltrations of the brain-tissue with blood, as in 
 hemorrhagic infarctions from emboli in other parts of the body, do not 
 usually occur, although considerable blood may be extravasated. Areas 
 of softening in which there is little extravasation of blood are usually 
 white or yellow in color {white or yellow softening). When much blood 
 is present, the process is frequently called red softening. The tissue in 
 the affected area gradually softens and may become diffluent. Microsco- 
 pically, the softened tissue is seen to consist of more or less fluid with 
 broken-down brain-tissue, fragments of nerve-fibres, droplets of myelin, 
 nerve-cells, shreds of neuroglia tissue and blood-vessels, and red and white 
 
 Eis. 69.— Degenerated Cells, Cholestearin Crystals and Corpora Amylacea prom Bbaih- 
 TissuE IN Embolic Softening. 
 ct, Fatty ganglion cells; h, corpoi-a amylacea; c, cell containing very large number of fat-drop- 
 lets (compound granular, or Gluge's corpuscle); d, cholestearin crystals. 
 
 blood-cells. Then evidences of degeneration are seen, in the presence of 
 fat granules and droplets, larger and smaller cells densely crowded with 
 droplets of fat (so-called Gbige's corjmscles or compound granular corpus- 
 cles). (See Fig. 69.) Various kiads of cells and cell-fragments, more or 
 less granular and fatty, and also corpora amylacea, blood-pigment, fat- 
 crystals and cholestearin crystals may be found. The walls of the blood- 
 vessels may also be in a condition of fatty degeneration (Fig. 70). The 
 
THE NEEVOUS ST STEM. 
 
 177 
 
 color of the softened mass will of eouise depend upon the relative 
 amounts of these elements. 
 
 The tissue may remain for a long time in the soft condition, or it may 
 be absorbed and replaced by a connective-tissue cicatrix, which may be 
 
 Fig. 70. — Blood-vessels from an Area op Embolic Softening of Brain. 
 The walls of the vessels, particularly the endothelial cells, contain fat droplets and granules. 
 
 more or less pigmented ; or a wall of connective tissue may form about 
 it, converting it into a well-defined cyst, with or without pigmented 
 walls; or the mass may dry and form a dense structureless nodule. Acute 
 inflammatory changes may occur about the dead tissue. In cases of 
 infectious emboli, numerous abscesses maybe formed in addition to their 
 mechanical action. 
 
 Thrombi are most frequent in the internal carotids, less so in the 
 middle cerebral, basilar, and vertebrals. They may occur, but still less 
 frequently, in other cerebral arteries. Emboli are most common in the 
 middle cerebral artery, next in the internal carotid, and then in the 
 basilar. The relative frequency with which embolism occurs in the mid- 
 dle cerebral artery is attributable to the directness with which the blood 
 passes into this artery from the heart. The great significance attaching 
 to embolism of the middle cerebral artery is evident when we remember 
 that its branches are terminal arteries, and are distributed to such import- 
 ant structures as the lenticular and caudate nucleus, the internal capsule, 
 and the optic thalamus. 
 
 Hyper cemia and Ancemia. — The appearance of the brain-tissue after 
 death does not always furnish reliable indications of its blood-contents 
 during life, though they are perhaps more to be depended on than the 
 appearance of the meninges. 
 
 Some of the more common conditions determining hypercsmia which 
 are mentioned above as influencing the meninges, apply also to the sub- 
 stance of the brain. In sections of hypersemic brains, the small blood- 
 points from the cut ends of small vessels are more numerous and con- 
 13 
 
178 THE NEEVOUS SYSTEM. 
 
 spicuous than under normal conditions, and the brain-tissue, particularly 
 the gray matter, may have a difEuse red color. If excessive, the convolu- 
 tions may be somewhat flattened, and the brain-tissue and pia mater 
 may be cedematous, and the ventricles contain fluid. The congestion 
 of the vessels may be general or localized. 
 
 Ancemia of the brain may be either local or general. It may depend 
 upon a general anasmia or upon general disturbances of the circulation, 
 such as mitral stenosis or regurgitation, or upon local interference with 
 the arterial blood-supply, such as complete or partial obstruction of the 
 arteries froni thrombi, emboli, inflammatory changes, spasmodic contrac- 
 tions, etc., or from tumors, exudations, and blood extravasations pressing 
 upon the vessels from without. In oedema of the meninges and in the 
 presence of internal hydrocephalus, the brain-tissue is apt to be aneemic. 
 The brain-tissue in ansemia looks whiter than usual, the contrast betvveen 
 the gray and white matter is less marked, and the small blood-points 
 usually seen on section from divided vessels may be very inconspicuous 
 or almost entirely absent. 
 
 (Edema of the brain-tissue may accompany either hypersemia or anss- 
 mia, and seems in most cases, though not always, to be dependent upon 
 conditions whicli induce these alterations in the blood content of tiie 
 brain. In some cases of marked impoverishment of the blood, a so-called 
 hydroBmic oedema of the brain is found. Very marked oedema of the 
 brain may exist without any accompanying brain symptoms. On the 
 other hand, persons may die comatose; this is seen with especial frequency 
 in acute and chronic alcohol poisoning, but may occur under other con- 
 ditions, and the post-mortem examination reveals nothing but oedema of 
 the brain-tissue, either with or without oedema of the pia mater. 
 
 Hemorrliage. — Hemorrhages in the substance of the brain may be 
 very small and punctate, and are then usually called capillary hemor- 
 rhages, or they may result in the collection in the brain-tissue of masses 
 of blood of considerable size, which are called apoplectic foci or clots. 
 These forms of hemorrhage may be associated, or a number of capilhiry 
 hemorrhages may join to form an extensive clot. 
 
 Capillary hemorrhages may look on section of the brain like the 
 severed ends of hypersemic blood-vessels, or the tissue about them may 
 be more or less tinged with blood. Microscopically, the peri-vasculav 
 spaces will be found distended with blood, which may have escaped into 
 them, and more or less broken down the brain-tissue. They may occur 
 singly, but are frequently m.ultiple, so that the brain-tissue is besprinkled 
 with blood-points. Degeneration of the extravasated blood may give rise 
 in later stages to reddish or brown or yellowish circumscribed discolora- 
 tion of the brain-tissue, due to granules and crystals of blood-pigment 
 intermingled with broken-down brain-tissue, with more or less fatty de- 
 generation of its elements. Capillary hemorrhages may be due to fatty de- 
 
THE XEEVOUS SYSTEM. 1Y9 
 
 generation of the vessels leading to rapture; or the extravasation may be 
 -due to diapedesis ; or it may depend upon conditions which we do not 
 understand. They frequently occur in the vicinity of apoplectic clots and 
 tumors; they may be due to thrombosis of the veins, or of the sinuses of 
 the dura mater ; they not infrequently occur in acute encephalitis, in 
 congestive hypersemia, in acute mania, and in delirium tremens, and 
 they may be associated with general diseases such as scurvy, purjjura 
 hsemorrhagica, typhus fever, pyemia, ulcerative endocarditis, etc.; they 
 may be associated with embolic softening. 
 
 A23opl6ctic foci may result from the coalesence of numerous capillary 
 hemorrhages: from injury, or from rupture of diseased arterie-, either 
 with or without changes in the blood pressure. Hemorrhages from injury 
 to the skull may occur as well without as with fracture, and may be situ- 
 ated over the vertex as well as at the base of the brain, and will vary in 
 extent and seat, depending upon the character and jioint of the injury 
 and the size of the vessels involved. The so-called spontaneous hemor- 
 rhages other than those of capillary origin, which give rise to masses of 
 blood and broken-down brain-tissue, may vary in size from that of a pea 
 to those occupying a large part of a hemisphere. They are due in a very 
 considerable proportion of cases to the rupture of small arterial aneur- 
 isms, but may arise from weakening of the walls of the artej-ies, from 
 arteritis, atheroma, or fatty degeneration. These latter forms of disease 
 doubtless give rise in most cases to the formation of the aneurisms whose 
 rupture is in so many cases the immediate cause of the hemorrhage. 
 Aneurisms of the cerebral arteries may be as large as a pea or hazel-nut, 
 but those most frequently met with and causing apoplexy are usually 
 small — called miliary aneurisms — and may be microscopic in size, vary- 
 ing from this up to that of a large pin's head or larger. They may be 
 saeculate or fusiform, and frequently exist in considerable numbers. Tliey 
 may occur in any of the small arteries of the brain, but are said to be 
 most frequent on the branches of the middle cerebral artery. It is as- 
 serted that the bursting of miliary aneurisms is the nearly if not quite 
 exclusive cause of the formation of spontaneous apoplectic clots, but this 
 we do not believe to be true. As to the immediate cause of rupture, 
 either of aneurisms or otherwise diseased blood-vessels in the brain, we are 
 in many cases entirely ignorant. In some cases it seems to be due to an 
 increased arterial tension in such diseases of the heart as induce this 
 change, as in the cardiac hypertrophy which may accompany some forms 
 of chronic diffuse nephritis; or it may result fi'om unusual exertion or 
 mental excitement ; but, as above stated, in many cases the immediate 
 inciting cause is not evident. 
 
 The most frequent seat of hemorrhage is in the opto-striate bodies 
 and the brain-tissue in their vicinity, and here they occur most often in 
 the parts supplied by the branches of the middle cerebral artery. 
 
180 THE NEEVOUS SYSTEM. 
 
 Hemorrhages frequently seriously affect otlier portions of the brain 
 than those immediately supplied by the ruptured vessels. Thus hemor- 
 rhages ill the cortical substance or beneath the pia mater may force their 
 way deep into the brain-substance ; or in hemorrhage in the braiu-sub- 
 stance the blood may burst into the ventricles or work its way into the 
 intermeuingeal space, and either at the seat of its occurrence, or in the 
 situations into which it is forced, it may give rise to serious compression 
 of the brain. Portions of the bi'ain containing large extravasations may 
 be enlarged, the tissue anaemic from pressure, the convolutions flattened, 
 and the surface dry. As the blood is poured out, the brain-tissue is 
 usually torn and lacerated, so that the apoplectic clot usually consists of 
 detritus of brain-tissue intermingled with blood. If, however, the blood 
 is poured out from a single vessel, the lacerated brain-tissue may be 
 pressed aside, and the greater portion of the red mass may consist of pure 
 blood-clot. 
 
 The appearances presented by hemorrhages in the brain vary greatly, 
 depending upon the time which has elapsed since their occurrence. If 
 life continue, the cedema which usually soon occurs in the vicinity of the 
 hemorrhage disappears, and the clot becomes drier and firmer; gradually 
 the blood undergoes the usual series of changes seen in extravasation: 
 the haemoglobin decomposes, forming granules and crystals of blood pig- 
 ment, the blood-cells and fibrin undergo degeneration and absorption; the 
 detritus of brain-tissue undergoes fatty degeneration. As these altera- 
 tions occur, the color changes to reddish-brown, orange, or yellow, and 
 the adjacent brain-tissue may be discolored by imbibition. 
 
 Inflammatory reaction may occur in the vicinity, either leading to 
 the formation of a more or less pigmented cicatrix, or to a cyst with yel- 
 lowish fluid contents and a fibrous, more or less pigmented wall. The 
 process of degeneration and absorption of the blood and broken-down 
 brain-tissue and their replacement by a cyst or by a cicatrix is a slow one, 
 and the cysts and cicatrices may resemble those formed at the seat of 
 embolic softening. Not infrequently we find in the brain of a person 
 dead from recent apoplexy, the remains of old clots presenting some one 
 of the above-described stages of absorption. The apoplectic cysts and 
 cicatrices persist for a long time after their formation. 
 
 Secondary Degenerations. — Lesions of parts of the brain which involve 
 the destruction of brain-tissue containing certain systems of motor-nerves, 
 owing, it is believed, to the separation of those nerves from their trophic 
 centres, are regularly followed after a time by degenerative changes in 
 these nerves below tlie seat of lesion. It is particularly lesions in the 
 central convolutions, the internal capsule, portions of the corona radiata, 
 and the pes pedunculi, which destroy the motor-fibres passing through 
 these parts, and are followed by degenerative changes in the fibres below. 
 The most important and frequent lesions followed by this effect are those 
 
THE NEEVOUS SYSTEM. 181 
 
 involving the anterior two-thirds or three-fourths of the internal capsule. 
 It will suffice merely bo naention these changes here, as they are considered 
 more in detail in the section devoted to lesions of the spinal cord. 
 
 INFLAMMATION OF THE BEAIN (ENCEPHALITIS). 
 
 It has been already mentioned that the brain-tissue about hemorrhages 
 and areas of embolic and thrombotic softening may undergo inflamma- 
 tory changes leading to the formation of new connective tissue. There 
 is a class of cases in which localized areas of the brain undergo softening, 
 with more or less extravasation of red and white blood-cells and hyper- 
 emia of the blood-vessels, so that the softened material consists, as seen 
 under the microscope, of detritus of brain-tissue in a condition of fatty 
 degeneration, with more or less pus-cells or pigment. When such areas 
 are red in color from intermingled blood-cells or pigment, the condition 
 is called red inflammatory softening. When fatty degeneration prevails, 
 and the red blood-cells or their derivatives are not abundant, the softened 
 area looks yellow or yellowish-white, and this is often called yellow in- 
 flammatory softening. The origin of these processes is very obscure, and 
 their inflammatory nature not well defined. 
 
 Abscess of the Brain. — In another class of cases the inflammatory 
 •character of the lesion is well defined, and manifests itself chiefly by the 
 formation of pus and the development of abscesses. These abscesses 
 may be single or multiple, and may be situated in any part of the brain. 
 They may be small or they may be from one to two inches in diameter, 
 ■and are sometimes so large as to occupy nearly the whole of a cerebral 
 lobe. They may be sharply circumscribed, or the walls may merge im- 
 perceptibly into the adjacent brain-tissue. In the early stages of the 
 formation of some abscesses, there is simply a dense infiltration of a cir- 
 ■cumscribed area of brain-tissue with pus-cells, and the part then presents 
 very much the appearance of brain in the condition of yellow softening. 
 The brain-tissue after a time may break down and degenerate, and we 
 may then have a diffluent, yellowish mass consisting of fluid, degenerated 
 and disintegrated nerve-elements, Gluge's corpuscles, and pus-cells, more 
 •or less fatty, and cholestearin crystals. The brain-tissue about the difflu- 
 ent mass may be denser than usual, and more or less infiltrated with pus; 
 •or shreds of tissue may hang ofE into the cavity. A connective-tissue 
 wall may form around the abscess, and the brain-tissue about this maybe 
 •dense or very soft. Old abscesses with connective tissue-walls may resem. 
 ble cysts formed from hemorrhage or softening, and may contain but a 
 small amount of clear or turbid serum. When occurring near the me- 
 ninges or the ventricles, abscesses may rapture, and the adjacent ventri- 
 cles or the pia mater may become infiltrated with pus. When occurring 
 near the surfaces of the brain, they may set up purulent inflammation of 
 
182 THE NEEVOUS SYSTEM. 
 
 the pia mater, or this membrane may become thickened and adherent 
 over them. 
 
 Abscesses of the brain may occur from direct injury or laceration of 
 the brain, or without fracture, or direct wound, as the result of severe 
 jarring as in a fall on the head. Next to injury, inflammation of the 
 bones of the skull, particularly of t!ie temporal bone from otitis media, 
 most frequently leads to abscesses of the brain; though not infrequently 
 they are formed as a result of otitis media without involvement of the- 
 bone. In some cases, abscesses of the brain seem to be secondary to 
 2Durulent or septic infliimmations in other parts of the body, as in 
 pyaemia, nlcerative endocarditis, gangrene of the lungs, cerebro-spinal 
 meningitis, etc., and are doubtless embolic in their origin. In many 
 cases we are not able to assign a cause for the formation of abscesses in 
 the brain; this is especially the case in the abscesses of tlie cerebellum. 
 
 Very frequently in acute meningitis there is an infiltration of pus-cells; 
 along the walls of the vessels which enter the brain from the fiia mater;, 
 and under a variety of conditions which we do not understand, as in some- 
 cases of typhoid fever, delirium tremens, erysipelas, and under many 
 other conditions, there are numerous and sometimes very large numbers- 
 of leucocytes scattered through the substance of the brain, sometimes, 
 around the ganglion-cells, sometimes along the vessels in the peri-vas- 
 cular sheaths. 
 
 Chronic interstitial encephalitis — sclerosis. — This lesion of the brain- 
 tissue may occur diffusely, occupying an entire lobe, or more or less of 
 the whole brain, or in circumscribed small areas. It consists essentially 
 in an increase of the connective-tissue elements, the neuroglia, and an 
 atrophy of the nerve elements, particularly the ganglion-cells, and the- 
 medullary sheaths of the nerves. With these changes are usually asso- 
 ciated the form ation of Gluge's corpuscles, corpora amylacea, granular 
 and fatty degeneration of the nerve-elements, and thickening and pro- 
 liferation of cells of the walls of the blood-vessels. The area's of sclerosis 
 may be very dense and hard, or gelatinous in consistency. 
 
 The diffuse form of sclerosis is most frequently seen in the brains of 
 drunkards and in general paralysis of the insane. 
 
 The circumscribed form of sclerosis, multiple sclerosis (sclerose en 
 plaque), is much more common than the diffuse form, and may occur in 
 the brain alone, or may be associated with a similar lesion in the spinal 
 cord. It is almost entirely confined to the medullary substance, and the- 
 areas of sclerosis vary in size from that of a pea to that of an almond. 
 They may be few or numerous, they may be white, grayish, or grayish- 
 red in color, and are usually, but not always, sharply outlined against the- 
 unaltered brain-tissue. Although in many cases the increase in the con- 
 nective-tissue elements seems to be the primary lesion, and the degenera- 
 tion of the nerve-elements secondary to this, it is quite possible that in 
 
THE NERVOUS SYSTEM. 183 
 
 some cases the increase in connective tissue may be secondary to a de- 
 generation of the nerve-elemen-ts from loss of nutrition, or from other 
 causes. 
 
 WOUNDS OF THE BRAIN. 
 
 The brain may be directly wounded by a foreign body, or indirectly 
 by fragments of bone driven into it, or it may be lacerated by severe con- 
 tusion without fracture or solution of continuity of the skull. It is very 
 difficult to estimate the degree of injury which must cause death, since 
 persons frequently die from slight, and may recover from very severe 
 wounds of the brain. In incised wounds of the brain, more or less hem- 
 orrhage occurs at the seat of lesion, and the brain-tissue in the vicinity 
 soon undergoes degenerative changes. These may be comparatively 
 sliglit or extensive. Inflammatory reaction may occur in the vicinity, 
 and the adjacent brain tissue as well as the hemorrhagic and degene- 
 rated area become infiltrated with pus-cells. Afer a time the injured and 
 degenerated area may become surrounded by new-formed connective tis- 
 sue, and the decomposed extravasated blood and detritus of brain-tissue, 
 more or less fatty, may be absorbed, and thus after a time the part heals 
 by a more or less pigmented cicatrix. The healing is in most cases very 
 slow and may occupy months or even years. The pia mater may par- 
 ticipate to a marked degree in the inflammatory healing process. Ab- 
 scesses may form near the seat of injury. 
 
 After wounds which involve the removal of portions of the cranial 
 bones, it is not uncommon after a few days to see a bleeding fungous 
 mass project through the opening. This mass, sometimes wrongly called 
 hernia cerebri, consists of degenerated brain-tissue, blood, and granula- 
 tion-tissue, with more or less pus. The brain-tissue below it is degene- 
 rated, broken-down, soft and purulent, and there is often abscess in the 
 adjacent brain-tissue. Such wounds may finally heal by the absorption 
 of the broken-down brain-tissue and blood, and its substitution by 
 granulation tissue. 
 
 Lacerations of the brain-tissue without fracture may appear shortly 
 after the injury as simple more or less circumscribed areas of capillary hem- 
 orrhage; the brain-tissue about these may degenerate, pus may form, 
 and abscesses be developed; or the degenerated and lacerated tissue may 
 be gradually replaced by granulation-tissue which finally forms a cicatrix. 
 The process of degeneration and softening and of healing in such lacera- 
 tions of brain-tissue may occur very slowly indeed, even occupying years, 
 and not infrequently the degenerative changes are very extensive and 
 progressive. In many cases, of course, the injury is so extensive or in- 
 volves such important parts of the organ, that very little or no inflamma- 
 tory or degenerative change takes place before the occurrence of death. 
 
 Encephalitis in the new-horn. — This condition, first described by Vir- 
 
184 
 
 THE NEEVOTJS SYSTEM. 
 
 chow, is said to consist in the formation of circumscribed collections of 
 cells of various sizes containing many fat-granules (granular corpuscles) 
 and forming yellowish masses from one mm. to six mm. in diameter, in 
 the brain-tissue. A more diffuse occurrence of granular corpuscles is 
 also described, but this is said by some observers to be physiological. The 
 nature of this lesion is but little understood, and is still the subject of 
 controversy. 
 
 Holes or cysts in the iram.— Larger and smaller holes may be found 
 in the brain-tissue from dilatation of the perivascular lymph-spaces, or 
 well-formed cysts may exist from hemorrhage, inflammatory softening, 
 hydatids, etc. There are, however, cases in which one or several holes 
 of varying size are found in the brain which cannot be determined to have 
 either of the above modes of origin. They may lie deep in the brain- 
 substance or close under the pia mater, or may communicate with the 
 ventricles. This condition is sometimes called porencepMUe, and may 
 co-exist with various mental aberrations, hydrocephalus, etc' , 
 
 / 
 
 4/ 
 
 a,tl'^-«<Jii»A,y^ 
 
 \ 
 
 -"^ 
 
 Fia. 71.— Syphilitic Obliterating Endarteritis of a Cerebral Artery, X 50 and reduced. 
 
 ' Consult Kundrat ; " Die Porencephalie," Graz, 1883, and Savage and White: 
 " On the Causes of Holes in the Brain," Trans. London Path. Soc, Vol. 34, p. 1, 
 1833. 
 
THE JMEEVOUS SYSTEM. 
 
 185 
 
 Syphilitic injlamnmtion of the brain sometimes results in the formation 
 of so-called gummy tumors. These are most frequently found near 
 the periphery of the brain, not infrequently connected with the men- 
 inges, and may be sharply circumscribed. The central portion of the 
 tumor is usually in a condition of cheesy degeneration, and in the peri- 
 phery we see fibrous tissue or a dense infiltration of small spheroidal cells. 
 
 Syphilitic inflammation of the brain very frequently occurs in a diffuse 
 form, characterized by the formation of a gelatinous grayish tissue con- 
 sisting of a more or less homogeneous, or granular basement substance 
 with numerous small spheroidal cells. The nerve-elements ai-e atrophied. 
 Obliterating endarteritis may occur as a result of syphilitic poisoning 
 (Fig. 71). 
 
 Tubercular inflammation of the brain substance usually manifests 
 itself in the formation of circumscribed masses of new tissue from five mm. 
 to six mm. in diameter, or larger. These may be single or multiple, are 
 most common in young persons, and very frequently occur in the cerebel- 
 lum. They are apt to occur in connection with tubercular inflammation of 
 
 Fig. 72.— Solitary Tubercle of Cerebellum, X 10. 
 a, Tubercle granula with giant-cells; 6, tubercle granula without giant-cells; c, diffuse tuber- 
 cle tissue; d, central cheesy mass; e, nerve tissue of the cerebellum. 
 
 other organs. They are frequently called solitary tubercles, and usually 
 consist of a dense central cheesy mass, around which is a grayish zone 
 containing tubercle granula, numerous small spheroidal cells, with occa- 
 sionally larger polyhedral cells and giant-cells (Fig. 72). They do not as a 
 
186 THE NERVOUS SYSTEM. 
 
 rule seem to be formed by an aggregation of miliary tubercles, although 
 these may be present in the periphery. Tubercle bacilli have been 
 found in these solitary tubercles. 
 
 Conglomerate and scattered miliary tubercles of the ordinary form 
 sometimes occur in the brain, usually in connection with tubercular in- 
 flammation of the meninges or ependyma. 
 
 LESIONS OF THE BRAIN IN CHRONIC PARALYSIS OF THE INSANE. 
 
 The changes in this disease are in the main those of chronic diffuse en- 
 cephalitis, but the appearances vary greatly and depend to some extent 
 upon whether the brain is examined in early or late stage of the disease. 
 According to Meyer, in the early stages of the disease, the convolutions, 
 particularly of the anterior cerebral lobes, are swollen, the gray matter con- 
 gested and softened in places. The brain-tissue is more or less infiltrated 
 with leucocytes. Patty degeneration of the walls of the capillaries and 
 punctate hemorrhages are also common. 
 
 In later stages of the disease, a great variety of changes may be ob- 
 served: hemorrhagic pacchymeningitis, thickening of the dura mater, 
 and close adhesions to the skull; thickening and opacities of the pia mater, 
 adhesions of the latter to the dura mater and to the brain-tissue. The 
 brain-tissue is apt to be atrophied, and the ventricles dilated and filled 
 with fluid. The pia mater may be oedematous, the ependyma thickened 
 and roughened. On microscopical examination, the neuroglia is found 
 to be increased in amount, the ganglion-cells shrunken and sometimes 
 pigmented; the nerve-fibres may also be atrophied, and the blood-vessels 
 in a condition of fatty or hyalin degeneration. There may be an accu- 
 mulation of fatty and granular cells along the walls of the blood-vessels. 
 Secondary degenerations in the spinal cord are not infrequently ob- 
 served. 
 
 It is very difficult to make positive and definite statements regarding 
 many such lesions of the brain as those just indicated, or in general of 
 brain lesions whose nature must be revealed by microscopical study, be- 
 cause our technical procedures in the study of the brain, even in normal 
 conditions, are still quite unsatisfactory and incomplete. The brain-tissue 
 is so delicate and liable to post-mortem changes, and the effects of differ- 
 ent preservative agents are so liable to variations, that great caution is 
 necessary in arriving at conclusions regarding the minuter lesions afEect- 
 ing the nerve-tissue of the brain. 
 
 HYPERTROPHY AND ATROPHY OF THE BRAIN. 
 
 True liypertropliy of the brain is rare and probably always congenital. 
 An increase in the size of the brain from the proliferation of the neu- 
 roglia sometimes occurs in children either before or after birth, less fre- 
 quently in youth, and very seldom in adults. The white substance of the 
 hemispheres is increased in amount. If it takes place before the ossifica- 
 
THE Js'EEVOUS SYSTEM. 18T 
 
 tioii of the cranium, the bones are separated at the sutures and fonta- 
 nelles; if after this, the inner table of the skull may be eroded and 
 thinned. "When the cranium is opened, the dura mater appears tense 
 and anaemic, the convolutions of the brain are flattened, the brain-sub- 
 stance is firm and ansemic, the ventricles are small, the ganglia and cere- 
 bellum are either of normal size or compressed. 
 
 The disease is usually very chronic, and destro3's life with symptoms 
 of .compression of the brain. There may, however, be acute exacerba- 
 tions. 
 
 Atrophy. — This may occur as a senile change; or in adults, in chronic 
 alcohol, opium, or lead poisoning, in chronic insanity, and in chronic 
 meningitis. In children who are much reduced by chronic diseases, 
 atrophy of the brain may accompany atrophy of the rest of the body." 
 
 The atrophy affects principally the cerebral hemispheres, and may be 
 uniform or more marked in some parts than in others. The convolu- 
 tions are small, the sulci broad, the ventricles usually dilated, the brain- 
 tissue firm, the gray matter discolored: the white substance grayish in 
 color; the blood-vessels may be dilated. The basal ganglia may be 
 small. Serum accumulates in the pia mateu and the ventricles; the pia 
 mater, and often the skull become thickened: the brain-tissue maybe 
 oedematous or contain small hemorrhages. The nerve-elements of the 
 brain-tissue are those most involved in the atrophy. 
 
 Pigmentation. — This may occur in any portion of the brain or its 
 meninges from the decomposition of extravasated blood. In persons 
 affected by malaria, the gray matter of the brain has sometimes an un- 
 usually dark or even blackish appearance. This color is due to the pres- 
 ence of black pigment granules within the capillary blood-vessels. The 
 obstruction to the vessels by masses of these pigment granules may cause 
 capillary apoplexies. The pigment may also be found in the walls, and 
 in the lumina of the vessels of the pia mater. 
 
 Pigmented patches of congenital origin are not infrequently seen in 
 the pia mater. They may be due to the presence of branching pigmented 
 cells. 
 
 Tumors of the Brain. 
 
 The most common tumors of the brain are gliomata. They are most 
 frequently found in the cerebrum, and may be small or large. They may 
 be sharply circuihscribed or mei-ge imperceptibly into the brain-substance. 
 They may be white and hard, or gray and soft or gelatinous. The softer 
 forms consist largely of neuroglia cells (Fig. 41), the harder forms contain 
 fewer cells and numerous interlacing fibrils. The blood-vessels of the 
 gliomata are often widely dilated. They are frequently the seat of hemor- 
 rhages and may soften and break down, and may then resemble apoplectic 
 clots. They are liable to undergo fatty and cheesy degeneration. 
 
188 THE NEEVOUS SYSTEM. 
 
 Not infrequently the gliomata are combined with sarcomata, forming 
 glio-sarcomata. 
 
 Sarcomata of various forms occur in the brain as jirimary tumors. 
 
 Circumscribed masses of dilated blood-vessels, angiomata, are not in- 
 frequently met with in the brain. 
 
 Myxoma, fibroma, lipoma, and osteoma are among the rarer forms of 
 brain tumors. 
 
 Endotheliomata {cliolesieatomata), in the form of glistening white 
 tumors, sometimes attain a large size. 
 
 Sarcomata and Oarcinomata not infrequently occur in the brain as 
 secondary tumors. Dermoid and other Cysts occur, but are rare. 
 
 Small masses of the gray matter of the brain sometimes occur in the 
 medullary jjortions of the brain, and localized hyperplasias of gray 
 matter have been described in the form of rounded nodules projecting 
 from the free surface of the brain or into the ventricles. 
 
 PARASITES. 
 
 Cysticercus and more rarely Echinococci are found in the brain. 
 
 MALFORMATIONS. 
 
 Gyclopia. — This malformation consists in an arrest of development 
 affecting the cerebrum, whicli, instead of separating into two hemispheres, 
 remains single, with one ventricle, and the rudiments of the eyes usually 
 become joined and form one eye. This single eye is in the middle of the 
 face, near the place of the root of the nose, in a single orbit. Over this 
 is an irregular body representing the nose. The rest of the face is well 
 formed. Or the eye-ball may be wanting entirely, or there are two eyes 
 joined together, or, more seldom, two separate eyes. The orbit is sur- 
 rounded by rudiments of four eye-lids. The frontal bone is single, the 
 nasal bones undeveloped; the ethmoid, vomer, and turbinated bones are 
 absent. The optic nerve is double, single, or absent. There may be 
 hydrocephalus. Such children are incapable of prolonged existence. 
 
 Anenceplialia. — This malformation may be of various degrees. The 
 brain may be entirely absent, and the base of the cranium is covered with 
 a thick membrane, into which the nerves pass. Or the membranes may 
 form a sort of cyst containing blood and serum, or portions of brain. 
 Of the cranial bones, only those which form the base of the skull are 
 present (Acrania). The scalp, usually, partly or entirely fails over the 
 opening in the skull; the eyes stand prominently out, and the forehead 
 slopes sharply backward. This malformation may occur in otherwise 
 well-developed children. 
 
 Hydrocephalus. — This lesion has been already considered above. 
 It is probable that in some cases liydroceplialus interims is due to 
 a primary partial anencepihalia, and that the accumulation of fluid 
 
THE NERVOUS SYSTEM. 189 
 
 is of secondai-y occurrence. In rare cases, only parb of one lateral 
 ventricle is hydrocephalic, giving to the head a protuberance on one side. 
 The viability of the foetus depends upon the degree of the hydrocephalus. 
 Hydrocephalufi externus is an accumulation of serum beneath the pia 
 mater, or, according to some authors, between the pia and dura mater. 
 It causes dilatation of the cranium and compression of the brain. It is 
 of very rare occurrence, and may also be secondary to partial anence- 
 phalia. 
 
 OepTialocele or Brain Hernia. — When abnormal openings exist in the 
 skull from malformation, the contents of the cerebral cavity are apt to 
 protrude in the form of larger or smaller sacs. Tliis may occur in cases 
 of well-marked anencephalia, or in cases in which the brain is well devel- 
 oped. The protruding sac formed of the meninges may or may not be 
 covered with skin. If the contents of the sac are simply fluid, the lesion 
 is called hydromeningocele; if composed of brain substance, enceplialocele; 
 if the sac contain both fluid and brain substance, it is called liydrence- 
 plialocele. The sacs may be very small or as large as a child's head. They 
 may j)rotrude from the top of the skull in acrania. They most frequently 
 protrude through openings in the occipital bone, often hanging down in 
 large sacs upon the neck; also at the root of the nose, along the line of the 
 sutures, at the base of the skull, and elsewhere. 
 
 Microcephalia. — This is an abnormally small size of the brain, with 
 a correspondingly small cranium. The diminution in size affects prin- 
 cipally the cerebral hemispheres, though the other parts of the brain are 
 also small. The convolutions are few and simple, the cavities often di- 
 lated with serum; on the membranes, there may be traces of inflamma- 
 tion. The cranium is small, the face large, the rest of the body small. 
 The malformation is in some cases caused by inflammation or dropsy of 
 the brain during foetal life. It is endemic in some countries, but single 
 cases may occur anywhere. The fcetus is viable. Absence or incomplete 
 development of portions of the brain may occur, not only in idiots, but 
 in i^ersons whose minds are perfect. 
 
THE SPIITAL COED. 
 
 THE MEMBRANES OF THE SPINAL CORD. 
 A.— THE DUEA HATER SPINALIS. 
 
 The dura mater spinalis, unlike that of the brain, does not serve as 
 periosteum to the bones forming the cavity, so that the lesions of the two 
 membranes differ somewhat. Hemorrhage may occur as the result of 
 injury between the dura mater and periosteum, or it may occur in tetanus, 
 as a result of circulatory changes induced by muscular spasm, or in the 
 asphyxia of new-born children. Small hemori'hages on the surfaces of 
 the membrane may occur, as the result of inflammation. 
 
 Serous fluid may accumulate outside of the dura mater, as a result of 
 post-mortem changes, or in connection with circulatory or inflammatory 
 changes in the membranes. 
 
 hiflainmafion. 
 
 Acute external Pacchymeningitis is almost always secondary to disease 
 or injury of the spinal column, and may result in collections of pus be- 
 tween the dura mater and periosteum, usually most abundant posteriorly. 
 Hemorrhagic pacchymeuvii git is occurs in the duramater spinalis, with the 
 formation of products similar to those observed in the brain, in the chronic 
 insane, and in drunkards. Siviple chronic pacchymeningitis interna, 
 with the formation of new connective tissue containing brain-sand, is not 
 infrequent. The new tissue may form minute iirojections or roughness 
 of the surface or, when more abundant, the jjsammomata. Tulercular 
 inflammation of the dura mater spinalis may occur in connection with 
 tubercular meningitis, or secondary to tubercular inflammation of the 
 vertebrse. 
 
 Tumors. — Filromata, lipomata, chondromata, myxomata, endothelio- 
 mata occur in the dura mater spinalis as primary tumors. C'arcinomata 
 and sarcomata, may occur as secondary tumors. Small plates of new- 
 formed hone are rarely found in the dura mater spinalis. 
 
 Parasites. — Echinococcus developing outside of the spinal canal may 
 
THE SPINAL COED. 191 
 
 perforate the dura mater ; or the cysts may lie between the dura mater 
 and the pia mater. 
 
 It is obvious that even small tumors in the spinal canal may give rise 
 to serious results from compression. 
 
 B. — THE PIA JIATER SPINALIS. 
 
 It is almost impossible in most cases in the pia mater, as well as in 
 the dura mater spinalis, and in the spinal cord, to judge with certainty 
 from the appearances after death of the blood content of the vessels, of 
 these parts during life. The same is true of abnormal quantities of se- 
 rum found after death. Tlie veins of the pia mater, especially in the 
 posterior region, may be greatly distended with blood after death, with- 
 out pre-existing disease; and the intermeningeal space may contain much 
 fluid under the same condition. 
 
 Hemorrhages may occur from injury in connection with severe con- 
 vulsions, or general diseases such as the hemorrhagic diathesis, scurvy, 
 small-pox, etc. The hemorriiages under these conditions, except from 
 injury, are not usually extensive. But in some cases of injury, or cere- 
 bral apoplexy; from the bursting of aneurisms of the basilar or vertebral 
 arteries; or in cases in which we cannot find a cause, a very large quantity 
 of blood may collect between the dura and pia mater, and in the meshes 
 -of or beneath the latter. 
 
 Inflammation. — Acute exudative spinal meningitis occurs under 
 essentially the same conditions and with essentially the same post-mor- 
 tem appearances as acute cerebral meningitis, though it is less frequent. 
 The exudations are apt to be most abundant in the posterior portions. 
 It may be associated with a similar inflammation of the pia mater cere- 
 bralis, and the inner surface of the dura mater may be involved. The 
 •disease may be circumscribed, but usually affects the entire length of the 
 membrane. 
 
 Tubercular Inflammation is usually most marked, when associated 
 with a similar condition of the pia mater cerebralis, in the upper portions 
 of the cord; but it may extend over the entire membrane. The conditions 
 under which it occurs and the character of the lesions are similar in both. 
 Chronic Spinal Meningitis is not infrequent, manifesting itself in the 
 formation of larger or smaller patches of new connective tissue or thick- 
 enings of the pia mater. The pia and dura mater may thus be firmly 
 united in places by adhesions, or the pia mater may become closely 
 adherent to the substance of the cord. 
 
 Not very infrequently large numbers of pigment-cells are found 
 in the pia mater spinalis, sometimes giving it a distinct gray or blackish 
 color. 
 
 Tumors. — Small plates of cartilage and lone are sometimes found in 
 pia mater. 
 
192 THE SPINAL COED. 
 
 Fibromata, inyxomata, sarcomata, and endotlieliomata have been 
 found. 
 
 Parasites. — Oysticercus sometimes occurs in the meshes of the pia 
 mater. 
 
 THE SPINAL CORD. 
 
 Hemorrhage. — -This is much less frequent than in the brain, but may 
 occur either as capillary apoplexy or as larger apoplectic clots. Capillary 
 hemorrhages, similar in appearance to those of the brain, may occur as 
 the result of injury, or near areas of softening or tumors, or may accom- 
 pany severe convulsions, as in tetanus. Apoplectic clots, which are 
 comparatively rare in the sjDinal cord, are usually small, commonly not 
 more than one ctm. in diameter, and are similar in their appearances and 
 in the changes subsequent to their formation, to those of the brain. They 
 are usually the result of injury; but may occur sjoontaneously, probably 
 in most cases as a result of inflammation, and are then most apt to occur 
 in the gray matter. Sometimes, however, hemorrhagic foci are found 
 in the spinal cord without traumatism or evidence of inflammatory 
 change. 
 
 INJURIES. 
 
 The spinal cord may be compressed or lacerated by penetrating 
 wounds, by fracture, or dislocation of the vertebrse, or by concussion, 
 without injury to the vertebra. The spinal cord is found simply disin- 
 tegrated, or there maybe much hemorrhage and the disintegrated nerve- 
 tissue be mixed with blood. If life continue, the nerve elements may 
 degenerate, Gluge's corpuscles, and free fat-droplets may form ; blood- 
 pigment may be formed, and when inflammation supervenes, more or less 
 pus may be intermingled with the degenerated detritus. There may be 
 marked changes in the minute structure of the cord without any change 
 being evident to the naked eye. 
 
 SECONDARY DEGENERATIONS IN THE SPINAL CORD. 
 
 When nerve-fibres of certain parts of the brain and of the spinal cord 
 are divided or destroyed from any cause, that portion of them which 
 becomes separated from its trophic centres degenerates. After a time- 
 frequently two to four weeks— the medullary sheath and axis-cylinder 
 disintegrate, becoming granular and fatty. These products of degenera- 
 tion may be in part absorbed at once, or may collect in cells, forming the 
 so-called compound granular corpuscles. After a still longer time- 
 sometimes several months — the degenerated areas become gray in color, 
 from the absorption of the degenerated myelin, harder, and somewhat 
 shrunken. These changes are partly due to the formation of new con- 
 nective tissue which takes the place of the degenerated nerve-fibres. 
 
 Since the affected portion of norve-tissue becomes gray.or translucent 
 
THE SPINA!, COED. 193 
 
 after the myelin is broken down and absorbed, and the new connective 
 tissue is formed, this is often called Gray Degeneration; or as the degene- 
 rated areas are harder than normal, it is sometimes termed Sclerosis. 
 
 Now it is found that this secondary degeneration takes place in the 
 direction in which the fibres conduct — in centripetal or sensory fibres, 
 upwards; in centrifugal or motor-fibres, downwards. Thus, we have 
 Descending Gray Degeneration [Descending Sclerosis), and Ascending 
 Gray Degeneration {Ascending Sclerosis). 
 
 Descending Gray Degeneration. — This change affects only the motor 
 nerve-fibres, and may reach but a short distance from the seat of lesion, 
 or may extend for a long distance, depending upon whether the severed 
 fibres run a short or long course before reaching their termination, i. e., 
 passing into ganglionic centres. Lesions of the brain, such as embolic 
 softenings and apoplectic clots, which destroy or interrupt any of the 
 motor nerve-fibres originating in the central convolutions, may be fol- 
 lowed by gi-ay degeneration of the portion of the fibres situated periphe- 
 rally to the lesion. These fibres pass through the corona radiata, anterior 
 portion of the internal capsule, pes pedunculi, pons, and thence to the 
 anterior pyramids where most of them decussate and pass to the poste- 
 rior part of the lateral columns of the opposite side. Those which do 
 not decussate form a narrow band at the inner part of the anterior 
 columns of the same side, constituting the columns of Tiirck. These 
 fibres which convey motor impulses from the brain to the cord form 
 a system called the pyramidal tract. There are also motor fibres in 
 the anterior columns, forming the so-called anterior root zones, which 
 maintain communications between different portions cf the gray* mat- 
 ter, and which are short. 
 
 Now a lesion in the brain or medulla, destroying the continuity of 
 the motor nerve-fibres of the pyramidal tract, will be followed by areas 
 of gray degeneration in the porterior part of the lateral column of the 
 opposite side, and in a narrow band near the anterior longitudinal fis- 
 sure of the same side. A lesion below the medulla, involving the fibres of 
 the pyramidal tract, will be followed by degeneration of the fibres on the 
 same side below the point of lesion. Lesions involving the fibres of the 
 anterior root zones will be followed by degenerations which extend but 
 a short distance, since these fibres soon communicate with their centres 
 in the gray matter. If a part only of the fibres in any of these regions 
 are interrupted, the amount of degeneration is proportionately small. 
 
 Ascending Gray Degeneration. — Any lesion interrupting the course of 
 the sensory nerve-fibres in the cord is followed by degeneration of the 
 central ends of the involved fibres, and increase of connective tissue, 
 about them. These fibres are in part situated in the posterior columns, 
 and form communications between different parts of the gray matter — 
 posterior root zones, and hence have not great length. Other sensory 
 13 
 
194 THE SPINAL COED. 
 
 fibres are grouped in a narrow band near the posterior longitudinal fis- 
 sure, forming the columns of Gall, while another set, forming the so- 
 called direct cerebellar trad, is situated in the periphery of the posterior 
 part of the lateral columns. 
 
 A lesion of the cord involving the severance or destruction of these 
 centripetal fibres will be followed by gray degeneration of the entire pos- 
 terior columns and the cerebellar tract for a short distance above the 
 lesion. The fibres of the posterior root zone being short, however, the 
 degeneration will, at a short distance above the lesion, become limited to 
 the columns of Goll, and the direct cerebellar tract in the lateral col- 
 umns. The degeneration may be traced along the columns of Goll to 
 the restiform bodies, and in the cerebellar tract to the cerebellum. Le- 
 sions involving the entire thickness of the cord will produce bilateral 
 degenerations. 
 
 It should be borne in mind, in looking for these secondary lesions, that 
 they are not developed until considerable time has elapsed since the pri- 
 mary lesion, and that, when small areas are involved, they are usually 
 inconspicuous. In any event, the lesions are apt to be more evident to 
 the naked eye in specimens hardened in chromic fluids than when fresh, 
 and microscopical examination is often necessary for their recognition. 
 
 INFLAMMATION. 
 ACUTE MYELITIS. 
 
 This lesion of the spinal cord, which is sometimes distinctly inflam- 
 matory in character and sometimes of a rather degenerative nature, is usu- 
 ally conSned to a comparatively limited longitudinal extent of the cord, 
 and hence is sometimes called transverse myelitis. When the cord is re- 
 moved and laid upon the table, if the lesion is marked, a flattening of 
 the cord at its seat may be observed; or on passing the finger gently along 
 the organ, the a£fected segment will be found softer than the rest of the 
 cord. On making a section through the diseased portion, the nerve-tis- 
 sue may be white or red or yellowish or grayish; it may be quite firm, but 
 is usually more or less softened and sometimes almost diflluent. ' 
 
 Microscopical examination shows different appearances depending 
 •upon the stage of the inflammatory or degenerative jirocess. There may 
 be much blood, or, if the lesion has existed for some time, blood pigment; 
 also fragments of more or less degenerated nerve-fibres and cells (Fig. 
 73), myelin droplets, free fat-granules and larger and smaller cells filled 
 with fat-granules (Glnge's corpuscles), pus-cells,granular matter, neuroglia 
 
 ' It should be remembered that a mechanical injury to the cord in removal, 
 such as crushing or bruising, may reduce the injured portion to a pulpy consist- 
 ency and thus produce appaarances somewhat similar to those of some forms of 
 inflammatory softening. 
 
THE SPINAL COED. 195 
 
 cells, and sometimes corpora amykcea. The various combinations of these 
 elements give rise to the different gross appearances which the diseased 
 part presents. In earlier stages of the lesion, the blood-vessels may be 
 dilated, the nerve-fibres and cells swollen; or the walls of the blood-ves- 
 sels may be thickened or fatty. 
 
 The lesion is apt to commence in the gray matter or at its edge, and 
 then extend first laterally and afterwards upwards and downwards. 
 
 Fio. 73.— Degenerated Tissue from Acute Myelitis, X 400 and reduced. 
 
 In a certain number of cases, the degenerated material may be 
 absorbed and a cicatrix or cyst formed. In the least extensive forms of 
 the lesion, there is apparently a regeneration of the nerve- fibres, and a 
 restoration of the functions of the cord. 
 
 Secondary gray degeneration, both asceading and descending, may 
 occur in this form, of myelitis, varying in extent according to the size of 
 the primary lesion. 
 
 Acute disseminated Myelitis runs a rapid course, and proves fatal in a 
 short time. The inflammation involves nearly the whole length of the 
 cord, but is more intense in some places than in others. The cord is 
 swollen and congested, it is infiltrated with pus-cells, the connective-tis- 
 sue framework is swollen, and the nerve-elements are degenerated. 
 
 Polinmyelitis anterior {Myelitis of the anterior horns). — This name 
 is applied to a group of cases which are characterized by clinical symp- 
 toms. indicating changes in the anterior gray cornua. The disease occurs 
 both in children and in adults, and varies in the severity, acuteness, and 
 duration of its symptoms. In many cases there is complete recovery, 
 and then we must suppose that the changes in the nervous tissue were 
 not destructive in their character. In other cases, the symptoms are 
 more permanent, indicating a destructive lesion. The lesions are not as 
 yet well established by actual observation. From the autopsies so far 
 recorded, we learn that the lesion is most frequent at the lumbar and 
 cervical enlargements of the cord, but may occur anywhere, and is often 
 in scattered patches. There is degeneration, shrinkage, pigmentation, 
 and atrophy of the ganglion-cells in the anterior gray cornua. There 
 
196 THE SPINAL COED. 
 
 may be an increase of connective tissue in the gray cornua, and in the- 
 anterior iind lateral columns. There may be degeneration and destruc- 
 tion of a considerable part of the anterior cornua; there may be atroph j 
 of the anterior nerve-roots. 
 
 CHEONIC MYELITIS. 
 
 Chronic Interstitial Myelitis. — Under this heading are embraced a 
 variety of lesions which probably differ from one another somewhat in 
 the nature of the changes involved, but more in the seat of the disease. 
 We shall consider without special classification the most important forms. 
 
 Chronic Transverse Myelitis. — In certain cases of pressure on the 
 spinal cord from a tumor or from displacement of the bones of the ver- 
 tebral column, etc., instead of becoming softened or undergoing acute 
 inflammatory changes, the cord becomes the seat of a localized formation 
 of new connective tissue with consecutive atrophy of more or less of the 
 nerve-elements in the gray and white matter. The cord becomes in this 
 way harder, and sometimes shrunken at the seat of lesion, and grayish in 
 color. This change may be followed by ascending and descending gray 
 degeneration. 
 
 Multiple Sclerosis. — This lesion, similar in its nature to multiple scle- 
 rosis of the brain, and often occurring with it, seems to belong, like 
 other chronic inflammations of the cord considered in this section, to the 
 group of chronic interstitial inflammations. It consists in the formation, 
 in more or less numerous, scattered, circumscribed areas, of new connec- 
 tive tissue, apparently derived from the neuroglia. The formation of 
 new connective tissue is accompanied by degeneration and atrophy of the 
 nerve-fibres and ganglion-cells. Whether the formation of new connec- 
 tive tissue is primary and the atrophy of the nerve-elements secondary, 
 or vice versa, it is difficult to say. The new connective tissue consists of 
 the characteristic branching neuroglia-cells surrounded by a more or less 
 dense network of fine fibrillse, many if not most of whicli seem to be 
 branches of the neuroglia-cells. Corpora amylacea and sometimes fat- 
 droplets, either free or contained in cells, may be present in the sclerosed 
 areas. 
 
 The areas of sclerosis may involve both gray and white matter, and 
 may be very small or large. If very small or in early stages of forma- 
 tion, they may not be recognizable by the naked eye, but when visible 
 they are grayish, translucent, and firmer than the surrounding tissue, 
 and may or may not present a depressed surface; they sometimes project 
 above the general level. The cause of this, as of other forms of so-called 
 idiopathic interstitial myelitis, is very obscure. 
 
 Posterior Spinal Sclerosis {Locomotor Ataxia). — This lesion (Fig. 74) 
 consists essentially in a degeneration and atrophy of the nerve-fibres and an 
 increase of connective tissue in the posterior columns of the spinal cord. 
 
THE SPINAL COED. 
 
 197 
 
 Uot infrequently the posterior portion of the lateral columns, the poste- 
 rior roots and cornua are also involved. Exceptionally a large part of 
 the lateral columns is involved, and also the anterior cornua. The change 
 
 Fig. 74. — Posterior-spinal Sclerosis — Upper Dorsal Region, X about 8. 
 The specimen was stained by Weigert's f uchsin method. (See methods of microscopical study 
 of cettrfil nervous system.) 
 
 usually commences in that portion of the posterior columns bordering on 
 the posterior cornua, but may involve, as above stated, the adjacent 
 
 -v.T(i.^. 
 
 Fie. 7.5.— Posterior Spinal Sclerosis. 
 Portion of sclerosed area shown in Fig. 74, more highly magnified. 
 
 parts. It is usually most marked in the lower dorsal and lumbar 
 legions. The sclerosis may extend upward to the restiform bodies, but 
 
198 THE SPINAL COED. 
 
 in the cervical region it is apb to be confined largely to the columns of 
 Goll, although there are exceptions to this. 
 
 When the lesion is well developed, the pia mater over the affected area 
 is usually thickened and adherent to the cord. In its early stages there 
 may be no change evident to the naked eye ; but when advanced, the 
 p'osterior columns may appear somewhat depressed, and grayish and 
 firmer than the rest of the cord. The microscopical appearances vary ^ 
 depending upon the stage and extent of the lesion. The walls of the 
 blood-vessels may be thickened ; there is more or less new connective 
 tissue consisting of neuroglia cells and very numerous interlacing, deli- 
 cate fibrils. There may be numerous corpora amylacea and fat-granule& 
 either free or collected in cells. The nerve-fibres may be numerous, but 
 separated more or less widely by the new connective tissue, or they may 
 be very few in number and irregularly scattered through the new tissue 
 (Fig. 75). The atrophy may involve the fibres of the posterior nerve- 
 roots and cornua, and even the ganglion-cells of the latter. 
 
 According to the recent researches of Linauer,' the columns of Clarke 
 in the dorsal region show in this disease a very constant and marked 
 diminution in the number of delicate fibrils which under normal condi- 
 tions surround the ganglion-cells. 
 
 In the rare cases in which the sclerosis extends to the lateral columns 
 and to the anterior cornua, the minute characters of the lesions are the 
 same. 
 
 There are other less important and less well understood forms of scle- 
 rosis of the whi,te matter anddegenerativeor inflammatory changes in the 
 gray matter of the cord; but so far as we know, the character of the le- 
 sions is essentially the same as those above described, except in their dis- 
 tribution. They are associated either with paralysis or changes in the 
 muscles, and the secondary changes are for the most part better known 
 than the primary alterations in the cord. Such lesions, which the scope 
 of this book does not permit us to enter into, are lateral sclerosis, periph- 
 eral sclerosis, the lesions involving muscular atrophy, etc. 
 
 Solitary tubercles and gicm?nata may occur in the spinal cord, but 
 are not common. Cysts may occur as a result of softening, or from un- 
 known causes. Sometimes very long narrow canals are found in the 
 spinal cord, even reaching nearly its whole length. Some of these are 
 evidently the dilated central canal, as they are lined with epithelium. 
 Others, however, have been found behind the central canal, and their 
 mode of origin is unknown. 
 
 Tumors. — Tumors of the spinal cord are not very common, much less, 
 so than tumors of the meninges. Fibromata, gliomata, sarcomata, find 
 neuromata have been described as primary tumors. Oarcinomata, as 
 
 ' Fortschritte der Medioin, Bd. ii.. No. 4, 1884. 
 
THE SPINAL COED. 199 
 
 secondary tumors, may occur. Tumors, of the meninges are apt to 
 secondarily involve the cord. 
 
 A remarkable form of new growth on the cord has been shown to one of us 
 (Delafield) by Dr. E. C. Seguin. The patient was a woman, thirty years of age. 
 Two years before her death she received a severe blow on the back of the head 
 After this, first one side and then all the limbs became paralyzed. From this 
 condition she recovered sufficiently to walk; but after a short time she again 
 grew worse, and both arms and legs were paralyzed aud.contractured. She died 
 of bronchitis. At the autopsy there were found two tumors on the spinal cord 
 .within the dura mater. 
 
 The upper tumor was on the anterior face of the cord just below the decussa- 
 tion of the medulla. It was of ovoid shape, and of the size of a pigeon's egg. It 
 was composed of branched connective tissue with many round cells. 
 
 The lower tumor was on the posterior face of the cord, at the upper part of 
 the lumbar enlargement. It was of the size and shape of a large, flattened cherry. 
 It was composed of portions of two spinal cords fused together, with their long 
 axes parallel to that of the normal cord. There were four patches of gray mat- 
 ter, having the shape of the cornua, containing ganglion-cells, and joined two 
 and two by regular gray commissures, in each of which was a central canal. The 
 gray portions were surrounded by tissue resembling the normal white substance 
 of the cord. 
 
 MALFORMATIONS. 
 
 The spinal cord may be double either in circumscribed portions, or over 
 a large part of its extent. It may be unusually long or short, or it may 
 be absent altogether (amyelia). This usually occurs with anencephalia. 
 Under these conditions a long connective-tissue sac filled with more or 
 less fluid may occupy the spinal canal. 
 
 Hydrorrliachis interna. — This abnormality consists in the dilatation 
 of 'the central canal of the spinal cord by fluid. This may be moderate, 
 or so extreme that but little of the substance of the cord is left, as a 
 thin shell around the central cavity. 
 
 Hydrorrliachis externa. — In this lesion there is an accumulation of 
 fluid between the meninges of the cord, causing more or less atrophy of 
 the latter. 
 
 Hydromyelocele — Spina Mfida. — In the majority of cases, hydror- 
 rhachis is accompanied by a more or less complete lack of closure of the spinal 
 canal posteriorly, so that the collections of fluid within, pouch outward 
 through the opening, in the form of a sac. The sac may be covered by 
 skin, or this may be absent, either from the beginning or as a result of 
 thinning and rupture. The walls of the sac may consist of the dura 
 mater and pia mater, or, in cases of hydrorrhachis externa, of the dura 
 mater alone; when both are present, they are usually more or less fused 
 together. Inside of the membranes of the sac, there may be a shell of 
 distended nerve-tissue of the cord, or the spinal cord may be split 
 posteriorly and the sides crowded sideways; or there maybe a rudi- 
 mentary fragment of the cord suspended in the sac or attached to 
 
200 THE SPINAL COED. 
 
 the walls; or the cord may be but little changed and remain inside the 
 spinal canal. The openings in the spinal canal may be due to the com- 
 plete or partial absence of the vertebral arches, or more rarely the sac 
 may protrude through openings between the completely formed arches. 
 Spina bifida most frequently occurs in the lumbar and sacral regions, but 
 it may occur in the dorsal or cervical regions; or the canal may be open 
 over its entire length. Very rarely it is open on the anterior surface. 
 The protruding sac may be very small or as large a child's head. The 
 fluid in the sac is usually clear, but may be turbid from flocculi of degene- 
 rated nerve-tissue. 
 
 THE PERIPHERAL NERVES. 
 
 Changes in Nerves after Division. — When nerves are divided or a 
 portion destroyed by injury, the nutrition of certain parts of the fibres is 
 interfered with, apparently because of their separation from their trophic 
 centres, and they suffer degeneration ; but after a time, if the condi- 
 tions be favorable, they may undergo regeneration and restitution of 
 function. The trophic centres of motor or efferent nerves are in the ante- 
 rior cornua of the spinal cord, while those of the afferent or sensory 
 nerves are in the spinal ganglia. As the degeneration of the nerve-fibres 
 occurs in that part which is severed from their trophic centres, it follows 
 that any division of motor-nerve fibres outside of the spinal cord will be 
 followed by degeneration of the entire separated portion of the nerve, 
 while a division of the sensory fibres between the ganglion and the spinal 
 cord will be followed by degeneration of the spinal end, but not of the 
 peripheral portion. In any mixed nerve outside of the spinal canal a 
 division will be followed by degeneration of all the fibres, both motor and 
 sensory. The degeneration not only affects the entire severed portion, 
 but it occurs at nearly the same time in all parts. The degeneration 
 consists in the bi-eakingup of the medullary sheaths into variously shaped 
 droplets, and the decomi^osition of these, with the formation of fat, which 
 may remain for some time either free or inclosed in cells, and finally be 
 absorbed. The axis cylinder, too, is, in many cases at least, more or less 
 completely destroyed. The neurilemma and its nuclei do not seem 
 usually to undergo degeneration, but may persist and form part of the 
 regenerated nerve when restitution occurs. 
 
 After a variable time, if the conditions are favorable, the divided ends 
 of the nerve may be united and a regeneration or new formation of 
 nerves in or about the severed portions may occur, so that the function 
 may be resumed. Considerable time is required, frequently months, for 
 the completion of the regenerative process. Degeneration of the nerves 
 not only follows mechanical injuries, such as incision, crushing or tear- 
 ing, and compression, as from a tumor or dislocation of the bones ; 
 but it may result from disease of the special nerve-centres with which the 
 
THE SPINAL COED. 201 
 
 nerves communicate ; from inflammation of the nerves themselves ; or 
 from causes which are unknown to us, as in certain forms of lead-poison- 
 ing, etc. 
 
 Acute Neuritis. — Primary acute inflammation of the nerves may 
 occur as the result of injury, or it may be secondary to an inflammatory 
 process in its vicinity^ although, owing to the dense, lamellar sheaths and 
 the special blood supply, the nerve-trunks may escape particiiDation in 
 even very sevei'e inflammatory processes in surrounding tissues. Tlie 
 inflamed nerve may be red and swollen and infiltrated with serum and 
 pus-cells. The process may undergo resolution or terminate in gangrene 
 and destruction of the nerve, or it may become chronic and result in the 
 formation of new connective tissue. 
 
 Chronic Neuritis. — This is essentially a chronic interstitial inflamma- 
 tion resulting in an increase of connective tissue in the nerve-sheath and 
 intra- fascicular bands. As a result of this, the nerve-fibres undergo 
 atrophy from pressure ; the medullary sheath, and finally the axis-cylin- 
 der, being in more or less of the fibres partially or completely destroyed. 
 
 Syphilitic and Tubercular Inflammation of the nerves is not common 
 except at their central ends, in connection with similar inflammations of 
 the meninges, or when they are secondarily involved in connection with 
 these inflammations in neighboring tissues. 
 
 Leprous Inflammation. — This consists in the formation within the 
 nerve of masses of new-formed tissue somewhat resembling granulation 
 tissue, in whose cells multitudes of characteristic bacilli are uniformly 
 found.' It constitutes the variety of leprosy known as lepra ancesthetica. 
 
 Fig. 76.— MtJLTiPLE Fibromata (False Neuromata) of Pkeumogastrio Nerve, one-quarter 
 natural size.^ 
 
 Tumors. — The tumors of the nerves are such as consist largely of, or 
 contain new-formed nerve-tissue — true ?i,euromata ; and the so-called 
 false neuromata (Figs. 76 and 77), which are for the most -p^Tt fibromata 
 or myxomata of the connective tissue of the nerve. Myxo-sarcomata 
 are less common, and primary sarcomata rare. The nerves may be 
 secondarily involved in sarcomata or carcinomata, though not infre- 
 
 ' See Leprosy. 
 
 ' This drawing is made from a specimen taken from a case described in the 
 American Journal of Medical Sciences, July, 1880, in which over 1 182 tumors were 
 found in the body. Fig. 77 shows the minute structure of the more typical of 
 the tumors. 
 
202 
 
 THE SPINAL COED. 
 
 qnently nerves pass through these tumors without being in the least 
 involved in their peculiar structure. 
 
 
 
 Fig. 77.— Fibroma (False Neuroma) of Lumbar Nerve, x 300. 
 The fibrous tissue was loose in texture and in places oedematous, so that it considerably re- 
 sembled mucous tissue. 
 
 METHODS OF PREPARATION OF NERVE-TISSUE FOR MICROSCOPICAL 
 
 STUDY. 
 
 The general methods of hardening have been already given on p. 41. 
 For minute study there is no one method of staining and mounting upon 
 which we can rely exclusively for the study of all lesions. A preliminary 
 examination of areas of inflammatory softening or of the disintegrated 
 tissue in apoplectic clots, or of the new-formed tissue in chronic liemor- 
 rJiagicjiacchy meningitis interna may be made by teasing portions of the 
 affected tissues in one-half-per-cent salt solution. Or the tissues in 
 these lesions or in any others in which fatty degeneration is suspected 
 may be placed for twenty-four hours in one-per-cent aqueous solution of 
 osmic acid, and then washed and teased in glycerin. In this way th& 
 myelin and the fat will be stained brown or black. Secondary and other 
 degenerations of medullated nerves may be studied by soaking the nerves 
 for twenty- four hours in one-per-cent solution of osmic acid, and then 
 staining with picro-carmin and teasing and mounting in glycerin. 
 Suppurative inflammation of the central nervous system and the mem- 
 branes, or the connective-tissue changes in general, may be studied in 
 
THE SPINAL COED. 203 
 
 sections from the tissues hardened in Miiller's fluid and alcohol, stained 
 double with hsematoxylin and eosin (see p. 44), and mounted in Canada 
 balsam. 
 
 A very valuable method for the study of any of the forms of chronic 
 interstitial inflammation of the central nervous system, with associated 
 atrophy of the nerve-flbres ; or for the identification of nerve-fibres in 
 true neuromata, or other tumors containing nerves, is the acid fuchsin- 
 staining of Weigert. The following is the mode of procedure in staining 
 by this method. The tissues must be well hardened in Miiller's fluid. 
 Alcohol may be used to complete the hardening. The staining agent is 
 the so-called acid fuchsin, which is rosanilin, in which one atom of H is 
 replaced by the radicle SO3H. It is really a sulphate of rosanilin. Thin 
 sections of nerve-tissues are stained for from one to twenty-four hours in a 
 saturated aqueous solution of the fuchsin. They are then rinsed for an 
 instant in water — each section should be handled separately — and then 
 dipped for an instant in a saturated alcoholic solution of caustic potash, 
 diluted with alcohol in the proportion of 1 to 10. The exposure to the 
 alkali should be brief, the sections being merely dipped in and moved to 
 and fro two or three times. A too long exposure will result in the com- 
 plete removal of the color from the specimen and the failure of the 
 operation. The sections are immediately transferred to a dish of pure 
 water, which is changed two or three times to insure complete removal 
 of the alkali. They are now dehydrated with alcohol, cleared up with 
 oil of cloves, and mounted in balsam. The nuclei may be stained by 
 hematoxylin before dehydration. The structural outlines are rendered 
 more distinct and the color intensified by dipping the sections for an 
 instant, after the removal of the potash, in a mixture of hydrochloric 
 acid and water, 1 to 5. In sections prepared in this way, the connective- 
 tissue elements are of a grayish or violet color, with indistinct outlines. 
 The nerve-fibres are of a light or deep distinct red. The nerve-cells are 
 not much stained, but usually stand out with distinctness. 
 
 The rationale of the process is as follows. The fuchsin stains the 
 tissues diffusely, all of the structural elements being colored alike red. 
 The potash removes the color from all of the structural elements, but 
 with different degrees of rapidity, the nerve-fibres holding it more tena- 
 ciously than other elements, so that if the action of the alkali be stopped 
 at the right moment, the differentiation is secured. 
 
 It is necessary to use a particular preparation of the acid fuchsin for 
 obtaining these results: namely, that known as the acid fuchsia S, of the 
 Baden anilin factory. This maybe obtained from Meyrowitz Bros., cor. 
 Fourth avenue and 23d street, New York. 
 
 This method is well suited for showing the nerve-fibres, and their 
 courses in normal nerve-tissues.' 
 
 ' Another most excellent method of demonstrating the nerve-fibres in the cen- 
 
204 THE SPINAL COED. 
 
 To demonstrate the presence of miliary aneurisms in or about apo- 
 plectic clots, it is usually necessary to macerate the brain-tissue in water 
 until the nerve elements disintegrate, and they may then be washed away 
 under a stream of water, leaving the blood-vessels with their aneurisms 
 exposed. 
 
 tral nervous system, both in health and disease, may be found described by Wei- 
 gert in " Fortschritte der Medicin," Bd. 2, No. 6, 1884. By this method the nerve- 
 fibres are stained black, while the remaining elements are of a yellowish or brown 
 color. 
 
THE RESPIRATORY SYSTEM. 
 
 THE LARYNX AND TRACHEA. 
 MALFOEMATIONS. 
 
 The larynx and trachea may be entirely absent in acephalic monsters. 
 The larynx may be abnormally large or small. The epiglottis also may 
 be too large, or too small, or may be cleft. There may be communica- 
 tions between the trachea and the oesophagus, and then the pharynx 
 generally ends in a cul-de-sac and the ossophagus opens into the trachea. 
 There may be imperfect closure of the original branchial arches, so that 
 there are fissures in the skin leading into fistulas which open into the 
 pharynx or trachea. The fissure in the skin is small, and is situated 
 about an inch above the sterno-clayicular articulation, usually on one or 
 both sides, more rarely in the middle line. Individual cartilages, as the 
 epiglottis, or one or more rings of the trachea may be absent, or there 
 may be supernumerary rings. The trachea may divide into three main 
 bronchi instead of two, and in that case two bronchi are given off to the 
 right lung and one to the left. The trachea may be on the left side of 
 the (Esophagus, or behind it. 
 
 INFLAMMATION". 
 
 Acute Gatarrhal Laryngitis. — Tliis occurs as an idiopathic inflam- 
 mation, as a complication of the exanthemata and the infectious diseases, 
 and is produced by the inhalation of irritating vapors and of hot steam 
 and smoke. The inflammation varies in its intensity in different cases. 
 The mucous membrane is at first congested, swollen, and dry; then the 
 mucous glands become more active and an increased quantity of mucus 
 is produced. There is an increase in the desquamation of the superficial 
 epithelial cells, and in the production of the deep cells. A few pus-cells 
 are found in the mucus and in the stroma of the mucous membrane. 
 For some reason inflammation of the larynx is frequently attended with 
 spasm of its muscles, thus producing attacks of suffocation. In severe 
 cases oedema of the glottis is developed. 
 
206 THE EESPIEATOEY SYSTEM. 
 
 After death, the congestion of the mucous membrane frequently dis- 
 appears altogether. 
 
 Chronic Catarrhal Laryngitis. — There is a thickening and increase 
 of the connective-tissue stroma of the mucous membrane. The epithelial 
 cells are deformed, and may desquamate so as to form superficial ulcers. 
 The mucous glands are swollen and prominent or may be inflamed and 
 form ulcers. The inflammation may extend to the perichondrium of the 
 cartilages. 
 
 Croupous laryngitis occurs most frequently as the lesion of diph- 
 theria; it may also complicate the exanthemata and the infections dis- 
 eases, or be due to the inhalation of steam or smoke, or it may occur as 
 an idiopathic inflammation. 
 
 The mucous membrane is swollen and congested. Its surface is 
 coated with a layer of fibrin and pus, and its stroma is infiltrated with 
 fibrin and pus. The epithelial cells may die and fall off with the false 
 membrane. The quantity of fibrin and pus produced varies in the dif- 
 ferent cases. 
 
 Inflamination of the submucous connective tissue occurs as: 
 
 (1) CEdema glottidis. Here we find the epiglottis swollen, and from 
 its base two bags of serum, formed of the aryteno-epiglottidean folds, 
 extend backward. This csdema is often sufficient to close the larynx and 
 cause death. It accompanies acute catarrhal laryngitis, small-pox, ty- 
 phoid fever, syphilitic and tuberculous ulcerations, facial erysipelas, and 
 perichondritis. 
 
 (3) Purulent inflammation may attack the same parts which are 
 implicated in oedema glottidis, and cause death in the same way. 
 
 Perichondritis. — Inflammation of the perichondrium of the cartilages 
 of the larynx may be idiopathic or secondary to inflammations of the 
 mucous membrane, especially tubercular and syphilitic inflammation. 
 It usually attacks first the cricoid cartilage, and extends later to the 
 other cartilages. The inflammation causes the production of pus and 
 separation of the perichondrium from the cartilage, with the death of 
 the latter. The cartilage is usually found ossifled, sometimes carious, 
 sometimes degenerated and softened without ossification. The pus 
 spreads to the submucous tissue, collects in abscesses, and may cause 
 death by suffocation, or may perforate the mucous membrane. When 
 the inflammation extends outward, abscesses and sinuses form on the 
 outside of the larynx, and may perforate through the skin of the neck. 
 Portions of the necrosed cartilages may find their way into the cavity of 
 the larynx and be coughed out, or may become fixed in the rima glottidis 
 and cause suffocation, or may pass into the bronchi. In other cases, the 
 portions of cartilage may be discharged outward through openings in the 
 skin. 
 
 Syphilitic Laryngitis. — Constitutional syphilis shows itself very fre 
 
THE EESPIKATOEY SYSTEM. , 207 
 
 quently in the larynx. It produces here simple catarrhal inflammation, 
 either acute or chronic. The chronic inflammations are attended with 
 the production of superficial and deep ulcers, irregular hypertrophy of 
 the stroma of the mucous membrane and perichondritis. Sometimes 
 mucous patches or condylomata are found. 
 
 Tuiercular Laryngitis presents us with lesions due partly to chronic 
 catarrhal inflammation and partly to the formation of tubercle tissue. 
 The chronic inflammation causes changes in the epithelium, superficial 
 ulcers, hypertrophy and ulceration of the mucous glands, hypertrophy 
 of the stroma, and perichondritis. The tubercle tissue is formed in the 
 stroma, close under the epithelium. It degenerates and softens in the 
 iisual way, and so produces large ulcers. Tubercular laryngitis is, as a 
 rule, associated with pulmonary phthisis. 
 
 TUMOES. 
 
 Retention Cysts of the mucous glands of the larynx may reach such a 
 size as to form sacs projecting into its cavity. 
 
 Papilloma is the most frequent form of tumor of the larynx. The 
 tumors grow most frequently from the vocal cords. They consist of a con- 
 nective-tissue stroma arranged so as to form papilla covered with epithe- 
 lium. 
 
 Fibromata, Lipomata, Myxomata, and Angiomata are occasionally 
 met with. 
 
 Chondromata grow from the normal cartilages and are usually mul- 
 tiple and sessile. They may project into the cavity of the larynx. 
 
 Sarcomata of the larynx have been seen in a considerable number of 
 •cases. They occur both in children and in adults. They are com- 
 posed of fusiform or round cells, with a stroma which varies in quantity 
 in the different cases. 
 
 Oarcinomata may invade the larynx from the tongue or the pharynx, 
 ■or may originate in it. They are composed of flat epithelial cells packed 
 together in the usual way. 
 
 In the trachea, tumors are of rare occurrence, but occasional exam- 
 ples of growths similar to those in the larynx have been met with. 
 
 THE LUNGS. 
 
 The lungs are composed of a connective-tissue stroma containing 
 blood-vessels, lymphatics, and nerves. This stroma is so arranged as to 
 inclose rounded and irregular spaces — the air-vesicles and air-passages; 
 to form a continuous membrane on the surface of the lung — the pul- 
 monary pleura; bands which divide up the lung into lobules — the septa; 
 and tubes by which the air enters the air-imssages and air-vesicles — the 
 bronchi. Bach lung, therefore, is made up of bronchi, air-passages, air- 
 vesicles, pulmonary pleura, blood-vessels, lymphatics, and nerves. 
 
208 THE EESPIEATOEY SYSTEM. 
 
 The lungs thus formed are contained within the thorax, each in its 
 separate canity. The walls of these cavities are formed by the ribs and 
 muscles, the diaphragm, and the mediastinum. Everywhere the cavi- 
 ties are lined by a connective-tissue membrane — the pleura. According 
 to its position, we distinguish the costal, the diaphragmatic, and the 
 mediastinal pleura. 
 
 The entire structure of the lungs, and with them the costal, dia- 
 phragmatic, and mediastinal pleura, may be the seat of morbid changes. 
 Or the different parts of the lung: the bronchi, the septa and pulmonary 
 pleura, the air-passages and vesicles, or the blood-vessels, may be dis- 
 eased separately or in various combination. Or the costal, diaphragma- 
 tic, and mediastinal pleura may alone be changed. 
 
 So we have to describe separately the lesions of the pleura, the bronchi, 
 the parenchyma of the lung, and its interstitial tissue, although these 
 lesions are often associated. 
 
 THE PLEUEA. 
 HYDE0TH0EA5. 
 
 Non-inflammatory accumulations of clear serum in the pleural cavi- 
 ties are of frequent occurrence. They are produced by the same causes 
 which effect dropsy in other parts of the body — lesions of the heart, 
 liver, and kidneys, and changes the circulation, and in the composition 
 of the blood. 
 
 If the amount of serum is small, it is of little consequence; if it is 
 large it may compress the lower lobes of the lungs and interfere with 
 respiration. 
 
 There may be changes in the endothelium of the parietal pleura. In- 
 stead of the regular endothelium, large and small flat cells of irregular 
 shape are found. 
 
 HEMOEBHAGE. 
 
 Extravasations of blood in the substance of the pleura are found in 
 persons who have died after suffering from the infectious diseases; and 
 as the result of injuries to the wall of the thorax. 
 
 Blood in large quantity in the pleural cavities is found after rupture 
 of aneurisms, of the heart and pericardium. 
 
 Bloody serum in the pleural cavities is not often found with ordinary 
 pleurisy. But with tubercular pleurisy and traumatic pleurisy it is not 
 infrequently present. 
 
 INELAMMATION". 
 
 The inflammations of the pleura are all spoken of by the common 
 name of jDleurisy. 
 
 All the different inflammations of the lung are capable of being ac- 
 
THE EESPIEATOEY SYSTEM. 209 
 
 companied by pleurisies, which begin in the pulmonary pleura and ex- 
 tend to the costal. 
 
 Besides these, however, there ai-e many pleurisies which belong pri- 
 marily to the costal pleura and extend from there to the pulmonary pleura. 
 
 Such pleurisies occur as idiopathic inflammutions, as complications of 
 various diseases, as the result of injuries, or are produced by the inflam- 
 mation of adjacent parts. 
 
 We can distinguish: 
 
 1. Pleurisy with the production of fibrin. 
 
 2. Pleurisy with the production of fibrin and serum. 
 
 3. Pleurisy with the production of fibrin, serum, and pus. 
 i. Chronic pleurisy with the formation of adhesions. 
 
 5. Tubercular pleurisy. 
 
 All the varieties of ^sleurisy can best be studied in the lesions which 
 are developed in and on the costal pleura. The lesions can be observed 
 in the human subject, and can be produced artificially in the lower ani- 
 mals. It is in these artificial pleurisies especially that we are able to see 
 the early changes produced by the inflammation, and to watch the pro- 
 cess step by step. 
 
 The free surface of the costal pleura is covered with a single layer of 
 flat cells — the endothelium. The pleura itself is formed of planes of 
 connective tissue, reinforced by elastic fibres. Connective-tissue cells 
 with large bodies and branching processes are present in considerable 
 numbers, being most abundant in the layers beneath the endothelium. In 
 the connective tissue are embedded blood-vessels, lymphatics, and nerves. 
 
 1. Pleurisy with the production of fiirin. Dry Pleurisy. Acute 
 
 Pleurisy. 
 
 This form of pleurisy is apt to involve circumscribed areas of the 
 costal; mediastinal, diaphragmatic, or pulmonary pleura, less frequently 
 the entire pleura of one side of the chest. While the inflammation is 
 going on, the affected portion of pleura is coated with fibrin, the surface 
 of the opposite portion of pleura is coated in the same way, and bands of 
 fibrin join the two together. After the inflammation has run its course, 
 we find the affected portion of pleura thickened by the formation of new 
 connective tissue, while bands of connective tissue extend between the 
 opposed pleural surfaces. 
 
 As an exceptional condition there is inflammation of the entire pleura 
 of one side, with the production of such an enormous amount of fibrin 
 as to compress the lung and cause death. 
 
 3. Pleurisy with the production of fibrin and serum. Pleurisy with 
 Effusion. Subacute Pleurisy. 
 This is the most common form of pleurisy. As a rule, it involves the 
 greater part of the pleura of one side of the chest. Sometimes, however, 
 14 
 
210 THE EESPIEATOET SYSTEM. 
 
 the pleura of both sides of the chest is involved, and then the pericardium 
 also is often inflamed. 
 
 While the inflammation is in progress, the surface of the affected 
 pleura is coated with fibrin, and bands of fibrin stretch between the 
 parietal and pulmonary pleura. In the pleural cavity is serum in vari- 
 able quantity. This serum is clear, or turbid from the presence of piis- 
 cells and flocculi of fibrin. The lung is compressed in different degrees 
 and positions according to the quantity of the serum, and the character 
 of the adhesions. 
 
 If the j)atients recover, the serum is absorbed, the fibrin disappears, 
 and there are left behind connective-tissue thickenings of the pleura"and 
 adhesions. 
 
 These two forms of pleurisy, although different in their clinical his- 
 tories, are yet anatomically essentially the same. In both of them we 
 find a regular sequence of changes. First, the production of fibrin and 
 a few pus-cells, either with or without serum. Second, a gradual absorp- 
 tion of the serum and fibrin. Lastly, the formation of permanent new 
 connective tissue in the form of adhesions or of thickenings of the pleura. 
 Throughout the whole process the tissue of the pleura is but little 
 changed, the products of inflammation, although they originate in the 
 tissue of the pleura, do not infiltrate it, but make their way to its surface, 
 there accumulate, and there undergo their diflierent changes. Variations 
 from the regular course of the inflammation are effected by the excessive 
 formation either of the fibrin, the pus, or the serum, and by the manner 
 in which these inflammatory products are absorbed. 
 
 If we endeavor to follow out the successive changes by which the 
 fibrin, pus and serum, make their appearance and then disappear, and the 
 way in which permanent new connective tissue takes their place, we en- 
 counter several difficulties. It is impossible to obtain autopsies which 
 will give the lesions belonging to each successive day of the disease; the 
 pleura does not really show well, if the patient has been dead more than 
 two or three hours before the autopsy; and in most cases the inflamma- 
 tion is too intense, its products are too abundant to be easily studied. 
 
 To obviate these difiiculties we must resort to the lower animals. By 
 injecting a solution of chloride of zinc into the pleural cavities of dogs, 
 we can excite pleurisies exactly resembling those which we see in the 
 human subject. By varying the amount of fluid injected, we can obtain 
 pleurisies of different degrees of intensity. By using a number of 
 animals, we can observe the course of the inflammation from hour to 
 to hour, and from day to day. 
 
 In such an artificial pleurisy the first change is congestion. The 
 pleura is of a uniform bright red color, its surface moist and shining. 
 There is, as yet, no serum and no fibrin. Already, however, the endo- 
 thelial cells have fallen off in patches, the superficial connective-tissue 
 
THE EESPIEATOEY SYSTEM. 211 
 
 cells are swollen and increased in number, and a few pus-cells are present. 
 Those are all the changes for from half an hour to six hours after the 
 irritant has been applied to the pleura. 
 
 The next step in the inflammatory process is the production of serum 
 and fibrin. The serum collects in the bottom of the pleural cavity, the 
 fibrin coats the pleura. As the fibrin is produced the pleura loses its 
 natural moist and shining appearance. The fibrin appears first in the 
 form of little granules, knobs, and threads between the edges of the endo- 
 thelial cells and overlying them. A few pus-cells are entangled in the 
 fibrin, and infiltrated in the superficial layers of the pleura. The swell- 
 
 If 
 
 'n 
 
 
 5.V 
 
 
 I 
 
 Fio. 78.— An Artificial Pleurisy of Twen'ty-four Hours' Duration, X 750 and reduced. 
 Swelling and growth of the connective-tissue cells in the pleura. 
 
 ing and new growth of the connective-tissue cells are now well marked. 
 The bodies of the branching cells are swollen, and small polygonal, nu- 
 cleated cells, arranged in rows between the fibres of the basement sub- 
 stance, make their appearance. By the end of twenty-four hours these 
 changes are fully developed (Fig. 78). 
 
 After this the production of fibrin, serum and new connective-tissue 
 cells continues, and by the third or fourth day the new connective-tissue 
 cells are present, not only in the superficial layers of the pleura, but also 
 in the layer of fibrin coating its surface and forming adhesions. 
 
 By the fourth or fifth day, the cells in the fibrin are still more numer- 
 ous, blood-vessels make their appearance, which can be injected from the 
 arteries of the pleura (Fig. 79). 
 
 After this the serum is gradually absorbed. The layer of fibrin and 
 cells on the surface of the pleura exhibits a constant decrease of fibrin 
 
212 
 
 THE EESPIEATOET SYSTEM. 
 
 and increase of cells, and becomes more intimately connected with the 
 surface of the pleura. 
 
 By the fourffienth day the fibrin has disappeared, and a basement sub 
 stance has been formed between the cells. Of the new cells the super- 
 ficial ones are changed into endothelium, the deeper ones into branching 
 
 Fig. 79.— Artificial Pleurisy on the Fifth Day, X 750 and reduced. 
 The layer of new tissue on the surface of the pleura. 
 
 cells. The changes in the adhesions between the pulmonary and costal 
 pleura are the same as those in the layer of fibrin coating the costal pleura. 
 
 The lesions of human pleurisy seem to be essentially the same as those 
 of the artificial pleurisy just described. But the inflammatory products 
 are formed in larger quantities, a much longer time is required for their 
 absorption, and the formation of new connective tissue follows more 
 slowly. 
 
 In these forms of pleurisy, therefore, two distinct processes take place. 
 
THE EESPIEATOET SYSTEM. 213 
 
 1. The blood-vessels are congested, and through their walls transude 
 the plasma of the blood and a few white blood-globules. 
 
 2. The superficial connective-tissue cells are increased in size and 
 number. 
 
 The products of the first of these processes, the fibrin and serum, are 
 regularly reabsorbed. 
 
 The product of the second of these processes, the new connective-tissue 
 cells, regularly increases until a layer of new connective tissue is formed. 
 
 The natural termination of such a pleurisy is the recovery of the 
 patient with thickenings of the pleura and adhesions. 
 
 The irregular terminations are : the death of the patient, the pro- 
 tracted existence of the fibrin and serum, and the change of the char- 
 acter of the inflammation so that pus is produced. 
 
 3. Pleurisy with the production offihrin, seru^n, and pus. Empyema. 
 This form of pleurisy may occur under several different conditions. 
 
 1. The inflammation is at the very outset of severe character with the 
 formation of pus. 
 
 2. A pleurisy with the production of fibrin and serum, either 
 gradually or suddenly, changes its character, and pus is formed. 
 
 3. Phthisical areas of softening, or abscesses of the lung, abscesses in 
 the wall of the thorax, or in the liver, or in the abdomen rupture into a 
 pleural cavity and set up an empyema. 
 
 4. The inflammation may be not only purulent, but also gangrenous 
 in character. The fluid in the pleural cavity, the fibrin and pus coating 
 the pleura, and the pleura itself may putrefy, with the production of 
 bacteria and the evolution of gases. This may take place either in a 
 closed pleura or in one which has been opened. 
 
 5. If there is an opening into a pleural cavity, either through the 
 lung or through the wall of the thorax, there is air in the pleural cavity 
 in addition to the inflammatory products. Such a condition is called 
 pyo-'pneum othorax. 
 
 In all these different cases the pleural cavity is partly or completely 
 filled with purulent fluid, and the lung is either compressed against the 
 vertebral column, or partly adherent to the chest-wall. Sometimes, 
 however, the purulent fluid is shut in by adhesions, either between parts of 
 he lung and the thoracic wall, or between the lung and the diaphragm, or 
 between the lung and the pericardium, or between the lobes of the lung. 
 
 The fluid in the pleural cavity is usually a thin, purulent serum, 
 composed of serum, pus-globules, endothelial cells, and pieces of fibrin. 
 But sometimes this fluid is very thick and viscid. 
 
 In empyema in its earlier stages, the lesions are the same as those in 
 pleurisy with effusion, with the addition of pus in the serum, the fibrin, 
 and the superficial layers of the pleura. 
 
214 THE EESPIEATOET SYSTEM. 
 
 In children, the inflammation may remain in this condition for a 
 long time, but in adults other changes in the pleura are soon developed. 
 
 These changes consist in the growth of a large number of small poly- 
 gonal and round cells, the basement substance is split up, and the pleura 
 is changed into a tissue resembling granulation tissue. 
 
 The pleura is thus considerably thickened. Its surface is coated with 
 fibrin and pus, or is bare like the surface of an ulcer. 
 
 In this condition the pleura may remain for months or years; its inner 
 layers formed of granulation tissue, its outer layers of densec onnective 
 tissue. 
 
 Sometimes the cell-growth is more active, necrotic changes are added, 
 and so there is a conversion of portions of the pleura into pus. Such a 
 suppuration may extend from the pleura to the fasciee, the muscles, the 
 skin, the diaphragm, or the lungs. Thus the pus may find an exit 
 through the wall of the thorax, into the peritoneal cavity, or into the lungs. 
 
 If the empyema becomes gangrenous, the pleural cavity contains foul 
 gases, the purulent serum is dirty and stinking, and swarms with bacte- 
 ria. The fibrin coating the pleura is of green or brown color. Portions 
 of the pleura itself may also become gangrenous. 
 
 In old cases, the thickening of the pleura may reach an enormous 
 degree, and it may become calcified. The perichondrium of the cartilages 
 and the periosteum of the ribs may become inflamed, with necrosis of 
 the cartilages and ribs, or a production "of new bone. 
 
 Empyema is, therefore, a very much more s'erious lesion than the two 
 forms of pleurisy just described. The lesions involve not merely the 
 surface of the pleura, but its entire thickness. When the pleura has 
 thus been converted into granulation tissue it is hardly possible for it to 
 return to a normal condition. 
 
 It is important to remember that in children the changes in the 
 pleura itself are less profound, and that in adults they become more and 
 more marked, according to the duration of the disease. 
 
 4. Chronic Pleurisy, ivith the formation of adhesions. 
 
 This form of pleurisy may follow one of the varieties of pleurisy jus* 
 described, it may be associated with emphysema and chronic phthisis, or 
 it may occur by itself. 
 
 After death the pulmonary and costal pleura are found thickened, 
 and joined together by numerous adhesions. These changes may involve 
 only a pai-t, or the whole of the pleura on one or both sides of the chest. 
 
 The thickened pleura is covered with endothelial cells which are in- 
 creased in size and number; the connective-tissue cells in the pleura are 
 also increased in number, and the blood-vessels are more numerous. 
 
 The adhesions are formed of connective tissue resembling that of the 
 costal pleura, containing blood-vessels and covered with endothelium. 
 
THE EESPIEATOEY SYSTEM. 
 
 215 
 
 5. Tuhercular Pleurisy. 
 
 In acute general tuberculosis, miliary tubercles are often present in 
 the pleura. In acute and chronic phthisis, besides the fibrin, pus, se- 
 rum, and new connective tissue so often produced, there may also be 
 miliary tubercles, or larger flat, cheesy nodules. 
 
 There are, however, cases of tubercular pleurisy which have the 
 ■characters of a local tubercular inflammation. Tubercles are either ab- 
 sent altogether from the rest of the body, or of secondary importance to 
 the pleurisy. 
 
 This form of pleurisy involves the pleura of one side of the thorax only. 
 
 
 
 Fig. 80.— Tubercular Pleurisy, X 90 and reduced 
 A vertical section o£ the costal pleura. 
 
 It may be rapidly developed, the patient dying at the end of two weeks; 
 or it may continue for months. It seems to be very fatal. 
 
 The inflammation maybe confined to the costal pleura, or may involve 
 ■also the diaphragmatic and pulmonary pleura. The gross appearance of 
 the lesion, varies. 
 
216, THE EESPIEATOEY SYSTEM. 
 
 1. The pleura is thickened, its surface is bare of fibrin ; it is of a bright- 
 red color from the congestion of the blood-vessels, and this red surface is 
 mottled with white dots— the miliary tubercles. In the pleural cavity is 
 bloody serum. 
 
 2. The pleura is thickened, it is thickly coated with fibrin, no tuber- 
 cles are visible to the naked eye; the pleural cavity contains clear serum. • 
 
 3. The pleura is thickened and the pleural cavity contains purulent 
 serum. 
 
 In all the cases, the changes in the pleura itself are essentially the 
 same. The thickened pleura is infiltrated with new connective-tissue 
 cells. Scattered through its entire thickness are tubercle granula, either 
 single or joined together by difEase tubercle tissue. The smaller blood- 
 vessels show a growth of their endothelial cells. 
 
 New Growths. 
 
 Fibroma. — Little white or pigmented fibromata of the size of a pin's 
 head are often present in the pulmonary pleura. 
 
 Larger fibrous tumors are formed in the deeper layers of the costal 
 pleura, and project into the pleural cavity. They may become detached 
 and are then found loose in the pleural cavity (Lebert). 
 
 Lipoma. — Patty tumors are formed beneath the costal pleura, and 
 project into the pleural cavity (Lebert). 
 
 Carcuiomata, Sarcomata, and LympJwmata are usually secondary to- 
 similar tumors in other parts of the body. 
 
 A peculiar form of primary new growth in the pleura has been de- 
 scribed by several observers.' It is associated with a pleurisy, with the 
 production of fibrin and serum. There is a difEuse thickening of the 
 costal pleura, or circumscribed nodules of different sizes. 
 
 The new growth seems to begin in the lymphatics of the pleura, which 
 are distended with flat, nucleated cells. 
 
 I (Delafield) have seen two of these cases. The first case was a 
 woman, fifty-three years old, who was ill with the symptoms of pleurisy, 
 with effusion, for four months. After death, the left pleural cavity was 
 found to be fall of bloody, purulent serum. The costal i-)leura was 
 moderately thickened and coated with a layer of fibrin and pus. Beneath 
 the fibrin and pus was a thin layer of granulation tissue. In tliis tissue 
 and in the pleura were anastomosing tubules filled with flat, nucleated 
 cells. The tubules looked like lymphatics. 
 
 The second case was a man, sixty-three years old, who had the symp- 
 toms of pleurisy with effusion, for four months. After death, the right 
 pleural cavity was found half full of bloody serum. The costal, 
 diaphragmatic, and pulmonary pleura were coated with fibrin, and con- 
 
 ' Bh-ch-Hirschfeld, Path. Anat., p. 768. E. Wagner, Arch. d. Heilkunde, xL 
 E. Schulz, Arch. d. Heilkunde, xv. Thierfelder, Atl. d. path. Hist., 4 Lief. 
 
THE EESPntATOET SYSTEM. 217 
 
 tained numerous white nodules, some of them as large as a pigeon's egg. 
 These nodules were formed of a connective-tissue stroma inclosing ir- 
 regular spaces and tubules filled with flat, nucleated cells. 
 
 It is very difficult to class these tumors; whether to call them by the 
 name of Carcinoma, Sarcoma, or Endothelioma is not easy to say. 
 
 THE BEONCHI. 
 
 Inflammation. 
 
 Acute Catarrhal Bronchitis is a disease of very common occurrence, 
 but one which seldom proves fatal. Our knowledge of its lesions is de- 
 rived from severe cases, from cases which are complicated by other dis- 
 eases, and from the symptoms which we observe during life. 
 
 The inflammation involves regularly the trachea and the larger and 
 medium-sized bronchi, less frequently the smaller bronchi also. As a 
 rule, the bronchi in both lungs are equally affected. 
 
 The first change seems to consist in a congestion and swelling of the 
 mucous membrane, with an arrest of the functions of the mucous glands. 
 This is attended with pain over the chest, a feeling of oppression, some- 
 times spasmodic dyspnoea, and a dry cough. After this, the mucous 
 glands resume their functions with increased activity, the congestion 
 diminishes, there is an increased desquamation of epithelium, an in- 
 creased formation of the deeper epithelial cells, and a moderate emigra- 
 tion of white blood-globules. Sometimes the red blood-globules also 
 escape from the vessels. The patient now has less pain and oppression, 
 the cough is accompanied with an expectoration of mucus mixed with 
 epithelium, pus, and sometimes blood. 
 
 After death the only lesions visible are the increased amount of 
 mucus, the growth of new epithelium, a few pus-globules infiltrating the 
 stroma, and the general congestion of the mucous membrane. The 
 whole process is a superficial one, not producing any changes in the walls 
 of the bronchi beneath the mucous membrane. 
 
 When the inflammation involves the smaller bronchi also, they may be 
 full of pus, but their walls are unchanged. 
 
 The filling of the small bronchi may result in the collapse of the 
 groups of air-vesicles to which they lead, and thus are produced areas of 
 atelectasis, which may be further changed by inflammatory processes. 
 
 Acute, intense, general Bronchitis, Capillary Bronchitis. 
 
 This is for convenience described here as a separate lesion, although 
 it is really almost always a broncho-pneumonia, from the extension of the 
 inflammation to the air-vesicles. 
 
 The trachea, and most of the bronchi are inflamed. In the trachea 
 and larger bronchi the inflammation is simply catarrhal, but in the 
 smaller bronchi there are other changes. Their walls are thickened and 
 
218 THE EESPIEATOBT SYSTEM. 
 
 infiltrated with cells, their cavities may be dilated, the air-vesicles snr- 
 rounding these bronchi are intensely congested or contain fibrin and pus. 
 Areas of atelectasis may be produced by the plugging of small bronchi. 
 The entire lung is large, heavy, and congested, and there may be fibrin 
 on the pulmonary pleura. 
 
 Such a general bronchitis is a very serious lesion, often causing death. 
 It is usually complicated by peri-bronchitic pneumonia and often by dif- 
 fuse pneumonia. 
 
 Chronic catarrhal Bronchitis. — This form of bronchitis may be the 
 sequel of one or more attacks of acute bronchitis. More frequently it is 
 associated with emphysema, heart disease, interstitial pneumonia, phthi- 
 sis, pleuritic adhesions, or the inhalation of irritating substances. 
 
 There is, in most cases, a constant production of mucus, pus, and 
 serum in considerable quantities, and these inflammatory products may 
 have a very foul odor. Less frequently these products are very scanty — 
 dry catarrh. ^ 
 
 In examining the bronchi in these cases after death, we are often 
 struck by the want of proportion between the symptoms and the lesions. 
 The same bronchi, which during life were constantly producing large 
 quantities of inflammatory products and injuring the patient's health, 
 after death may be but little changed from the normal. In other cases, 
 however, the lesions are more marked. 
 
 The bronchi contain mucus and pus, they may be congested, their 
 walls are often trabeculated. The epithelium is deformed and desqua- 
 mating, with a production of new cells in the deeper layers. The 
 mucous glands are enlarged. The connective-tissue stroma is thickened 
 and infiltrated with cells. There may be cylindrical dilatation of one or 
 more bronchi. Very frequently the epithelial cells of the air- vesicles and 
 air-passages are increased in size and number. 
 
 Acute croupous Bronchitis occurs as a lesion of diphtheria, as associated 
 with croupous laryngitis, as the result of the inhalation of hot steam, 
 with lobar pneumonia, and sometimes as an idiopathic disease. 
 
 The bronchi are lined or filled with a mass of fibrin, pus, and de- 
 squamated epithelium. Fibrin and pus may also be found beneath the 
 epithelium and infiltrated in the stroma. 
 
 Chronic croupous Bronchitis is attended with the formation in one or 
 more bronchi of masses of fibrin which are expectorated by the patient 
 in the form of branching casts of the bronchi. The disease is a very 
 chronic one, and is often associated with phthisis. After death the 
 bronchi are said to be found but little altered from the normal. 
 
 Broncldectasia. 
 
 Dilatation of the bronchi presents itself under three forms: the cylin- 
 drical, the fusiform, and the sacculated. 
 
THE EESPIEATOEY SYSTEM. 219 
 
 The cylindrical dilatation is a uniform enlargement of one or more 
 bronchi for a considerable part of their lengths. It is found in bronchi 
 of every size, but most frequently in the medium sized. 
 
 The fusiform dilatation is a mere variety of the cylindrical. The 
 bronchus is uniformly dilated for a short distance, and then resumes its 
 natural size. Several such dilatations may be found in the same bronchus. 
 
 The sacculated dilatations form the largest cavities. These cavities 
 communicate with one side of the bronchus, the peripheral portion of 
 the bronchus may be obliterated. The bronchus leading to the cavity 
 may be of normal size, or dilated, or stenosed, or even completely oblite- 
 rated. Such sacculated dilatations may reach a very large size, and may 
 communicate with each other. 
 
 Any inflammatory process which involves the thickness of the wall of 
 a bronchus seems to be capable of producing dilatation of that bronchus. 
 
 In acute general bronchitis and broncho-pneumonia in children, 
 cylindrical dilatation of a number of the medium-sized bronchi is often 
 produced. 
 
 In the persistent broncho-pneumonia of children, such dilatations 
 reach a still greater development. 
 
 In acute and chronic phthisis, tubercular inflammation gives rise to 
 sacculated dilatations, which expand with time and are made still larger 
 by the destruction of the adjacent lung tissue. 
 
 Chronic bronchitis may lead to cylindrical or sacculated dilatations, 
 sometimes of great size. 
 
 The walls of these dilatations may preserve the characters of the wall 
 of the bronchus more or less altered by inflammation, or these characters 
 may be altogether lost. The dilatations may contain mucus and pus, or 
 they may be empty. 
 
 New Growths. 
 
 Ossification of the walls of the bronchi is sometimes found. 
 
 Lipoma in the submucous connective tissue has been described by 
 Eokitansky. 
 
 Carcinoma of the walls of the bronchi may occur as a secondary le- 
 sion, but as a primary growth it is very rare. 
 
 Langhans' describes a primary carcinoma of the lower end of the 
 trachea, and the large bronchi in a man forty years old. The lower end 
 of the trachea and the large bronchi showed a general thickening of their 
 walls with flat tumors projecting inwards. The new growth was com- 
 posed of a stroma inclosing cavities filled with cells. The cells were 
 small, nucleated, polygonal or cylindrical in shape and packed closely to- 
 gether. Apparently the new growth originated in the mucous glands. 
 
 ' Virohow Arch., liii., p. 470. 
 
220 THE RESPIEATOEY SYSTEM. 
 
 I (Delafield) have seen one case of new growth of the lower end of the 
 trachea and large bronchi, which I hardly know how to name. The pa- 
 tient was a woman, twenty-seven years old, who suffered for seven months 
 from cough, constantly increasing dyspncea, and progressive emaciation. 
 After death , the wall of the lower end of the trachea was found to be thick- 
 ened. Its inner surface Avas studded with minute papillary outgrowths. 
 The epithelial cells were increased in size and number, and in some places 
 were replaced for considerable spaces by a regular layer of pavement 
 epithelium. The mucous glands were hypertrophied. The wall of the 
 trachea from the basement membrane to the cartilages was thickened by 
 new connective tissue. 
 
 The walls of the large bronchi were very much thickened and their 
 cavities nearly obliterated. The entire wall was thickened with new 
 connective tissue. The epithelial layer was thickened, and in places re- 
 placed by patches of pavement epithelium. The' mucous glands were 
 enlarged . 
 
 Sarcomata of the walls of the bronchi occur as secondary growths, and 
 as prolongations of similar growths in the mediastinum. 
 
 Primary sarcoma of the bronchi seems to be rare. 
 
 Hesse' describes a form of lympho-sarcoma, forming nodules around 
 the bronchi, as of common occurrence among the miners in some cobalt 
 and nickel mines. 
 
 THE LUNGS. 
 
 Malformations. 
 
 One or both lungs may be entirely wanting, or only partially devel- 
 oped. In some of the cases with only one lung the patients have grown 
 up to adult life. 
 
 A peculiar degeneration, by which the lung is converted into a num- 
 ber of sacs containing air and serum, the sacs communicating with the 
 bronchi, has been seen in a few instances. 
 
 The lobes may be subdivided by deep fissures. An accessary lobe, 
 separated from the lung, between the base of the left lung and the dia- 
 phragm has been described by Kokitansky. 
 
 There may be hernia of the lung, with absence of part of the wall of 
 the thorax. 
 
 There may be transposition of the lungs, with similar changes in the 
 position of the heart and the abdominal viscera. 
 
 Injuries. Perforations. 
 
 Severe contusions of the thorax may produce rupture of the lungs, 
 with extravasation of blood into the pleural cavities. 
 
 The lungs may be wounded by a fractured rib, and by penetrating 
 
 ' Arch. f. Heilkunde, xix., p. 160. 
 
THE EESPIEATOEY SYSTEM. 221 
 
 weapons and projectiles. Such injuries often produce bleeding into the 
 lung tissue and inflammatory changes. The lungs, however, exhibit a 
 considerable degree of tolerance for such injuries, and the patients often 
 recover. 
 
 Collections of pus in the pleural cavities, the mediastinum, the liver, 
 the spleen, the kidneys, and the peritoneal cavity may perforate the 
 lungs. 
 
 Congestion and (Edema. 
 
 These two conditions are regularly associated with each other in the 
 lungs, although one or the other of them may preponderate in different 
 cases. 
 
 A moderate degree of congestion and oedema of the posterior portions 
 of the lungs is often found as a result of post-mortem changes. 
 
 In persons who have been comatose from any cause for some hours 
 before death, congestion and oedema of the lungs are regularly developed. 
 
 With disease of the heart, kidneys and lungs, the congestion, and es- 
 pecially the oedema, may be excessive. The lungs may be so completely 
 infiltrated with serum as to be unaerated. Such a solid oedema of the 
 lungs is sufficient of itself to cause death. It has been asserted by Welch' 
 that the cause of such an excessive oedema is a paralysis of the left side 
 of the heart, while the force of the right heart is unimpaired. Such an 
 ■explanation seems to be plausible. 
 
 Patients confined to bed for a considerable length of time may develop 
 congestion of the dependent portions of the lungs — hypostatic congestion. 
 The affected portion of lung is shrunken, congested, and imperfectly 
 aerated. 
 
 Hemorrhage. 
 
 Extravasations of blood within the air-cavities are found with the 
 general diseases which produce a disposition to bleeding in different parts 
 of the body. 
 
 Blood from the bronchi or from cavities may be inspired into the air- 
 vesicles. 
 
 Valvular lesions of the heart, especially of the mitral valve, are often 
 iicoompanied by the production of hemorrhagic infarctions in the lungs. 
 These infarctions are circumscribed, of rounded or wedge-shaped form, 
 from the size of a walnut to that of an orange. They are of dark-red 
 color, unaerated, the air-passages distended with blood, and are often 
 surrounded by a zone of pneumonia. They may be situated in any part 
 of the lungs, but are most common in the lower lobes. When they are 
 near the surface of the lungs, a circumscribed pleurisy is often produced. 
 
 Such infarctions may produce death; they may become gangrenous, 
 
 ' Virchow's Archiv, 73. 
 
222 THE RESPIEATOBY SYSTEM. 
 
 or the blood may become absorbed, or they may be gradually changed 
 into a smaller mass of pigmented fibrous tissue. 
 
 It is probable that these infarctions are produced either by thrombo- 
 sis of branches of the pulmonary artery, or by rupture of the capillaries. 
 
 Infarctions of smaller size, and with more disposition to be surrounded 
 by inflammatory changes, are produced by emboli from the right side of 
 the heart, and from thrombi in the veins of pysemic patients. These in- 
 farctions are usually situated near the surface of the lung. 
 
 Hemorrhages with rupture of the lung-tissue are produced by severe 
 contusions, by penetrating wounds, and by the rupture of aneurisms. 
 
 Emphysema. 
 
 Emphysema is of two kinds — vesicular and interlobular. 
 
 1. Vencular Emphysema is a permanant dilatation of the air-pas- 
 sages and vesicles of the lung. 
 
 A temporary dilatation of the air-passages and vesicles may be pro- 
 duced in a variety of ways. The bronchi may be partially obstructed, 
 so that the air does not readily escape, and the lungs are found unnaturally 
 inflated after death. Part of the lungs may be rendered solid by pneumo- 
 nia, oedema, or compression; and the rest of the lung is dilated. For 
 some reason, death may take place with the lungs excessively dilated, 
 and this condition remains after death. None of these conditions con- 
 stitute true emphysema. 
 
 Permanent dilatation of groups of air-vesicles often accompanies 
 chronic phthisis and is then one of the lesions of that disease. 
 
 In true emphysema, the lesions are dif£use,^involving the whole of 
 both lungs. The lungs are large, often overlapping the heart and liver, 
 sometimes pushing down the diaphragm. The air-vesicles and air-pas- 
 sages are so much dilated that they are readily seen with the naked eye, 
 or several of them may be fused together, so as to form cavities of some 
 size. The lungs may be pale and anaemic, or congested, or oedematous. 
 
 The walls of the air-vesicles are often thinned, and this atrophy may 
 go on to complete absorption of the walls, so that a number of vesicles are 
 converted into a common cavity. But, instead of these changes, the 
 walls of the vesicles may remain of normal thickness, or may even be 
 thickened. It is said that the capillaries in the walls of the vesicles be- 
 come obliterated and degenerated, but this is certainly not always the 
 case. We have frequently made complete artificial injections of the ves- 
 sels and found all the capillaries intact, although sometimes small and 
 with the spaces between them increased in size. There must, however, 
 always be some mechanical obstruction to the circulation of the blood 
 through emphysematous lungs, as evidenced by the venous congestion 
 which is produced in other parts of the body. 
 
 The bronchi are regularly the seat of chronic catarrhal inflammation. 
 
THE EESPIEATOEY SYSTEM. 223 
 
 Thickening of the pulmonary pleura, pleuritic adhesions, and bands of 
 fibrous tissue penetrating the lung are often found; and chronic miliary 
 tuberculosis is not infrequently added to the other lesions. 
 
 When there is much bronchitis, a chronic pneumonia often exists, 
 with the production of new epithelial cells on the walls of the Tesicles; 
 not, however, in sufficient numbers to fill their cavities. 
 
 The secondary lesions of emphysema are very important; they are 
 due to the difficult passage of the blood through the lungs. 
 
 The capillaries of the pia mater may be dilated and tortuous, the pia 
 itself thickened, and an increased amount of serum present beneath the 
 pia. 
 
 The right ventricle of the heart may be dilated, with or without hyper- 
 trophy. The liver and the kidneys may be in the condition of chronic 
 congestion. 
 
 Very often we find, as associated lesions, chronic endocarditis, endar- 
 teritis, cirrhosis of the liver, and atrophied kidneys. 
 
 Interlobular emphysema is not usually a lesion of much importance. 
 It occurs most frequently with whooping cough. In rare cases, there is 
 rupture of the pulmonary plura and pneumothorax, or the air may pass 
 into the mediastinum, and from thence into the neck, producing general 
 subcutaneous emphysema. 
 
 A remarkable case of interlobular emphysema and inflammation of 
 the interlobular septa in a child after whooping-cough is described by 
 Dr. W. P. ISTorthrup.^ 
 
 Atelectasis. 
 
 A collapsed and unaerated condition of portions of lung-tissue is 
 either congenital or acquired. 
 
 (1.) In congenital atelectasis, portions of the lung are firm, non-crepi- 
 tant, of a dark-blue or purple color, depressed and smooth on section. 
 These portions can usually be artificially inflated, and then cannot be 
 distinguished from the surrounding pulmonary tissue. This condition is 
 produced by the inability of the child after birth to fully inflate its lungs, 
 either from want of sufficient vitality or from obstruction of the bron- 
 chi. If the child lives for some time and tlie collapsed lobules are not 
 inflated, they become hard and dense. 
 
 (2.) In young children, the smaller bronchi may become obstructed 
 by the inflammatory products of bronchitis, and the corresponding air- 
 vesicles will then collapse. We then find scattered through the lungs 
 collapsed lobules like those in the new-born child. Inflammatory changes 
 may be subsequently developed in the collapsed lobules. 
 
 (3.) In adults, large or small portions of lung-tissue may become col- 
 
 ' American Journal of Medical Sciences, July, 1883. 
 
224 THE EESPIEATOET SYSTEM. 
 
 lapsed as the result of bronchitis, of stenosis of a large bronchus, of com- 
 pression of a bronchus, of paralysis of the pneumogastric, of compression 
 of the lungs by fluid or by new growths, and of long-continued feeble- 
 ness of the act of respiration. 
 
 Gangrene of the Limgs. 
 
 It is customary to distinguish two forms of gangrene of the lung: the 
 circumscribed and the diffuse; yet both can occur together. 
 
 Circumscribed gangrene occurs in the form of one or more rounded 
 or irregular masses of variable size. The gangrenous portion of lung 
 is at first brown and dry. The surrounding lung-tissue is congested, or 
 cedematous, or infiltrated with blood, or inflamed. If the gangrenous 
 focus is near the pleura, the latter will be coated with fibrin. Gradu- 
 ally the gangrenous portion of lung assumes a dirty-green color and a 
 putrid odor. It becomes soft, broken down, and separated from the sur- 
 rounding lung. The blood-vessels may be obliterated by thrombi, or 
 eroded, so that there are profuse hemorrhages. 
 
 Such a gangrenous process may extend to the adjacent lung tissue, or 
 a zone of gray or red hepatization or of connective tissue may be formed. 
 
 The fluid from the gangrenous lung may pass into the bronchi and 
 be expectorated; or it may run from one bronchus into another, and set 
 up new gangrenous foci, or a diffuse gangrene. 
 
 The pulmonary pleura may be i^erforated, and a gangrenous pleurisy 
 produced. 
 
 Diffused gangrene may follow the circumscribed form; it may com- 
 plicate lobar pneumonia, or occur as an idiopathic condition. A large 
 part of a lobe or of an entire lung becomes greenish, putrid, and soft, 
 and the pulmonary pleura is inflamed. There may be hemorrhages from 
 eroded vessels. There may be general septicaemia. 
 
 Inflammation. 
 
 The word 'Pneumonia' is employed as a general term, to designate 
 all the inflammations of the lungs. Anatomically, there are five varie- 
 ties of pneumonia: intra-alveolar pneumonia, interstitial pneumonia, 
 broncho-pneumonia, syphilitic pneumonia, and tubercular jineumonia. 
 The terms croupous and catarrhal should not be applied to designate any 
 of the inflammations of tlie lung-tissue. 
 
 For practical purposes, it is more convenient to divide the cases of 
 pneumonia into clinical groups. "We will, therefore, describe: 
 
 Lobar jDneumonia. 
 
 Secondary and complicating pneumonia. 
 
 The pneumonia of heart disease. 
 
 Broncho-pneumonia. 
 
 Interstitial pneumonia. 
 
THE KESPIEATOEY SYSTEM. 225 
 
 Syphilitic pneumonia. 
 Acute miliary tuberculosis. 
 Clironic miliary tuberculosis. 
 Acute phthisis. 
 Chronic phthisis. 
 
 /. Acute Lobar Pneumonia. 
 
 The inflammatory process is from the first a diffuse one, involving 
 the greater part of one or more lobes. The situation of the inflamma- 
 tion can be seen from the following figures compiled by Juergensen from 
 6,666 cases: 
 
 Eight lung, 53.7^. Left lung, 38.23^. 
 
 Upper lobe, 13.15^. Upper lobe, 6.96^. 
 
 Middle lobe, 1.77^. Lower lobe, 22.73^. 
 
 Lower lobe, 22.14^. Whole lung, 8.54^. 
 
 Whole lung, 9.3o^. 
 
 Both lungs, 8.07^. 
 
 Both upper lobes, 1.09^. 
 
 Both lower lobes, 3.34^. 
 
 In rare cases, nearly the whole of both lungs will become inflamed at 
 the very onset of the disease. 
 
 The inflammatory process involves regularly the air-vesicles, the air- 
 passages, the bronchi, the interstitial connective tissue, and the 
 pulmonary pleura. It passes through four stages: congestion, red hepa- 
 tization, gray hepatization, and resolution. 
 
 (1) Congestion. — The affected portion of lung is somewhat swollen 
 and dense, congested, and (Edematous. The air-spaces contain granules, 
 reticulated fibrin, pus-cells, red blood-cells, and epithelial cells. The 
 quantity of these inflammatory products, however, is very small — not 
 sufiicient to fill the air-spaces. The epithelial cells on the walls of the 
 air-vesicles are swollen, the capillary plexus contains a large number of 
 white blood-cells. 
 
 This first stage of congestion lasts usually only a few hours ; from 
 clinical experience it seems probable that it may last for one or two days. 
 It is succeeded by 
 
 (2) Red Hepatization. — The affected portion of lung is now com- 
 pletely solid and unaerated. It is also increased in size, often so much 
 increased as to compress the tininfiamed lobe of the same lung, to push 
 downward the diaphragm, or to give the surface of the lung an imprint 
 of the ribs. The cut surface of the lung is of a uniform red color, or 
 mottled with hemorrhagic spots. When fresh, it is dry and granular; as 
 decomposition commences, it is covered with a thick, reddish fluid. The 
 granules are plugs of inflammatory matter contained in the air-spaces. 
 
 15 
 
226 
 
 THE EESPIEATOET SYSTEM. 
 
 The pulmonary pleura is coated with fibrin, and there may be a little 
 serum in the f)Ienral cavity. 
 
 The air-vesicles and air-passages are distended with fibrin, pus, epithe- 
 lium, and red blood-globules (Fig. 81). The fibrin is coagulated in the 
 form of a network or of granules; it is most abundant in the most severe 
 
 Fig. 81. — Lobar Pneumonia, Red Hepatization, X 850 and reduced. 
 A single air-vesicle with its blood-vessels artificially injected. 
 
 cases. The pus-cells are numerous, the epithelial cells but few. The small 
 bronchi are filled with pus and fibrin. The larger bronchi are lined or 
 filled with fibrin and pus, or their mucous membrane is congested and 
 coated with mucus. The interstitial connective tissue is infiltrated with 
 fibrin and pus. 
 
 In my own experience, about one-fourth of all the fatal cases have 
 died in the stage of red hepatization at periods varying between twenty- 
 four hours and eleven days. 
 
 (3) Oray Hejmtization. — Red hepatization gradually changes into 
 gray hepatization, not uniformly, but in such a way that the lung is first 
 mottled red and gray, and then completely gray. 
 
 The surface of a section of the lung is usually dry, as in red hepatiza- 
 
THE EESPIKATOET SYSTEM. 227 
 
 tion, but in some cases, even within one hour after death, there is an 
 abundant exudation of grumous fluid. This dejDends upon the small 
 amount of fibrin and the large amount of pus, not upon an infiltration 
 of the lung-tissue with pus. 
 
 The change in the color of the lung is due to the diminished conges- 
 tion and the loss of color of the extravasated red blood-globules. 
 
 The products of inflammation within the air-spaces are the same as 
 in red hepatization, but they are more closely packed together, the walls 
 of the vesicles are more compressed, the epithelial cells and pus-cells are 
 swollen and infilti'ated with granules and small fat-globules. 
 
 I have found the condition of mottled red and gray hepatization in 
 about one-half the fatal cases at from the second to the eighteenth day 
 of the disease; the condition of complete gray hepatization, in about one- 
 fourth of the cases, from the fourth to the twenty-fifth day of the disease. 
 
 (4) Resolution. — If the jaatients recover, the lung passes from the 
 condition of gray hepatization into that of resolution. In this condition 
 the lung seldom comes under observation, but occasionally the patients 
 die from some complicating condition. 
 
 In such cases of commencing resolution, we find that the disappear- 
 ance of the inflammatory products occurs in many separate places, so that 
 the lung is mottled with areas of comiDlete and incomplete hepatization, 
 and aerated lung tissue. The fibrin seems to be absorbed, the pus and 
 epithelium to degenerate; and partly by expectoration, partly by absorp- 
 tion, the air-spaces become cleared of all inflammatory products. 
 
 in the regular cases, the walls of the bronchi and of the air-spaces re- 
 main unchanged, so that when the patients have recovered, and the pro- 
 ducts of inflammation have been absorbed, the lungs return to a normal 
 condition. 
 
 Modifications of the Inflammatory Process. 
 
 (1) The lung may remain in the condition of gray hepatization for several 
 weeks without any attempt at resolution. It then becomes very firm, dry 
 and white. The air-vesicles remain filled with fibrin, pus, and epithelium. 
 
 (2) In lungs which are already the seat of emphysema and chronic 
 bronchitis, lobar pneumonia is characterized by the presence of an un- 
 usual number of epithelial cells. 
 
 (3) The quantity of fibrin produced may be so great that the walls of 
 the vesicles are compressed, the blood ceases to circulate in them, and 
 even an artificial injection does not fill the vessels. 
 
 In rare cases, such a compression of the vessels is followed by the 
 death of small portions of lung-tissue. These necrotic portions become 
 separated from the surrounding lung, which is infiltrated with pus and 
 in this way abscesses are formed. 
 
 (4) The pus-cells may not only be present within the air-spaces, but 
 they may also infiltrate to a moderate extent the walls of the air-vesicles. 
 
228 THE EESPmATOEY SYSTEM. 
 
 (5) In rare cases the air-vesicles, instead of being filled with the ordi- 
 nary inflammatory products, contain organized connective tissue with 
 basement substance and cells, and new blood-vessels which can be arti- 
 ficially injected. 
 
 (6) The inflammation of the larger bronchi may be unusually devel- 
 
 ^^Q 
 
 
 '-£1- 
 
 t 
 
 r 
 
 
 TC\^ 
 
 j«V«S=^^^/"" i/^Xj 
 
 / 
 
 \ ^^ . 
 
 Fig. 82, — Acute Lobak Pneumonia -with the Production of Organized Tissue in the 
 
 Air-Spaces, X 130 and reduced. 
 
 Section of a number of air-vesicles containing organized tissue. 
 
 oped; either catarrhal inflammation with the production of a large amount 
 of mucus, or croupous inflammation with large cords of fibrin. 
 
 (7) The inflammation of the pleura may be unduly developed, either 
 during the progress of the pneumonia, or while it is subsiding. Both the 
 pulmonary and costal pleura are then coated with fibrin, and there is a 
 considerable amount of serum in the pleural cavity. 
 
 (8) There may be gangrene of portions of the inflamed lungs. 
 
 The presence of a characteristic form of micrococci in lobar pneu- 
 monia has been detei-mined by numerous observers. First described by 
 Klebs,' they have been observed by Eberth,' Koch,'' Fried! an der,* Leyden, 
 
 ' Klebs, Arch. f. exp. Path., 1877, Bd. iv., p. 420. 
 ^Eberth, Deutsch. Arch. f. klin. Med., Bd. 28, 1881. 
 » Koch, Mitt. a. d. k. Gesundheits-Amt, Bd. I., p. 1, 1881. 
 
 ^ Friedlaader, Virch. Arohiv, Bd. 87, 1882 ; also, Fortschritte der Medicin, Bd. 
 I., No. 22, 1883; Bd. II., No. 10, 1884. 
 
THE EESPIEATOET SYSTEM. 
 
 229 
 
 and many others. Recording to Priedliinder, whose researches on this 
 subject have been most exact and extensive, these micrococci are con- 
 stantly present in the lungs in the earlier stages of the disease, sometimes 
 in very large numbers. They are spheroidal or ellipsoidal in shape, some 
 ■of them nearly 1 ;u in the longest diameter, frequently are joined together 
 
 
 Fig. 83.— Orgakized Tissue in an Aie-Vesicle, X 830 and reduced. 
 
 in pairs, sometimes in chains of three or four. They are sometimes, but 
 not always, surrounded by a broad mucin-like capsule. They are found 
 not only in the exudation in the lung after death, but they may be de- 
 tected in the sputum,' and have been found by Giinther and Leyden' in 
 the sanguinolent fluid drawn from the consolidated lung mifra Wi'toii, with 
 an hypodermic needle. 
 
 Pure cultures of the micrococci have been made, especially by Fried- 
 lander, who found that they grew in characteristic form in gelatinized 
 bouillon. 
 
 ' Ziehl, Centrbl. f. d. med. Wiss., 1883, No. 35, and 1884, No. 7. 
 
 ' Gtinther and Leyden, Deutsch. med. 'Wochenschr., Bd. 9, p. 4, 1883. 
 
230 THE KESPEBATOET SYSTEM. 
 
 Inoculation of the jjure cultures in Friedlander's experiments gave 
 markedly different effects in different animals. Injections of the pure 
 cultures, diffused through distilled water, into the lungs of thirty-two 
 mice regularly produced death in from eighteen to twenty-eight hours. 
 After death the pleural cavities contained turbid fluid, the lungs were red, 
 nearly empty of air, and contained scattered areas of red consolidation. 
 The spleen was swollen dark red, other organs normal. The character- 
 istic micrococci were found in the fluid in the pleural cavity, in the exuda- 
 tion, in the lung, and in the blood. In dogs and guinea-pigs, the results 
 were inconstant and not so pronounced, while in rabbits the inoculations 
 were negative. There was considerable difference in the size of the micro- 
 cocci as found in man and in animals as a result of the inoculation of 
 pure cultures. 
 
 While the above experiments and observations would tend to confirm 
 the belief in the infectious nature of lobar pneumonia, we cannot con- 
 sider them as yet sufficiently definite and extensive to prove it.' 
 
 The micrococci may be stained in anilin-gentian-violet solution, dif- 
 ferentiated by dilute iodine solution by Gram's method (see p. 90), and 
 mounted in balsam. This method is applicable both to sections of tissue, 
 and to fluids dried on to the cover-glass. 
 
 Ziehl recommends, for the staining of the pneumonia micrococcus in 
 sputum, an aqueous solution of gentian-violet, and the examination of 
 the stained specimen in water. 
 
 //. Secondary and Complicating Pneumonia. 
 
 Inflammation of the lungs occurs frequently as a complicating condi- 
 tion with lesions of the brain and spinal cord, with pyaemia, with the 
 continued fevers, after injuries and surgical operations, and in patients 
 who are confined to bed for a long time from any cause. 
 
 The pneumonia developed in these cases may follow one of two dif- 
 ferent types. 
 
 (1) Part of the lung, usually the posterior portion, is congested, leath- 
 ery, only partly aerated, and mottled by irregular patches of red or gray 
 hepatization which have no relation to the bronchi. In the hepatized 
 portions of lung, the air-spaces are filled with pus and fibrin. 
 
 (3) The inflammation has the characters of a broncho-pneumonia. 
 The small bronchi are filled with pus, their epithelium is altered, their 
 
 ' Considerable bibliography regarding the infectious nature of pneumonia may 
 be found in an article on the subject by Mendelson in Zeitschrift fiir klin. Med.,. 
 Bd. 7, p. 178, 1884. See also the discovery of pneumonia microconci beneath the 
 floors of a prison hospital in which many cases of pneumonia had developed. 
 Emmerich, Fortschritte der Medicin, Bd. 2, No. 5, 1884. 
 
THE EESPIEATOEY SYSTEM. 
 
 231 
 
 walls are infiltrated with ptis, and around each bronchus is a zone of air- 
 vesicles filled with pus and fibrin. The lung is mottled with little whi- 
 tish nodules, corresponding to the bronchi and the peri-bronchitic zones, 
 and between these there may be a difEuse hepatization. 
 
 ///. The Pneumonia of Heart Disease. 
 
 Lesions of the aortic and mitral valves, and dilatation of the left ven- 
 tricle, often produce a diffuse, chronic inflammation of both lungs of a 
 peculiar character. This condition is often called pigment induration 
 or brown induration, but it is really a chronic pneumonia. 
 
 The lungs are diminished in size, and of a peculiar yellowish-pink 
 color, mottled with spots of black or brown pigment. They are not con- 
 gested, but are of a dry, leathery consistence; or portions of them may 
 be in the condition of a smooth red hepatization. The appearance of 
 these lungs may be modified by the presence of hemorrhagic infarctions; 
 by the pre-existence of emphysema; or by oedema. 
 
 Minute examination of these lungs shows four separate pathological 
 conditions. 
 
 ^'^::^M^ 
 
 ^—""s^ 
 
 Fig. 84.— The Pnecmonia Of Heart Disease, X 850 and reduced. 
 An air-vesicle from a child's lung. 
 
 (I) A change in the capillaries in the walls of the air-spaces. These 
 capillaries are dilated and tortuous, so that they project into the cavities 
 of the vesicles. The degree of the dilatation varies in the different 
 lungs; in some it is very marked, in others but slight. 
 
232 THE EESPIEATOET SYSTEM. 
 
 (2) A thickening of the walls of the air-spaces due partly to the dila- 
 tation of the capillaries, partly to a growth of smooth mirscle, and partly 
 to a growth of connective tissue. The degree of the thickening varies 
 very much in different cases. 
 
 (3) A formation of black or brown pigment in the shape of granules 
 and small masses. This is deposited in the walls of the vesicles, in the 
 interstitial connective tissue, and in the new cells within the vesicles. 
 
 (4) A formation of cells within the air-spaces. The walls of the 
 vesicles are coated with a layer of flat, nucleated cells. Similar cells, or 
 swollen and granular cells, are present in the cavities of the vesicles. If 
 these cells are numerous, the cavities of the vesicles are filled, and there 
 results a smooth, red hepatization. 
 
 IV. BroncJw- Pneumonia. 
 
 Whenever the parenchyma of the lung is inflamed, there is regularly 
 some degree of bronchitis present, so that, strictly speaking, every pneu- 
 monia is a broncho-pneumonia. In most of such cases the changes in 
 the bronchi are superficial. Mucus, pus, or fibrin are found on the sur- 
 face of the mucous membrane, the epithelial cells undergo various chan- 
 ges, the mucous glands are swollen, the blood-vessels are congested, but 
 the wall of the bronchus is not changed except by the infiltration of a 
 few pus-cells. 
 
 There are cases, however, in which these superficial changes are ac- 
 companied by inflammation of the entire wall of the bronchus; an inflam- 
 mation which extends directly outwards and involves the air-vesicles 
 surrounding each bronchus. Such an inflammation involves nearly all 
 the bronchi of both lungs, being most intense in the smaller bronchi. 
 The size and number of the zones of peri-bronchi tic pneumonia vary; 
 and the condition of the lung may be farther complicated by the existence 
 of a diffuse pneumonia which has no direct relation to the bronchitis. 
 
 Broncho-pneumonia of this character is very common in children un- 
 der flve years old, as an indiopathic condition and as a complication of 
 other diseases. It is, in fact, the regular pneumonia of childhood, lobar 
 pneumonia being comparatively rare. In adults such a broncho-pneu- 
 monia is not very common. 
 
 Cases of this kind in which the pneumonia is of small extent are often 
 called "capillary bronchitis." 
 
 The trachea and the larger bronchi are congested and coated with 
 mucus. The smaller bronchi contain pus, their walls are thickened and 
 infiltrated with cells, and they may be dilated. Around many of the 
 small bronchi are narrow zones of congestion or heiDatization. The rest 
 of the lungs is congested and cedematous. 
 
 Or the zones of peri-bronchitic pneumonia are larger, so that a 
 
THE EESPIEATOBT SYSTEM. 
 
 233 
 
 section of the lung is mottled with little whitish nodules, each nodule 
 corresponding to a cut bronchus surrounded by its zone of iDneumonia. 
 
 Or between these zones of peri-bronchitic pneumonia are areas of dif- 
 fuse hepatization which render portions of the lung completely solid (Fig. 
 85). 
 
 
 
 J. 
 
 r^ 
 
 
 
 w/- 
 
 
 
 ^-^M- -^ 
 
 -W'-^ ^ 
 
 i) 
 
 ) 
 
 ^3. 
 
 
 
 >; -^' I' 
 
 I ,' 
 
 r- 
 
 ^•^3, 
 
 
 
 J) 
 
 
 'J 
 
 r _. 
 
 Fig. 85.— Broncho-pketjmonia in a Child, X 7S0 and reduced. 
 Air-vesicles in the diffuse hepatization. 
 
 Or there may be areas of atelectasis corresponding to occluded 
 bronchi. 
 
 There is often a thin layer of fibrin on the pulmonary pleura. The 
 bronchial glands are the seat of simple or tubercular inflammation. 
 
 The dilatation of the bronchi is not constant. When present, it is of 
 the cylindrical character and inTolves the medium-sized bronchi for a 
 considerable part of their length. Such dilated bronchi are each of them 
 surrounded by a narrow zone of pneumonia; the intervening lung-tissue 
 may be still aerated or hepatized. 
 
 In these peri-bronchitic zones of pneumonia, the thickening and celhilar 
 infiltration which exist in the walls of the bronchi extend also to the 
 
334 
 
 THE EESPIEATOET SYSTEM. 
 
 walls of the air-spaces (Fig. 86). These walls are thickened and infiltrated 
 Avith cells, while the cavities of the vesicles are filled with pus and epi- 
 thelium, or with tissue resembling granulation tissue. In the diffuse 
 hepatization, the air-vesicles are filled with epithelium, pus, and fibrin in 
 varying proportion and quantity; the walls of the air-spaces remain 
 unchanged. 
 
 The portions of lung which are not hepatized are congested and 
 cedematous. The cavities of the vesicle's are diminished by the enlarged 
 capillaries, the epithelium is swollen, and in many vesicles a few pus or 
 epithelial cells are to be found. 
 
 Such a broncho-pneumonia differs from the ordinary lobar pneumonia 
 very decidedly. The inflammatory process is not a superficial one, resnlt- 
 
 
 
 •5 
 
 A. 
 
 As 
 
 4351. 
 
 ^O^ 
 
 ^ 
 
 
 
 Fig. 86.— BnoNoao-PNEUMONiA in an Adult, X 850 and reduced. 
 Ad air-vesicle containing organized tissue in a zone of peribronehitic pneumonia. 
 
 ing only in filling the bronchi and air-space? with inflammatory products, 
 but it affects also the tissue of the lung, infiltrating the walls of the 
 bronchi and of the air-spaces. 
 
 This interstitial character of the inflammation seems to be the reason 
 why the disease is often protracted and sometimes succeeded by a chronic 
 inflammation. This chronic condition (ve will call ' Persistent Broncho- 
 -Pneumoiiia.' 
 
THE EESPIEATOET SYSTEM. 
 
 235 
 
 The original acute broncho-pneumonia is succeeded by a chronic in- 
 flammation involving especially the interstitial tissue. 
 
 This inflammation may involve only some of the smaller bronchi and 
 small zones of vesicles around them, and then a section of the lung will 
 seem to be studded with fibrous nodules. Or all the bronchi of some 
 part of the lung will be inflamed, the peri-bronchitic zones of pneumonia 
 will become continuous, and so part of a lobe or an entire lobe becomes 
 converted into a dense mass of connective tissue. The air-vesicles are 
 obliterated by the new connective tissue, the interlobular septa and the 
 pulmonary pleura are thickened, and the inflamed bronchi may be di- 
 lated. The blood-vessels, however, are, for the most part, not obliterated, 
 so that the lung does not become necrotic or degenerated, although oc- 
 casionally areas of cheesy degeneration exist. 
 
 V. Interstitial Pneumonia. 
 
 This term is applied to a chronic form of inflammation involving 
 the walls of the air-spaces and of the bronchi, the connective septa, and 
 the walls of the blood-vessels. Permanent new connective tissue, dense 
 and ofteu pigmented, is produced in these situations. The cavities of 
 the air-spaces are deformed and obliterated, and the epithelial cells on 
 
 Fig. 87.— Interstitial Pneumonia of Chronic Phthisis, X 90 and reduced. 
 
 their walls are increased in size and number (Fig. 87). The pulmonary 
 pleura is often thickened and the bronchi dilated. 
 
 Such an interstitial pneumonia forms part of the lesions of broncho- 
 
336 THE EESPIEATOEY SYSTEM. 
 
 pneumonia, of syphilitic pneumonia, and of phthisis. It is often as- 
 sociated with emphysema, with chronic bronchitis, and with pleuritic 
 adhesions. It may be produced by the inhalation of coal-dust and other 
 irritative substances. 
 
 Suppurative interstitial pneumonia is sometimes produced in cases of 
 septicsemia. The pulmonary pleura is coated with fibrin, the bronchi con- 
 tain pus, portions of the lung are hepatized, and the interlobular septa 
 are infiltrated with pus. 
 
 VI. Syphilitic Pnetimotiia. 
 
 Persons suffering from inherited or acquired syphilis sometimes 
 develop inflammations of the lungs which seem to be due to the syphilitic 
 infection. The lungs may then be afEected in several different ways. 
 
 sf 
 
 
 
 
 
 
 M'i 
 
 /.v~>.. 
 
 f& 
 
 1 
 
 
 
 
 "'■Vi 
 
 '^■M. 
 
 
 
 ■ .;> 
 
 '. H 
 
 
 •:••:•.•; ?;;j; 
 
 1 
 
 
 
 o 
 
 
 f;''; ''■:-.'\T ii-'. -■ .'.-'',-;" ' •■■■■<; 
 
 1/ i 
 
 
 Fig. 88.— Interstitial Syphilitic Pneumonia, X 170 and reduced. 
 
 1. There is an interstitial pneumonia beginning around the larger 
 bronchi and blood-vessels at the root of the lung, and extending to the 
 walls of the air-spaces and interstitial connective tissue, so that the central 
 portions of one or both lungs are converted into a dense mass of connective 
 tissue (Fig. 88). 
 
 2. There is an interstitial pneumonia, with the formation of gummy 
 tumors. 
 
THE EESPIEATOET SYSTEM. 237 
 
 3. There is an inflammation of the wall of the trachea and of the larger 
 bronchi. There are ulcers in the mucous membrane, their walls are very 
 much thickened, and their cavities are narrowed. 
 
 4. There are circumscribed areas of interstitial inflammation around 
 the smaller bronchi, forming small, hard, peri-bronchitic nodules. 
 
 5. There is a diffuse hepatization involving lobules, or an entire lobe. 
 The affected portion of the lung is white or grayish. The walls of the air- 
 vesicles are infiltrated with cells, and their cavities are filled with epi- 
 thelial cells. 
 
 6. There may be a broncho-pneumonia, like the ordinary broncho- 
 pneumonia of children; or a lobar pneumonia, like that of adults. 
 
 7. There may be an obliterating endarteritis of branches of the 
 pulmonary artery, with the formation of white infarctions surrounded 
 by zones of connective tissue. ' 
 
 Vn. Acute Miliary Tulerculosis. 
 
 The acute development of miliary tubercles in the lungs is usually only 
 part of general tuberculosis, although the lesion may be most extensive 
 in the lungs. 
 
 Both lungs are usually involved, but the distribution, number, size, 
 and character of the miliary tubercles differ in different cases. 
 
 The larger bronchi are the seat of catarrhal inflammation; the lung- 
 tissue is congested; the air-spaces contain epithelium, pus, and fibrin in 
 small quantity. 
 
 The tubercles are found in the parenchyma of the lung, in the connec- 
 tive tissue forming the septa, along and in the walls of the bronchi and 
 blood-vessels, and in the pulmonary pleura. 
 
 They are scattered singly through the lungs, or aggregated in groups. 
 They may be separated by considerable interspaces, or so close together 
 that the lung is rendered nearly solid. Some are so small and trans- 
 parent that they can hardly be seen with the naked eye; others are larger 
 and more opaque. In children's lungs, large masses are found of the 
 same structure as miliary tubercles. 
 
 When we examine miliary tubercles as they exist in different lungs, it 
 becomes evident that they are not all of the same structure. We find: 
 
 1. Miliary tubercles composed entirely of amorphous granular mat- 
 ter, with a few shrunken cells and an external zone of pus-cells. These 
 cannot be said to have any definite anatomical structure. In some of 
 them, the outlines of the walls of the air-spaces are still visible; in others, 
 they are lost in the cheesy mass. 
 
 2. Miliary tubercles composed of a group of air-spaces of which the 
 walls are infiltrated and the cavities filled (Fig. 89). The walls of the air- 
 spaces are infiltrated with granulation tissue or tubercle tissue; as the in- 
 
 ' Hiller, Charite-Annalen, 1884, p. 184. 
 
238 
 
 THE EESPIEATOET SYSTEM. 
 
 filtration progresses, the blood-vess^s are obliterated. Such an infiltration 
 may involve symmetrically the whole of the wall of an air-space, or only 
 a portion of the wall. The cavities of the air-spaces are filled with tu- 
 bercle-tissue, or with epithelium, fibrin, and pus. 
 
 
 
 Fig. 89.— a Miliary Tobeecle, X 300 and reduced, 
 Involving only two air-vesicles, oi: which the walls are infiltrated and the cavities filled with tuber- 
 cle-tissue. 
 
 In some of these tubercles, the tubercle-tissue, both in the walls of the 
 air-spaces and in their cavities, is well developed (Fig. 90); then they 
 look like little tumors replacing the lung-tissue. In others, the outlines 
 of the walls of the vesicles are preserved, granulation tissue predomi- 
 nates, the cavities of the vesicles contain pus, epithelium, fibrin, and less 
 tubercle-tissue (Fig. 91); then the tubercles look like little areas of a 
 compoi-ite hepatization. 
 
 In adults such tubercles are small, but in children they may reach a 
 large size. 
 
 3. Miliary tubercles, formed by the infiltration of the wall of a bron- 
 
THE EESPIEATOEY SYSTEM. 
 
 239 
 
 chiole or air passage with tubercle-tissue, or granulation tissue. This 
 infiltration is apt to involve only one side of the bronchiole or air pas- 
 sage. It may be confined to this or it may extend to the walls of the ad- 
 jacent vesicles. These vesicles may i-emain empty, they may be dilated. 
 
 
 
 
 1? J 
 
 
 
 
 Si^f 
 
 
 Fig. 90. — A Miliary Tubercle, x 300 and reduced, 
 formed of several air-vesicles filled with tubercle-tissue and surrounded by a zone of granulation 
 
 tissue. 
 
 •or they may be filled with tubercle-tissue or with epithelium, fibrin, and 
 pus. 
 
 4. Miliary tubercles, formed by the infiltration of the walls of small 
 bronchi with tubercle-tissue or granulation tissue. The infiltration 
 ■often extends to the surrounding air-spaces so as to form tubercles of large 
 size. 
 
 In all these miliary tubercles, there is often cheesy degeneration of the 
 central portions. 
 
 Tubercle bacilli can be demonstrated in most of these miliary tu- 
 bercles, especially in those which have undergone cheesy degeneration 
 (Fig. 92). 
 
240 
 
 THE EESPIEATOEY SYSTEM. 
 
 Fig. 91.— a Miliary Tubercle, X 300 and reduced, 
 Formed of a number of air-vesicles, some containing tubercle-tissue, others pus and epithelium. 
 
 . f 
 
 ^ "s 
 
 n ff » ^ * tsT.O * 
 
 
 Fig. 9'3.— Miliary Tubercle in Lung of Child, X 600 and reduced, 
 
 Showing the Bacillus tuberculosis in the contents of the air-vesicles and in their thickened walls. 
 
 (The size of the bacilli relative to other elements is shghtly exaggerated.) 
 
THE EESPIEA.T01JY SYSTEM. 
 
 241 
 
 YIII. Chronic Miliary Tuberculosis. 
 
 This form of tuberculosis is in most cases a local lesion limited to the 
 lungs. Or if other parts of the body — the larynx, the intestines, and the 
 peritoneum — are involved, the lung lesion is still the primary one. 
 
 There are two sets of cases of chronic miliary tuberculosis. 
 
 1. Miliary tubercles scattered singly through the lungs (Fig. 93). 
 
 V^« /» f'/i 
 
 
 Fig. 93.— An Old Miliary Tubercle, X 90 and reduced, 
 converted into fibrous tissue. 
 
 They may be few or numerous; in both lungs, or only in part of one 
 lung. The lungs are regularly the seat of emphysema and chronic bron- 
 chitis, sometimes of bronchiectasise. 
 
 3. Miliary tubercles aggregated in groups and accompanied by a dif- 
 fuse growth of tubercle tissue or connective tissue (Fig. 94). These 
 tubercles also may be confined to the apex of one lung, or may involve 
 a large part of both lungs. Bronchiectasise, often of large size, are very 
 commonly present. The rest of the lung is frequently emphysematous, 
 and the bronchi are the seat of chronic catarrhal inflammation. 
 
 In both these forms of chronic miliary tuberculosis, there are often 
 developed, as secondary lesions, tubercles in the larynx, pleura, perito- 
 neum, liver, spleen, kidneys, and small intestine. In some cases these sec- 
 ondary tubercular lesions are of more importance than the primary lesion 
 of the lung. 
 
 The miliary tubercles are hard and dense. Tbey are formed in the 
 16 
 
24:2 THE KESPntATOKT SYSTEM. 
 
 same situations as acute jmiliary tubercles, and have the same diversity of 
 shape. 
 
 Some are formed entirely of dense connective tissue. 
 
 Some are formed of well-developed tubercle tissue, which infiltrates 
 the walls of the air spaces and fills their cavities. 
 
 Some look as if they had originally been formed of tubercle tissue 
 which had afterwards undergone cheesy degeneration, or been replaced 
 by granulation tissue or connective tissue. 
 
 The difEuse consolidation of the lung between the tubercles is effected 
 partly by a simple, partly by a tubercular interstitial pneumonia. 
 
 M 
 
 
 N, 
 
 / 
 
 
 
 
 i ^•"^s-^J^ ■»" 
 
 
 
 Fig 94 — 1^ ^c recation of Miliary Tubercles X 90 and reduced 
 
 The new connective tissue is formed in the walls of the air-spaces, the 
 bronchi, and the blood-vessels, and in the interlobular septa and pulmo- 
 nary pleura. Much of it is a dense, fibrillated tissue with few cells, but 
 well supplied with blood-vessels. In other places it is like granula- 
 tion tissue. It is often pigmented. The air-spaces are compressed, 
 deformed, and obliterated by the pressure of the new tissue (Pig. 95). 
 
 The tubercle tissue both infiltrates the walls of the vesicles and fills 
 their cavities. It either projects into the cavities as outgrowths from 
 their walls, or is formed within them. It contains very few vessels. 
 
 The combination of these processes results in the solidification of por- 
 tions of the lung. These portions are contracted and dense. They are 
 made up of miliary tubercles, difEuse tubercle, granulation tissue, and 
 connective tissue. 
 
 The cavities so often found in these lungs are sacculated or cylindri- 
 
THE EESPIEATOET SYSTEM. 243 
 
 cal bronchiectasiee, apparently due to a cellular, infiltration of the walls 
 of the bronchi as in broncho-pneumonia. 
 
 
 * ' • f ^, '- "■ SV 
 
 
 Fig. 95.— Diffuse Tubercular Inflammation, x 300 and reduced, 
 producing diffuse consolidation of the lung. 
 
 ZJT. Acute Filth isis. 
 
 This term is used to designate a lesion of the lungs of a very compos- 
 ite character. The air-spaces, the bronchi and the blood-vessels are the 
 seat of a variety of tubercular and inflammatory changes which result in 
 the consolidation of a considerable part of tlie lung. 
 
 After death we find a part of one or of both lungs consolidated, 
 but this consolidation is not of a uniform appearance. Much of it looks 
 like ordinary red hepatization, or the hepatization is of a peculiar grayish 
 color, different from that of lobar pneumonia. In this diffuse hepatiza- 
 tion are other portions of solidified lung of different appearance. They 
 are of white or yellow color, denser than the surrounding hepatization, 
 or softened at their centres. These white nodules are of various size and 
 shape. The smallest are hardly larger than an air-vesicle, the largest 
 include a considerable portion of a lobe. Their size and shape are 
 made more evident by an artificial injection of the blood-vessels, for 
 while the vessels of the diffuse hepatization are easily filled, those of the 
 nodules are not. 
 
 Some of these white nodules are scattered irregularly through the 
 lung like miliary tubercles. Some are situated around the smaller bron- 
 chi. Some correspond to a single air-passage or a group of air-passages. 
 Some are large, and look like a diffuse infiltration, but are really made 
 up of a number of small nodules close together. 
 
2ii THE EESPIEATOEY SYSTEM. 
 
 In some cases, these nodules soften, break down, and form cavities. 
 
 The bronchi of the affected lung are also changed. They may be 
 congested and coated with mucus; they may be filled with pus, epithe- 
 lium, and fibrin, which sometimes undergo cheesy degeneration; they 
 may be the seat of cylindrical or sacculated dilatation. 
 
 We must consider separately the diffuse hepatization, the nodules, 
 and the bronchi. 
 
 (1) The diffuse hepatization. This is of a red color, but smoother 
 than in lobar pneumonia, or gray, or semi-translucent. The walls of the 
 air-spaces are unchanged, their blood-vessels are easily injected. The 
 cavities of the air-spaces are partly or completely filled with inflamma- 
 tory products — fibrin, pus, epithelium, granules, and a transparent, 
 coagulated substance. The epithelial and pus cells are often swollen 
 and filled with coarse granules. 
 
 This diffuse hepatization seems to have no tendency to cheesy degen- 
 eration or necrosis. It is capable of resolution if the patient recovers. 
 
 (2) The nodules. They vary in their size, their shape, and their 
 structure. They are close together or widely separated. Some are sur- 
 rounded by diffuse hepatization, others by nearly normal lung. Even 
 those which present the same appearance to the naked eye are not all of 
 the same nature. 
 
 {a) The smallest nodules are composed of a single air-passage or air- 
 vesicle filled with tubercle-tissue, while the walls of the air-spaces are 
 not infiltrated. 
 
 (b) Other nodules are miliary tubercles, with the variety of position, 
 size, and shape already described. 
 
 (c) Nodules formed around the smaller bronchi. 
 
 Some of these are of the same character as those in broncho-pneumo- 
 nia. The cavity of the bronchus is filled with pus, its walls are infiltrated 
 with cells, around it is a zone of air-vesicles filled with pus, epithehnm, 
 and fibrin, or new connective tissue. 
 
 In others, the peri-bronchitic zone is composed of vesicles filled and 
 infiltrated with tubercle-tissue. 
 
 {d) Nodules composed of a group of air-spaces in the condition of 
 coagulation necrosis (Fig. 96). These nodules seem to be of the same 
 character as the so-called white infarctions, and to be produced by the 
 occlusion of small arteries by obliterating endarteritis. 
 
 These areas of coagulation necrosis are of variable size; their blood- 
 vessels cannot be injected. The outlines of the walls of the vesicles are 
 visible, but are very thin. The cavities of the air-spaces are filled with 
 coagulated fibrin, or with pale, shrunken epithelial cells and shrivelled 
 nuclei. 
 
 Around each area of coagulation necrosis is a zone of air-spaces filled 
 with pus, epithelium, and fibrin, or with tubercle-tissue (Pig. 97). 
 
THE EESPERATOET STSTEM. 
 
 245 
 
 These areas of coagulation necrosis are dead tissue, which can never 
 return to a natural condition. They may undergo cheesy degeneration, 
 or they may soften, break down, and form cavities. 
 
 (3.) The bronchi. 
 
 
 Fig. 96.— An Area op Coagulation Necrosis surrounded by a Zone ow Pneumonia, 
 X 40 and reduced. ' 
 
 The smaller bronchi may undergo cylindrical dilatation, as in bron- 
 cho-pneumonia, as the result of a cellular infiltration of their walls. 
 
 Or there may be tubercular infiltration, with cheesy degeneration of 
 the walls of either small or larger bronchi. This results in the forma- 
 tion of sacculated bronchiectasise, produced partly by the dilatation of 
 ^ bronchus, partly by the destruction of its wall. Such cavities may be 
 rendered still larger by becoming continuous with softened areas of coag- 
 ulation necrosis. 
 
 X. Ghroiiic Phthisis. 
 
 The lesions of chronic phthisis are essentially the same as those of 
 
246 
 
 THE EESPIEATOKT SYSTEM. 
 
 acute phthisis, but yet their slow development and long continuance give 
 them a somewhat different character. We may still distinguish the dif- 
 fuse pneumonia, the nodules, and the changes in the bronchi. 
 
 • (1) The difEuse pneumonia presents a more complicated and varia- 
 ble character than in acute phthisis. 
 
 We find in different lungs and in different parts of the same lung: 
 
 Fig. 97.— Tubercle Tissue around ah Area op Coagulation Necrosis, x 850 and reduced. 
 
 (a) The air-spaces filled with swollen and fatty epithelium (Fig. 98), 
 or with fibrin and pus, while their walls are unchanged and their blood- 
 vessels remain pervious. 
 
 (5) The air-spaces are filled and distended with compact fibrin and 
 shrivelled pus and epithelium. Their walls are compressed and thin, or 
 thickened and infiltrated with cells. The blood-vessels can be only very 
 imperfectly injected. This condition may be succeeded by complete 
 cheesy degeneration. 
 
 (c) The walls of the vesicles are thickened, their cavities are filled 
 with new connective tissue often containing new vessels (Figs. 99 and 100). 
 This new connective tissue may look like an outgrowth from the wall 
 of the vesicle, or as if it was formed free in its cavity. 
 
 (d) There is a diffuse interstitial growth of fibrous tissue and granu- 
 lation tissue in the walls of the air-spaces, the bronchi and the blood 
 
THE BKSPIEATOET SYSTEM. 
 
 247 
 
 Tessels, and in the septa. By this new tissue the air-spaces are com- 
 pressed and deformed or completely obliterated (Fig. 101). 
 
 (2) The nodules. 
 
 These, as in acute phthisis, consist of areas of coagulation necrosis, 
 peri-bronchitic nodules, and miliary tubercles. 
 
 The tubercles may preserve their characteristic structure, or undergo 
 cheesy degeneration, or be changed into fibrous tissue. 
 
 The areas of coagulation necrosis undergo cheesy degeneration, or 
 
 Fig. 98.— Chronic Phthisis, X 850. 
 An air-vesiole filled with fatty epithelium. 
 
 soften and form cavities. They are surrounded by tubercle tissue, or 
 granulation tissue, or connectiye tissue. 
 
 The peri-bronchitic nodules are much the same as in acute phthisis, 
 
 (3) The bronchi. 
 
 The changes in the bronchi in chronic phthisis form a very impor- 
 tant part of the morbid process. 
 
24:8 
 
 THE EESPIEATOET SYSTEM. 
 
 Fig. 99.— Chronic Phthisis, X 850 and reduced. 
 Growth of connective tissue within an air-vesicle. 
 
 
 Fig. 100.— Chronic Phthisis, x 850 and reduced. 
 Growth of connective tissue within an air-vesicle. 
 
THE EESPIEATOET SYSTEM. 249 
 
 (a) The larger bronchi may be the seat of a chronic catarrhal inflam- 
 mation, accompanied by the production of large quantities of mucus and 
 pus. 
 
 (b) The bronchi of all sizes may be inflamed, with the production 
 •of new cells in their walls, in addition to the inflammatory changes of 
 their inner surfaces. Such a cellular infiltration of the walls of the 
 bronchi is often followed by dilatation— either fusiform or sacculated. 
 
 (c) Tubercle granula and granulation tissue are found in the walls 
 •of the bronchi. These tissues may degenerate, soften, and thus form 
 ulcers. 
 
 (d) The entire thickness of the wall of a bronchus may become the 
 
 / 
 
 
 
 I I 
 / 
 
 ' iM 
 
 ir 
 f 
 
 'r ^^'"''^" , ^ ^ 
 
 
 ,^ 3 
 
 9'fmy^-fA 
 
 
 Fig. 101.— Interstitial Pnedmonia as Chhonio Phthisis, X 850 and reduced. 
 
 seat of inflammation of a peculiar charactei*. The surface of the mucous 
 membrane is coated with pus, the epithelial layer can no longer be seen, 
 the wall of the bronchus is infiltrated with cells. The inflammatory 
 products undergo cheesy degeneration, so that we find the inner surface 
 of the bronchus coated with cheesy matter, while its wall is also changed 
 into cheesy matter. Such a condition of the bronchus is usually fol- 
 Jowed by sacculated dilatation. 
 
 The cavities of chronic phthisis, therefore, are formed by the dilata- 
 Tiion of inflamed bronchi, by the softening of areas of coagulation 
 necrosis, or by the combination of both these processes. 
 
250 
 
 THE EESPIEATOET SYSTEM. 
 
 When cavities are once formed, they are apt to continue and to become 
 larger as the disease goes on. Their walls may be converted into granu- 
 lation tissue, which ulcerates in some places and proliferates in others ; 
 or portions of the wall become necrotic ; or all active processes cease and 
 the wall of the cavity is formed of new connective tissue. The lung- 
 tissue between the cavities becomes compressed and altered in various 
 ways. As the cavities increase in size, they touch and open into each 
 other. In this way large portions of the lung may be converted into a 
 dense mass honey-combed with cavities. 
 
 TUMORS. 
 
 Dermoid Cysts have been found in the lungs in a few instances. 
 
 Fibromata have been described by Eokitansky. 
 
 Encliondromata may occur both as primary and secondary tumors. 
 The primary tumors are small and are believed to originate in the car- 
 tilages of the bronchi. The secondary tumors often attain a very large 
 size. 
 
 J 
 
 K 
 
 Fig. 103. — Primary Carcinoma of the Lung, X 300 and reduced. 
 
 Osteoma is very rare. A case is described by Luschka.' 
 Sarcomata as secondary tumors are of not infrequent occurrence. 
 A primary adeno-sarcoma is described by Weichselbaum.' 
 
 ' Virch. Arch., x., p. 500. 
 = Virch. Arch., 85, p. 559. 
 
THE EESPIEATOKY SYSTEM. 251 
 
 LympJiomata are found in cases of leukEemia and pseudo-leukgemia. 
 
 Carcinoma as a secondary growth may have the form of nodules or 
 of diffuse infiltration. Primary carcinoma of the lung has been described 
 by a number of authors. The new growth (Pig. 103) is in the form of 
 small nodules surrounded by pneumonia. As the result of the new 
 growth and the pneumonia, a considerable part of both lungs maybe 
 rendered solid. The bronchial glands are infiltrated and there may be 
 secondary nodules in the pleura. 
 
 The new growth seems to originate in the air-spaces. Their walls 
 are thickened, their cavities are lined with cylindrical epithelium, or 
 filled with cylindrical and polygonal cells, some of which undergo 
 colloid degeneration. 
 
 Or it may originate in the small bronchi.' 
 
 Parasites. 
 
 Ecliinococci occur in the lungs in their ordinary cystic form. The 
 sacs may suppurate and discharge through the pleura, the bronchi^ the 
 wall of the chest, or the diaphragm. 
 
 In bronchiectasiae and in gangenous cavities in the lungs, vegetable 
 parasites of various kinds have been described — both moulds and bacteria.'' 
 
 The Bacillus tuberculosis is regularly found in the walls and con- 
 tents of cavities in acute and chronic phthisis, sometimes in enormous 
 numbers. They are also often present in great numbers in the nodules 
 of tubercular inflammation, particularly when these are softening and 
 beginning to break down to form cavities. See Tuberculosis. 
 
 THE MEDIASTINUM. 
 
 The anterior mediastinum is situated in front of the pericardium, 
 between it and the sternum. At its superior part the two layers of 
 pleura separate somewhat to inclose the vestiges of the thymus gland ; 
 behind the second piece of the sternum they are in contact, but below 
 this the left pleura recedes from its fellow towards the left side, leaving 
 an angular space of some breadth. The triangularis sterni muscle 
 bounds this space in front. 
 
 The posterior mediastinum, stretching from the pericardium to the 
 bodies of the vertebrae, incloses between its layers the lower part of the 
 windpipe and gullet, the thoracic duct, the descending aorta, the 
 azygos vein, the pneumogastric nerve, and some lymphatic glands. 
 
 INBLAMMATION. 
 
 Suppurative inflammation may occur either in the anterior or pos- 
 
 • Virch. Arch., Bd. 83, p. 77. 
 « Virch. Arch., Bd. 66, p. 330. 
 
252 THE EESPIEATOEY SYSTEM. 
 
 tei'ior mediastinum. It may be caused by fractures, caries, or necrosis of 
 the sternum and vertebrse, by perforation of the oesophagus, by suppura- 
 tion of the lymphatic glands, by pleurisy ; or may occur without dis- 
 coverable cause. 
 
 The pus may infiltrate the connective tissue, or may form abscesses 
 which may attain a large size. The inflammation may extend to the 
 pleura or the pericardium ; the abscesses may displace the heart, the 
 lungs, or the sternum ; or they may perforate through the skin, into a 
 pleural cavity, the oeosphagus, the trachea, or a bronchus. 
 
 TUMORS. 
 
 The most common form of new growth in the mediastinum is that 
 known by the names of Lymphoma, Lympho-Sarcoma and Lymjsh- 
 adenoma. 
 
 These tumors are confined to the mediastinum, or they are associated 
 with similar growths in other parts of the body in the disease called 
 " pseudo-leuksemia." 
 
 Persons between the ages of twenty and thirty years seem to be the 
 most liable to the growth, but it is also not uncommon in children. 
 
 The growth begins in the lymphatic glands in the mediastinum, and 
 at the root of the lung. It increases at first slowly, then more rapidly 
 and gradually infiltrates the adjoining tissues. In this way the walls 
 of the trachea, bronchi, and aorta, the pericardium, the pleura, and the 
 lung become infiltrated with the growth. The tumoi* also compresses 
 the surrounding organs. 
 
 The growth is composed of a connective-tissue stroma infiltrated with 
 small round cells, the relative quantity of cells and stroma varying in 
 the difEerent cases. 
 
 Besides this form of tumor there may also occur in the mediastinum, 
 tumors similar to those which grow in the pleura and behind the perito- 
 neum, tumors which resemble both the sarcomata and carcinomata 
 and which are difficult to classify. 
 
 Teratoma myomatodes. — Under this name Virchow describes a very 
 remarkable tumor. It grew rapidly in a man, aged twenty-two, of good 
 constitution and physical development. The right pleural cavity was nearly 
 filled with a solid growth. There were similar growths, of smaller size, 
 on the left rib, in the liver, spleen, and kidneys. The mediastinal tumor 
 consisted of two portions, a larger and a smaller. The larger portion 
 consisted of solid tissue, in which were a few cavities. It was very vas- 
 cular. Part of it was composed of dense fibrous tissue. The greater 
 portion, however, consisted of loose connective-tissue fibres, of fusiform 
 cells, and of large, many-nucleated cells. Some of the fusiform cells 
 were small and of the usual appearance ; but many were large, and 
 
THE EESPIEATOEY SYSTEM. 253 
 
 presented striations like those of yoang Toluntary muscle. The smaller 
 portion of the tumor looked like a multilocular cystoid. The cysts va- 
 ried much in size, and contained serum, colloid matter, and blood. 
 Some of the cysts contained a thick, white material, in which were 
 hairs, epidermis scales, ciliated epithelium, and cholesterin. In the 
 fibrous tissue about these cysts were pieces of hyalin cartilage. Near the 
 surface of the tumor the tissue consisted of a fibro-cellular stroma form- 
 ing alveoli filled with epithelium. The tumor on the third left rib con- 
 sisted of connective-tissue fibres and cells, muscle-cells, cysts, alveoli 
 filled with epithelium, and a small portion of tissue resembling foetal 
 lung. 
 
THE VASCULAR SYSTEM. 
 
 THE HEART. 
 THE PERICARDIUM. 
 
 liiTJUltlES. 
 
 The pericardium may be wounded by penetrat:ing weapons, by gun- 
 shot wounds, and by fragments of bone. It may be ruptured by severe 
 contusions of the thorax, and by rapid extravasation of blood into the 
 pericardial sac. 
 
 Perforations may be produced by empyema, by mediastinal abscesses, 
 by abscesses of the chest-wall and of the liver, by aneurisms of the aorta, 
 and by suppurative inflammation of the pericardium. 
 
 DROPSY. 
 
 In most post-mortems, we find a little serum, from one-half ounce to 
 one ounce, in the pericardial sac. This serum is usually clear and of a 
 light yellow color ; if decomposition has commenced, it may be of a 
 reddish color, or it may be slightly turbid from the falling ofi of the 
 pericardial epithelium. 
 
 Large accumulations of serum are found as part of general dropsy 
 from heart-disease, kidney-disease, etc. The serum is clear and of a 
 light yellow color. Hydro-pericardium is usually moderate in comparison 
 with the accumulations of serum in the other serous cavities ; some- 
 times, however, there is a very large amount of serum, which hinders the 
 movements, and interferes with the nourishment of the heart. 
 
 HEMOKEHAGE. 
 
 Extravasations of blood in the cavity of the pericardium are pro- 
 duced by wounds and rupture of the heart, rupture of the aorta and of 
 aneurisms, and occur with pericarditis. Small extravasations in the 
 substance of the pericardium are found with scurvy, purpura, fevers, etc. 
 
THE YASCtTLAE SYSTEM. 255 
 
 PJSTEUMOKATOSIS. 
 
 Air or gas in the pericardium is sometimes found as a post-mortem 
 appearance, accompanied with drying of portions of the pericardium. 
 
 Wounds or paracentesis of the pericardium; the perforation of ulcers 
 of the stomach, cavities of the lungs, and ulcers of the oesophagus may 
 admit air into the pericardial cavity. In purulent pericarditis, with foul, 
 decomposing exudation, gases may be evolved. 
 
 INFLAMMATION. 
 
 Pericarditis is very rarely a primary lesion. It is most frequently 
 associated with rheumatism and Bright's disease, but is also found with 
 pneumonia, pleurisy, phthisis, endocarditis, pyaemia, and may be pro- 
 duced by injuries. 
 
 The inflammations of the pericardium resemble those of the pleura. 
 They usually begin acutely or subacutely, but may become chronic. 
 There is a greater disposition to the escape of blood from the vessels than 
 in pleurisy, so that the inflammatory products are often mixed witli 
 blood. The inflammatory process usually begins at the base of the heart 
 and from there extends over the rest of the pericardium. 
 
 We may distingirish: 
 
 1. Pericarditis ivith the prodaction of fibrin. — In the milder exam- 
 ples of this form of pericarditis, the pericardium is congested, or also 
 studded with minute hemorrhages, its surface is roughened by the depo- 
 sition of a thin layer of fibrin. In the more severe cases, the entire sur- 
 face of the pericardium is covered with a thick layer of fibrin, and there 
 are fibrinous adhesions between the visceral and parietal pericardium. If 
 the inflammatiou continues for any length of time, the pericardium itself 
 becomes thicliened and infiltrated with cells, and the wall of the heart 
 may also undergo inflammatory changes. 
 
 If the patient recovers, the fibrin may be absorbed, and the pericar- 
 dium return to its normal condition. Or, instead of this, as the fibrin 
 disappears there is a growth of new connective tissue which forms perma- 
 nent thickenings and adhesions of the pericardium, which may after- 
 wards become calcified. 
 
 3. Pericarditis tuith the proditction of fibrin and a good deal of serum. 
 — In these cases the pericardium is coated with fibrin, but in addition 
 there is a large effusion of serum into the pericardial sac. This serum 
 accumulates at first between the floor of the pericardium and the lower 
 surface of the heart, and as it increases, distends the pericardial sac in 
 all directions, pushing the heart upwards and forwards. The pericar- 
 dial sac may be so much distended as to compress the trachea, the left 
 bronchus, the oesophagus, or the aorta. If the patients recover, the se- 
 rum is absorbed and permanent adhesions and thickenings are left. 
 
 3. Pericarditis loith the production of fibrin, serum, and a good deal 
 
256 THE VASCULAE SYSTEM. 
 
 of pus. — This variety may liave the purulent character from the outset, 
 or it may begin as one of the forms just described, and afterwards assume 
 the purulent character. These latter cases are apt to run a chronic 
 course. 
 
 In the chronic cases, the pericardial sac contains a large amount of 
 purulent serum. The pericardium is coated with fibrin and is itself 
 thickened and infiltrated with cells. The walls of the heart may be the 
 seat of interstitial myocarditis. In some cases, the products of inflamma- 
 tion undergo putrefactive changes; in some cases, the serum is absorbed 
 and the fibrin and pus undergo cheesy degeneration; in some cases, ex- 
 tensive connective-tissue adhesions and calcific plates are formed. 
 
 4. TuiercyJar Pericarditis. — The varieties of pericarditis already 
 mentioned may be associated with a production of tubercle-tissue in the 
 the thickness of the pericardium. Such a tubercular pericarditis may be 
 localized, or may be associated with tubercular inflammation in other 
 parts of the body. 
 
 TUMOES. 
 
 Fihrornata sometimes are developed in the pericardium. They are 
 often of polypoid form, and from atrophy of the pedicle may become free 
 in the joericardial sac. 
 
 Sarcomata and Carcinomata occur as secondary growths either from 
 continuous infiltration or as metastatic tumors. 
 
 Cysts of the visceral pericardium have been described. 
 
 Endothelioma. There may be a growth of flat cells arranged in anas- 
 tomosing tubules which look like lymphatics, in the pericardium, resem- 
 bling similar growths in the pleura. 
 
 THE HEART. 
 
 MALFORilATIONS. 
 
 The malformations of the heart are usually closely connected with 
 malformations of the aorta and pulmonary artery. They depend on ar- 
 rest of, or abnormal development; on endocarditis, myocarditis, throm- 
 bosis, or mechanical causes. 
 
 I. The common arterial trunk is only partially, or not at all, separated 
 into aorta and pulmonary artery. The divisions between the heart cavi- 
 ties are at the same time defective. 
 
 1. Tliere is one ventricle and no auricle. 
 
 2. There is one ventricle and one auricle. 
 
 3. There is one ventricle and two auricles; the aorta is alone or in- 
 completely sejjarated from the pulmonary artery. 
 
 II. The trunk of the pulmonary artery, or of the aorta, is stenosed or 
 obliterated, and from the obstruction to the current of blood the develop- 
 ment of the septa, between the heart cavities, is prevented. 
 
THE VASCPLAU SYSTEM. 257 
 
 1. The aorta, at its origin, or iu the ascending portion of the arch, 
 is stenosed or closed. The pulmonajy artery gives off the descending 
 aorta, and supplies the carotids and subclavians. The foramen ovale re- 
 mains open, or there is no septum between the auricles. The ventri- 
 cular septum is also usually defective. The right ventricle is hyper- 
 trophied. 
 
 2. The pulmonary artery is stenosed or closed. Its branches are sup- 
 plied by the aorta, through the ductus arteriosus. The ventricular sep- 
 tum is defective, the foramen ovale is open, or the auricular septum 
 defective. 
 
 III. The malformation affects the aorta and pulmonary artery after 
 they are more fully developed. 
 
 1. There is stenosis of. the aorta between the left subclavian and 
 ductus arteriosus, or just at the opening of the ductus arteriosus. The 
 descending aorta is then a continuation of the pulmonary artery. 
 
 3. The aorta gives off all its branches from the arch, but the descend- 
 ing aorta is a continuation of the pulmonary artery; or the carotids 
 may spring from the aorta, the subclavians from the pulmonary artery. 
 
 3. The vessels are transposed; the pulmonary artery arises from the 
 left, the aorta from the right ventricle; the pulmonary veins empty into 
 the left, the vense cavae into the right auricle; or the veins also may be 
 transposed. The septa are defective. 
 
 IV. The aorta and pulmonary artery are normal, but the cardiac 
 septa are defective. 
 
 1. The foramen ovale remains partly open. This condition may con- 
 tinue through life without giving any trouble. 
 
 2. The ductus arteriosus may remain open for many years; this also 
 may cause no disturbance. 
 
 3. There is a small or large opening in the ventricular septum. This 
 may give rise to no symptoms, unless disease of the heart or lungs be 
 superadded. 
 
 V. Either of the auriculo-ventricular orifices may be entirely closed. 
 The foramen ovale remains open, and the ventricular septum is de- 
 fective. 
 
 VI. The valves of the different orifices of the heart may be absent or 
 defective. The arteries or the ventricles are usually defective at the 
 same time. 
 
 The aortic and pulmonary valves may consist of two large or four small 
 leaves, instead of the usual three. The edges of the semilunar valves 
 may be fenestrated. These alterations are usually of no significance. 
 
 Generally speaking, the existence of openings between the two aui-i- 
 cles or the two ventricles, admitting some admixture of venous and arte- 
 rial blood, produces no marked change in the circulation. If, however, 
 the passage of the current of venous blood into the right heart is in any 
 17 
 
258 THE VASCULAE SYSTEM. 
 
 way interfered witli, the consequences are very serious. Cyanosis is 
 produced, the skin is of a bluisli color, the small veins and capillaries are 
 dilated, exudation of serum and hypertrophy of connective tissue takes 
 place, especially in the fingers and toes. 
 
 Besides the malformations already mentioned, we fllay find: 
 
 Entire absence of the heart. 
 
 Abnormal septa and cordse tendinese in the heart cavities. 
 
 Abnormal shapes of the heart. 
 
 Abnormal positions of the heart. 
 
 a. There is a smaller or larger defect in the walls of the thorax, so that 
 the heart projects on the outside of the chest; the pericardium is usually 
 absent. 
 
 i. The diaphragm is absent, and the heart is in the abdominal cavity. 
 
 c. The heart is in some part of the neck or head; this occurs only in 
 fcBtuses very much malformed. 
 
 d. The heart is transposed, being on the right side. 
 
 Very rarely two more or less perfect hearts are found in the same 
 thorax. 
 
 CHANGES IN POSITION. 
 
 Changes in the position of the heart are congenital or acquired. The 
 congenital malpositions have already been mentioned. 
 
 The acquired malpositions are caused by: 
 
 1. Hypertrophy of the heart; its long axis approaches the horizontal 
 direction. 
 
 3. Changes in the thoracic viscera. Emphysema of both lungs 
 pushes the heart downward. Emphysema, pleurisy with effusion, or 
 pneumo-thorax of one side, push the heart to the other side. Pleurisy or 
 chronic pneumonia, producing retraction of one side of the thorax, draws 
 the heart to that side. New growths, aneurisms, and curvatures of the 
 spine displace the heart in various directions. 
 
 3. Changes in the abdomen. Accumulations of fluid and new growths 
 in the abdomen, and tympanites, may push the heart upward. 
 
 VrOUNDS AND EUPTUEES. 
 
 Wounds of the heart are produced by penetrating instruments, by 
 bullets, and by fragments of bone. The right ventricle is the more 
 frequently wounded; next, the left; rarely, the auricles. 
 
 The wound may penetrate into the cavities of the heart, or only pass 
 partly through its wall, or a bullet, or the broken end of a weapon may 
 be imbedded in the wall. If the wound penetrates into a cavity, and is 
 gaping, death follows instantly, and the pericardium is found filled with 
 blood. If the wound be small and oblique, the blood may escape gradually, 
 
THE VASOULAE SYSTEM. 259 
 
 and death may not ensue for several days. In rare cases, adhesions are 
 formed with the pericardium, and the wound cicatrizes. Wounds which do 
 not penetrate may cause death by the inflammation which they excite, or 
 may cicatrize. 
 
 Bullets and foreign bodies may become encapsulated in the heart- 
 wall, and remain so for years. 
 
 Ruptiores of the heart-wall occur in various ways. 
 
 1. Severe contusions of the thorax may produce rupture, usually of 
 one of the auricles. 
 
 2. Spontaneous rupture occurs usually in advanced life. Rupture is 
 most frequent in the left ventricle and, in a considerable proportion of 
 cases, near the apex. There is usually one rupture, but sometimes 
 more. The rupture is usually oblique and larger internally than ex- 
 ternally. The heart-wall, near the seat of rupture, may be infiltrated 
 with blood, or blood may infiltrate the subpericardial fat. The heart- 
 wall may be of normal thickness, or thin: it is usually soft and in a con- 
 dition of fatty infiltration or degeneration. The rupture very frequently 
 takes place when the patient is quiet. Death may be almost instantaneous 
 or may not ensue for several hours. 
 
 Fatty degeneration leading to rupture of the heart may be general, or 
 it is frequently circumscribed and due to obliterating endarteritis, 
 atheroma, thrombosis, or embolus of one of the coronary arteries, whereby 
 a portion of the heart-wall is deprived of nourishment, and degenerates. 
 Or rupture of a branch of one of the coronary arteries may induce rupture 
 of the heart- wall. Acute and chronic myocarditis, with or without the 
 formation of abscess or cardiac aneurism, or the presence of tumors in 
 the heart-wall, or hydatids, may lead to the rupture. 
 
 3. In very rare cases, rupture is produced by stenosis of the aorta and 
 ■dilatation of the heart-cavities. 
 
 4. Rupture of the papillary muscles and tendons may be produced by 
 fatty degeneration, or inflammatory or ulcerative processes. 
 
 ATROPHY. 
 
 Atrophy of the walls of the heart may be accompanied with no change 
 in the size of its cavities; or with dilatation (the same as passive dilata- 
 tion); or, more frequently, with diminution in the size of the cavities. 
 
 The atrophy involves most frequently all the cavities of the heart, but 
 may be confined to one or more of them. 
 
 The muscular tissue appears normal, or brown from the presence of 
 little granules of pigment in the muscular fibres, which are sometimes 
 present in large numbers; or the muscular fibres may undergo fatty de- 
 generation; or there may be an abnormal accumulation of fat beneath 
 the pericardium; or there may be a peculiar gelatinous material beneath 
 the pericardium, this consists of fat which has undergone mucous de- 
 
260 THE VASCULAJB SYSTEM. 
 
 generation. The heart may be so mnch atrophied as to weigh four 
 ounces. 
 
 The causes of atrophy of the heart are: 
 
 1. It is a congenital malformation; the heart of an adult then looks 
 lilse that of an infant. 
 
 2. Any chronic and exhausting disease, repeated hemorrhages, old 
 age, typhus fever, dysentery, etc., may produce atrophy. 
 
 3. Chronic pericarditis, with large serous effusion, or with thicken- 
 ing of the pericardium, producing constriction of the coronary arteries. 
 
 4. Stenosis, atheroma, calcification, or thrombosis of the coronary 
 arteries may produce partial or total atrophy. 
 
 5. Myocarditis, with fatty or fibrous degeneration. 
 
 6. Mitral stenosis may cause atrophy of the left ventricle. 
 
 HTPEKTEOPHT. 
 
 All the cavities of the heart may have their walls hypertrophied, 
 or the thickening may involve one or more. While the wall of a ventri- 
 cle is thickened, its cavity may retain its normal size — simple hypertrophy , 
 or be dilated — eccentric hypertrophy ; or it may be contracted — concentric 
 hypertrophy. 
 
 Care should always be exercised in judging of this condition, for a 
 firmly contracted heart seems to have a small cavity and thick walls. 
 The existence of such a condition as concentric hypertrophy is denied 
 by some authors. Eccentric hypertrophy is the most common form. 
 Simple hypertrophy is not common, but may occur in connection with 
 the atrophied kidneys of chronic diffuse nephritis. The muscle-tissue 
 in hypertrophied hearts is firmer and denser than normal, and is apt to 
 have a darker color. Patty degeneration may, however, be associated 
 with it, giving the walls a lighter appearance. It is probable that the 
 increase of tissue in the hypertrophied heart- wall is the result of increase 
 both in size and number of the muscle-fibres. 
 
 Hypertrophy of both ventricles increases both the length and breadth 
 of the lieart. Hypertrophy of the left ventricle (alone) increases its 
 length. The apex is then lower and further to the left than usual. Hy- 
 pertrophy of the right ventricle (alone) increases the breadth of the heart 
 toward the right side; but sometimes the right edge of the heart retains 
 its normal situation, and the apex is displaced to the left. With large 
 hypertrophy of both ventricles, the base of the heart may sink, so that 
 its long axis approaches a horizontal direction. 
 
 Hypertrophied hearts may weigh from forty to fifty ounces, or even 
 more. 
 
 Hypertrophy of the heart may depend upon a variety of causes: 
 
 1. Changes in the valves; either insufficiency or stenosis in the valves 
 
THE VA8CULAJB SYSTEM. 261 
 
 leading from a cavity, and insuflSciency in valves leading to a cavity, may 
 induce hypertrophy of its walls. 
 
 'i. Obstruction to the passage of blood through the arterial system, 
 as in atheroma and other diseases of the intima, congenital or acquired 
 stenosis of vessels, pressure of tumors, etc., on vessels; certain forms of 
 chronic diffuse nephritis, especially atrophied kidneys, lead to hypertro- 
 phy of the left ventricle, and sometimes secondarily to hypertrophy of 
 the right ventricle. 
 
 3. Obstruction to the passage of blood through the pulmonary ar- 
 tery by stenosis or by certain diseases of the lungs, particularly emphy- 
 sema and chronic phthisis, may lead to hypertrophy of the right ventri- 
 cle, and secondarily, of the right auricle and left ventricle. 
 
 4. Any cause, whether muscular or nervous, which increases the 
 rapidity and force of the heart's contractions, may produce hyper- 
 trophy. 
 
 5. Dilatation of the ventricles, from any cause, is frequently followed 
 by hypertrophy. 
 
 6. Pericarditis may produce hypertroi^hy by inducing softening and 
 dilatation of the ventricles, or by leaving adhesions, which obstruct the 
 heart's action. Chronic myocarditis also may lead to hypertrophy. 
 
 Finally, for some cases of hypertrophy no satisfactory cause can be 
 found. 
 
 It should be borne in mind that an increase in the amount of fat in 
 and about the heart may make the organ appear larger, when there may 
 be actually a- considerable decrease in the amount of muscle-tissue. 
 
 DILATATION. 
 
 Dilatation may be combined with hypertrophy — active dilatation; or 
 there may be no increase of muscle tissue, but a thinning of the walls 
 proportionate to the dilatation of the cavity— /jflsstVe dilatation. 
 
 Either one or all of the heart cavities may be dilated, the auricles 
 most frequently; next the right ventricle; least often the left ventricle. 
 Active dilatation has been considered under hypertrophy. 
 
 Passive dilatation may be produced by: 
 
 1. Changes in the valves. Mitral or aortic stenosis or insufficiency 
 may produce dilatation of the auricles and right ventricle. Pulmonary 
 ■stenosis or insufficiency may produce dilatation of the right auricle and 
 right ventricle. Aortic insufficiency, with or without stenosis or mitral 
 insufficiency, may produce dilatation of the left ventricle. Dilatations 
 from. these causes are often succeeded and compensated for by hypertro- 
 phy of the heart's walls. 
 
 2. Changes in the muscular tissue of the heart- walls: Serous infil- 
 tration from pericarditis, myocarditis, fatty degeneration and infiltration, 
 •atrophy of the muscle-fibres, may all lead to dilatation. 
 
262 THE VASCULAR SYSTEM. 
 
 3. A heart which is abeady hypertrophied may, from degeneration 
 of the muscle, become dilated. 
 
 4. Acute exudative inflammations of the lungs and acute pleuritic 
 exudations, by rendering a large number of vessels suddenly imperme- 
 able to the blood-current, may produce sudden stasis in the pulmonary 
 artery and dilatation of the right heart. 
 
 5. There are curious cases of acute and chronic dilatation of the ven- 
 tricles, for which no mechanical cause can be found, and which are very 
 fatal. 
 
 DEGENEKATIOKS. 
 
 Parenchy matous degeneration. — This lesion frequently occurs in ty- 
 phoid and typhus fever, pyaemia, erysipelas, and other infectious diseases, 
 as well as in the exanthemata, as a result of burns, and under a variety 
 of other conditions. It is characterized by the presence in the muscle- 
 fibres of the heart of greater or less numbers of albuminous granules of 
 various sizes, most of them very small. They are not as refractile as 
 fat-droplets, and are insoluble in ether, while swelling up and becoming 
 almost invisible under the influence of acetic acid. Sometimes they are 
 so abundant as to conceal the striations of the fibres. The degeneration 
 is usually quite uniformly diffused through the heart, whose walls are 
 softer than normal and of a grayish color. This lesion may be associated 
 with or followed by fatty degeneration. 
 
 Fatty degeneration — This consists in the transformation of portions of 
 the muscle-fibres of the heart into fat, which collects in the fibres in larger 
 and smaller droplets, sometimes few in number, sometimes so abundant 
 as to entirely destroy or conceal the normal striations (Fig. 103). These 
 
 Fig, 103.— Fatty Degeneration of the Heakt Muscle, teased. 
 
 droplets are soluble in ethei-, and remain unchanged on treatment with 
 acetic acid. 1'his degeneration is sometimes quite universal, but is more 
 apt to occur in patches, giving the heart muscle a mottled appearance. This 
 mottling may usually be best seen on the papillary muscles. The degener- 
 ated areas have a iiale-yellowish color, and the muscle-tissue is soft and 
 flabby; but when moderate or slight in degree, the gross appearance may 
 be little changed, and the microscopical examination be necessary for its 
 determination. This degeneration may lead to thinning of the walls oi' 
 
THE VASCTTLAE SYSTEM. 
 
 263- 
 
 to rupture of the heart, or to inability to fulfil its functions. It is not 
 infrequently the cause of sudden death. 
 
 It may be secondary to hypertrophy of the heart, to inflammation of 
 the heart-muscle, or to pericarditis; to disturbances of the circulation in 
 the coronary arteries by inflammation, atheroma, etc. It may be due 
 to deteriorated conditions of the blood in wasting diseases, excessive 
 hemorrhages, exhausting fevers, leukaemia, etc., or to poisoning with 
 phosphorus and arsenic. It may occur in otherwise apparently healthy 
 persons. 
 
 Lipomatosis of the heart, which should be clearly distinguished from 
 fatty degeneration, consists of an unusual accumulation of fat, either about 
 the heart or between the muscle-fibres (Fig. 104). The subpericardial fat. 
 
 Fig. 104. — Lipomatosis op Heart, X ( 
 The lesion is excessive; the heart-musole being to a large extent atrophied. (The fat-cells are 
 represented, for the sake of cfearness, of relatively too large size.) 
 
 which may be present in considerable quantity under normal conditions, 
 may be so greatly increased in amount as to form a thick envelope, inclos- 
 ing nearly the entire organ. Sometimes the accumulation of fat extends 
 into the walls of the heart, between the muscles, causing atrophy of the 
 latter, frequently to a very great extent, so that the function of the heart 
 is seriously interfered with. This occurs sometimes in general obesity, 
 or as a result of chronic pericarditis, or in drunkards, or in debilitated 
 or old persons. 
 
 Mucous degeneration or transformation of the subpericardial fat is 
 sometimes found in persons much emaciated by chronic disease. 
 
 Amyloid degeneration of the endocardium or the walls of the blood- 
 vessels and intermuscular connective-tissue septa is a not very infrequent, 
 but usually not very important lesion. 
 
264 THE VASCULAR SYSTEM. 
 
 Calcification of the products of inflammation in pericarditis, or of 
 connective-tissue membranes in chronic pericarditis, sometimes occurs, 
 and in the latter case the heart may be more or less inclosed by a calca- 
 rious shell. The muscle-fibres of the heart-wall may, though rarely, be- 
 come densely infiltrated with salts of lime. 
 
 Myomalacia. — When, through obliterating endarteritis, atheroma, 
 thrombosis, or embolus of a branch of the coronary arteries, the blood 
 supply is cut oflE from a circumscribed portion of the heart-wall, the 
 tissue in the affected area may undergo fatty degeneration leading to 
 rupture. Or instead of extensive fatty degeneration, the muscle-fibres 
 may break down into a granular detritus, and the connective tissue about 
 them suffer retrograde metamorphosis, so that the whole affected area 
 may be soft and yellowish-white, or grayish in color. If, as not infre- 
 quently occurs, there is considerable extravasation of blood, the degene- 
 rated area may be of a dark-red color. Under these conditions the wall 
 may rupture; or acute inflammatory processes may occur; or the degene- 
 rated tissue may be gradually absorbed, and replaced by new connective 
 tissue which gradually grows dense, shrinks, and assumes the characters 
 of cicatricial tissue. This may occur in any part of the heart-wall or in 
 the papillary muscles. When the heart- wallis involved, the new-formed 
 connective tissue may yield to the blood pressure from within, and an 
 aneurism of'the heart be formed. 
 
 INFLAMMATION. 
 
 Undocai'diiis. 
 
 The endocardium is a connective-tissue membrane, which lines the 
 cavities of the heart and forms its valves. Its inner surface is covered 
 with a layer of endothelial cells. It is but poorly supplied with vessels, 
 and the inflammations which attack it are of the cellular variety. The 
 ordinary piroducts of inflammation, pus, fibrin, and serum are scanty or 
 absent altogether. The connective-tissue cells and basement substance 
 are principally concerned in the inflammatory processes. The new tissue 
 thus produced is prone to degeneration and calcification. The roughen- 
 ing of the endocardium due to the inflammation often causes a coagula- 
 tion of fibrin on the inflamed surface. 
 
 In foetal life it is the endocardium of the right heart, in extrauterine 
 lite that of the left heart which is regularly inflamed. 
 
 The endocardium which forms the valves is that which is most fre- 
 quently inflamed, but the other portions of it are by no means exempt. 
 
 We distinguish : 
 
 (1) Acute endocarditis, which occurs most frequently with rheu- 
 matism. It may attack a heart which was previously healthy, or one in 
 which the lesions of chronic endocarditis already exist. 
 
THE VASCULAR SYSTEM. 265 
 
 In some cases the only lesion is a simple swelling of the valves. They 
 are thick and succulent, but their siTrfaces remain smooth. The base- 
 ment substance is swollen, and there is a moderate production of new 
 connective-tissue cells. 
 
 In other cases, the growth of connective-tissue cells is very much 
 more marked, the basement substance is split up, and little cellular, 
 fungous masses project from the free surface of the endocardium. On 
 these roughened surfaces the fibrin of the blood is deposited, and so 
 vegetations of considerable size may be formed. 
 
 In still other cases the cell growth, while in some places it forms vege- 
 tations, in other places rapidly degenerates, and thus portions of the 
 valves are destroyed. 
 
 In some cases of this disease, the patients recover, and the valves 
 seem to return to a normal condition; in other cases the valves are left 
 permanently damaged; and in still others chronic endocarditis follows 
 the acute form. 
 
 (2) Malignant eiidocaj-diiis (acute ulcerative endocarditis) seems 
 to have the characters of an acute infectious disease rather than those of 
 a local inflammation, but for convenience we describe it as a form of 
 endocarditis. 
 
 It may occur as an independent disease, or be associated with the 
 puerperal condition, rheumatism, pneumonia, and other diseases. 
 
 It may attack hearts previously healthy, or those in which the lesions 
 of chronic endocarditis already exist. 
 
 In the endocardium there is a marked cell-growth, and also a degene- 
 ration, which in some places produce large vegetations, in others deep 
 destruction of tissue. In this way, the surface of the endocardium is 
 rendered ragged and irregular — an irregularity rendered still more marked 
 by the deposition of fibrin from the blood . 
 
 The mitral valve and its chordte tendineae seem to be the most fre- 
 quent seats of this lesion, but other parts of the endocardium are not in- 
 frequently affected. 
 
 Colonies of micrococci are constantly found in this disease in and upon 
 the vegetations, on the surfaces of the ulcers, in the infiltrated endocar- 
 dium, or in the vessels of the valves, and to these maybe attributed the 
 destructive character of the local process (Fig. 105). 
 
 A very frequent accompaniment of acute ulcerative endocarditis is 
 the formation of multiple abscesses in the spleen, kidneys, brain, skin, 
 or abscess in the heart- wall. In these secondary abscesses, colonies of 
 micrococci may usually be found. If they are examined in early stages, 
 masses of micrococci may be found blocking up some of the small arteries, 
 and around these'will often be found a more or less circumscribed area of 
 tissue in the condition of coagulation necrosis. These areas with their 
 contained bacteria may act as irritants, and lead to the development of a 
 
266 
 
 THE VASCULAE SYSTEM. 
 
 purulent inflammation which results in abscess. It is probable that 
 these abscesses in ulcerative endocarditis do not always arise from cardiac 
 emboli, but may precede the heart lesion. 
 
 Although very constantly associated with this disease, our knowledge 
 of the micrococci is not yet extensive enough to enable us to assert posi- 
 tively that they are its cause, although the necrotic changes which seem 
 
 Fig. 103.— Malignant Endocarditis, X 700 and reduced. 
 Section of vegetation showing colonies of micrococci, stained with fuchsin. 
 
 uniformly to occur in tissues in which they have found lodgment as 
 emboli, speak very strongly in favor of this view. Whether or not the 
 micrococci in this disease are identical with those found more or less 
 constantly in numerous other diseases, or in any one of them, cannot be 
 decided at present, in the absence of conclusive culture experiments.' 
 (For method of staining these micrococci, see p. 90.) 
 
 (3) Chronic Endocarditis may succeed acute endocarditis, or the in- 
 flammation may be chronic from the outset. It affects most frequently 
 the aortic and mitral valves, and the endocardium of the left auricle and 
 ventricle; similar changes in the right side of the heart being much less 
 frequent. 
 
 ' We have seen a case, reported by Dr. J. Lewis Smith and Dr. W. P. North- 
 rup to the New York Pathological Society, October 33d, 1884, of a child five and 
 one-half years of age, which died after a severe illness, lasting about ten days, 
 whose nature was obscure. The temperature ranged from the normal to 105°. 
 At the autopsy, nine hours after death, numerous ecchymoses were found be- 
 neath the skin, pleura, and pericardium, sub-pial hemorrhage on both sides of 
 brain, and small extravasations in the liver and spleen. A pyriform polypus 
 about two ctm. long and one ctm. wide hung from the edge of the mitral into 
 the ventricle; smaller vegetations, which seemed to rest on an ulcerated base, 
 were found on the mitral and on the papillary muscles. The vegetations pre- 
 sented the appearances common to ulcerative endocarditis, except that the masses 
 of bacteria, which were clustered in enormous numbers about and in the vege- 
 tations, were not micrococci, but were filamentous, being from 0.7 to 1.0 /t long 
 and very slendei". They were mostly grouped in twos, end to end, and in some 
 cases in longer chains. Bacilli were not found in other organs. No cultures were 
 made. 
 
THE VA8CTJLAE SYSTEM. 26T 
 
 There are two main anatomical yarieties of chronic endocarditis, 
 which may occur separately or together. 
 
 1. The endocardium is thick and dense, its surfaces are smooth or 
 covered with small, hard vegetations or ridges; it is often infiltrated with 
 the salts of lime. 
 
 3. There is a growth of connective-tissue cells in the endocardium 
 with a splitting up of the basement substance. Some of the new cells 
 continue to live, others degenerate. By the combination of such a cell- 
 growth and destruction, the endocardium is in some places destroyed, in 
 others changed into projecting vegetations. Fibrin is deposited on the 
 roughened surfaces. After a time, the condition is further complicated 
 by the deposition of the salts of lime in the new tissue and the endocar- 
 dium. All these changes may extend to the wall of the heart beneath the 
 endocardium. 
 
 The most important result of chronic endocarditis is its efEect on the 
 heart valves, producing insuflBciency and stenosis. The changes in the 
 valves are followed by changes in the walls and cavities of the hear^ 
 and disturbances of the circulation throughout the body. 
 
 (4) Tuiercular Endocarditis may occur in connection with tuber- 
 cular pericarditis or general miliary tuberculosis. The tubercles may be 
 small and single, or grouped in masses, and show the usual degenerative 
 changes. 
 
 DEGENERATION-. 
 
 It is not uncommon to find, especially in old persons, changes in the 
 valves, which seem to be simply degenerative. The valves are a little 
 thiclcened, they are denser than the normal, their tissue is infiltrated 
 with fat and granular matter, or with the salts of lime. 
 
 Myocarditis. 
 
 The inflammatory changes in the walls of the heart involve primarily 
 the interstitial tissue and blood-vessels, the muscle-fibres being seconda- 
 rily affected by atrophic and degenerative changes. 
 
 There is a change in the muscle-fibres by which they are broken into 
 rectangular fragments with a collection of granular matter around the 
 nuclei, the entire tissue becoming dense and translucent. This change 
 is sometimes called "parenchymatous myocarditis," but its inflammatory 
 nature is doubtful. 
 
 Interstitial Myocarditis may be acute and purulent, or chronic with 
 the formation of new connective tissue. 
 
 Acute purulent Myocarditis may be diffuse, infiltrating the wall of the 
 heart with pus. This occurs as a complication of scarlatina and from 
 unknown causes. 
 
 More frequently the purulent inflammation is circumscribed, produc- 
 
368 THE VASCULAE SYSTEM. 
 
 iiig abscesses. These occur with pysemia, ulcerative endocarditis, diph- 
 theria, an'd other infectious diseases. They are of difierent sizes, and 
 either single or multiple. They seem to be regularly produced by the 
 lodgment of infectious emboli in small yessels. The contents of the ab- 
 scesses consist of pus, broken down muscle-tissue, and bacteria. These 
 abscesses may open into the pericardial sac and set up a purulent peri- 
 carditis; or into a heart-cavity, giving rise to thrombi in the heart and 
 emboli in different parts of the body; or the wall of the heart is weak- 
 ened by the abscess, so that it ruptures, or an aneurismal sac is formed; 
 or an abscess in the interventricular septum may establish an opening 
 between the ventricles; or the suppurative process may extend upwards 
 and form an abscess in the connective tissue at the base of the heart. 
 
 In rare cases, the patients recover, the contents of the abscesses 
 become dry and hard, and inclosed by a wall of fibrous tissue. 
 
 Clironic Inierstitial Myocarditis may be secondary to pericarditis or 
 endocarditis, to obliterating endarteritis of the branches of the coronary 
 artery, or may occur by itself. There is a growth of new connective 
 tissue or of granulation tissue between the muscular fibres, with atrophy 
 and degeneration of the muscle. This growth may be in the form of 
 circumscribed patches, or diffused over a considerable part of the wall of 
 the heart. Such an interstitial inflammation is often followed by dilata- 
 tion of the cavities of the heart, by the formation of aneurisms of the 
 wall of the heart, and of thrombi in the cavities of the heart. 
 
 Syphilitic Myocarditis is accompanied by the growth of connective 
 tissue or granulation tissue in the wall of the heart between the muscular 
 fibres, and to this may be added the formation of gummy tumors. The 
 pericardium and endocardium may also be thickened, and pericardial 
 adhesions may be formed. 
 
 CHANGES IN THE VALVES. 
 
 Fenestration of the valves is usually a change productive of no bad 
 consequences. It occurs in the aortic and pulmonary valves. The valves 
 are thinner than usual, and close to their free edges are small slits ex- 
 tending from the centre to the attached edges of a leaf. 
 
 Anctirisms of the valves are produced in two ways: 
 
 (1) They are the result of endocarditis. One of the lamella? of the 
 leaf of a valve is destroyed and the other lamella is converted into a sac 
 filled with blood. These aneurisms are found in the aortic valve, pro- 
 jecting into the ventricle; and in the mitral valve, projecting into the 
 auricle. Not infrequently the wall of the aneurism gives way, so that 
 there is a rupture entirely through the valve. 
 
 (2) The entire thickness of a leaf of ii valve is converted into a sac 
 filled with blood. This occurs in the aortic, mitral, and tricupsid valves; 
 its cause is unknown. 
 
THE YASCULAE SYSTEM. 269 
 
 Hemorrhage in the substance of the valves is sometimes found in 
 very young children. It does not appear to have much clinical im- 
 portance. 
 
 ANEURISM OF THE HEAET. 
 
 Sacs filled with blood, situated in the walls of the heart, and com- 
 municating with its cavities, are formed in several different ways. 
 
 (1) In consequence of inflammatory processes in the endocardium 
 and muscular tissue, a small or large portion of the wall is converted into 
 fibrous tissue. The portion thus changed no longer resists the pres- 
 sure of the blood from, within, and is driven outward. Such a pouch may 
 be a circumscribed sac, communicating with the heart-cavity by a small 
 opening, or may look like a dilatation of part of the ventricle. The wall 
 of such an aneurism becomes thinner as the sac increases in size. It is 
 composed of the endocardium, new fibrous tissue, visceral pericardium, 
 and sometimes the adherent parietal pericardium. The walls may cal- 
 cify; or rarely they become so thin as to rupture externally or into the 
 right ventricle. The sacs may contain fluid blood or be filled up with 
 fibrin. 
 
 Such aneurisms are usually situated in the wall of the left ventricle; 
 rarely in that of the left auricle. If they are in the septum, they may 
 project into the right ventricle. They are usually single; sometimes two 
 or three are found in the same heart. 
 
 (2) Fatty degeneration of the heart-wall may reach such a point that 
 the wall yields, and is pouched out into an aneurismal sac. 
 
 (3) Endocarditis and myocarditis, or fatty degeneration, may so 
 soften a portion of the heart-wall that the endocardium and part of the 
 muscular tissue is ruptured, and a ragged cavity is formed. This form 
 of aneurism usually does not attain a large size, but soon ruptures exter- 
 nally, and causes the death of the patient. 
 
 THROMBOSIS OE THE HEAET. 
 
 It is very common to find after death, in the heart-cavities, yellow, 
 succulent, semi-translucent masses. They are most common and of firm- 
 est texture in persons who die of acute inflammatory diseases. They may 
 adhere quite firmly to the walls of the heart, and may extend in long, 
 branching cords into the vessels. They are formed in the last hours of 
 life, and just after death. They have no clinical or pathological impor- 
 tance. 
 
 Coagulations of the fibrin of the blood in the heart do, however, occur 
 during life, and may exist for years. If the fibrin adheres to the valves 
 in small masses, these are called vegetations; if it coagulates in the heart 
 cavities in larger bodies, they are called thrombi, or heart polypi. 
 
 Such thrombi are found in all the heart-cavities. They form flattened 
 
270 THE VASCULAE SYSTEM. 
 
 masses firmly adherent to the endocardium; or rounded bodies in the 
 spaces between the trabeculse; or have a polypoid shape and arc attache^d 
 by a narrow pedicle, or are free in the cavity. 
 
 They are usually found in connection with some valvular lesion, which 
 prevents the free circulation of blood through the heart. 
 
 They are firm, dry, and of a whitish color, they may soften and break 
 down at their centres, so as to look like cysts filled with pus, or they 
 may calcify. They are usually entirely unorganized, consisting simply 
 of fibrin. 
 
 I, Delafield, have observed one case in which the thrombi were dis- 
 tinctly organized. The patient was a man found dead in the street, con- 
 cerning whom no history was obtained. 
 
 Sometimes sarcomatous and carcinomatous tumors in different parts 
 ■of the body are accomjianied by the formation of thrombi in the lieart- 
 cavities which are composed jiartly of coagulated blood, partly of tissue, 
 like that of the primary tumor. 
 
 TUMOKS. 
 
 Primary tumors in the heart are rare; but sarcomata, myxomata, fibro- 
 niata, and lipomata may occur. Rhaidoinyomata, probably congenital, 
 may occur in the heart-wall as circumscribed nodular masses. A cavern- 
 ous tumor of this kind has been described. Secondary tumors, as a result 
 of metastasis or of continuous growtli from adjacent parts, are not very 
 infrequent. These are usually carcinomata or sarcomata. Secondary 
 cliondromata have been observed. 
 
 PARASITES. 
 
 Echinococcus sometimes occurs in the heart-wall and may perforate 
 into the cavities. Oysticercus cellulosise has been observed. 
 
 THE BLOOD-VESSELS. 
 ATROPHY AND HYPERTROPHY. 
 
 Atrophy of the blood-vessels may involve the entire trunk or some of 
 its elements. It may occur as a part of general malnutrition of the body, 
 or in connection with atrophy of particular organs, or as an accompani- 
 ment of various diseases of the vessels themselves. 
 
 Hypertrophy, which is especially seen in the arteries, may occur in 
 the establishment of a collateral circulation upon the closure of arterial 
 trunks, or it may occur as the result of increased blood-pressure, as in 
 some forms of hypertrophy of the heart. 
 
 DEGENERATION. 
 
 Fatty degeneration. — This may occur in the walls of otherwise unal- 
 tered vessels, or in those which have undergone a variety of inflamma- 
 
THE VASCULAR SYSTEM. 27 
 
 tory or degenerative changes. It may occur either in the intima or 
 media or both, and may be so extensive as to form a very prominent 
 gross lesion, or so little developed as to require the microscope for its 
 recognition. When marked, especially if occurring in the intima of large 
 vessels, smaller and larger spots or stripes or patches may be seen, of a 
 yellowish -white color, usually sharply circumscribed, and sometimes 
 smooth, sometimes roughened on the surface. It is most apt to occur in 
 the aorta, but may be found in any of the vessels. In moderate degrees of 
 the lesion, we find on section that the cells of the intima contain fat-drop- 
 lets in greater or less number. When further advanced, not only are the 
 cells crowded with fat-droplets, but the intercellular tissue also may be 
 more or less densely infiltrated with them , Sometimes the infiltration is 
 so dense that the tissue breaks down, and there may be an erosion of the 
 surface, forming a so-called fatty ulcer. When the media is involved, the 
 muscle-cells contain fat-droplets. It may lead to the formatien of aneu- 
 rism or to rupture of the vessels. 
 
 Calcification usually occurs in vessels otherwise diseased, and may in- 
 volve either the intima or media. It consists in the deposition of salts 
 of lime either in the cells or intercellular substance. The lime may be 
 in the form of larger or smaller granules or in dense translucent plates. 
 
 Amyloid degeneration, which may affect all the coats of the arteries, 
 but especially the intima and media, will be considered under the lesions 
 of the organs in which it most commonly occurs. 
 
 THE ARTERIES. 
 
 INFLAMMATION. 
 ACUTE AETEBITIS. 
 
 Acute inflammation of the walls of the arteries is, in the majority 
 of cases, the result of injury, or of an inflammation in the vicinity of the 
 vessel, or of the lodgment within it of some foreign body of an irritat- 
 ing or infectious nature. The inflammatory process may be largely con- 
 fined to the inner layers of the vessel — endarteritis— ov it may com- 
 mence in the outer l&^ens,— periarteritis — or it may involve the entire 
 wall. 
 
 The blood-vessels in the outer layers may be congested, the tissue 
 cedematous and infiltrated with pus-cells, and the entire wall may 
 become necrotic. The intima, if this layer is involved, loses its natural 
 gloss, looks dull and swollen. It may become infiltrated with pus from 
 the outer layers, and it may become necrotic. Under these conditions 
 thrombi usually form, and in these may occur the various changes which 
 have been already described on p. 52. 
 
i! 1 li THE VASCULAE SYSTEM. 
 
 CHEONIC ARTERITIS. 
 
 In chronic arteritis, all the coats of the yessel may be involved, but in 
 most cases the lesion is either largely confined to or most marked in the 
 intima — endarteritis. The disease may supervene upon an acute inflam- 
 mation of the artery, or it may be chronic from the beginning. Tlie 
 inflammation may occur in patches or in irregular segments of the ves- 
 sels, of various lengths, or it may occur diffusely. It may be limited to 
 single arterial trunks, or it may affect more or less all the arteries of the 
 body. Arteries which are the seat of slight degrees of chronic inflam- 
 mation may appear to the naked eye but slightly, or even not at all 
 changed, or the walls may seem stiffer than usual, and remain widely 
 open when cut across. "When the lesion is more marked, whitish patches 
 or areas of distinct thickening of the wall may be seen, which sometimes 
 visibly encroach upon the lumen of the vessel (Fig. 106). Microscopical 
 
 
 Fjg. 106.— Cheonic Endarteritis, X about 15, 
 In one of the cerebral arteries. The amount of thickening of the intima is moderate. 
 
 examination shows that the thickening of the wall is due to the forma- 
 tion of new connective tissue, mostly in the intima. The new tissue 
 may be soft and gelatinous in character and contain few or many cells ; 
 or it may be very dense and hard and contain very few cells. The 
 endothelial layer of the intima may remain intact over the thickened 
 area. Parts of the vessel not distinctly thickened may contain an 
 unusual number of small spheroidal cells. Sometimes the musculosa 
 and adventitia as well as the intima show at the seat of thickening an 
 increase of new connective tissue. The increase of connective tissue in 
 the intima, particularly of smaller arteries, may be so great as to encroach 
 seriously upon the lumina, and even lead to their obliteration — endarteritis 
 olliteraiis (Pig. 107). Obliterating endarteritis is very common in the 
 interstitial inflammation of organs such as the kidney, liver, etc., as a part 
 of the general new formation of connective tissue. Arteries which are 
 the seat of chronic arteritis are not infrequently the seat of secondary 
 acute inflammatory changes, so that, in addition to the formation of con- 
 
THE VA8CULAE SYSTEM. 
 
 273 
 
 neetive tissue they may become infiltrated with small spheroidal cells, 
 which may lie singly or in clusters in the various layers, and particularly 
 along the blood-vessels of the adventitia. 
 
 Arteries which are the seat of chronic endarteritis are liable to suffer 
 
 Fig. 107. — Chronic Obliterating Endarteritis, X about 15. 
 The lesion is excessive, almost entirely closing the lumen of the vessel. There is in this case a 
 moderate degree of periarteritis. 
 
 a series of degenerative changes consisting chiefly of fatty degeneration, 
 calcification, or the breaking down of the degenerated tissue, and the 
 
 Fig, 108.— Atheroma of the Aorta, tvith Degeneration of New-formed Tissue, X about 10. 
 a, Adventitia; b, media; c, new tissue developed in the intima; d, degenerated area; e, area of 
 softening; g, fat-droplets in softened area. 
 
 formation of inclosed softened areas (Pig. 108), or erosions or ulcer-like 
 openings in the intima. To the varied alterations produced in the walls 
 of the arteries by combinations of these inflammatory and degenerative 
 changes the name atheroma is frequently applied. 
 18 
 
274 THE VASCULAE SYSTEM. 
 
 When fatty degeneration supervenes upon chronic endarteritis, the 
 thickened areas may have a light-yellowish color, and the microscopical 
 examination will show a greater or less amount of fat in and between the 
 cells of the intima or the new tissue produced therein. Should the 
 fatty degeneration be extensive, the basement substance and the cells may 
 gradually disintegrate, and larger and smaller irregular cavities may be 
 formed in the walls, filled with fat-droplets and tissue detritus. 
 
 These softened areas, sometimes called atheromatous cysts, frequently 
 also contain cholestearin, and there may be partial calcification of their 
 contents, or of the tissue of the arterial wall about them. Sometimes 
 the wall of the artery, instead of undergoing simple fatty degeneration, 
 or in connection with this change, becomes in circumscribed localities 
 looser in texture by the conversion of the muscular and connective 
 tissue into a finely fibrillar substance which may persist for some time or 
 break down, forming an atheromatous cyst. These atheromatous cysts 
 may, through a degeneration of the tissue inclosing them, open into the 
 lumen of the vessel, forming the so-called atheromatous ulcers. Frag- 
 ments of tissue from the edges of these ulcers, or from the contents of 
 the cysts, may be carried into the circulation, forming emboli. Fibrin- 
 ous thrombi are prone to form upon the roughened surface of the 
 intima, or upon the surface of the erosions. Very frequently the calci- 
 fication is so extensive that large hard calcareous plates are formed in 
 the walls and may project inward, forming roughened surfaces on which 
 thrombi are deposited. Fatty degeneration and calcification of the 
 media and thickening of the adventitia may occur in connection with 
 atheroma of the intima. Sometimes the vessels by these changes become 
 greatly deformed so that over considerable areas the entire wall may be 
 altered, presenting raised and roughened surfaces interspersed with cal- 
 careous plates, erosions, thrombi, etc. Chronic endarteritis and athe- 
 roma is most common and marked in the aorta, but it may occur in 
 smaller arteries, particularly in the cerebral and coronary arteries. 
 
 Arteritis as a result of syiihilis is of frequent occurrence. This may 
 lead to partial or complete obliteration of the lumen of the vessel by 
 a thickening of the intima (Fig. 71), or it may involve all the arterial 
 coats. Histologically the new tissue formed in syphilitic arteritis is iden- 
 tical in most cases with the product of simple chronic inflammation ; 
 but when arteries are involved in the growth of gummy tumors, the 
 cheesy degeneration characteristic of the latter often affects the vessels 
 also. Syphilitic arteritis is apt to affect smaller vessels, and the de- 
 generative changes do not form so prominent a feature as in other forms. 
 
 In tubercular inflammation, the walls of the arteries, particularly the 
 smaller ones, may be thickened, and their Inmina obliterated. 
 
 The results of arteritis vary greatly, depending upon the size and situ- 
 ation of the affected vessel, and the extent and particular form which the 
 
THE VASCITLAE SYSTEM. 275 
 
 lesion assumes. The vessels may become dilated by a yielding to the 
 blood-pressure of their weakened walls, and aneurisms of various kinds 
 may be thus produced. Thrombi and emboli may be induced by means 
 of the roughened surfaces, common in endarteritis, particularly of the 
 larger vessels. On the other hand, obliterating endarteritis may cause a 
 partial or entire shutting oS of the blood-supply to a part, and a more or 
 less serious interference witli its nutrition or even its death. Hyper- 
 trophy of the left ventricle of the heart may accompany extensive arteritis, 
 as a result of the increased rigidity of the walls of the vessels, or the di- 
 minution of their lumina. 
 
 It is important to remember that a very slight contraction of arteries 
 which have undergone a considerable degree of obliterating endarteritis 
 may produce, for the time being, the same effect upon the part supplied 
 by them with blood that a permanent occlusion would do. Such an oc- 
 clusion of the vessels, and cutting off of the blood-supply may be of the 
 greatest significance, even though it be but temporary, if it involve 
 branches of the coronary or cerebral arteries. Although it is not yet 
 proven that temporary contraction of partially occluded arteries is a 
 sufficient or frequent cause of sudden death, there are cases of sudden 
 death with the symptoms of heart-failure or with the symptoms of 
 hemiplegia, in which the only discoverable lesions are obliterating endar- 
 teritis, respectively, of the coronary or cerebral arteries. We have seen 
 cases of sudden death occurring with symptoms of hemiplegia, in which 
 there was at some point of the middle cerebral artery considerable, 
 although not complete, obliteration of the vessel, but no evidence of de- 
 generation of the brain-tissue supplied by it. ' 
 
 The causes of chronic arteritis und atheroma are in many cases not 
 understood. It may commence in an acute process, or it may be slow in 
 its development. It is very common in old people, and seems often to 
 be of no particular significance. On the other hand, it may, as we have 
 seen, particularly in the smaller arteries, be associated with syphilis, tuber- 
 culosis, or interstitial inflammation of organs. 
 
 DILATATION' AND ANBUEISM. 
 
 (I) Cirsoid aneurism consists in the dilatation and lengthening of 
 large or small arteries. The walls of the artery are thinned, the vessel is 
 tortuous, and in places sacculated. These changes are most frequent in 
 small arteries, especially the temporal and occipital; they involve the 
 trunk of the vessel and its branches, or may extend to the capillaries and 
 small veins. They form larger or smaller tumors beneath the skin. 
 
 > Consult Conheim and v. Schulthess-Rechberg: " ITeber die Folgen d. Kranz- 
 arterienverschliessung fiir das Herz," Virch. Archiv, Bd. 85, p. 503; also Leyden: 
 " Ueber d. Sclerose der Coronar-Arterien u. d. davon abhangigen Krankheitszu- 
 stande," Zeitsch. £. klin. Med., Bd. vii., pp. 459 and 539. 
 
2Y6 THE VASCULAE SYSTEM. 
 
 Earely they are found in the larger arteries, and even in the aorta. 
 
 (3) The ordinary aneurism is a dilatation of the coats of the artery 
 over a larger or smaller part of its course. Such dilatations are usually 
 due to chronic endarteritis and atheroma. According to their shape we 
 may distinguish two varieties: the diffuse and the circumscribed. 
 
 {a) The diffuse, cylindrical, or fusiform aneurism consists in a uni- 
 form dilatation of all the coats of an artery, so that it assumes the shape 
 of a fusiform or cylindrical swelling. In the walls of the dilated portion 
 of the vessel there are often smaller circumscribed dilatations. The 
 wall of the aneurism is atheromatous or calcified; the middle coat maybe 
 atrophied. The arch of the aorta is the most common seat of this form 
 of aneurism; but the entire length of the aorta, or parts of any other 
 arteries, may be dilated in the same way. 
 
 (5) The circumscribed or sacculated aneurism consists either in a 
 dilatation of the entire circumference of an artery over a short portion of 
 its length, or in a dilatation of only a small portion of one side of the 
 wall, so that the aneurism looks like a swelling attached to one side of 
 the artery. The aneurism commences as a dilatation of all the coats of 
 the vessel; but as soon as it attains any considerable size, the middle coat 
 atrophies, so that the wall is composed of the inner and outer coats; or the 
 inner coat is destroyed by endarteritis, so that the outer coat alone forms 
 the wall of the aneurism. As the aneurism increases in size, it presses upon 
 and causes the destruction of the neighboring tissues and viscera, and 
 portions of these tissues and viscera become incorporated with or take 
 the place of the wall of the aneurism. The cavity of the aneurism is 
 filled with fluid or clotted blood, or with layers of fibrin which adhere 
 closely to its wall. The communication between the aneurism and the 
 artery may be small or large. If arterial branches are given off from the 
 aneurism, they may remain open, or become plugged with fibrin; or 
 their walls are thickened and their cavities narrowed by endarteritis. 
 Death is produced by the pressure and interference of the aneurism with 
 the adjoining viscera, or by rupture. The rupture may allow enough 
 blood to escape to destroy life, or the blood may be held in by the soft 
 parts, and a second false aneurism formed about the original one. 
 
 Dissecting aneurisms are those in which, owing to a solution of con- 
 tinuity of the inner layers of the artery, the blood gets between the media 
 and adventitia, and forces its way for a greater or less distance between 
 them. Or, it may separate the media into two layers. 
 
 AliTEUBISMS OF THE DIPFEEBlirT ARTERIES. 
 
 The aorta may be dilated over its entire length; or there may be dif- 
 fuse or circumscribed dilatations at any portion of its course; or there 
 may be several aneurisms situated at different points. The ascending 
 portion of the arch of the aorta may be uniformly dilated in a fusiform 
 
THE VASCULAR SYSTEM. 27T 
 
 shape; or there may be circumscribed dilatations on its anterior wall; or, 
 more rarely, on its posterior wall. The sacculated aneurisms may be of 
 all sizes, and may rupture within the pericardium; or they may form a 
 cavity^in the upper part of the ventricular septum, and communicate by 
 openings into the pulmonary artery and left ventricle; or they may dilate 
 downward between the visceral and parietal pericardium, in front of the 
 heart, pushing that organ backward. They may perforate into the right 
 or left auricle or right ventricle, the superior vena cava, or the pulmon- 
 ary artery; or they may reach a large size, press on and erode the right 
 side of the sternum and adjoining ribs, project under the skin, and even 
 rupture externally. 
 
 The transverse portion of the arch may be dilated in a fusiform 
 shape; or there may be sacculated aneurisms at any point in its wall. 
 The sacculated aneurisms usually reach a considerable size. They press 
 on the sternum and ribs in front, or on the oesophagus, trachea, and 
 bronchi behind. The large arteries given off from the arch may be oc- 
 cluded. They cause death by pressure on the air-passages, the oeso- 
 phagus, and the vena cava; or may rupture externally or into the oeso- 
 phagus, trachea, bronchi, or pleural cavities. 
 
 On the abdominal aorta we usually find aneurisms sacculated. If 
 they are situated high up, they may project into the pleural cavities; if 
 lower down, into the abdomen. They may compress and displace the 
 viscera, vessels, and nerves, and erode the vertebrae. They may rupture 
 behind the peritoneum, into the peritoneal cavity, the pleural cavities, the 
 inferior vena cava, the lungs, the colon, the pelves of the kidney, or the 
 posterior mediastinum. 
 
 Tlie coronary arteries may be dilated throughout, or may be the 
 seat of small sacculated aneurisms. These may rupture into the peri- 
 cardium, or may cause rupture of the heart- wall. 
 
 The pulmonary arteries are rarely the seat of aneurisms. Diffuse 
 and circumscribed dilatations, however, sometimes occur on the main 
 trunk and on the two principal branches of the artery. They do not 
 usually reach a large size, but may cause death by rupture. General 
 dilatation of all the branches of the pulmonary artery is more common. 
 It is found in connection with stenosis of the mitral valves, and with 
 compression or induration of the lung-tissue. 
 
 Of the other arteries of the body, there is hardly any one which may 
 not become the seat of an aneurism, but those of the popliteal artery are 
 most common. 
 
 STENOSIS. 
 
 Stenosis and obliteration of the aorta, at the point of entrance of the 
 ductus arteriosus, has been described in a considerable number of cases. 
 The situation of the stenosis is either exactly at the entrance of the 
 
278 THE VASCTJLAE SYSTEM. 
 
 ductus arteriosus, or close on either side of this point. The degree of 
 stenosis Taries. The aorta may be entirely closed and converted into a 
 solid cord for a length of half an inch; or there may be a circular con- 
 striction through which there is a larger or smaller opening. The con- 
 striction is uniformly circular; or there is a septum springing from the 
 concave side of the vessel at the opening of the ductus arteriosus; or 
 there is a cicatricial-like contraction of the aorta. The walls of the 
 aorta at this point may be thickened and sclerosed. The ductus 
 arteriosus may be closed or open. Above the constriction the aorta is 
 usually dilated; below it, it is normal, dilated, or stenosed. 
 
 Stenosis of the aorta produces hypertrophy of the left ventricle, and, 
 later, of the right ventricle, with venous congestion throughout the bodyl 
 or there may be a collateral circulation developed between the arteries 
 given ofE above and below the constriction; or there may be rupture of 
 the aorta, the right ventricle or auricle. 
 
 This condition is found at all ages, but is produced during foetal life, 
 or in the first year of extra-uterine life. It is probable that it 
 may be caused after birth by an abnormal closure of the ductus arte- 
 riosus. This vessel normally becomes closed without the formation of a 
 thrombus. If a thrombus is formed, it may extend into the aorta and 
 obstruct it; or the ductus arteriosus is filled with a thrombus, but in- 
 creases for a time in size; afterward, as the thrombus is absorbed, the 
 vessel contracts and draws the walls of the aorta together. 
 
 Stenosis of the aorta and of some of the other arteries has been ob- 
 served in a few rare cases, without any known cause. 
 
 Endarteritis, with the production of atheromatous and calcareous 
 patches, may obstruct or entirely obliterate the smaller arteries. This is 
 especially seen in the arteries of the leg, foot, and brain, and in the 
 coronary arteries. The writer (T.M.P.) has seen a case in which the 
 subclavian was completely occluded in this way. 
 
 Narrowing of the aorta and of all its branches, with thinning of the 
 arterial coats, is found as a congenital condition. It usually occurs in 
 females, in connection with imperfect development of the whole body. 
 
 Stenosis from thrombosis or embolism is treated of elsewhere. 
 
 RUPTUEES AND WOUNDS. 
 
 Rupture of arteries is found under the following conditions: 
 1. Patty degeneration or endarteritis, with atheromatous changes, 
 may so soften and destroy the inner and middle coats of an artery as to 
 admit of its rupture. The aorta, just above the valves, is the most fre- 
 quent seat of this lesion. The rupture may run in any direction: its 
 edges are irregular and jagged. The blood may burst through all the 
 coats of the aorta at the same point; or, more frequently, the external 
 coat remains and the blood is infiltrated in the middle coat and between 
 
THE VASCULAR BTSTEM. 279 
 
 it and the external coat. In this way, a dissecting aneurism is formed, 
 which may extend along the aorta for a considerable distance. After a 
 short time, the external coat usually gives Way at some point, and the blood 
 escapes. In rare cases, life is prolonged for some time, the rupture being 
 closed by a new membrane. 
 
 We also find ruptures from fatty degeneration and atheroma in the 
 arteries of the brain and lungs ; in the coronary arteries, the cceliac 
 axis, the mesenteric arteries, and in the arteries of the extremities. 
 
 3. In rare cases, stenosis of a portion of the aorta may cause rupture 
 at some point between the seat of stenosis and the heart. 
 
 3. Contusions, wrenchings, and severe falls may rupture the walls of 
 an artery, either partially or completely, produciiig traumatic or dis- 
 secting aneurisms, or completely severing the vessel. 
 
 4. Penetrating wounds may injure or entirely sever an artery. If 
 the vessel be lauge and the injury severe, death from hemorrhage is the 
 usual result. A small artery may become closed, or be the seat of a false 
 aneurism. 
 
 In the healing of a wounded artery, two conditions co-operate. The 
 vessel retracts and contracts, and a thrombus is formed within it. The 
 contraction may be alone sufficient to close the vessel; its coats thicken, 
 and the iriner surfaces finally are fused together; or the blood coagulates, 
 and forms a thrombus in the vessel near the wound. This thrombus 
 later becomes organized, and the vessel is converted into a fibrous cord. 
 
 Spurious or false aneurisms are found most frequently connected with 
 vessels of the extremities. Wlren an artery is wounded, the blood escapes 
 into the surrounding soft parts, and a cavity is formed filled with blood 
 and broken-down tissue. This condition may -terminate in several ways. 
 
 a. The wound in the artery may heal, and the effused blood be ab- 
 sorbed. 
 
 b. The efiused blood and broken tissues may become gangrenous and 
 the surrounding soft parts be inflamed. 
 
 c. A sort of sac-wall may be formed by the soft parts, while the wound 
 •of the artery remains open, so that we have an aneurismal sac through 
 which the blood is constantly pou.ring. 
 
 5. If an artery be wounded, and at the same time the vein which ac- 
 companies it, we have as the result the conditions called aneurismal varix 
 and varicose aneurism. In aneurismal varix, the artery and vein become 
 adherent at the seat of injury, so that the arterial blood passes directly 
 into the vein. There is a smooth, rounded opening between the two 
 vessels, the vein is dilated into a sac, and the veins emptying into it are 
 dilated and tortuous. 
 
 In varicose aneurism, the artery and vein do not communicate di- 
 rectly, but a false aneurismal sac is formed between the vessels, into 
 which the blood is poured before passing into the vein. 
 
280 THE VASCULAK SYSTEM. 
 
 Varicose aneurism may also be produced by the spontaneous rupture 
 of an aneurism into a vein. Tlie aneurism presses against the vein, be- 
 comes adherent, and finally ruptures into it. This condition has been 
 observed between the aorta and pulmonary artery; the aorta and inferior 
 and superior vena cava; the popliteal artery and vein; the femoral artery 
 and vein; the splenic artery and vena azygos; the internal carotid and 
 sinus cavernosus. Even in cases of perforation by aortic aneurisms, life 
 is usually prolonged for some time. 
 
 6. Destructive inflammation or tumors of the surrounding tissues 
 may invade and destroy a portion of the wall of an artery. Thus ulcera- 
 tion of the trachea, bronchi, bronchial glands, and oesophagus, or 
 tumors of these parts, may perforate the aorta; gangrene of the lungs, 
 the pulmonary arteries; ulcer of the stomach, the gastric arteries, etc. 
 
 Tumors. — Secondary tumors, chiefly carcinomata and sarcomata, 
 may occur in the walls of the arteries by continuous growth from with- 
 out, involving first the external layers. To these layers they are usually 
 confined, for the densityof the inner layers affords such marked resistance 
 to the infiltration of the tumor-cells that they are apt to pass intact 
 through the tumor which grows around them. More frequently, the 
 arteries become secondarily involved in the growth of malignant tumors, 
 by the occurrence, within them, of emboli formed by larger and smaller 
 masses of tumor-cells. 
 
 These emboli are usually of small size, and are apt to get into the cir- 
 culation by growing through the walls of the veins into their lumina. 
 Large emboli from tumors are most apt to occur in the branches of the 
 pulmonary artery. The emboli, formed as they are for the most part by 
 cells capable of growth and proliferation, are apt to soon form connection 
 with the walls of the vessels, and by the growth into them of blood-vessels 
 from the vasa vasorum to find the conditions necessary for their develop- 
 ment, and they may thus soon involve the entire wall of the vessel, and 
 grow out into adjacent parts. 
 
 THE VEINS. 
 
 DILATATION. 
 
 Dilatation of the Veins, or Phlebectasia, presents itself under a va- 
 riety of forms. 
 
 (1) Simple Dilatation. — The vein is uniformly dilated in a cylindrical 
 or fusiform shape; its length is not increased; its walls are of normal 
 thickness, or thinned; the valves increase in size, or are insufficient, or 
 atrophy, or are torn. 
 
 (2) Cirsoid Dilatation. — The vein is imiformly cylindrically dilated, 
 but is also increased in length, so that it assumes a very tortuous course. 
 The walls are normal, thickened, or thinned. 
 
THE VASCULAR SYSTEM. 281 
 
 (3) Varicose Dilatation. — A circumscribed portion of the wall of the 
 vein is dilated so as to form a globular sac. The sac communicates with 
 the vein through a large or small opening. The wall of the sac is formed 
 of the coats of the vein, which preserve their normal thickness, are thick- 
 ened or thinned; the middle coat may disappear entirely. There may be 
 only one such dilatation, or there may be a number on the same vein, or 
 a number of veins may be affected at the same time. The vein may be 
 otherwise normal, or, more frequently, is dilated in the cirsoid form. 
 
 (4) Anastomosing Dilatation. — A number of contiguous and anasto- 
 mosing veins are dilated, both in the cirsoid and varicose forms. The 
 vein then looks like a series of cavities separated by thin partitions. The 
 dilatations of the same vein become adherent to each other and to those 
 of the adjoining veins; portions of the wall of the dilated parts may dis- 
 appear, and we find a number of cavities containing venous blood, and 
 separated from each other by thin partitions. The course of the vein can 
 no longer be followed out. 
 
 Spontaneous cure of dilatations of the veins is not common, and usu- 
 ally occurs only in the lesser degrees of the lesion. Most phlebectasias in- 
 crease steadily in size and extent. Very frequently thrombi form in the 
 dilated veins, and either partially or completely fill them, and these in rare 
 cases may become organized, or the clots may dry and become calcified, 
 forming phleboliths (see p. 53), and by the formation of new connective 
 tissue in the walls, they may become inclosed in a fibrous capsule with the 
 obliteration of the vessel. The wall of the dilated sac may become so thin 
 that it finally ruptures, and the blood is discharged externally. Some- 
 times inflammation is set up in the tissues surrounding the vein, and we 
 find both the surrounding tissues and the wall of the vein the seat of 
 purulent infiltration or fibrous thickening. The parts of the body from 
 which the dilated veins draw their blood may exhibit the results of 
 chronic venous congestion, oedema, hyperaemia, and hypertrophy or ulce- 
 ration. 
 
 When occurring in mucous membrane, dilated veins are usually associ- 
 ated with persistent catarrh. There is hardly one of all the veins of the 
 body which may not be dilated. The hemorrhoidal veins, the veins of the 
 leg and thigh; those of the pelvis and pelvic viscera; those of the spermatic 
 cord, scrotum and labia; those of the abdominal wall; those of the neck 
 and arms; are the ones most frequently found in this condition. 
 
 The causes of dilatation are principally some mechanical obstruction 
 to the passage of the blood through the veins towards the heart; but 
 changes in the walls of the vessels from inflammation or injury, etc., are 
 not without influence. 
 
 WOUNDS. KUPTUKE. 
 
 Wounds of the veins usually heal by a simple contraction and an ad- 
 
282 THE VASCULAR SYSTEM. 
 
 hesive inflammation of their walls: sometimes by the formation of a 
 thrombus. Eupture of the veins may be produced by sevei'e contusions 
 and crushings of the body, and by violent falls. Perforation of a vein 
 may be produced by suppuration of the soft parts, and the invasion of 
 the walls of the vessel; by the pressure of an aneurism or of a new growth; 
 by the thinning of the wall of the vein in phlebectasia. 
 
 INFLAMITATION. 
 
 Inflammation of the veins, phlelitis, may involve chiefly the external 
 layers — periphlebitis, or the internal — endoplileiitis, or, as is very fre- 
 quently the case, the entire wall may be affected. Phlebitis may be 
 •caused by the presence of a thrombus, by injuries, or by an inflammation 
 of the surrounding tissues. Thrombosis of the vein, either primary or 
 secondary, is a very constant accompaniment of phlebitis. 
 
 Acute phlelitis may commence as a suppurative periphlebitis or as a 
 result of inflammatory processes about the vessel. The outer layers of 
 the venous wall are congested, swollen, infiltrated with serum and pus. 
 The inner coats may become infiltrated with pus, they may become 
 necrotic and disintegrate. A thrombus is constantly formed under these 
 ■conditions, which may for a time stop the circulation, and keep the pro- 
 ducts of inflammation and degeneration from mixing with the blood, but 
 the thrombus itself is prone to disintegration, and thus the exudations and 
 decomposing fragments of tissue may enter the circulation. 
 
 On the other hand, owing to the presence of irritating or infectious 
 material within the vein and the formation of a thrombus, the inflamma- 
 tory process may be at the commencement an endophlebitis, but usually, 
 if the inflammation be at all severe, the entire wall of the vessel will 
 eventually be involved. The pus-cells in both oases doubtless come from 
 emigration from the vasa vasorum. Acute phlebitis may terminate in 
 the absorption of the thrombus, and the return of the vein to its normal 
 condition; in the obliteration of the vein; or portions of the thrombus 
 may become detached, and find their way as emboli into various parts of 
 the body. The most important results of jDhlebitis are usually those 
 which depend upon the introduction into the blood of these emboli, or 
 ■of septic material (see thrombosis and embolism, p. 51, and pysemia). 
 
 Chronic periphlebitis produces thickening, principally of the outer 
 ■coats of the veins, but the inner coats may also be involved. The sur- 
 rounding tissue may be also thickened and coalesce with the walls of the 
 vein. There may or may not be thrombosis. 
 
 Chronic endophlebitis is a not very common lesion, of the same gen- 
 eral character as chronic endarteritis. More or less circumscribed patches 
 ■of new connective tissue are formed in the inner coats, which may 
 undergo fatty or calcareous degeneration. 
 
 Tubercular inflammation of the walls of the veins may occur as an 
 
THE VASCULAK SYSTEM. 283 
 
 extension of the process from without. This is not infrequent in the 
 pulmonary veins, and Weigert has recently called attention to the fact 
 that in acute miliary tuberculosis the growth of tubercle tissue into the 
 lumina of these veins from tubercular lymph-glands is of frequent 
 occurrence, and readily explains the topography and mode of occurrence 
 of the general disease. The tubercle bacilli which are present in the 
 tubercular tissue growing into the lumen of the veins, find thus an easy 
 distribution. 
 
 Syphilitic inflammation may involve the walls of the veins either as 
 gummy tumors or as more diffuse thickenings. 
 
 TUMOES. 
 
 Primary tumors of the veins are rare. Small leiomyoviata have been 
 described in the saphenous and ulnar veins. A myosarcoma as large as 
 a man's fist has been described, situated in the dilated vena cava inferior. 
 The veins are not infrequently secondarily involved by sarcomata and 
 carcinomata, and sometimes by cliondromata. Tlie thin walls of the veins 
 oSer comparatively little resistance to the encroachment of malignant 
 tumors which thus gain access to the circulation, and may form metas- 
 tases in various parts of the body. 
 
 PARASITES.- 
 
 Ecliinococcus is sometimes found in the veins, having either developed 
 there or perforated from without. 
 
 Two species of distojna {liver flitke) occur in man. D. hepaticum 
 occurs rarely in man, and while usually found in the bile-ducts, may occur 
 in the vena cava. D. hcematobium is very common in man in Egypt and 
 in other parts of Africa, and usually occurs in the portal vein or its 
 branches, and frequently in other veins. 
 
 THE CAPILLARIES. 
 
 The walls of the capillaries are so thin and so intimately connected 
 with the surrounding tissues that their lesions are studied most appro- 
 priately among the diseases of the several organs. Dilatation of the new^ 
 formed capillaries in tumors, granulation tissue, etc., and fatty degen- 
 eration of their walls, may be mentioned here as readily observed lesions 
 occurring under a variety of conditions. The changes which we assume 
 to occur in the walls of the smaller veins and capillaries in exudative 
 inflammation by reason of which fluids and blood-cells pass through 
 them, are not yet sufficiently understood to be described with definite- 
 ness. 
 
 THE LTMPH-TESSELS. 
 
 The smaller lymph-vessels can hardly be treated as independent 
 structures, since their walls are so closely joined with the tissues through 
 
284 THE VASCULAE SYSTEM. 
 
 which they pass ; the lymph radicles indeed being nothing more than 
 the spaces in the connective tissue in which the variously-shaped con- 
 nective-tissue cells lie. In the larger lymph-vessels we find a moderate 
 number of more or less independent lesions. 
 
 INFLAMMATION {Lymphangitis). 
 
 Inflammation of the larger lymph-vessels is usually secondary, and 
 connected with some wound or injury. Owing, it is believed to the 
 entrance into the lymph-trunk of some septic material or bacteria, the 
 vessels, sometimes for a considei-able distance away from the wound, 
 become red, tender, and painful. Under these conditions, the micro- 
 scopical appearances which the vessels present vary. In some cases the 
 redness disappears after death, and we find no appreciable alteration. 
 In other cases we find the walls of the lymph-vessels more or less densely 
 infiltrated with pus-cells, and the lumen may contain variable quantities of 
 pus and fibrin and desquamated endothelium. The tissue about the 
 vessels may also be infiltrated with serum and pus. These changes may 
 undergo resolution and the vessel be restored to its normal condition ; 
 or the vessel-wall and surrounding tissue may die or become involved in 
 abscess; or new connective tissue may form in and about the vessel, 
 sometimes with obliteration of its lumen. The lymph-glands may par- 
 ticipate in the inflammatory process. 
 
 Inflammation of the lymph-vessels may occur as the result of dissection 
 and other wounds, and the bites of venomous reptiles. It may occur in 
 the uterine lymphatics in the phlegmonous form of puerperal fever, and 
 under other conditions. 
 
 Tubercular Lymphangitis. — Tubercular inflammation occurs both in 
 large and small lymph-vessels. Miliary tubercles and diffuse tubercle 
 tissue may form in the walls and project into the lumen of the larger 
 trunks ; or in the smaller vessels the new growth may entirely fill the 
 lumen, and grow in this, with more or less involvement of the walls. 
 This may occur independently, but it is most frequently seen in connec- 
 tion with tubercular inflammation of adjacent tissues. Thus from tuber- 
 cular lymph-glands in the vicinity of the thoracic duct there may be a 
 direct extension of the tubercular inflammation, an involvement of the 
 walls of the duct, and a growth of tubercle tissue into its lumen. 
 Such growths in the thoracic duct have been shown by Weigert to be 
 frequent in acute general miliary tubercnlosis, and very satisfactorily 
 explain, on the hypothesis of the bacterial origin of the disease, the dis- 
 semination of the tubercles. In the vicinity of tubercular ulcers in the 
 intestines, furthermore, we often see the subserous lymph-vessels, 
 which pass from the vicinity of. the ulcers, distended with the products 
 of tubercular inflammation, andlooking like dense white knobbed cords. 
 
 Syphilitic inflammation of the lymph-vessels not infrequently occurs 
 
THE VASCULAE SYSTEM. 285 
 
 in the Ticinity of syphilitic ulcers in the primary stage. In later stages 
 there may be thickening of the walls of the Tessels and the develop- 
 ment of gummy tumors in and about them. 
 
 LTMPHANGIECTASIS. 
 
 Dilatation of the lymph-vessels occurs under a variety of conditions. 
 It may be congenital, or it may be due to some hindrance to the flow of 
 lymph onward, as by jsressure from any cause, or from the occlusion of 
 the vessels by inflammation, or it may be produced by unknown causes. 
 If the dilated vessels form a circumscribed mass, this is often called a 
 lymphangioma. In certain forms of elej>Jiantiasis and in macroglossia 
 the dilatation of the lymph-vessels is an important factor. Its occur- 
 rence is not infrequent in the labia, prepuce, and scrotum. 
 
 TUMOES. 
 
 The relation of the endothelium of the lymph-vessels and spaces to 
 endotheliomata has been already mentioned on p. 133. 
 
 The dissemination of malignant tumors through the lymph-channels 
 is of frequent occurrence and is particularly marked in the case of carci- 
 noma.' In the vicinity of carcinomata, the lymph-vessels are not infre- 
 quently crowded with the tumor-cells forming white irregular cords; or 
 small masses of the tumor-cells may be found in the lymph-vessels, either 
 near to or remote from the tumor. White irregular networks are often 
 formed in this way beneath the pleura in carcinoma of the lung (Fig. 48), 
 or beneath the capsule of the liver. Transverse sections of lymph- vessels 
 thus distended show sometimes swelling a.nd detachment of the endothe- 
 lium and a crowding of the lumen with tumor-cells. Whether or not 
 the endothelium participates in the new formation of the characteristic 
 carcinomatous cells is not known. 
 
 THE LYMPH-GLANDS. 
 
 It is well, in studying the lesions of the lymph-glands, to remember 
 that they are structures so placed in the course of the lymph-vessels that 
 the lymph, in flowing towards the larger central trunks, passes through 
 them, undergoing a sort of filtration, as it percolates through the trabec- 
 ulse of the lymph-sinuses. If this simple fact be borne in mind, the dis- 
 -eases of the lymph-glands, which are, in the majority of cases, secondary, 
 are much more readily understood. Particles of pigment which in any 
 way get into the lymph- vessels are carried along until a lymph-gland is 
 reached, and here they are, in part at least, deposited among the trabeculse 
 ■of the sinuses, while the lymph passes on and out of the efferent vessels. 
 The same thing occurs when cells from malignant tumors, bacteria of 
 various kinds, etc., gain access to the lymph-vessels, and also, as there is 
 good reason for believing, in the case of many infectious materials which 
 
286 THE TASCULAE SYSTEM. 
 
 our present knowledge does not enable us to definitely associate with 
 bacteria. These various materials, filtered out of the lymph by the 
 glands, may act in a variety of ways to produce lesions in them. 
 
 INFLAMMATION. 
 
 Acute Inflammation of the lymph-glands usually occurs in con- 
 nection with some inflammatory process in the region from which its 
 lymph is gathered. The glands are, in the majority of cases, swollen, 
 reddened, and softer than normal, and often the seat of smaller and 
 larger hemorrhages. Sometimes one, sometimes several glands of a cluster 
 are afEected. 
 
 The microscopical examination shows the most prominent change to 
 be a great increase in the number of cells in the follicles and cords, as 
 well as in the lymph-sinuses. These cells are, in part, small and 
 spheroidal, and similar to those normally filling the meshes of the folli- 
 cles; in part, large polyhedral or variously-shaped cells, with prominent 
 nuclei; the latter cells are most abundant in the lymph-sinuses. In ad- 
 dition to this, there is swelling of the endothelial cells of the reticulum 
 of the sinuses. The blood-vessels may be distended with blood, or there 
 may be blood, in greater or less quantity, free in the sinuses and folli- 
 cles. The origin of the large number of new cells which may form in a 
 very short time is not yet definitely known. They may be emigrated 
 leucocytes or their derivatives; they may be derivatives of the endothe- 
 lium of the reticulum; or they may be in some cases, at least in part, cells 
 which have been brought into the gland, through the afferent trunks, 
 from some external inflammatory focus. The capsule of the glands, and 
 not infrequently the connective tissue about them, may also be infiltrated 
 with round cells. 
 
 Acute inflammation may terminate in resolution, the new cells dis- 
 appearing either by fatty or other degeneration, or by being carried off 
 in the lymph, and the gland return to its normal condition. This is 
 the rule in the less intense forms of inflammation. On the other hand, 
 the inflammatory process may become ijurulent and so intense as to lead 
 to the formation of abscess, usually with a gi-eater or less involvement of 
 the tissue about the gland. There may be at first numerous small ab- 
 scesses which coalesce to form larger ones. These ahscQasea— buboes — 
 may open externally or internally, or they may become dried and con- 
 verted into cheesy masses which may calcify and, by a chronic inflamma- 
 tion in their periphery, become inclosed by dense connective tissue. 
 Sometimes, instead of abscess being formed, the tissue of the inflamed 
 glands becomes necrotic and breaks down, inducing more orless severe in- 
 flammatory or necrotic changes in the tissues in their vicinity. 
 
 In still other cases, acute inflammation of the lymph-glands passes 
 into the chronic form. 
 
THE VASCULAE SYSTEM. 287 
 
 Moderate degrees of inflammation in the lymph-glands are very com- 
 mon in connection with various forms of inflammation in neighboring 
 parts. Thus simple pharyngitis, gastro-enteritis, erysipelas, simple 
 purulent inflammation, etc., are often associated with this lesion of the 
 glands. The lymph-glands of children are, as a rule, more easily affected 
 by moderate inflammations in neighboring parts than are those of adults. 
 Purulent inflammation of the lymph-glands is most frequently associated 
 with severer forms of inflammation of adjacent or related parts, espe- 
 cially those of an infectious character, syphilitic inflammation, poisoned 
 wounds, pysemia, etc. In a certain number of cases, we find bacteria in 
 the inflamed lymph-glands, either singly or in zoogloea colonies, which 
 have presumably something to do with the lesion. 
 
 Chronic Inflammation. — This is characterized by an increase of the con- 
 nective-tissue elements of the gland, with a gradual and commensurate 
 disappearance of the lymphoid cells. The reticulum of the follicles and 
 sinuses becQmes thickened and fibrous, and in the trabeculae and capsule 
 new connective tissue is formed until, in advanced cases, the entire gland 
 may be more or less completely converted into a mass of connective 
 tissue. This condition is very frequently seen in the lower tracheal and 
 in the bronchial glands, apparently as a result of the lodgment in them 
 of respired pigment particles; but it may occur in any glands, either as a 
 result of repeated moderate degrees of inflammation, or from causes 
 which we do not know. In some cases, the glands are greatly enlarged, 
 and the new tissue contains many large cells, while in other cases the con- 
 nective tissue is dense and contains but few cells. 
 
 Pigmentation. — The pigment which is very frequently found in 
 lymph-glands may be derived from the haemoglobin of the blood, either 
 in the glands themselves, or in remote jiarts, or it may be formed of various 
 materials introduced into the body from without, such as the fiignients 
 used in tattooing; respired dust particles of various kinds, coal, stone, 
 iron, etc. The pigment particles, which usually first lodge in the lymph- 
 sinuses, may collect here in large quantities, either in the reticulum or 
 the cells lying in its meshes; they may penetrate the follicles and cords 
 and find permanent lodgment there. They usually induce a greater or 
 less degree of chronic inflammation, so that in extreme cases, such as are 
 frequently seen in the bronchial glands, nothing is finally left of the 
 gland but a more or less deeply pigmented mass of dense connective 
 tissue. The function of the gland is of course, in this way, partially or en- 
 tirely destroyed. The pigment in these cases appears to reach the gland 
 in part by being carried along free in the lymph-current, in part by be- 
 coming inclosed in leucocytes and being transported by them. Pigmen- 
 tation of the glands is most marked in those about the root of the lungs 
 which are frequently of a mottled gray or a black color, but it may oc- 
 cur in the mesenteric and other glands. Under similar conditions, the 
 
288 THE VASCFLAE SYSTEM. 
 
 diffuse lymphatic structure in the lungs and liyer may be similarly pig- 
 mented. 
 
 Inflammation of the Lym2}li- Glands with Cheesy Degeneration.^T\\\s 
 lesion of the lymph-glands, which is distinct from the above-mentioned, 
 comparatively infrequent cheesy degeneration of the contents of old ab- 
 scesses, commences with changes similar to those above described in sim- 
 ple inflammation. The gland in this condition is swollen, and feels harder 
 than normal; on section it has a u.niform, reddish-gray color. Mi- 
 croscopical examination reveals a great increase in the number of paren- 
 chyma cells, some small and spheroidal, others larger and polyhedral. 
 Sometimes the larger cells are multinuclear, and not infrequently the re- 
 ticular framework and the capsule are thickened. As the process advan- 
 ces, the characteristic necrotic changes make their appearance. We may 
 find at first a greater or less number of the cells converted into a strongly 
 refractile material, and the nuclei no longer capable of being stained. 
 Then larger and smaller masses of cells undergo cheesy degeneration 
 with complete destruction of the blood-vessels, reticulum, and the sphe- 
 roidal and other cells, and their conversion into a granular material. A 
 section through the gland in this condition shows the cut surface mot- 
 tled with irregular-shaped, larger and smaller opaque white patches, 
 which indicate the areas of cheesy degeneration. These patches may 
 Increase in size and coalesce, so that a large part of, or even the entire 
 gland, may be converted into a more or less dense cheesy mass which 
 may be surrounded by the thickened cajDsule. 
 
 In this condition they may remain for a long time, and not infre- 
 quently, owing to the involvement of a series of associated glands, either 
 simultaneously or one after another, and the increase of connective tis- 
 sue about them, we find large irregular nodular masses made up of a con- 
 geries of similarly affected glands. 
 
 On the other hand, the cheesy material may soften and break down, 
 and by the establishment of purulent and necrotic inflammation about 
 them, abscesses may form, which may open externally. These abscesses 
 may heal; but usually the healing is difficult and slow, and long-contin- 
 ued suppurations, frequently with the development of flstulffi, are very 
 common. Under these conditions, the inflammation may assume a tu- 
 bercular character. Instead of softening, the cheesy material in the 
 glands may become dry and hard, and undergo calcification. 
 
 Cheesy inflammation of the lymph-glands is most common in the cer- 
 vical, bronchial, and mesenteric groups, but may occur anywhere. It is 
 most apt to occur in badly nourished young persons, who in addition to 
 the lesion of the lymph-glands, are very liable to suffer from chronic in- 
 flammations of the mucous membranes, skin, periosteum, joints, and the 
 subcutaneous and other connective tissues. This general condition is 
 known as scrofula, and the lesion of the glands is sometimes called scro- 
 
THE VABCULAE SYSTEM. 289 
 
 fulous inflammation. It is not infrequently associated with tubercular 
 inflammation of the glands, either as an independent lesion or as a part 
 of a general tuberculosis, and by some writers tuberculous and scrofulous 
 inflammation of the lymph-glands are considered to be identical. In a 
 considerable proportion of cases, however, of so-called scrofulous inflam- 
 mation of the lymph-glands, there is no formation of tubercle tissue, and 
 we find no tubercle bacilli, so that we must consider this class of cases 
 as simply inflammatory, with a tendency to cheesy degeneration. 
 
 Tubercular inflammation may occur in connection with simple in- 
 flammatory changes in the lymph-glands, or with the form of inflamma- 
 tion which tends to cheesy degeneration. It may be local, confined to the 
 glands, or it may occur in connection with general acute miliary tuber- 
 culosis or with tubercular inflammation of single organs. It may occur 
 in single glands or in several glands of the same group, or in groups situ- 
 ated in different parts of the body. In its simple and acute form, there 
 may be no evident change to the naked eye in the appearance of the 
 glands, or they may be besprinkled with small grayish-white translucent 
 spots. Under these conditions, the glands may be reddened and soft, or 
 swollen and denser than normal. In more advanced forms of the lesion, 
 the tubercles coalesce, and undergo a greater or less degree of cheesy de- 
 generation. Under these conditions, the cheesy areas are evident to the 
 naked eye as more or less sharply circumscribed, opaque whitish areas, 
 frequently surrounded by an irregular, more translucent grayish zone of 
 tubercle tissue, which merges insensibly into the adjacent tissue. The 
 entire gland may become involved, and more or less completely converted 
 into a cheesy mass, in the periphery of which a zone of tubercle tissue 
 may or may not be evident. 
 
 Microscopically the small nodules or miliary tubercles are seen to con- 
 sist of more or less circumscribed collections of small spheroidal, or more 
 frequently larger polyhedral cells, with or without well-defined giant-cells. 
 They usually commence to form in the follicles and lymph-cords of the 
 nodes, and from these may spread and involve the entire surrounding 
 tissue. Tlie cheesy degeneration, which here as elsewhere is apt first to 
 involve the central portions of the tubercles, presents the usual appear- 
 ances. Tubercle bacilli may be found in the edges of the cheesy areas, 
 or in the tubercle tissue about them. 
 
 Simple inflammatory changes regularly occur in the periphery of the 
 tubercles. There is an increase of cells in the lymph sinuses and follicles, 
 and a more or less marked swelling, and apparently a proliferation of the 
 cells of the reticular tissue of the gland. In cases in which the process 
 is chronic, there is often marked increase in the connective tissue of 
 the glands: the reticular tissue becomes dense and fibrous, and the 
 trabeculse and capsule are thickened. The tubercles themselves, instead 
 19 , 
 
290 THE VASCULAE SYSTEM. 
 
 of undergoing cheesy degeneration, may become fibrous or be converted 
 into a hyalin material. 
 
 Tlie cheesy material may dry and shrink, and become inclosed by a 
 capsule of dense connective tissue and become calcified; or it may soften, 
 and thus cavities be formed in the glands filled with grumous material; 
 or inflammatory changes may be induced in the vicinity of the glands, 
 leading to abscesses. On the other hand, hyperplastic inflammation in 
 the periphery of the affected glands may result in their becoming bound 
 together into a dense nodular mass. 
 
 When cheesy degeneration has occurred, to the naked eye tuberculous 
 lymph-glands may not be distinguishable from those in scrofulous' in- 
 flammation, but in some cases the nodular character of the new tissue 
 around the cheesy centres is evident. The process is usually a slow and 
 chronic one, except when occurring in connection with acute miliary 
 tuberculosis in other parts of the body. It may occur in any of the 
 glands, but is most frequent in those of the bronchial, mesenteric, and cer- 
 vical regions. 
 
 Syphilitic Inflammation. — The lesions of the lymph-glands, which 
 occur in connection with syphilitic poisoning, vary greatly, depending 
 upon the stage of the disease. In the primary stages, the lymph-glands 
 in the region of the seat of infection are ajDt to present the lesions of an 
 ordinary acute inflammation with a tendency to the assumption of the 
 purulent form. 
 
 In the secondary stage of the disease, the glands of other regions, 
 neck, elbow, axilla, etc., are frequently swollen and hard. On micro- 
 scopical examination, there maybe an increase of connective tissue in the 
 capsule and trabeculse, but the chief change is in the accumulation in the 
 follicles and lymph sinuses of larger and smaller spheroidal and poly- 
 hedral cells. The reticular tissue may be thickened, and the walls of the 
 blood-vessels infiltrated with cells. In this condition, the glands may 
 remain for a long time, not tending to form abscess; or they may undergo 
 resolution through degeneration and absorption of the cells. 
 
 In the tertiary stage of the disease, the glands may be the seat of chronic 
 inflammation characterized by the formation of gummy tumors. Under 
 these conditions, they may form large firm nodular masses by the grow- 
 ing together by new connective tissue of several altered glands. The gross 
 and microscopical characters of gummata of the lymph-glands are in the 
 main similar to those in other parts of the body (see p. 105). 
 
 There are important changes in tlie lymph-glands which occur as 
 local manifestations of general diseases, such as typlioid fever, leprosy, 
 etc., which will be considered under the heading of tliese diseases. 
 
 Degenerative clianges in the lymph-glands, with the exception of those 
 above described, are not of great frequency nor significance. 
 
 Atrophy is a very regular occurrence in old age. In this condition. 
 
THE VASCULA.E SYSTEM. 291 
 
 the glands are small, hard, and, unless pigmented, white. Microscopical 
 examination shows a marked diminution in the number of parenchym- 
 cells, while the reticulum and the capsule and trabeculse may be thick- 
 ened. There may be an accumulation of fat around the gland in con- 
 nection with senile atrophy. 
 
 It should be remembered, in this connection, that the lymph-glands as 
 well as the lymphatic tissue' in general, in children are more voluminous 
 and contain a greater number of parenchyma cells than in adults. 
 
 Amyloid degeneration of the blood-vessels and reticulum of the lymphs 
 glands occurs under the conditions which favor this change in general- 
 It may occur in connection with amyloid degeneration of other parts of 
 the body, or by itself. It may occur in glands otherwise normal or in 
 those which are the seat of other lesions; thus in simple chronic or tuber- 
 cular inflammation. It is frequently found in the mesenteric glands in 
 connection with waxy degeneration of the intestinal mucous membrane. 
 
 Hyalin degeneration of the external layers of the smaller arteries and 
 the capillaries of the lymph-glands and also of the parenchyma cells oc- 
 curs occasionally in old age or in connection with wasting diseases. The 
 vessels and cells are swollen and converted into a translucent, strongly 
 refractile substance resembling amyloid optically, hut not responding to 
 its micro-chemical tests. By the accumulation of this material the un- 
 involved parenchyma of the glands may be compressed and atrophied. 
 
 Hyperplasia of the Lymph-glands [Lymphoma). 
 
 In addition to the considerable enlargements of the lymph-glands in 
 inflammation which have been described above, they become enlarged 
 under a variety of conditions which we do not understand. This lack 
 of knowledge of the etiology, together with our ignorance of the func- 
 tion of the lymph-glands, and the morphological similarity or even 
 identity which these enlarged glands present, render it very difficult to 
 decide upon the exact nature of the change, and in many cases to 
 distinguish one form from another. 
 
 In the first place, there is a class of cases in which, sometimes 
 slowly, sometimes with great rapidity, the lymph-glands of certain 
 
 ' What we call lymphatic tissue embraces not only the lymph-glands and the 
 less complex, but still well-defined structures found in the stomach, intestines, 
 tonsils, and elsewhere, and called lymph-follicles; but also the less well-defined, 
 irregular masses of tissue resembling that of lymph-follicles, which, as Arnold has 
 shown (Virchow's Archiv, Bd. 80, p. 315; Bd. 82, 894; Bd. 83, 289; Bd. 87, p. 114), 
 is widely disseminated in variable amounts in different parts of the body; in the 
 lungs, beneath the pleura and elsewhere; in the liver, kidneys, etc. Although 
 the exact nature of these more diffuse masses of lymphatic tissue is but little 
 understood, as indeed is that of the lymph follicles and glands themselves, there 
 is reason to believe that they are analogous structures and prone to be affected by 
 similar deleterious agencies. 
 
292 THE TASCULAE SYSTEM. 
 
 regions, especially the abdominal, axillary, cervical, and inguinal, enlarge 
 not infrequently to an enormous extent. They may be either hard or 
 soft, even almost fluctuating; the individual glands may be distinct or 
 merged into one another. Sometimes the glands in nearly all parts of 
 the body are affected. Microscopically we find that the enlargement is 
 due, in the soft varieties, to an enormous increase of small spheroidal and 
 polyhedral cells, and a growth of the reticular tissue. It is a new for- 
 mation of lymphatic tissue, but the normal relations of follicles, cords, 
 and lymph-sinuses is not preserved. In the harder varieties, there is a 
 thickening of the reticular tissue in addition to an increase of cells. In 
 very rare cases, portions of the glands may become cheesy. Sometimes 
 larger and smaller hemorrhages occur in the glands, especially in the 
 softer forms. In addition to these changes in the lymph-glands, there 
 is, in a considerable proportion of cases, a new formation of lymphatic 
 tissue in greater or less quantity in other parts of the body, in the sjileen, 
 in the gastro-intestinal canal, in the marrow of bones, in the liver, kid- 
 neys, etc., and the number of leucocytes in the blood and in other parts of 
 the body is increased. This general condition is known as leickmrnia and 
 will be considered under the general diseases. The enlarged lymph-glands 
 in this disease may be called, for convenience, leukcBinic lympJiomata. 
 
 In the second place, there is a form of disease in many respects, par- 
 ticularly in the lesion of the lymph-glands, identical with leukaemia. 
 There is, however, usually a less prominent involvement of the spleen 
 and other lymphatic structures, and what is more striking, no increase 
 in the number of leucocytes in the blood. This is called Hodglcin's dis- 
 ease or pseudo-Ieiokceinia, and the enlarged lymph-glands may in this case 
 be called pseudo-leuhcBinic lymphomata. The lesions of the lymph-glands 
 are identical in both diseases, and it is convenient to assign different names 
 to them simply because, for reasons which we do not at all understand, 
 they seem to arise under difEerent conditions, and to be associated with a 
 constant difference in the character of the blood. 
 
 Tumors. — Sarcomata occur in the lymph-glands as primary and 
 secondary tumors, and these may be of various forms: spindle-celled, 
 large and small round-celled, and angio-sarcomata. It is not easy in 
 many cases to distinguish morphologically between the small round- 
 celled sarcomata and the above-described lymphomata. Fibromata, myxo- 
 mata, and cliondromata occur in the lymph-glands, but are rare. Endo- 
 theliomata are described, but are not common. Secondary carcinomata are 
 of frequent occurrence, the form of the cells and the nature of their growth 
 depending upon the seat and character of the primary tumors (Fig. 50). 
 
 Parasites. — Aside from various forms -of bacteria which are not in- 
 frequently found in the lymph-glands, thus in diphtheria, S23lenic fever, 
 typhoid fever, tuberculosis, etc., 7??arm, tr ichince, -cind pentastomum have 
 been described. 
 
THE ALIMEKTART OANAL. 
 
 THE MOUTH. 
 
 MAlFOEMATIOiq^S. 
 
 Malformations of the li]3 and cheeks are usually associated with de- 
 fective formation of the bones of the mouth. The entire process is gen- 
 erally due to an arrest of development. 
 
 (1) The lower jaw is absent; the upper jaw and hard palate small and 
 imperfectly formed; the temporal bones nearly touch in the median line. 
 The lower part of the face is, therefore, wanting; the mouth is absent, or 
 small and closed posteriorly; the tongue is absent. Such a malforma- 
 tion is rare; the foetus is not viable. 
 
 (2) The face remains in its early foetal condition of a large cleft; 
 the mouth and nose form one cavity; the orbits may be united in the 
 same cavity. The fcetus is not viable. 
 
 (3) There is a cleft in the upper lip, upper jaw, and hard palate 
 The cleft corresponds to the point of junction of the processes of the 
 superior maxilla with the intermaxillary bone. There may be one cleft 
 or two, one on either side of the intermaxillary bone. The cleft involves 
 the lip alone, or the lip and superior maxilla, or the lip, maxilla, and 
 palate. There may be a single or a double cleft in the palate; and the 
 cleft may involve either the hard or soft palate, or both. If there are, 
 two clefts of the lip and maxilla, the portion of lip and bone between 
 them may be small, or entirely absent, so as to leave a large open space. 
 The soft palate may be entirely absent. This is a common malforma- 
 tion, and does not endanger life. 
 
 (4) Earely we find a cleft involving the middle of the lower lip, and 
 sometimes extending into the inferior maxilla. 
 
 (5) Either the inferior, the superior, or both maxillary bones may be 
 abnormally small. 
 
 (6) The edges of the lips may be partly or completely joined together. 
 The opening of the mouth may be only a round hole. 
 
 (7) The lips may be absent or imperfectly developed. 
 
294 THE ALIMENTAET CANAL. 
 
 (8) The corners of the mouth may be prolonged by clefts in the 
 cheeks nearly to the ears. 
 
 HTPEKTROPHT. 
 
 The skin of the cheeks and lips may be hypertrophied in connection 
 with elephantiasis of the face. 
 
 There may be a thickening of the lips alone, so that they appear dou- 
 ble. This thickening may be due to an increase of all the anatomical 
 elements of the lips; or there may be an increase and dilatation of the 
 lymphatic vessels, giving to the growth a soft, (Edematous character. 
 
 INFLAMMATION". 
 
 Catarrhal Stomatitis is found most frequently in children. It is pro- 
 duced by a great variety of local and constitutional causes. Of the con- 
 ditions which are seen during life, the congestion, increased production 
 of mucus, and swelling of the mucous membrane, but little remains after 
 death. 
 
 During life, the congestion and swelling of the mucous membrane are 
 well marked. There are often white patches, produced by the death of 
 the superficial epithelial cells. There may be an increased production of 
 mucus, which runs constantly from the mouth, or, instead of this, the 
 entire mucus membrane is unnaturally dry. 
 
 The only structural changes which can be demonstrated are the de- 
 generative changes of the epithelial cells and the production of pus-glob- 
 ules, which infiltrate to a moderate degree the stroma of the mucous 
 membrane and appear on its surface. 
 
 Croupous Stomatitis is produced by local irritants, by extension of 
 the same form of inflammation from the pharynx, and it occurs with the 
 exantliematous fevers and with diphthei'ia. 
 
 Portions of the mucous membrane are swollen, and congested, and 
 covered with a false membrane. This false membrane is composed of a 
 thickened layer of epithelium in the condition of coagulation necrosis, 
 and of fibrin and pus in variable relative quantity. The stroma of the 
 mucous membrane is infiltrated with pus and fibrin, and portions of it 
 may become necrotic. 
 
 STOMATITIS ULCEROSA.' [Stoviacace. Stomatite Ulcero-membraneiise.) 
 
 This form of stomatitis occurs regularly in children between the ages 
 of four and eight years, and in adults between the ages of eighteen and 
 twenty-five years. It is apt to occur in localized epidemics, in hospitals 
 and asylums, and among soldiers and sailors. Some of the forms of mer- 
 curial stomatitis seem to be identical with this form of inflammation. 
 
 'Bergeron: "Stomatite ulcerosa." Union Medicale, 1859. Bohn: " Mund- 
 krankheiten der Kinder," 1880. 
 
THE ALIMENTAET .CANAL. 295 
 
 The inflammation begins at tlie margin of the gams of the lower jaw. 
 The gums are swollen and coated with a grayisli, soft matter, composed 
 of bacteria and detritus. Then follows destruction of tissue, the gums 
 are destroyed around the teeth, and these fall out; the inflammation ex- 
 tends to the lips, cheeks, and tongue. The ulcers are coated with a 
 thick, soft, gray membrane. The surrounding soft parts are swollen, 
 and there may be necrosis of the jaws.' 
 
 GANGRENE. 
 
 Gangrene of the lips and cheeks, or noma, is most frequent in ca- 
 chectic children as a consequence of the abuse of mercury. Much more 
 rarely it occurs in adults after typhus and other exhausting diseases. 
 The disease begins in the mucous membrane of the cheeks near one of 
 the corners of the mouth. The mucous membrane becomes black and 
 gangrenous; the gangrene extends rapidly through the entire thickness 
 of the cheek, and produces perforation; it extends laterally in all direc- 
 tions. 
 
 Syphilitic Stomatitis. — As a result of syphilis, there may be produced 
 €ither the so-called mucous patches or gummy tumors. In the mucous 
 patches, we find at first the epithelial layer thickened and the papillse of 
 the stroma swollen and infiltrated with cells. This may be followed by 
 desquamation of the epithelium and ulceration of the stroma. 
 
 The deeper gummy tumors may also soften and form ragged ulcers of 
 some size. 
 
 Tubercular Stomatitis commences with the formation of miliary 
 tubercles or of larger tubercular masses in the stroma of the mucous 
 membrane. These masses soon degenerate, soften, and form ragged 
 ulcers resembling very closely syphilitic ulcers. 
 
 TUMORS. 
 
 Adenomata are formed in the mucous membrane covering the mouth, 
 lips, and soft palate. The tumors are rounded, usually small, sometimes 
 as large as a hen's egg. They may be situated in the thickness of the 
 mucous membrane, or project in a polypoid form. They are formed by 
 an hypertrophy of the normal mucous glands. The glandular acini are 
 increased in number and size, the epithelial cells are increased in number 
 and may undergo colloid degeneration. 
 
 Papillomata occur most frequently at the edges of the lips, but are 
 also found on the gums, the floor of the mouth, and the cheeks. They 
 are formed of hypertrophied papillte, covered with thickened epidermis. 
 They very often ulcerate. 
 
 'R. Volkmann, Virch. Arch., Bd. 50, p. 143, describes five cases of inflamma- 
 tion of the mucous glands of the lower lip. The lip was swollen and hard, the 
 mucous glands and their ducts were dilated. 
 
296 THE ALIMEHTAEY CANAL. 
 
 Carcinomata are of frequent occnrrence. They may be found at any 
 part of the mucous membrane of the mouth, but as a rule begin in the 
 edge of the lower lip. 
 
 They may originate in an ulcerating papilloma, or as a flat, superficial 
 growth from the deeper layers of the epithelium, or as deep nodules 
 starting in the mucous glands. They are composed of large masses of 
 epithelial cells, closely packed together, often forming nests, and arranged 
 in anastomosing tubular masses. The stroma surrounding these masses 
 is inf:ltrated with cells. In a few cases the infiltration of the stroma 
 with small round cells may be very marked, so marked that the epithe- 
 lial growth may be obscured. The new growth increases in size, ulcerates* 
 infiltrates the adjacent tissues, and may give rise to metastatic tumors. 
 
 Angiomata are found in the lips. They may be congenital or devel- 
 oped after birth. 
 
 Fibromata, Lifomata, and Encliondromata have been seen in a few 
 cases in the lips. When they appear in the mouth they usually grow 
 from the bones. 
 
 THE TONGUE. 
 
 MALFORMATIONS. 
 
 Absence of the tongue is found in connection with the extreme de- 
 fects of development of the face already mentioned. 
 
 The anterior portion of the tongue may be absent while its base 
 remains. The lower jaw is then small. 
 
 The tongue may be partly or completely adherent to the floor of the 
 mouth. The frenulum may be abnormally short, or may extend to the 
 tip of the tongue. In rare cases, the sides of the tongue are adherent;, 
 or its upper surface may be adherent to the roof of the mouth. 
 
 HTPERTEOPHY. 
 
 Makroglossia, or hypertrophy of the tongue, is almost always a con- 
 genital lesion, and is especially common in cretins. The tongue is so 
 large that the cavity of the mouth cannot contain it, it is protruded 
 through the lips and displaces the jaws. Tlie lips may also be hypertro- 
 phied in the same way. 
 
 There is an hypertrophy of all the anatomical elements which make 
 up the tongue, and in addition to this there may be a dilatation of the 
 lymphatic vessels. 
 
 INFLAitllATIOK. 
 
 Inflammations of the tongue may be associated with similar changes 
 in the mouth, or may occur by themselves. 
 
 Superficial Inflammation. — Inflammation involving only the mucous 
 membrane of the tongue may occur as an acute or chronic jjrocess. 
 
THE ALIMENTAET CANAL. 297 
 
 The acute forms present no marked lesions. 
 
 The chronic forms result in an increased production of epithelium 
 and an hypertrophy of the papillES of the tongue. 
 
 A moderate development of such an inflammation is not infrequently 
 associated with derangements of the stomach. The tongue is large, its 
 surface is irregular from the hypertrophy of the papillse. There may be 
 no change in the epithelium, and then the surface of the tongue is clean 
 and red; or the epithelium is increased and the tongue is covered with a 
 white fur. 
 
 More severe forms of the disease also occur, especially with syphilis. 
 The hypertrophied papillae and increased' epithelium then alter very 
 decidedly the appearance of the tongue. 
 
 ParencUynudoiis Glossitis may be produced by mercurial poisoning, 
 by injury, or by unknown causes. The tongue is swollen, the muscular 
 and connective portions are congested and infiltrated with serum and pus. 
 The inflammation may stop at this point, or it may go on to the forma- 
 tion of an abscess. 
 
 Syphilitic Inflammation. — In persons suffering from constitutional 
 syphilis there may be mucous patches on the surface of the tongue ; or 
 gummy tumors in its stroma, which often sofKen and form deep ulcers; 
 or a diffuse, chronic inflammation of the surface of the tongue with 
 hypertrophy of the jjapillEe. 
 
 Tubercular Glossitis. — There may be a tubercular inflammation of 
 the connective tissue of the tongue just beneath the epithelial layer, 
 resulting in the formation of tubercle granula and granulation tissue. In 
 this way tumors of some little size are formed, which may remain un- 
 changed for some time, or may degenerate, soften, and form ulcers. 
 
 TUMOES. 
 
 Cysts. — The most common forms of cysts are the sacs beneath or 
 partly in the substance of the tongue (ranula). They are formed by 
 dilatation of the ducts of the submaxillary and sublingual glands ; or 
 make their appearance in the connective tissue beneath and in the 
 tongue. 
 
 Angioma. — Cavernous vascular tumors are found in the substance of 
 the tongue and projecting from its surface. 
 
 Lipoma and Fibroma are rare. They form nodules in the substance 
 of the tongue, or project in a polypoid form. Composite tumors, com- 
 posed largely of fat, are found in the tongue as a congenital condition. 
 
 Lupus occurs in the form of nodules and ulcers at the base of the 
 tongue. 
 
 Sarcomata are rare in this situation. I have seen one such tumor in 
 a young child. It formed a nodule as large as a chestnut, and was com- 
 posed of round and fusiform cells. 
 
298 THE ALIMENTARY CANAL. 
 
 Carcinoma. — This form of new growth may begin in the tongue or may 
 extend to it from the adjacent tissues. The growth is composed of large> 
 flat epithelial cells packed closely together in anastomosing tubular 
 spaces and surrounded by a connective-tissue stroma. 
 
 THE PHAEYNX AND THE (ESOPHAGUS. 
 
 MALEOEJIATIONS. 
 
 Fistulous openings from the pharynx, running between the muscles, 
 and perforating the skin, have been seen in rare instances. These 
 fistulas are so small as to have no practical interest. 
 
 The oesophagus may be entirely absent, or its lower portion may be 
 present, and joined to the pharynx by a solid cord ; or the pharynx, or 
 the lower part of the oesophagus, may be continuous with the trachea ; 
 or the entire oesophagus may be represented by a solid cord. 
 
 Diverticula of the pharynx, dilatations of the oesophagus^ and 
 division of the middle portion of the oesophagus into two branches have 
 all been observed. 
 
 INFLAMMATION. 
 
 Catarrhal and Croupous Pharyngitis are usually associated with the 
 same forms of inflammation in the mouth, and have the same characters. 
 
 Submucous Pliaryngitis may occur with inflammations of the mucous 
 membrane, with caries of the cervical vertebrae, with inflammation of 
 the cervical and parotid glands, with periostitis of the cranial bones, or 
 may be idiopathic. It may result in swelling and oedema, in induration, 
 or in suppuration. It is most important when it afEects the posterior 
 wall of the pharynx, and forms retro-pharyngeal abscesses. Such 
 abscesses may cause death by suffocation. 
 
 Catarrhal CEsophagitis may be either acute or chronic. The chronic 
 form may produce ulceration, or relaxation and dilatation of the walls, 
 or hypertrophy of the muscular coat. 
 
 Croupous CEsophagitis is found with croup of the pharynx, and after 
 the exanthemata and otlier severe diseases. 
 
 Irritating and caustic acids and alkalies destroy larger or smaller 
 portions of the mucous membrane. The necrosed portions are of a 
 black or whitish color, surrounded by a zone of intense congestion. If 
 the patient recover, the patches of membrane which have been destroyed 
 slough, fall ofE, and leave a granulating surface. In this way, dangerous 
 stenosis of the oesophagus may be produced. 
 
 Foreign bodies, which are swallowed and become fixed in the oeso- 
 phagus, cause inflammation of the mucous membrane and of the adjoin- 
 ing soft parts. The inflammation may go on to produce abscesses 
 
THE ALIMENTARY CANAIi. 299 
 
 around the oesophagus, or to destroy the wall of the canal, and the for- 
 eign body finds its way into the trachea, aorta, or pericardium. 
 
 Inflammation of the submucous tissue of the oesophagus, apart from 
 the cases just mentioned, is not common. It may cause the formation 
 of abscesses, or of fibrous tissue, which may produce stenosis. 
 
 ULCERATION. 
 
 Ulceration of the pharynx occurs in rare cases as the result of catar- 
 rhal inflammation. More frequently it is produced by syphilis, either in 
 the form of superficial ulcers or of deep and extensive destructions of tis- 
 sue from the softening of gummy tumors. 
 
 Lupus also sometimes attacks the upper part of the pharynx, and 
 produces extensive ulceration. Ulceration of the oesophagus is not com- 
 mon, but a few cases of simple perforating ulcer have been described.' 
 
 Foreign bodies in the oesophagus may perforate its wall, as already 
 mentioned. Perforation of the oesophagus from without may be produced 
 by inflamed bronchial glands, by cavities and gangrene of the lungs, by 
 abscesses in the mediastinum, by abscesses accompanying caries of the 
 vertebrae, and by aneurisms of the aorta. Cases have been described of 
 rupture of the wall of the oesophagus by violent coughing and vomiting, 
 but it seems probable that there was really some previous disease to 
 account for the rupture. 
 
 DILATATION.' 
 
 Simple cylindrical dilatation of the oesophagus is usually the result of 
 long-continued stenosis of the oesophagus or of the cardiac end of the 
 stomach ; although not nearly all the stenoses are followed by dilatation. 
 These dilatations are formed at first immediately above the stenosis and 
 then extend upwards. Only in rare cases does the dilatation involve 
 the whole length of the tube. The entire wall of the dilated portion of 
 the oesophagus is thickened, and there may be polypoid outgrowths from 
 the mucous membrane. 
 
 In rare cases there is cylindrical dilatation of part or of the whole of 
 the oesophagus without a stenosis or any discoverable cause. In these 
 cases the dilatation is usually greatest near the middle of the oesophagus 
 and diminishes upwards and downwards, so that the oesophagus has a 
 fusiform shape. The dilatation may reach a very considerable degree, 
 the walls of the oesophagus are thickened; its mucous membrane may be 
 covered with papillary outgrowths or ulcerated. 
 
 The Sacculated Dilatations of the a3sophagus are of two kinds : 
 those due to pressure, and those due to traction. 
 
 'Graefe u. Walther, Jour. f. Chh-. u. Augenheilk., Bd. 19. Med. Chir. 
 Trans., Vol. 36. Eokitansky, Path. Anat. 
 
 ' Ziemssen, Cyclopaedia of Medicine, viii., p. 47. 
 
300 THE ALIMENTAET CANAL. 
 
 The dilatations due to pressure are situated in the f)osterior wall of 
 the pharynx, just at its junction with the oesophagus. The smaller sacs 
 are from the size of a pea to that of a hazel-nut ; the larger sacs may 
 reach an enormous size, and hang down between the oesophagus and the 
 vertebral column, the opening into the oesophagus remaining compara- 
 tively small. It is supposed that a limited area of the wall of the 
 oesophagus loses its power of resistance against the pressure exercised upon 
 it in each act of swallowing ; it then is forced outward by the pressure, 
 and so there is formed first a protrusion and then a sac. "When a sac 
 is formed the food enters it, accumulates there, and so the sac becomes 
 larger and larger. 
 
 The dilatations due to traction are situated on the anterior wall of 
 the oesophagus, at a point nearly corresponding to the bifurcation of the 
 trachea. They are of funnel-shape with the small end outward. Their 
 length varies from two to twelve millimetres, the width of the opening 
 into the oesophagus is from six to eight millimetres. 
 
 These dilatations are due to inflammation of the parts adjoining the 
 oesophagus, especially of the bronchial glands, followed by adhesions to 
 some part of the anterior wall of the oesophagus. These adhesions then 
 contract and draw the wall of the oesophagus outwards, and in this way 
 the dilatations are formed. 
 
 At a later time these sacs may perforate into the bronchi, the 
 lungs, the pleural cavity, the pericardium, the aorta or pulmonary artery. 
 
 STEATOSIS. 
 
 Congenital Stenosis. — Besides the defects of development of the oeso- 
 phagus which are incompatible with life, there may be a congenital ste- 
 nosis of some part of it which causes difficulty in swallowing, but yet does 
 not destroy life. 
 
 Stenosis iy compression is not uncommon. Tumors of the neck 
 and mediastinum, and aneurisms of the aorta are the usual causes. 
 
 Stenosis iy obstruction. — Foreign bodies may be lodged in the oeso- 
 phagus. Tumors may hang down from the pharynx into the oesopha- 
 gus, or may be situated in the wall of the oesophagus. Inflammation of 
 the oesophagus, due to the ingestion of irritating poisons, produces cica- 
 tricial stenoses. A few cases of stenosis due to syphilitic inflammation 
 have been reported. 
 
 TUMORS. 
 
 The veins of the oesophagus may be enormously dilated. They may 
 rupture, and so give rise to hemorrhage.' 
 
 Cysts. — Small retention cysts of the follicles of the mucous membrane 
 
 ' Bristowe, Trans. London Path. Soc,, 1856. 
 
THE ALIMENTARY CANAL. 301 
 
 are sometimes found. Van Wyss' describes a cyst as large as an apple 
 attached to the' posterior wall of the oesophagus, one and one-half inches 
 aboTethe stomach. It was filled with ciliated epithelium. 
 
 Papillomata of small size may be found in considerable numbers 
 throughout the entire length of the oesophagus, or may occur singly. 
 Large papillary tumors are more rare. 
 
 Fibromata grow from the periosteum of the bones at the base of the 
 skull, and project into the cavity of the phitrynx and posterior nares in 
 the form of large polypoid tumors. Small fibrous tumors are formed in the 
 submucous connective tissue of the oesophagus. Tumors, which attain a 
 very large size, originate in the submucous connective tissue on the ante- 
 rior wall of the lower part of the pharynx, and as they grow hang down 
 into the oesojihagus. 
 
 Lipomata of small size are sometimes found in the wall of the ceso- 
 phagus. 
 
 Myomata composed of smooth muscle may grow in the muscular coat 
 of the oesophagus and attain a considerable size." 
 
 Carcinomata may originate at any part of the wall of the pharynx and 
 oesophagus. They are composed of flat epithelial cells closely packed 
 together in masses in the usual_way. In the oesophagus the new growth 
 begins in the deeper layers of the mucous membrane, and grows so as to 
 encircle the tube for a length of one or more inches. The tumor remains 
 as a fiat infiltration, or it ulcerates, or it projects inwards in large fun- 
 gous masses. The growth may extend up and down the oesophagus and 
 even involve the pharynx or stomach. 
 
 The ulcerative process may extend outwards so as to produce perfora- 
 tion into the air passages, the lungs, pleurae, pericardium, and large blood- 
 vessels. 
 
 The new growth may extend outward and infiltrate the surrounding 
 soft parts, so that the oesophagus is surrounded by large, solid, cancerous 
 masses. Metastatic tumors are also sometimes formed. 
 
 Adenoma. — A polypoid adenoma composed of tubules lined with 
 cylindrical epithelium, and growing from the anterior wall of the oeso- 
 phagus, has been described by "Weigert.^ 
 
 I have seen one tumor, the size of a chestnut, growing in the soft 
 palate, which was composed of a stroma of connective and mucous tissue 
 in which were irregular, anastomosing tubules filled with small, poly- 
 gonal, nucleated cells. It could be called an adenoma or a carcinoma. 
 
 Another comi^osite tumor grew from the mucous membrane of the 
 
 ' Virch. Arch., Bd. 51, p. 143. 
 
 "Vh-oh. Arch., Bd. 43, p. 137. Med. Times and Gazette, Nov. 28th, 1874. 
 Glasgow Med. Journal, Feb., 1873. 
 = Virch. Arch., Bd. 67, p. 516. 
 
302 THE AlIMENTAET CANAL. 
 
 pharynx, behind the left tonsil. It filled the pharynx, below the level of 
 the palate. It liad the gross appearance of a myxo-sarcoma, the central 
 portions being very soft. It was composed of connective tissue, mucous 
 tissue, fat, sarcomatous tissue, and irregular tubules lined with small, 
 polygonal ei^ithelial cells. Some of the tubules were distended with masses 
 of hyalin matter. The whole structure resembled that of the tumors 
 so often found in the parotid region, tumors which can be called 
 'Adenoid Myxo-Sarcomata.' 
 
 Sarcoma. 
 I have seen one case in which there was a diffuse growth involving 
 both the tonsils, the posterior and lateral walls of the pharynx, the base 
 
 Or 
 
 ■^ , 
 
 :c - _ r - fe '*,-^c &;c?^ O'^'^*' ^"'^T-s. 
 
 c ^- ^ ^ ,i: ^ 
 
 r 
 
 ^ ^ .. 
 
 ^.J^ 
 
 
 '^ 
 
 
 
 c 
 
 r 
 
 
 - C' /i 
 
 -T 
 
 Ci' o. 
 
 Fio. 109,— Diffuse Saeooma of the Pharynx, X 850 and reduced. 
 
 of the tongue, and the epiglottis. The new growth replaced the mucous 
 membrane, infiltrated the soft parts for a short distance, and projected 
 inwards in polypoid masses. It was composed of small, polygonal, nu- 
 cleated cells, contained in a very delicate nucleated stroma (Fig. 109). 
 
 THE STOMACH. 
 
 IIALFOEMATIONS. 
 
 Malformations of the stomach are not common. The organ may be 
 entirely wanting in acephalous foetuses. It may be of various degrees of 
 
THE ALIMENTAJJY CANAL. 303 
 
 smallness, sometimes no larger than the duodenum. It may be divided 
 into two halves by a deep constriction in the middle. The pyloric orifice 
 may be stenosed or entirely closed. The stomach may be outside of the 
 abdominal cavity from a hernial protrusion through the diaphragm, or 
 at some point in the abdominal wall. It is found on the right side, in- 
 stead of the left, when the other viscera are transposed, and the position 
 of the cardiac and pyloric orifices is correspondingly inverted. 
 
 POST-MORTEM OHAKGES. 
 
 In adults, the stomach after death is of a grayish or pinkish color, 
 sometimes mottled with red ecchymoses. The mucous membrane is 
 soft, and the epithelium easily brushed ofE. At the fundus, the food is 
 usually found collected, and here the mucous membrane is the softest. 
 It is very common to find the epithelium removed from the entire fun- 
 dus of the stomach, so that all that portion of its wall is grayer and thinner, 
 there being a sharp dividing-line between the two portions. Sometimes 
 this post-mortem softening process goes on to destroy all the coats of the 
 stomach, and even the adjoining portion of the diaphragm. In this way, 
 the contents of the stomach may be emptied into the pleural cavity by 
 a large, ragged opening in the stomach and diaphragm. When the 
 softening affects all the coats of the stomach, the softened portion is not 
 sharply limited. The entire thickness of the affected portion of the 
 wall is converted into a gray or yellow semi-transparent jelly, or into a 
 blackish, broken-down pulp. 
 
 This softening is most frequent in children, but also occurs in adults, 
 usually in connection with severe and exhausting diseases. 
 
 A similar post-mortem softening of the wall of the oesophagus has 
 been described by Moxon.' 
 
 INJURIES. 
 
 Perforating wounds of the stomach usually give rise to a fatal peritoni- 
 tis. It is possible, however, for the wound to heal, or a gastric fistula 
 may be formed. 
 
 Kupture of the stomach may be produced by severe blows or falls. 
 
 HEMORRHAGE. 
 
 Small extravasations of blood in the wall of the stomach are frequently 
 fouifd in persons who have died from one of the infectious diseases. 
 
 Hemorrhage into the cavity of the stomach may be produced in a 
 variety of ways. 
 
 In ulcers of the stomach, there may be bleeding from the small ves- 
 sels of the ulcer, or from the perforation of a larger artery. 
 
 In cancer of the stomach, there may be bleeding from the tumor. 
 
 1 Trans. Lond. Path. Soc, 1870, p. 159. 
 
304 THE ALLMEM^TART CANAL. 
 
 Some cases of chronic gastritis are characterized by general bleeding 
 from the mucous membranes of the stomach. 
 
 Cirrhosis of the liver is not infrequently attended with lai'ge hemor- 
 rhages from the mucous membrane of the stomach. 
 
 Small aneurisms of the arteries in the wall of the stomach may rupture 
 internally. 
 
 In yellow fever and some of the other infectious diseases, there is 
 hemorrhage into the cavity of the stomach. 
 
 Patients may vomit blood during life, and after death no lesion to ac- 
 count for the bleeding be found. 
 
 INFLAMMATION". 
 
 Acute catarrhal gastritis, as we see it after death, is usually due to thq 
 ingestion of irritating substances, or forms part of the lesions of cholera 
 morbus. If we can judge from clinical symptoms, it occurs during life 
 as a temporary condition from a variety of causes. 
 
 After death the mucous membrane is found congested and swollen, or 
 the congestion may have disappeared. The mucous membrane is coated 
 with an increased amount of mucus, especially at the pyloric end of the 
 stomach. Sometimes there are a number of minute white dots in the 
 substance of the mucous membrane. 
 
 The structural changes in the mucous membrane consist simply in a 
 swelling of the cells of the gastric tubules, a slight infiltration of the 
 stroma with pus- cells, and a swelling of the patches of lymphatic cells. 
 Tlie little white dots, when they are present, are composed of small foci 
 of pus between the gastric tubules, with degeneration and destruction of 
 some of the tubules. 
 
 Chronic catarrhal gastritis is a very common disease. There is, how- 
 ever, no very close relation between the severity of the symptoms during 
 life, and the extent of the lesions found after death. 
 
 In some cases, chronic alcoholism, or the abuse of drugs, or the mode 
 of life of the patient seem to be the causes of the lesion. Chronic 
 phthisis, chronic Bright's disease, cirrhosis of the liver, and fatty liver 
 are often accompanied by chronic gastritis. Organic disease of the heart 
 or pressure on the ascending vena cava produce a form of chronic gas- 
 tritis characterized by intense general congestion. 
 
 After death the stomach is found either empty or still containing food. 
 It is of normal size, or dilated, or small, sometimes hardly larger than the 
 duodenum. Its inner surface is coated with a thick layer of tenacious 
 mucus, most abundant at its pyloric end. The mucous membrane is 
 congested, or white, or slate-colored, or mottled with small white spots. 
 It is of normal thickness, or thinned, or thickened, or there are little 
 polypoid projections from its surface, or there is cystic dilatation of the 
 gastric tubules. The connective tissue and muscular coats remain un- 
 
THE ALIMENTAEY CANAL. 305 
 
 changed, or they are thinned and relaxed, or they are hypertrophied. 
 The hypertrophy may be diffuse, or it is confined to the pyloric end of 
 the stomach, and may then produce stenosis of the pylorus. 
 
 The minute lesions consist principally in changes in the mucous 
 membrane. The cells of the gastric tubules are swollen, degenerated, and 
 broken down. The tubules are atrophied and deformed, or dilated into 
 cysts. The patches of lympathic tissue about the blind ends of the 
 tubules are increased in size. The connective tissue between the tubules 
 is infiltrated with cells, and increased in quantity. 
 
 Croupous gastritis is of rare occurrence. It is found in children with 
 croupous inflammation of the pharynx and oesophagus, and is then usually 
 in small patches. In adults, it is almost always secondary to typhus, pye- 
 mia, puerperal fever, cholera, dysentery, the exanthemata, and irritating 
 poisons. The false membrane is in small j^atches, or may line a large 
 part of the stomach. The disease is usually not diagnosticated during 
 life, the symptoms of the primary disease diverting attention from the 
 gastritis. 
 
 I have seen one case of idiopathic croupous gastritis in an adult. A 
 man, forty-six years old, was in good health until eight days before his 
 death. At that time he caught cold, had pains over his bowels, tender- 
 ness over the liver, constipation, cough with mucous expectoration, tem- 
 perature 102^°, pulse 120. On the day of his death, the 8th day of the 
 disease, the temperature was 100°, pulse 112, tongue dry, abdomen tym- 
 panitic and tender, and he died in a prolonged attack of syncope. At 
 the autopsy all the viscera were examined. Excepting evidences of 
 bronchitis in the lungs, there were no lesions save in the stomach. About 
 two-thirds of the internal surface of the stomach, including the lesser 
 curvature and anterior and posterior walls, appeared to be covered with a 
 thick false membrane, which did not quite reach to the cardiac or pyloric 
 orifices. Minute examination showed that there was a layer of exudation 
 on the internal surface of the mucous membrane. This exudation con- 
 sisted of fibrillated fibrin and lymphoid cells, dipping into the mouths of 
 the follicles. Beneath the exudation the mucous membrane was thick- 
 ened and altered. A large number of lymphoid cells separated the 
 follicles, and even replaced them entirely. The submucous layer was 
 very much thickened by the presence of lymphoid cells, fibrillated fibrin, 
 and fibrous tissue. The muscular coat was separated into layers by 
 groups of lymphoid cells. 
 
 Wilks and Moxon' mention a similar case in a man with chronic 
 Bright's disease; and a case of both croupous gastritis and colitis with 
 abscess of the liver. 
 
 Suppurative or Phlegmonous Gastritis. — A formation of circum- 
 
 'Path. Anat., p. 381. 
 30 
 
306 THE ALIMENTARY CANAL. 
 
 scribed collections of pus may occur in the connective-tissue coat of the 
 stomach, as it does in other parts of the body, in puerperal fever and the 
 infectious diseases. 
 
 Idiopathic suppurative gastritis is a disease of rare occurrence. 
 Leube' has collected 31 cases, of which 26 were males and 5 females. In 
 some of the cases the inflammation was ascribed to the excessive use of 
 alcohol, in others to a wound in the region of the stomach, in others to 
 some error in diet. 
 
 Fagge' describes a case in a male of fifty-one years of age, without 
 discoverable cause. 
 
 Silcock^ describes a case in which the gastritis followed the operation 
 of gastrostomy. 
 
 I have seen one case occurring in an adult male, without any known 
 cause. 
 
 The suppurative inflammation seems to begin in the connective-tissue 
 coat of the stomach. From thence it may extend to the glandular coat 
 and produce perforations, or outward to the muscular and peritoneal 
 coats. In some cases there is added a local or general peritonitis. 
 
 The inflammation may involve one or more circumscribed areas and 
 so produce abscesses, or it may be a diffuse process involving the whole 
 extent of the wall of the stomach. 
 
 Toxic Gastritis. — The mineral acids, the caustic alkalies, arsenic, 
 corrosive sublimate, and the metallic salts, phosphorus, camphor, and all 
 other irritating materials, cause different lesions of the stomach, accord- 
 ing to their quantity, their strength, and the length of time that has 
 elapsed before death. 
 
 In large quantities, they destroy and convert into a soft, blackened 
 mass both the mucous membrane and the other coats, so that perforation 
 may take place. In smaller quantities, they produce black or white 
 sloughs of the mucous membrane, surrounded by a zone of intense con- 
 gestion. If death does not soon ensue, the ulcerative and cicatricial pro- 
 cesses which follow such sloughs, may contract and deform the stomach 
 in various ways. 
 
 If the poisons are of less strength, they produce a diffused congestion 
 of the mucous membrane, with catarrhal or croupous exudation on its 
 surface, and serous infiltration of the submucous coat (see chapter on 
 poisons). 
 
 ULCERS OF THE STOMACH. 
 
 1. TJlb Chronic j^erf orating Ulcer. — This form of ulcer is often seen; 
 according to Brinton, in five per cent of persons dying from all causes. 
 
 ' Leube, Zienissen's Cyclopaedia, vii., p. 157. 
 = Trans. Lond. Path. See, 1875, p. 81. 
 3 Trans. Lond. Path. See, 1883, p. 90. 
 
THE AlIMENTAET CAl^AL. 
 
 307 
 
 It occurs in females nearly twice as frequently as in males. As regards 
 the age, Brinton concludes that the liability of an individual to become 
 the subject of gastric ulcer gradually rises, from what is nearly a zero at 
 the age of ten, to a high rate, which it maintains through the period of 
 middle life; at the end of which period it again ascends, to reach its 
 maximum at the extreme age of ninety. Lebert gives one hundred and 
 ninety-eight cases in which the ulcers were found at the autopsy, as fol- 
 lows: 
 
 AGE. 
 
 NUMBER OF CASES. 
 
 AGE. 
 
 ITOMBER OF OASES. 
 
 15 to 20 years . ... ... 
 
 20 
 
 48 
 S8 
 43 
 
 50 to 60 years 
 
 60 to 70 years 
 
 29 
 
 20 to 30 years 
 
 30 to 40 years 
 
 19 
 
 70 to 80 years 
 
 5 
 
 40 to 50 years 
 
 
 
 Hauser' gives thirty autopsies from Erlangen of ulcers which were 
 still open, as follows: 
 
 AGE. 
 
 NUMBER OF CASES. 
 
 AGE. 
 
 NUMBER OF OASES. 
 
 20 to 30 years 
 
 30 to 40 years 
 
 8 
 3 
 3 
 
 
 7 
 
 fiO to 70 years 
 
 8 
 
 
 70 to 80 years. ....... 
 
 6 
 
 
 
 Moore'' gives the following table of the fatal cases of ulcer of the 
 stomach occurring at St. Bartliolemew's Hospital from 1867-1879: 
 
 POSITION. 
 
 Near pylorus 
 
 Greater curve near pylorus 
 Near pylorus 
 
 Pylorus I 
 
 (( 
 
 It 
 Lesser curve near pylorus. 
 
 Cardiac end 
 
 Near pylorus 
 
 Posterior wall 
 
 CAUSE OF DEATH. 
 
 Perforation. 
 
 Hemorrhage. 
 
 Exhaustion. 
 
 Phthisis. 
 
 ti 
 
 Exhaustion. 
 
 Perforation. 
 
 Sinus in liver to lung. 
 
 Hemorrhage. 
 
 Perforation. 
 
 Goodhardt" describes an ulcer of the stomach which proved fatal from 
 hemorrhage in an infant at birth. 
 
 The situation of these ulcers, according to Brinton, is as follows: 
 in 43 per cent, the posterior surface; in 27, the lesser curvature; in 16, 
 the pyloric extremity; in 6, both the anterior and posterior surface; in 5, 
 
 'Das chron. Magengesch., 1883. 
 
 2 Trans. Lond. Path. Soc, 1880, p. 110. 
 
 5 Trans. Lond. Path. Soc, 1881, p. 79. 
 
308 THE ALIMENTARY CANAL. 
 
 the anterior surface only; in 2, the greater curvature; in 2, the cardiac 
 pouch. Thus about 86 ulcers in every 100 occupy the posterior surface, 
 the lesser curvature, and the pyloric sac. 
 
 As regards the number of ulcers, two or more are present in about 31 
 per cent; there may be two, three, four, or even five ulcers. In cases 
 of multiple ulcers, the ulcers are often developed successively. 
 
 In size the uloers vary from one-quarter of an inch to five or six inches. 
 
 They are usually of circular shape, sometimes oval, sometimes two or 
 more are fused together. 
 
 The perforation is largest in the mucous membrane. It may remain 
 confined to this, or extend outwards and involve the connective tissue, 
 muscular and peritoneal coats, its diameter becoming smaller as it ad- 
 vances. The ulcer looks like a clean hole punched out of the wall of the 
 stomach. Its floor shows no active inflammatory changes. Its edges 
 may be in the same condition, or they may be thickened by the growth 
 of connective tissue and cells. The rest of the mucous membrane of the 
 stomach is apt to be in a condition of chronic catarrhal inflammation. 
 
 The ulcer may perforate directly through the wall of the stomach, 
 and the contents of the latter are discharged into the peritoneal cavity. 
 Or adhesions are formed between the wall of the stomach and the 
 neighboring viscera, so that the bottom of the nicer is closed. Or, if the 
 liver, the intestines, or the abdominal wall become adherent, they maybe 
 invaded by the ulcerative process, and cavities or fistnlse are formed com- 
 municating witl; the stomach. Or, if the adhesions are incomplete, a 
 local peritonitis and collections of pus may bo developed. 
 
 During the progress of the ulcer, there maybe repeated small hemor- 
 rhages from the erosion of small blood-vessels; or large hemorrhages 
 from the erosion of large arteries. 
 
 In many cases these ulcers cicatrize, and such a cicatrization may 
 produce various deformities of the stomach. 
 
 It is very diflicult to understand how these ulcers are produced. It 
 seems probable that the nutrition of a circumscribed joart of the wall of 
 the stomach is interfered with, and that this portion is then destroyed 
 by the action of the gastric juice. But we are still ignorant of the way 
 in which the obliteration of the arteries is effected. It has indeed been 
 demonstrated in animals that an artificial embolism of the branches of 
 the gastric arteries will produce ulcers of the stomach; and in the human 
 stomach we occasionally meet with cases of embolism of the branches of 
 the gastric artery and ulcers. But the clinical history of most cases of 
 ulcer of the stomach will not correspond with such a method of causa- 
 tion. A chronic obliterating endarteritis would seem to be a more prob- 
 able cause. 
 
 Hemori'liagic erosions occur as rounded spots or narrow streaks, 
 formed by a loss of substance pf the mucous membrane. The mucous 
 
THE AlIMENTAET CANAL 309 
 
 membrane at these points is congested, soft, and covered by small blood- 
 clots. The destruction of the mucous membrane is usually superficial, 
 but may involve its entire thickness. The number of these erosions may 
 be so great that the entire internal surface of the stomach is studded 
 with them. They give rise to repeated hemorrhages, and are accom- 
 panied by catarrhal inflammation of the rest of the mucous membrane. 
 
 They occur at all periods of life, even in infants. Their usual seat is 
 the pyloric portion of the stomach. 
 
 They may be idiopathic. Usually, however, they occur in connection 
 with some serious general disease. 
 
 Follicular ulcers somewhat resembling the ulcers of the small intes- 
 tine are occasionally met with. They are produced by changes in the 
 aggregafjons of lymphatic tissue, which are situated about the blind ends 
 of the gastric tubules. 
 
 DILATATIOSr. 
 
 Very considerable degress of dilatation of the stomach are found at 
 autopsies without stenosis of the pylorus, or any other mechanical cause 
 to account for them. It is usually difficult to determine how long these 
 ■dilatations have existed and how mucli effect they have in causing death. 
 Nine such cases are recorded by Goodhart.' 
 
 Acute dilatation of the stomach with vomiting of very large quantities 
 of thin fluid has been observed in a few cases. ^ It is a very curious con- 
 dition, the dilatation of the stomacli being developed suddenly and 
 without discoverable cause. 
 
 Of the mechanical causes which produce dilatation of the stomach, 
 stenosis of the jiylorus is the most common. Such a stenosis may be 
 effected by a tumor, by chronic inflammation and thickening, and bythe 
 oicatrization of ulcers. Less frequently obstructions of the small and 
 large intestines act in the same way. 
 
 Some forms of chronic gastritis are attended with dilatation of the 
 stomach without stenosis. 
 
 In rare cases circumscribed, sacculated dilatations are jjroduced by 
 the presence of foreign bodies — portions of woodj metal, etc. 
 
 TUMOES. 
 
 Papilloma. — It has already been mentioned, that in some cases of 
 chronic gastritis, there are small, polypoid hypertrophies of the mu- 
 ■cous membrane. Besides these, we find polypoid tumors which may 
 reach a considerable size. They are composed of a connective-tissue 
 
 ' Trans. Lend. Path. Soc, 1883, p. 88. 
 
 ^ Trans. Lond. Path. Soc, Vol. iv. and Vol. xxxiv., p. 82. Hughes Bennett, 
 Practice of Medicine. Fagge, Guy's Hospital Reports, Vol. xviii., p. 1. Andral, 
 €linic[ue Medicale. 
 
310 THE ALIMENTAET CANAL. 
 
 stroma arranged so as to form tufts covered 'vvitli cylindrical epithelium, 
 111 some cases, there are also tubules lined with cylindrical epithelium 
 so that the tumor has partly the structure of an adenoma. Fibromata 
 of small size are sometimes found in the connectiye-tissue coat. Lijjo- 
 mata are formed in the submucous connective tissue in the shape of 
 rounded or polypoid tumors. They usually project inwards, but some- 
 times outward beneath the peritoneum. They may also appear in the 
 form of numerous yellow nodules beneath the mucous membrane. 
 
 Myomata occur in the form of rounded tumors which originate in the 
 muscular coat, but may gradually separate themselves from it and project 
 inwards or outwards. The submucous myomata are at first small tumors 
 lying loosely attached in the submucous tissue. As they grow larger 
 they push the mucous membrane inward and take the shape of polypoid 
 tumors. Lympliomata in the wall of the stomach are seen in some cases 
 of leukaemia. 
 
 Sarcomata are said to occur in the wall of the stomach in rare in- 
 stances. It must be admitted that in some of the tumors of the wall of 
 stomach, which are ordinarily called cancerous, the structure is not well 
 defined and it is possible that some of them are sarcomata. 
 
 A myo-sarcoma growing outwards from the greater curvature of the 
 stomach is described by Brodowski.' The tumor weighed twelve pounds. 
 It was composed largely of smooth muscle-cells. There was a secondary 
 tumor in the liver. 
 
 Adenoma. — It has been already mentioned that in some of the papil- 
 lary tumors of the mucous membrane there is a considerable growth of 
 tubules lined with cylindrical epithelium. 
 
 Besides these, we find in the submucous coat circumscribed tumors 
 composed of tubules like those of the gastric mucous membrane. 
 
 Small tumors resembling the pancreas have also been seen in the sub- 
 mucous and subserous coats. 
 
 Carcinoma of the stomach is almost always primary. But very few 
 secondary cases have been recorded. ° 
 
 Primary carcinoma of the stomach is of the colloid variety, or 
 common cancer, or cancer with cylindrical epithelial cells, or it is pig- 
 mented. 
 
 Colloid cancer is composed of a connective-tissue stroma, arranged so- 
 as to form cavities of different sizes, which contain colloid matter and 
 polygonal cells. It infiltrates first the submucous connective tissue and 
 then extends inwards and outwards. In this way, there is formed a 
 diffuse thickening of the pyloric end of the stomach rather than a cir- 
 cumscribed tumor. Sometimes the whole of the wall of the stomach is 
 
 ' Virch. Arch., Bd. 67, p. 337. 
 
 2 Virch. Arch.. Bd. 38 and 86, p. 159. Trans. Path. See, London, 1876, p. 264. 
 
THE ALIMENTAET CANAL. 311 
 
 changed in this way. Secondary tumors are usually situated in the 
 peritoneum. 
 
 Carcinoma with cylindrical epithelial cells. These tumors are formed 
 of a connectiye-tissue stroma, which may contain numerous round cells, 
 and of tuhules lined with cylindrical epithelium, like that of the mu- 
 cous membrane of the stomach. In these tumors the new growth seems 
 to begin in the gastric tubules. As the arrangement of the tubules 
 is more or less regular, these tumors may be called adenomata or carcino- 
 mata (see Fig. 46, p. 143), 
 
 Common cancer is formed of a connective-tissue stroma, inclosing 
 rounded and tubular spaces filled with small, polygonal nucleated 
 cells. In some cases this structure is well marked; in others, the stroma 
 is abundant and filled with round cells, the spaces are very small, and 
 the epithelial cells few. It may then be difficult to distinguish between 
 inflammatory thickening, sarcoma, and carcinoma. 
 
 Both these forms of carcinoma, common cancer and cancer with 
 cylindrical cells, run the same course as regards their gross appearance, 
 their situation, and their development of metastatic tumors. 
 
 About sixty per cent of these tumors are situated at the pyloric end 
 of the stomach, on the lesser curvature or on the posterior wall. The 
 cardiac end of the stomach, the greater curvature, or nearly the entire 
 wall of the stomach may also be the seats of the new growth, but not as 
 frequently. 
 
 The new growth usually follows one or other of three types: 
 
 (1) There is a circumscribed, flat tumor formed in the deeper layers 
 of the mucous membrane and pushing this membrane inwards. After a 
 time, the mucous membrane over the centre of the tumor dies, the de- 
 structive process involves the tumor also, and so an ulcer with thickened 
 edges is formed. In some cases the new growth extends laterally and 
 outward, while the central destruction still continues; then the ulcers 
 reach a large size, their walls and floor are thick, and peritoneal adhe- 
 sions are formed over them. In other cases the ulcer perforates com- 
 pletely through the wall of the stomach, unless the opening is closed by 
 adhesions to the neighboring viscera. 
 
 (2) Large rounded tumors are formed, often several inches in dia- 
 meter, which project into the cavity of the stomach. 
 
 (3) There is a diffuse, flat infiltration of the deep layers of the mucous 
 coat, of the connective-tissue coat, and, sometimes, of the muscular coat, 
 which does not ulcerate and hardly forms a tumor. This infiltration 
 may be confined to the pyloric end of the stomach, or may involve nearly 
 the whole of its wall. 
 
 There is in most of the cases a good deal of chronic catarrhal inflam- 
 mation of the mucous membrane. 
 
 If the pylorus is obstructed, the stomach is often dilated. 
 
312 THE ALIMENTAEY CAJSTAL. 
 
 The new growth may extend from the stomach to the oesophagus, but 
 it very seldom involves the duodennm. 
 
 Metastatic tumors are very common. The liver, the lymphatic glands, 
 and the peritoneum are the parts most frequently affected, but such 
 metastases have been seen in nearly every part of the body. 
 
 DEGEN"EilATIONS. 
 
 Oalcification of the mucous membrane of the stomach sometimes 
 occurs as a metastatic process in connection with extensive diseases of 
 the bones. 
 
 Waxy Degeneration sometimes involves the blood-vessels of the mucous 
 membrane. 
 
 THE INTESTINES. 
 
 MALFOEMATIONS. 
 
 Diverticula of the intestines occur in several different ways: 
 
 (1) The abdomijial walls are cleft asunder at the navel. The ileum 
 opens through this cleft by a narrow aperture in its wall. The lower 
 portions of the ileum and the colon are small or entirely closed. 
 
 (2) There is an opening in the abdominal wall as before, but there is 
 not a direct opening into the ileum. There is a long diverticulum of 
 the ileum, with an open end projecting into the opening in the abdomi- 
 nal wall. 
 
 (3) The abdominal wall is closed. There is a diverticulum of the 
 ileum connected with the navel by a solid cord. 
 
 (4) There is an unattached diverticulum of the intestine. This is 
 much the most common form. The diverticula occur only in the lower 
 part of the ileum. They usually spring from the convex surface of the 
 intestine, more rarely from its attached border. In the latter case, they 
 are joined to the mesentery by a fold of peritoneum. The diverticulum, 
 forms a pouch, one to six inches long, of about the same diameter as the 
 intestine, smallest at its free extremety. 
 
 Such diverticula never interfere with the functions of the intestines. 
 They sometimes form part of a hernia. If they remain attached by a 
 fibrous cord to the navel, this cord may be the cause of incarceration of 
 a portion of the intestines. 
 
 Cloacse consist in the union of the rectum, bladder, and organs of 
 generation in a common outlet. 
 
 (1) Simple CloaccB are: (a) Complete, and consist in the common 
 opening of the urethra or ureters, the vagina, and the rectum into the 
 closed bladder, or into a sinus opening outward, which represents either 
 the vagina or the rectum. {h) Incomplete. The rectum opens into 
 the vagina, the bladder, or the urethra, while the lower part of the rec- 
 tum is closed or absent. 
 
THE ALIMENTARY CANAL. 318 
 
 (2) OloaccB coiiibinecl with deft Hadder. (a) The simple cleavage of 
 the intestines is combined. with cleft bladder. The anterior abdominal 
 wall from the umbilicus to the symphysis, the symphysis, and the ante- 
 rior wall of the bladder are absent; the gap is filled with a membrane 
 which represents the posterior wall of the bladder. Onto this membrane 
 open the ileum, ureters, and vagina, {b) The intestine is perfectly 
 formed, but the rectum opens into a common sinus with the ureters and 
 vagina; or the ureters open into the cleft bladder, and the rectum and 
 external genitals are united; or the ureters open into the rectum, and the 
 latter terminates normally. 
 
 (3) Cloacm combined with abdominal hernia. There is a hernial sac 
 containing all the abdominal viscera. At the lower end of the sac is an 
 opening leading into a sinus in which open the lower end of the ileum, 
 the bladder or urethra, and the ureters. The rectum is absent. 
 
 Atresia Ani consists in a deficient development of the colon or rec- 
 tum. The entire colon may be absent; the rectum may be absent, or 
 represented by a solid cord; or the upper or lower part of the colon may 
 be absent, or separated by a solid cord. 
 
 More rarely, blind terminations of the small intestines are found, and 
 sometimes a narrowing so complete as to close the canal. 
 
 The intestines are also found abnormally shortened in various de- 
 grees. 
 
 INCARCERATION. 
 
 (1) The most common form is that in which a portion of intestine is 
 strangulated by a fibrous band. Such fibrous bands are produced by 
 peritonitis, or are remains of foital growth. They pass from the intes- 
 tines to the abdominal wall, or from one part of the intestines to another. 
 The intestine becomes in some way caught under one of these bands, and 
 is compressed by it. The stricture thus produced may cause a gradual 
 accumulation of fseces in the intestine above it, and may last for a long 
 time before death ensues. In other cases, the stricture interferes at once 
 with the circulation of the blood; the intestine is intensely congested, 
 becomes gangrenous, and death takes place with the sym^jtoms of general 
 peritonitis. 
 
 (3) A portion of intestine becomes caught in some abnormal open- 
 ing in the mesentery or omentum, or in the foramen of Winslow, or be- 
 tween the two layers of the mesentery. We have seen a case in which 
 twelve feet of intestine had passed through a small opening in the 
 mesentery. 
 
 (3) A coil of intestine makes half a turn at its base, so that the two 
 sides of the loops cross at its base. In this way, the lumen of the intes- 
 tine is completely closed, and the vessels are compressed, so that con- 
 gestion, peritonitis, and gangrene result. This form of incarceration 
 
314 THp; ALIMENTAET CANAL. 
 
 is most frequent in tlie ascending colon. In the small intestine it only 
 occurs when the gut is fixed by old adhesions. 
 
 (4) A portion of the intestine, with its mesentery, makes one or more 
 complete turns on itself, closing the canal, and compressing the yessels. 
 
 (5) A portion of the intestine makes a half or entire turn about its 
 long axis. This is very rare, and only occurs in the colon. 
 
 (6) The mesentei-y of a part of the intestine is long au^, oose, in 
 sequence of a dragging down of the intestine by a hernia or by habitual 
 constipation. The portion of intestine thus permitted to hang down is 
 habitually filled with fseces, and by its pressure on some other part of the 
 intestine produces an incomplete stricture. 
 
 INTUSSUSCEPTIOK. 
 
 This change of position consists in the invagination of one portion of 
 intestine in another portion. Usaally this takes place in the direction 
 of the peristaltic movements, from above downward; more rarely, in the 
 opposite direction. 
 
 The parts are found in the following condition : There are three por- 
 tions of intestine, one within the other. The inner portion is continuous 
 with the intestines above the intussusception; its peritoneal coat faces 
 outward. The outer portion is continuous with the intestine below; its 
 peritoneal coat also faces outward. The inner portion is turned inside 
 out, its mucous membrane is in contact with the mucous membrane of 
 the outer portion. In rare cases, the intussusception is complicated by 
 the invagination of a second portion of intestine in the inner tube, and 
 even by a third intussusception into the second one. These changes oc- 
 cur both in the large and small intestine; most frequently the lower part 
 of the ileum is invaginated in the colon. The invaginated portion may 
 be from a few inches to several feet in length. The lesion is most fre- 
 quently found in early childhood. 
 
 The intussusception, by the draggging and folding of the mesentery 
 which it produces, causes an intense congestion of the parts, and even 
 large hemorrhages between the coats of the intestine. The congestion may 
 induce fatal peritonitis, or gangrene of the intestine, or chronic inflam- 
 mation and adhesions, and the patient lives for a considerable time with 
 symptoms of stricture. In other cases, the invaginated portion of intes- 
 tine sloughs, the outer and inner portion become adherent, and the pa- 
 tient recovers, with or without some degree of stricture. 
 
 Besides this grave form of intussusception, we often find, especially in 
 children, one or more small invaginations not attended with congestion 
 or inflammation. These are formed during the death agony, or immedi- 
 ately after death. 
 
THE JlLIMENTAET CANAL. 315 
 
 TRANSPOSITION. 
 
 The position of the intestines may be the opposite to that which is 
 usually found. The transposition may affect all the abdominal viscera, 
 or only a single yiscus is transposed. 
 
 WOUNDS, RUPTURES. 
 
 Penetrating wounds of the intestine usually prove rapidly fatal, either 
 from shock or from peritonitis. Sometimes, however, the wound becomes 
 closed by the formation of adhesions with the neighboring parts. Some- 
 times the wound in the intestines becomes adherent at the position of 
 the wound in the abdominal wall, and an intestinal fistula is formed. 
 
 Eupture of the small intestine is not infrequently produced by severe 
 blows on the anterior abdominal wall. It is noticeable that such blows 
 may not produce any marks or ecchymoses of the skin. Such ruptures 
 usually prove fatal very soon, but sometimes the i^atient lives several days, 
 and the edges of the rupture undergo inflammatory changes. 
 
 Strictures of the intestine are sometimes followed by rupture of the 
 dilated intestine at some point above the stricture. 
 
 THE SMALL INTESTINE. 
 INFLAMMATION. 
 
 Acute Catarrlial Inflammation of the greater part of the small intes- 
 tine is developed as part of the lesion of cholera morbus, and after the 
 ingestion of irritant poisons. 
 
 Acute inflammation of the duodenum accompanies gastritis, and 
 occurs as an idiopathic condition. 
 
 Acute inflammation of the ileum occurs as an idiopathic condition, 
 and accompanies inflammation of the colon and of the solitary and 
 agminated glands. 
 
 In many of these cases we infer the existence of the inflammation 
 from the clinical symptoms. 
 
 After death, the most marked lesions are the increased production of 
 mucus and the congestion. In very severe cases the inflammation may 
 extend to the peritoneal coat. 
 
 Chronic Catarrlial Inflammation of the small intestine accompanies 
 heart disease, phthisis, emphysema, cirrhosis of the liver, and Bright's 
 disease. The intestine is coated with an increased amount of mucus, it 
 is often congested, there may be a general thickening of all its coats. 
 
 Croupous Inflammation is produced by irritant poisons; it is associ- 
 and with croupous colitis, and it occurs as an idiopathic disease. The 
 mucous membrane is coated with fibrin, its stroma is infiltrated with 
 fibrin and pus, and this infiltration extends to the connective tissue, 
 muscular and peritoneal coats. 
 
316 THE AlIMENTART CANAL. 
 
 Supptirative inflammation of the submucous connective-tissue coat is 
 said to occur in rare cases. It is usually metastatic. It takes the form 
 of purulent foci of variable extent, which perforate either inward or 
 outward. 
 
 THE SOLITARY AND AGMINATED GLANDS. 
 
 It is not uncommon to find in healthy adults who have died from 
 accidental causes, a considerable swelling of the solitary and agminated 
 glands of the ileum without any reason which we can discover to account 
 for this swelling. 
 
 Extensive burns of the skin may be followed by a very marked swell- 
 ing of the solitary and agminated glands. 
 
 In jDersons who have died from the infectious diseases it is not 
 uncommon to find these glands swollen. 
 
 In children, swelling of these glands, often followed by softening and 
 the formation of ulcers, accompanies many of the catarrhal inflammations 
 of the large and small intestine. 
 
 In pulmonary phthisis we very frequently find changes in the solitary 
 and agminated glands of the small intestine, less frequently in the soli- 
 tary glands of the colon. The changes seem to be of the same character 
 as those which take place in tubercular inflammation of lymphatic 
 glands in other parts of the body. 
 
 The glands become swollen, their elements are multiplied, tubercle 
 granula are formed, the central jDortions of the glands become cheesy. 
 The cheesy degeneration extends, it is followed by softening and by death 
 of the miTCons membrane over the glands, the softened tissue is discharged 
 into the intestine, and ulcers are formed with overhanging edges. After 
 this, the ulcer shows no tendency to heal., but on the contrary, becomes 
 larger, usually extending laterally so as sometimes to nearly encircle the 
 gut. After death, we find, in different patients, these ulcers in all their 
 stages of develoiDment. They vary much as to the proportion between 
 the tubercular and the ordinary inflammatory changes. In some the 
 tubercle granula are numerous, in others they are few or even absent 
 altogether. The tubercle bacilli are very constantly found in them. 
 There is also usually a tubercular inflammation of the peritoneum over 
 the ulcers, and sometimes of the lymphatics and glands of the mesentery. 
 Although these ulcers often reach a large size, it is but very seldom that 
 they perforate into the jDeritoneal cavity. 
 
 Ulcers of the Duodenum . — A few cases have been recorded in which 
 extensive burns of the skin have been followed within a few days, by the 
 formation of deep ulcers of the duodenum. It is still uncertain how 
 these ulcers are produced. 
 
 Chronic perforating ulcers, resembling the chronic ulcers of the 
 
THE ALIMENTAEY CAJTAL. 317, 
 
 stomach, are found in the daodenum. They are associated with similar 
 ulcers in the stomach or occiir by themselves. 
 
 Some curious ulcers of the upper part of the small intestine are 
 described by Israel." There were five ulcers, from two and one-half 
 to ten centimetres long, encircling the intestine, with irregular, granu- 
 lating surfaces. 
 
 EMBOLI. 
 
 Emboli have been found in the superior mesenteric artery in a number 
 of cases ; in the inferior mesenteric artery they are less frequent. They 
 produce an intense venous congestion of the entire wall of the intestine, 
 with hemorrhage into its cavity and its wall. 
 
 THE LARGE INTESTINE. 
 INFLAMMATION. 
 
 The mucous membrane of the large intestine is very frequently the 
 seat of acute and chronic inflammatory processes. The larger number of 
 these belong to the condition which is described clinically under the 
 name of dysentery. The inflammation affects most frequently the rectum, 
 sometimes the entire length of the colon, sometimes only the upper part 
 of the colon. 
 
 Acute catarrhal colitis. — The mucous membrane is swollen and con- 
 gested, there is an increased production of mucus, there may be a large 
 transudation of serum, there may be some bleeding from the capillary 
 vessels. The epithelium desquamates, and the connective tissue and 
 glandular coats are infiltrated with a moderate number of pus-cells. 
 
 There are curious cases of catarrhal colitis occurring in old and feeble 
 persons, which are very fatal. After death, we find the mucous membrane 
 soft and black, and the entire wall of the gut soft and easily torn. The 
 intestine looks almost gangrenous, but yet does not seem really to be so. 
 What the real nature of these cases is I do not know, although I have 
 seen several of them. 
 
 Ohronic catarrhal colitis may succeed acute colitis, or it may begin as 
 a chronic affection. Either a portion or the entire length of the colon 
 may be involved, and the lesion is found developed in diiierent degrees 
 in different cases. The glandular coat is thickened by the growth of 
 connective tissue between the tubules, or the tubules may become 
 atrophied, and the glandular coat is then thin. There may be a com- 
 plete destruction of the glandular coat at different points, so that ulcers 
 of different sizes are formed. The solitary follicles in the wall of the in- 
 testine may be inflamed and softened, and in this way also small round 
 ulcers are formed. The connective-tissue coat is thickened; this thicken- 
 
 'Charite-Annalen, 1884, p. 707. 
 
318 THE ALIMENTAET CANAl. 
 
 ing is uniform, or it is more marked at some places than others, so that 
 little polypoid tumors are formed, which project into the cavity of the 
 colon. The muscular and peritoneal coats are also thickened. 
 
 Croupous Colitis. — This form of inflammation may inTolye the rec- 
 tum alone, or the entire length of the colon, or only its upper portion. 
 The mucous membrane is congested and swollen, and coated with a layer 
 of false membrane, the connective tissue between aud beneath the 
 glandular tabules is infiltrated with fibrin and pus, and in severe cases, 
 the inflammation involves the muscular and peritoneal coats also. The 
 inflammation is usually more intense at some places than at others, so 
 that the surface of the mucous membrane shows the false membrane in 
 isolated patches. Less frequently there is a uniform coating with the 
 false membrane. In mild cases, as the inflammmation subsides, the 
 products of inflammation are absorbed, and the wall of the intestine 
 returns to its normal condition. In more severe cases, the quantity of 
 the inflammatory products is so great that portions of the wall of the 
 intestine become necrotic. This necrosis may involve only the glandu- 
 lar coat, or it may extend deeper into the wall of the intestine. The 
 necrosed tissue after a time sloughs away, leaving behind ulcers of dif- 
 ferent sizes and depths. After this the ulcers may cicatrize, or their 
 floors and walls may remain in the condition of granulation tissue for an 
 indefinite length of time. When the latter is the case, there is added 
 a chronic inflammation of the wall of the intestine between the ulcers, 
 with changes in the mucous membrane, and thickening of the connective 
 tissue and muscular coats. 
 
 Tlie solitary foUides. — In children, the lymphatic glands in the wall 
 of the large intestine frequently become swollen, soften, and form ulcers 
 in cases of catarrhal colitis. In adults, such changes are not common 
 except in the dysentery of armies. In army dysentery, the changes in the 
 solitary follicles often form the principal part of the lesion, although 
 catarrhal or croupous inflammations are usually associated with them. 
 The intestine is thickly studded with small, round ulcers, originating in 
 the destructive changes in the solitary follicles. But these ulcers show 
 a disposition to increase in size and to remain as chronic ulcers for a 
 long time. 
 
 The ccBcum. — Catarrhal inflammation of the csecum is not uncommon. 
 It is usually produced by an habitual accumulation of fseces in this part 
 of the intestine. The course of the inflammation is chronic, but marked 
 by acute exacerbations. At first the mucous membrane undergoes the 
 ordinary changes of chronic catarrhal inflammation; then there is a slow 
 suppurative inflammation which extends through the wall of the intes- 
 tine, and produces ulcers aud perforations. Through these perforations 
 the fseces may pass into the peritoneal cavity, or the perforations are 
 
THE AI.IMENTAE\' CANAL. 319 
 
 partly closed by adhesions, and abscesses are formed, or sinuses into the 
 surrounding soft parts. 
 
 The rectum. — Besides the inflammatory changes already described as 
 existing in the colon, we sometimes find a suppurative inflammation of 
 the connective tissue which surrounds the rectum, either associated with 
 lesions of the mucous membrane or occurring by itself. 
 
 The vermiform appendix. — The most frequent form of inflammation 
 of the appendix is a suppurative one. The appendix is swollen and con- 
 gested; its walls are infiltrated with pus; at some points there may be 
 necrosis and sloughing of portions of its wall. Within the cavity of the 
 appendix we find fecal concretions, or foreign bodies, or nothing. Such 
 an inflammation may terminate in resolution, but more frequently it sets 
 up an inflammation of the surrounding tissues. This inflammation may 
 be either a local or general peritonitis, or a suppurative inflammation of 
 the soft parts about the appendix. 
 
 Less frequently there is a chronic inflammation of the mucous mem- 
 brane of the appendix, followed by constriction of its upper portion, 
 while the lower part is dilated into a cyst filled with mucus and serum. 
 
 Syphilitic ulcers produced by changes in the solitary and agminated 
 glands of the small intestine are sometimes found in infants. 
 
 In adults, the lower end of the rectum is the part of the intestine 
 which is the most frequent seat of syphilitic ulceration. Most of these 
 ulcers seem to be the result of unnatural coitus, or of infection from 
 specific sores of the vulva; but some of them seem to be due to the soft- 
 ■ening of gummy tumors. 
 
 TUllOKS. 
 
 Myoma. — Tumors composed of smooth muscle and connective tissue 
 grow in the muscular coat and project inwards. They may be large 
 enough to obstruct the intestine, and may then give rise to intussuscep- 
 tion. In the duodenum, such tumors may obstruct the common bile- 
 duct. Less frequently, these tumors project outwards into the perito- 
 neal cavity. 
 
 Lipomata may be developed from the submucous coat and grow 
 inwards, or from the subserous coat, and project outwards into the peri- 
 toneal cavity. 
 
 Polyjjoid Tumors, projecting into the cavity of the intestine and 
 ■composed of connective tissue and covered with epithelium, are frequently 
 found. They are associated with catarrhal inflammation or occur by 
 themselves. They are found throughout the intestinal tract, and may be 
 .single or multiple. They grow from the submucous coat, and project 
 inwards. Some of them are small, solid, connective-tissue tumors, covered 
 by the mucous membrane which they have pushed inwards. Others are 
 •of the same character, but of large size. In others, the connective 
 
320 THE ALIMENTARY CAifAL. 
 
 tissue is ari'anged in branching tufts, covered with cylindrical epithe- 
 lium, and in these last tumors there may also be tubules lined with cylin- 
 drical epithelium, giving to the growth the characters of an adenoma. 
 
 Adenomata are found in tlie duodenum and colon. They form fiat infil- 
 trations of the wall of the intestine, or project inwards as polypoid tumors. 
 They are composed of tubular follicles, like those of the intestinal mu- 
 cous membrane and of a connective-tissue stroma. In some of these 
 tumors the tubules have a tolerably regular shape and arrangement- 
 there is no infiltration of surrounding tissue; the tumor is of benign 
 nature. In other tumors, the tubules are irregular in shape, and arrange- 
 ment, and the growth infiltrates the surrounding jDarts. There is no 
 sharp dividing line between these tumors and the carcinomata. 
 
 Carcinomata are found in the colon and the duodenum, and are of three 
 varieties. 
 
 1. The new growth is composed of tubules lined with cylindrical epi- 
 thelium. It begins as a fiat infiltration of the submucous coat, which 
 soon surrounds the intestine, infiltrates the whole thickness of the wall 
 of the gut, and may extend to the surrounding soft piarts. Fungous 
 masses project int:o the cavity of the intestine, wliile at the same time 
 ulcerative and destructive processes are going on. According to the ex- 
 act arrangement of the growth, there is more or less stenosis of the in- 
 testine. 
 
 2. Tlie growth has the characters of colloid cancer, and forms a diffuse 
 infiltration of the intestinal wall, completely surrounding it and often 
 extending over a length of several inches. 
 
 3. At the anus, there is sometimes a carcinomatous growth, with flat 
 epithelial cells (eiiithelioma), like similar growths in the skin, which in- 
 volves the lower end of the rectum. 
 
 Lymplioma. — Tumors composed of tissue resembling that of the 
 lymphatic glands originate in the solitary and agminated follicles and in 
 the intestinal wall in cases of leukgemia and pseudo-leuksemia. 
 
 Similar tumors are found as an idiopathic lesion, both in the large and 
 small intestine. These tumors are irregular diffuse growths infiltrating 
 the wall of the intestine, the mesentery, and the neighboring glands, and 
 reaching a considerable size. They often ulcerate internally and pro- 
 duce dilatation or stenosis of the intestine. It is hard to tell whether 
 some of these tumors should be called lymphomata or sarcomata. 
 
 CONCRETIONS. 
 
 There are sometimes found in the intestines round, oval, or irregular 
 masses of firm consistence. They are usually small, but may reach the 
 size of a man's fist. They ai-e composed of fecal matter, mucus, bile, the 
 carbonate and phosphate of lime, and triple phosphate. They may pro- 
 duce iniiammation, ulceration, and perforation. 
 
THE ALIMENTAET CANAL. 321 
 
 PARASITES. 
 
 Mycosis Intestinalis. — Under this name have been described a number 
 of cases in which inflammation of the intestines occurred as one of a 
 group of lesions.' In these cases, there are found ecchymoses of the skin 
 and mucous membranes; patches'of fibrin in the stomach, small intes- 
 tine, and colon; serum in the peritoneal cavity; swelling of tiie spleen 
 and lymphatic glands; and sometimes inflammation of the lungs. The 
 intestinal lesions are most marked in the small intestine and the upper 
 part of the colon. The mucous membrane is studded with small brown- 
 ish patches. At the centres of these patches, the wall of the intestine is 
 infiltrated with pus, and around the centres it is infiltrated with blood. 
 Bacilli resembling those of anthrax are found in the intestinal lesions and 
 in other parts of the body. It is believed that the disease is a form of 
 anthrax. 
 
 Ascaris lumbricoides is found in the small intestine, either singly 
 or in considerable numbers. In rare cases, a number of worms may 
 form a mass which produces inflammation, ulceration, and perforation. 
 
 Oxynris vermicularis is found in large numbers in the rectum. 
 
 Tricocephalus dispar is found in the caecum. 
 
 Ankylostomum duodenale is found in the duodenum, and may give 
 rise to considerable hemorrhages. 
 
 Trichina spiralis is found in its adult condition in the small intes- 
 tine. 
 
 Pentaslomum denticulatum occurs in the submucous tissue of the 
 small intestine in an encapsuled condition. 
 
 Cysticercus cellulosm has been seen, in a few oases, on the mucous 
 membrane. 
 
 Tcenia solium, Tmnia mediocanellafa, and Bothrioceplialus latus 
 are all found in the small intestine. 
 
 Very large numbers of various forms of bacteria are regularly found 
 in the intestinal cavity intermingled with its contents, and clinging to 
 its walls. 
 
 THE PERITONEUM. 
 
 The free surface of the parietal peritoneum is covered with a single, 
 layer of flat, polygonal nucleated cells. Beneath these cells are succes- 
 sive planes of connective tissue extending down to the muscles and fascise. 
 These planes are formed of a fibrillated basement substance, reinforced 
 by elastic fibres, and of brandling cells. Embedded in the connective 
 .tissue are the nerves, blood-vessels, and lymphatics. The lymphatic 
 system is very extensive. 
 
 The omentum consists of fibrillated connective tissue arranged so as 
 
 ' Viroh. Arch., Bd. xxi., p. 579; xxx., p. 366; lii., p. 541. Zeitschr. f. Bio- 
 logie, v., 139. Arch. d. Heilkunde, xv. Arch. f. klin. Med., xii., p. 517. 
 31 
 
322 THE alhientaet caistal. 
 
 to form a mesh-work. The trabeculse of the mesh-work are completely 
 covered by large, flat cells. In the basement substance, beneatli the 
 endothelium, are branching cells. In tlie larger trabecalse are blood- 
 vessels, lymphatics, and fat. Sometimes we find on the larger trabeculse 
 little nodules formed of polygonal or branched cells. 
 
 MALFOEilATIOWS. 
 
 Arrest of development of the peritoneum occurs in the shape of fis- 
 sures in the mesial line, or external to it ; in the case of the diaphragm 
 being absent, of a fusion with the pleura ; and as defective development 
 of the mesentery, the omentum, and the other folds of the peritoneum. 
 
 Excess of development occurs in the shape of unusual length of the 
 mesentery, the omentum, and the other folds of the peritoneum; or of 
 supernumerary folds and pouches. These are chiefly found in the hypo- 
 gastric, iliac, and inguinal regions and near the fundus of the bladder. 
 There is access to these sacs by a well-deSned fissure, or ring, which is 
 frequently surrounded by a tendinous band lying in the duplicature. 
 They may give rise to internal incarceration of the intestines. 
 
 INFLAMMATION". 
 
 The very great extent of the peritoneum, and the readiness with 
 which its lymphatic system absorbs foreign matters from the peritonal 
 cavity, render peritonitis a most severe and dangerous form of inflamma- 
 tion. 
 
 If the greater part of the peritoneum is inflamed, we call the lesion a 
 general ]3eritonitis. If only a circumscribed area is involved, it is a local 
 peritonitis. The course of the inflammation may be rapid or slow, so 
 that we speak of acute and chronic inflammation. The inflammation 
 may be attended with the production of tubercle tissue, and then it is a 
 tuiercular j^eriton if is. 
 
 I. Acute Peritonitis. 
 
 The acute inflammations of the peritoneum may occur as idiopathic 
 lesions without discoverable cause ; but much more frequently they are 
 directly due to some appreciable cause. 
 
 Wounds and contusions of the wall of the abdomen ; wounds, ulcers, 
 new growths, incarcerations, intussnscejjtions, ruptures, perforations and 
 inflammations of the stomach and intestines ; inflammation of the ver- 
 miform appendix ; injuries, ruptures, and inflammations of the uterus, 
 ovaries and Fallopian tubes ; rupture and inflammation of the bladder ; 
 inflammation of and about the kidneys ; abscesses and hydatid cysts of 
 the liver ; inflammation of the gall-bladder and large bile-ducts ; throm- 
 hosis of the portal vein ; inflammations of the spleen, pancreas, lym- 
 phatic glands, retroperitoneal connective tissue, vertebrae, ribs and pel- 
 
THE ALIMENTAET CANAL. 
 
 323 
 
 yic bones ; septiceemia and the infectious diseases ; and chronic Bright's 
 disease, are all ordinary causes of acute peritonitis. 
 
 According to the exact cause of the inflammation, the peritonitis is at 
 first either local or general. A local peritonitis may remain circum- 
 scribed, or it may spread and become general. 
 
 We can distinguish two anatomical forms of acute peritonitis. 
 
 (1) Cellular Peritonitis. 
 
 This form of peritonitis may be produced by any irritant which does 
 not act too energetically. It can be excited in dogs by injections of 
 very small quantities of a solution of chloride of zinc. In the human 
 subject we find it with perityphlitis, with circumscribed abscesses in the 
 peritoneal cavity, and in cases of puerperal fever which die within forty- 
 eight hours after the development of symptoms. 
 
 After death we find the entire peritoneum of a bright-red color. 
 
 ¥m. 110.— Acute Cellulak Peritonitis, Human Omentum, X 750 and reduced. 
 
 from the congestion of the blood-vessels, but there is no fibrin, no 
 serum, no pus, no other lesions visible to the naxed eye. Minute 
 examination, however, shows a very marked change in the endothelial 
 cells. They are increased in size and number, and the new cells coat the 
 surface of the peritoneum, and project outwards in little masses (Fig. 110). 
 
324 THE ALIMENTARY CANAL. 
 
 (2) Exudative Peritonitis. 
 
 The. ordinary form of a'cute peritonitis is attended with the pro- 
 duction of serum, fibrin, and pus, and with changes in the endothelium 
 and connective-tissue cells. 
 
 If we inject a solution of chloride zinc, or of some other irritant into, 
 the peritoneal cavity of a dog, we find that by the end of one or two 
 hours inflammatory changes are evident. There is a little serum in the 
 peritoneal cavity, a general congestion of the peritoneum, and little 
 knobs and threads of fibrin on its surface. Tliere are no marked 
 changes in the endothelium or connective-tissue cells, but pus-cells are 
 present in moderate numbers in the stroma, just beneath the endothe- 
 lium, and white blood-cells in the vessels. 
 
 After the lapse of twenty-four hours, the lesions are more marked. 
 The congestion of the peritoneum is much more decided, there is more 
 serum in its cavity, and a thicker layer of fibrin and pus on its surface. 
 Minute examination shows that two distinct sets of changes are going 
 on at the same time : (1) a production of fibrin, serum, and pus ; (2) 
 a swelling and multiplication of the endothelial cells. If the inflam- 
 mation is very intense, the pus and fibrin are most abundant; if the 
 inflammation is milder, the changes in the endothelium are more 
 marked. The fibrin coagulates on the free surface of the peritoneum. 
 The white blood-cells collect in large numbers in the blood-vessels, and 
 as jDus-cells infiltrate the stroma and collect on its surface. There is no 
 special change in the connective-tissue cells. The endothelial cells may 
 remain in place, although their edges and corners are separated by 
 pus-cells and knobs of fibrin; or the endothelium falls off in large 
 patches; or the surface of the peritoneum is covered with numerous cells 
 which look like endothelial cells more or less deformed. But few dogs 
 survive the third day of an acute artificial peritonitis. 
 
 In the human subject, if death takes place before the third day, both 
 the gross and minute changes are the same as those seen in the dog. 
 There are present the same general congestion, the pus, fibrin, and 
 serum, the desquamation and multiplication of the endothelial cells. 
 
 In many cases of peritonitis, however, death occurs between the sixth 
 and fourteenth days of the disease. The appearance of the peritoneum 
 at this period of the inflammation is not always the same. The congestion 
 of the blood-vessels may persist, it may be very intense and accompanied 
 with extravasations of blood, or it may be entirely absent. There may 
 be a thin coating of fibrin and pus gluing together neighboring surfaces 
 of peritoneum, or this layer may be very thick. The production of pus 
 may be superficial, or it may infiltrate the whole thickness of the jierito- 
 neum and the subperitoneal connective tissue. The quantity of purulent 
 serum in the peritoneal cavity may be small or large, and this serum may 
 
THE ALIMENTARY CANAL. 
 
 325 
 
 contain few or many pus-cells, or the serum may be of a dirty brown 
 color, and filled with bacteria. When the purulent serum is shut in by 
 adhesion, it is often thick and yellow, like the pus of an abscess. 
 
 The minute appearances differ from those seen at an earlier stage, 
 chiefly in the larger amount of inflammatory products, and in the changes 
 
 Cr., .JL 
 
 FiGt. Ill,— Human Omentum, X 750 and reduced. 
 Acute Peritonitis of eight days' duration. 
 
 in the fixed connective-tissue cells. During the first three days of an. 
 acute peritonitis, the connective-tissue cells are but little changed, but 
 by the seventh day there is a marked increase in their size and number. 
 
 Acute peritonitis may prove fatal by the fourteenth day ; or it may 
 be succeeded by chronic peritonitis; or the patients recover and perma- 
 nent connective-tissue adhesions and thickenings of the peritoneum are 
 left behind. Recovery is most common when the peritonitis has been a 
 local one. 
 
 II. Chronic Peritonitis. 
 
 We find the following varieties of chronic peritonitis. 
 
 1. Cellular Peritonitis. 
 This form of peritonitis is found as a complication of chronic endo- 
 carditis, of cirrhosis of the liver, of chronic pulmonary phthisis and of 
 acute general tuberculosis. 
 
326 
 
 THE ALIMENTARY CANAL. 
 
 Neither fibrin nor pus are present, but there may be clear serum in 
 the peritoneal cavity. The peritoneum may look normal to the naked 
 eye, or it may be studded with very minute, translucent nodules. 
 
 Minute examination shows changes in the endothelial cells and the 
 connective-tissue cells. These cells are everywhere increased in number 
 and altered in shape; or to speak more guardedly, the surface of the peri- 
 toneum is covered with cells which look as if they were derived from the 
 endothelium and connective-tissue cells (Fig. 113). Some are large flat 
 
 
 Fig. 112.— Human Omentum, X 750 and reduced. 
 Chronic cellular peritonitis, -with pulmonary phthisis. 
 
 cells; some smaller polygonal cells; some irregularly fusiform; some large, 
 granular masses containing a number of nuclei. Although these new 
 cells are found over most of the surface of the peritoneum, yet they are 
 more numerous in little patches, which are scattered here and there. 
 
 2. Peritonitis -with Adhesions. 
 
 There may be a formation of j)ermanent adhesions without the pro- 
 duction of fibrin or pus. It is often, indeed, difficult to tell whether old 
 peritoneal adhesions are due to the form of chronic peritonitis of which 
 we are now speaking, or whether they are the result of an acute peritoni- 
 tis. But there are some cases in which the mode of development of the 
 adhesions seems evident (Fig. 113). 
 
 If, from perityphlitis or some other cause, a collection of pus is shut 
 in in some part of the peritoneal cavity, we may find the rest of the 
 peritoneum smooth and shining, no serum, fibrin, or pus, no thickening; 
 
THE ALIMENTAET CANAL. 327 
 
 but the neighboring surfaces of the peritoneum are attached to each 
 other by adhesions. These adhesions are in the shape of threads and 
 membranes, often of the most extreme tenuity. They are formed, of a 
 fibrillated basement substance, the fibrils crossing each other in all direc- 
 tions. In the basement substance are cells, some fusiform and stellate, 
 but most of them look like large branching cells, of which the cell-bodies 
 have become fused with the basement substance, while the nuclei remain. 
 Close to these adhesions the peritoneum may appear normal to the 
 naked eye, but if it is put in water, very fine threads and membranes 
 
 
 ^ 
 
 
 :M;^^^*IH'.^^ ^^^ 
 
 Fig. 113.— Chronic Peritonitis with Adhesions, X 750 and i educed. 
 Parietal Peritoneum. 
 
 will float upward from its free surface. Minute examination shows that 
 the connective-tissue cells are increased in size and number, that the 
 •endothelial cells are replaced by cells of a great variety of shapes, and 
 that the thin little threads and membranes on the surface are formed of 
 large branching cells. 
 
 Such a peritonitis with adhesions appears to be a more advanced 
 •stage of the cellular peritonitis just described, but the inflammation, 
 instead of stopping at the production of cells alone, goes on to the for- 
 mation of membranes. 
 
 "We sometimes find in the same patient chronic iDleiirisy with adhe- 
 sions and chronic peritonitis with adhesions. 
 
328 THE ALIMENTAET CANAL. 
 
 3. Chronic Peritonitis ivith Thickening of the Peritoneum. 
 
 This form of peritonitis occurs quite frequently sis an idiopathic 
 lesion. It may involve the greater part of the peritoneum or be confined 
 to the capsules of the liver and spleen. 
 
 The most marked feature of the lesion is the thickening of the peri- 
 toneum — a thickening which may reach as much as an inch. The outer 
 portions of the thickened jieritoneum are composed of dense connective- 
 tissue, the inner layers of granulation tissue. The surface of the perito- 
 neum is smooth or covered with fibrin. There may also be connective- 
 tissue adhesions between different parts of the peritoneum. The perito- 
 neal cavity contains clear or purulent serum. 
 
 In some cases the parietal peritoneum is principally involved; in 
 others, the peritoneum of the stomach, intestines, liver, and spleen. The- 
 thickening of the capsule of the liver is attended with a diminution in 
 the size of that viscus. 
 
 4. Chronic Peritonitis ivith the Production of Fibrin, Serum, and Pus, 
 This form of peritonitis may follow acute peritonitis, may be due to 
 lesions of tlie abdominal viscera, or may occur without known cause. 
 
 The abdominal cavity contains purulent serum, either free or shut 
 in by adhesions. The surface of the peritoneum is coated with fibrin and 
 connective-tissue adhesions. The coils of intestine, and all the neighbor- 
 ing surfaces of the peritoneum are matted together partly by fibrin, 
 partly by permanent adhesions. 
 
 5. Hemorrhagic Peritonitis. 
 
 This occurs most frequently as a local inflammation. It involves the 
 peritoneum behind and around the uterus in the female, and that cover- 
 ing the recto-vesical excavation in the male. The affected portion of th& 
 peritoneum is covered with layers of new membrane infiltrated with 
 blood. The membranes are formed of connective tissue containing nu- 
 merous blood-vessels and infiltrated with blood. The extravasations of 
 blood may form tumors of considerable size. 
 
 General hemorrhagic peritonitis is described by Friedreich.' In two- 
 cases of ascites, which had been frequently tapped, he found the visceral 
 and parietal peritoneum covered with a continuous membrane of a dif- 
 fuse yellowish-brown color, mottled with extravasations of blood. The 
 membrane was thickest over the anterior abdominal wall. It could be 
 separated into a number of layers. These layers were composed of blood- 
 vessels, masses of pigment, branching cells, and fibriliated basement sub- 
 stance. h\ many places the extravasated blood was coagulated in the 
 shape of round, hard, black nodules. The entire new membrane could 
 be readily stripped off from the peritoneum. 
 
 ' Viroh. Arch., Bd. 58, p. 35. 
 
THE ALIMENTARY CANAL. 329 
 
 6. Tubercular Peritonitis. 
 
 This occurs as one of the lesions of acute general tuberculosis, with 
 chronic pulmonary phthisis, witli tubercular inflammation of the genito- 
 urinary tracts, and as a local inflammation. 
 
 The gross appearance of the lesion varies. 
 
 When tubercular peritonitis occurs as one of the lesions of general 
 tuberculosis, there are numerous small miliary tubercles, increase in the 
 size and number of the endothelial and connective-tissue cells, and some- 
 times a little fibrin. Some of the miliary tubercles are composed of 
 tubercle tissue, others of round and polygonal cells. 
 
 As a complication of tuberculosis of the genito-urinary tract, we find 
 the peritoneum studded with miliary tubercles, coated with fibrin, and 
 serum is also present in the peritoneal cavity. 
 
 As a complication of chronic phthisis, there are miliary tubercles in 
 the peritoneum of the small intestine immediately over tubercular ulcers 
 of the mucous membrane. There may also be thickening of the peri- 
 toneum and permanent adhesions. 
 
 Local tubercular peritonitis usually follows one of three types. 
 
 (1) Tubercular ascites. — The peritoneum is thickened, it is studded 
 with masses of tubercle tissue in the form of miliary tubercles, or of 
 large, flat masses. The omentum may be much thickened. There are 
 bat few adhesions, but there is a large amount of turbid serum. There 
 may be at the same time tubercular jjleurisy, or tubercles in the spleen, 
 or in the lymphatic glands. 
 
 (2) Tubercular peritonitis with the production of a large amount of 
 fibrin. The peritoneum is studded with miliary tubercles. It is coated 
 with a thick layer of soft gelatinous fibrin, which mats together all the 
 neighboring peritoneal surfaces, so that the abdominal cavity seems to be 
 filled with a large boggy mass composed of all the viscera adherent to 
 each other, and with the interstices between them filled with fibrin. 
 
 (3) Tubercular peritonitis with adhesions. The peritoneum is thick- 
 ened and there are numerous connective-tissue adhesions. All the ab- 
 dominal viscera are firmly matted together, and there may be collections 
 of pus shut in by the adhesions. The adherent coils of intestine may 
 ulcerate and open into each other. There are miliary tubercles, or large 
 tubercular nodules or plates. 
 
 TUMORS. 
 
 Fibromata are developed from the subperitoneal connective tissue, and 
 project inwards into the peritoneal cavity. They are found beneath the 
 parietal peritoneum and that covering the intestines. Such tumors may 
 reach a very considerable size. 
 
 Lipoma. — Oirdumscribed tumors composed of fat -tissue are formed 
 beneath the intestinal and parietal peritoneum. These tumors may be- 
 
330 THE ALIMEHTAET CANAL. 
 
 come changed into fibrous tissue, or calcified. Their pedicles may be- 
 come atrophied so that they are left free in the peritoneal cavity. 
 
 When they grow beneath the parietal peritoneum, they may form fat 
 herniffi. At the umbilicus, in the ingainal canal, along the vas deferens, 
 in the crural ring, and in the foramen obturatorium fatty tumors may 
 grow, project outwards under the skin like hernise, and by drawing the 
 peritoneum after them into a pouch, may open the way for a future intes- 
 tinal hernia. 
 
 Plexiform Aug io- Sarcoma. — Very large tumors, resembling in their 
 gross appearance colloid cancer, have been described by Waldeyer.' They 
 are formed by a new growth of blood-vessels with a production of gelat- 
 inous tissue from their adventitia. 
 
 Carcinoma of the peritoneum is either secondary and primary. The 
 primary tumors assume the character of colloid cancer, or of common 
 cancer. 
 
 The colloid form frequently involves the greater part of the perito- 
 neum, and forms a large mass which distends the abdomen. The omen- 
 tum is changed into a large gelatinous mass; the subjacent muscles, the 
 lymphatic glands, and the liver are infiltrated with the new growth, and 
 soft gelatinous masses project into the peritoneal cavity. The umbiH- 
 cus is sometimes invaded, so as to project outward in the form of a semi- 
 translucent tumor. The appearance of the new growth is that of a soft, 
 jelly-like mass embedded in a fibrous stroma. The minute structure is 
 that of a connective-tissue stroma, arranged so as to form cavities of 
 different sizes. These cavities are filled with a homogeneous, gelatinous 
 basement substance and with polygonal cells. 
 
 Common carcinoma appears in the form of numerous small noduleS 
 scattered everywhere in the inner layers of the peritoneum. These 
 nodules are small, firm, and white, and are composed of a fibrous- stroma 
 inclosing cavities filled with polygonal cells. With the formation of these 
 nodules, there are often associated a general thickening of the perito- 
 neum, an accumulation of serum in the peritoneal cavity, and adhesions. 
 
 Endotheliomata of the peritoneum have been observed in cases with 
 similar growths in the pleura (page 216). 
 
 Sarcomata appear in the form of solitary, slowly-growing tumors 
 behind the peritoneum or between the folds of the mesentery. 
 
 These retro-peritoneal sarcomata are found both in children and 
 adults. They usually originate behind the peritoneum covering the pos- 
 terior part of the abdominal wall. At first they grow slowly inwards, 
 pushing forward the peritoneum and abdominal viscera. After a time 
 they assume a more infectious character, infiltrating the soft parts with 
 
 ' Virch. Arch., Bd. Iv., p. 134. 
 
THE AMMENTAEY CANAL. 
 
 331 
 
 ':^'''^'K^~ "^-",^-^1;. ^-^-^^-?' 
 
 c J" 
 
 |.1;^.:4. .- 
 
 
 Fig. 114.— Section of a Reteo-Peeit'onbal Sarcoma, X ITO and reduced. 
 
 J 
 
 
 
 5 Ji 
 
 
 .-, "t^ 
 
 ^iS: 
 
 3) 
 
 ^^ 
 
 Fig. 115.— Section of a Eeteo-Peritoneal Sarcoma, X 850 and reduced. 
 
332 THE ALIMENTAEY CANAL. 
 
 which they come in contact, and forming metastatic tumors in the liver 
 and other viscera. 
 
 These tumors are composed of a stroma and cells. The cells are 
 large, of cuboidal shape, and often undergo fatty degeneration, when 
 they become swollen. The proportion between the cells nd the stroma 
 and the arrangement of the cells varies in the different cases and in dif- 
 ferent parts of the same tumor (Figs. 114 and 115). 
 
 The stroma may be abundant, and the cells scattered irregularly, 
 each cell in a little cavity of its own. The stroma may be abundant, but 
 the cells are collected in masses, as in a carcinoma. 
 
 The cells are abundant and close together, but each cell is surrounded 
 by a thin partition of connective tissue. The blood-vessels are numerous, 
 and the cells are arranged around them with some regularity. 
 
 From the above description, it will be seen that these tumors are 
 of peculiar structure, and perhaps do not really belong to the sarcomata. 
 
 PARASITES. 
 
 EcMnococci can be formed in their regular way at any part of the vis- 
 ceral and parietal peritoneum, or be free in the peritoneal cavity. These 
 cysts may be small, or so large as nearly to fill the abdominal cavity. 
 
 Cysiicercus ceUiclosce may also be developed in the subperitoneal con- 
 nective tissue. 
 
THE LIYEE. 
 
 MALFORMATIONS. 
 
 Congenital malformations of the liver are not common, and are of 
 little i^ractical importance. Tlie organ may be entirely wanting; the 
 lobes may be diminished or increased in number; its form may be al- 
 tered, so that it is rounded, flattened, triangular, or quadrangular. The 
 gall-bladder or gall-ducts may be wanting, the ductus choledochus may 
 be double, both ducts emptying into the duodenum, or one emptying 
 into the duodenum, the other into the stomach. The single ductus 
 choledochus may also empty into the stomach. Owing to abnormal open- 
 ings in' the diaphragm or the abdominal parietes, the liver may suffer 
 ■displacement upward or forward. In congenital transposition of the 
 viscera, the liver is found on the left side, the stomach and spleen on 
 the right side. 
 
 Small, isolated bodies, having the same structure as the liver, have 
 been found in the suspensory ligament. 
 
 ACQUIEED CHANGES IN SIZE AND POSITION. 
 
 As a result of tight lacing, yery marked changes are sometimes pro- 
 duced in the shape of the liver. By the narrowing of the base of the 
 thorax, the organ is compressed from side to side, and its convex surface 
 is pressed against the ribs. In consequence of this, there are found 
 ridges and furrows on its convex surface. In consequence also of the 
 ■circular constriction, a part of the right, and usually of the left lobe 
 also, becomes separated by a depression. Over this depressed and thinned 
 portion of the liver, the capsule is thick and opaque. In extreme cases, 
 the depressing and thinning reach such an extent that there is only a 
 loose, ligamentous connection between the separated portion and the 
 liver. 
 
 A series of depressions are sometimes found on the upper surface of 
 the right lobe of the liver, running from front to back, apparently caused 
 by folds of the organ. 
 
 Structural changes in the liver may induce changes in its size and 
 
334 THE LIVEE. 
 
 shape. It may be increased in size by tumors, hydatid cysts, abscesses, 
 fatty and amyloid degeneration, by congestion, and sometimes by cirrho- 
 sis, etc. 
 
 It may be diminished in size by atrophy, by cirrhosis, by acute paren- 
 chymatous degeneration, etc. 
 
 Changes in the position of the liver are produced by alterations in 
 its size, by pressure downward from the thoracic cavity, and upward 
 from the abdomen, by the constriction of tight lacing, by tumors or 
 circumscribed serous exudation between the liver and diaphragm, by 
 curvature of the spine. 
 
 The liver is readily turned, by pressure from above or below, on its 
 transverse axis. The transverse colon may be fixed above the liver so as 
 to push it backward, downward, and to the right. Thei-e are a few 
 cases recorded of dislocated and movable livers. Those occurred in 
 women who had borne children, and whose abdominal walls were lax. 
 With ascites it is not uncommon to find the liver quite movable. 
 
 AN-IIMIA AND HYPEREMIA. 
 
 Anceinia of the liver may be general or partial. It may be due to 
 general ansemia or to local disturbances of the circulation, such as swell- 
 ing of the cells in parenchymatous or other degeneration, pressure of 
 tumors, etc. The organ appears pale, often of slightly yellowish or 
 brownish color. It may be harder than usual, and smaller. 
 
 Hypercemia of the liver is either an active or a passive process. In 
 health, the amount of blood in the liver varies at different times, being 
 regularly increased during the process of digestion. When the digestive 
 process is unduly influenced by the ingestion of spirits, spices, etc., the 
 hypersemia assumes abnormal proportions, and, when this is often repeated, 
 it may lead to structural changes in the organ. Severe contusions over 
 the region of the liver sometimes cause a hypersemia, which may result 
 in suppurative or in indurative inflammation. In hot climates and 
 in malarious districts, active and chronic hyperaBmia of the liver are 
 frequent, and often cause structural lesions. In scurvy, also, the liver 
 is sometimes congested. Cessation and suppression of the menses and 
 of hemorrhoidal bleeding may cause hyperaemia of the liver. In all these 
 varieties of active congestion, the liver is enlarged, of a deep-red color, 
 and blood flows freely from its cut surface. 
 
 The passive congestions of the liver are produced by some obstruction 
 to the current of blood in the hepatic veins. Valvular diseases of the 
 heart, emphysema and fibrous induration of the lungs, large pleuritic ef- 
 fusions, intra-thoracic tumors, angular curvature of the spine, aortic 
 aneurisms pressing on the vena cava, and constrictions of the vena cava 
 and of the hepatic veins, may all produce a chronic hyperemia of the 
 liver. In all these cases, as the congestion affects principally the hepatic 
 
THE LIVEE. 
 
 335 
 
 veins, we find the centre of each acinus congested and red, while its peri- 
 phery is lighter colored. This gives to the liver a mottled or nutmeg 
 appearance {Nutmeg liver). The liver-cells in the centre of each acinus 
 are frequently colored by little granules of red or black pigment, and 
 the cells at the periphery become fatty, so that the nutmeg appearance is 
 still more pronounced. A liver in this condition is usually of medium 
 size, but may be smaller or larger than normal. 
 
 
 .»,.V 
 
 
 
 V'VJ'I i 
 
 s^l 
 
 
 ^1 •'^ 
 
 .1"- 
 
 
 4 
 
 Fig. 116.— Chronic Congestion of the Livek. X 300 and reduced. 
 Complete atrophy of the liver-cells at the centre of a lobule, u, Dilated vena centralis; &, 
 dilated capillaries filled with blood; c, portal vein surrounded by connective tissue; d, gall-ducts; 
 e, atrophied liver-cells; g, nearly normal liver-tissue. 
 
 "When the congestion is long continued, the veins at the centre of each 
 acinus may become permanently dilated, the hepatic cells in their meshes 
 become atrophied (Pig. 116), so that the centre of each acinus consists 
 only of dilated capillaries and new connective tissue; or, the dilatation and 
 atrophy of the liver-cells may, in circumscribed portions of the organ, 
 involve the entire acinus. In long-continued congestion, the liver is 
 usually smaller than normal, and may be slightly roughened or uneven 
 on the surface; but it is sometimes enlarged. The peculiar nutmeg ap- 
 pearance may be very well marked, or it may not be evident, the organ 
 being of a dark-red color. 
 
33 6 THE LIVEE. 
 
 WOUNDS, EUPTUEB, AND HEMOEEHAGE. 
 
 Wounds of the liver induce hemon-hage, which, if life continue, is 
 followed by inflammation. Serious wounds of the liver are usually fatal, 
 but recovery may occur even after the destruction of a considerable por- 
 tion of the organ. 
 
 Rupture of the liver may be produced by severe direct contusions, or 
 by falls. It may be produced in children by artificial delivery. The rup- 
 ture usually involves both the capsule and a more or less considerable 
 portion t)f the liver-tissue. It is commonly accompanied by large hem- 
 orrhage, and is usually fatal. 
 
 Hemorrhage. — Extravasations of blood in the substance of the liver, 
 or more frequently beneath the capsule, are found in new-born childrea 
 after tedious or forcible labors. In adults, hemorrhage, except as the 
 result of injury, is uncommon. Extravasations of blood are sometimes 
 seen in malignant malarial fevers, especially in tropical climates; in 
 scurvy, purpura, and phosphorus poisoning; and bleeding may occur in 
 and about soft tumors, abscesses and echinococcus cysts. It may also 
 occur as a result of thrombosis of the hepatic vein. 
 
 LESIONS OF THE HEPATIC AETEET. 
 
 The hepatic artery is in rare cases the seat of aneurisms which may 
 attain a large size. Such aneurisms may displace the liver-tissue, com- 
 press the bile-ducts so as to cause jaundice, and may rupture into the 
 stomach or abdomen. 
 
 Owing to its abundant anastomoses, emboli of the branches of the 
 hepatic artery usually induce no marked lesions, but they sometimes result 
 in hemorrhagic infarctions. 
 
 LESIONS OF THE POSTAL VEIN. 
 
 Thrombosis, Bmbolism, and Inflammation. — Thrombosis of the 
 branches of the portal vein may Oe produced by weakening of the circu- 
 lation from general debility — marasmatic thrombi; by pressure on the 
 vessel from without, as in cirrhosis, tumors, gall-stones, dilatation of the 
 bile-ducts, etc. ; by injury; by the presence of foreign materials within the 
 vessel ; and as a result of inflammation of its wall, or of embolus. The 
 thrombus may form in the vessels in the liver, or be propagated into them 
 from without. It may partially or entirely occlude them. The clot 
 may become organized as a result of endophlebitis and a permanent oc- 
 clusion of the vessel ensue. If the clot be a simple, non-irritating one, 
 leading to occlusion, the consequences are usually more marked in the 
 ■ abdominal viscera than in the liver itself. The branches of the hepatic 
 artery form sufficient anastomoses to nourish the liver-tissue and prevent 
 its necrosis even in complete occlusion of the portal vein, and if occlu- 
 sion occur slowly, the organ may continue to perform its functions. 
 
THE LIVEE. 337 
 
 But this obliterative form of thrombosis is usually attended by ascites, 
 enlargement of the spleen, dilatation of the abdominal veins, and some- 
 times by hemorrhage from the stomach and intestines. 
 
 In another class of cases, in addition to the local and more mechanical 
 effects of a thrombus, there may be necrotic changes and suppurative in- 
 flammation in the walls of the vessels, or in the liver-tissue about them. 
 The thrombi are apt to soften and break down, and the fragments may 
 be disseminated through the smaller trunks of the portal vein. In this 
 way, by the distribution through the smaller vessels of a disintegrated 
 thrombus from a large trunk, or by the introduction into the branches 
 of the portal vein of purulent or septic material from some of the abdomi- 
 nal viscera, or from wounds, multiple foci of purulent inflammation in 
 the portal vein, and multiple abscesses involving the liver-tissue may be 
 produced. In many cases, the presence of bacteria may be detected in 
 the inflammatory foci. 
 
 These soft thrombi of the portal vein and the accompanying pylephlebi- 
 tis and abscess may be caused in a variety of ways: 1. Ulceration of the in- 
 testines and stomach, abscesses of the spleen, suppurative inflammation of 
 the mesentery and mesenteric glands, inflammation and ulceration of 
 the bile-ducts from gall-stones, inflammation of the umbilical vein in in- 
 fants, may all induce thrombi in their respective veins, which may be 
 propagated to the portal vein, or may give rise to purulent or septic em- 
 boli. Two cases are recorded in which a fish-bone in the portal vein in- 
 duced suppurative inflammation in that vessel. One of these cases, oc- 
 curring in Bellevue Hospital, in 1867, was reported by Dr. Janeway. 
 Male, 47; dying, after a four weeks' illness, in a typhoid condition, with 
 lesions of sero-fibrinous peritonitis and chronic diffuse nephritis. There 
 were numerous small abscesses in the right lobe of the liver, two in the left 
 lobe. The left division of the joortal vein contained a firm red and white 
 clot, over an inch long; the right division was lined with a firm throm- 
 bus. The walls of the vein were thickened and contained purulent fluid. 
 A fish-bone, two inches long, its centre covered by a thrombus, lay half 
 in the mesenteric and half in the portal vein. 
 
 In certain cases of thrombosis and inflammation of the portal vein, the 
 cause cannot be discovered. 
 
 In infants, inflammation of the umbilical vein may not only induce 
 inflammation of the portal vein and abscesses in the liver, but multiple 
 abscesses in various parts of the body, and acute peritonitis may be in- 
 duced. 
 
 Rupture of the Portal Vein, with fatty degeneration of its walls, has 
 occurred in a few instances. 
 
 Chronic Endoplilelitis, with atheroma and calcification, may occur in 
 the walls of the portal vein, giving rise to thrombosis. 
 
 Dilatation of the Portal Vein, either uniform or varicose, may occur 
 23 
 
338 THE LIVEE. 
 
 in various parts of the vessel or its branches. It may be caused by destruc- 
 tion of the liver-capillaries in cirrhosis, or by occlusion of the vein by 
 thrombi, tumors, etc. 
 
 THE HEPATIC VEINS. 
 
 The hepatic veins present lesions similar to those of the portal vein 
 and its branches, but they are much less frequent. They may be dilated 
 by obstruction to the passage of venous blood into the heart. They may 
 be the seat of acute and chronic inflammation, and soft thrombi and 
 suppurative inflammation may be produced by abscesses in the liver. 
 
 ATKOPHY OP THE LIVER. 
 
 Atrophy of the liver may affect the entire organ, or be confined to some 
 part of it. General atrophy may occur in old age as a senile change, or 
 may be induced by starvation or chronic exhausting diseases. The or- 
 gan is diminished in size, is usually firm, and the acini appear smaller 
 than usual. Microscopically, the change is seen to be due to a diminu- 
 tion in size of the liver-cells, and, hand in hand with this, there occurs 
 frequently an accumulation of pigment granules within the atrophied 
 cells. The cells may entirely disappear over circumscribed areas, leav- 
 ing only shrivelled blood-vessels and connective tissue; or, in some cases, 
 there may be an increase of connective tissue, in connection with the 
 atrophy of the cells. When much pigment is formed in the cells, the 
 lesion is often c&Wed pigment ah'0j)7iy. 
 
 Essentially the same changes may occur in circumscribed portions of 
 the liver, as the result of pressure from new connective tissue in cirrho- 
 sis, from tumors, hydatids, amyloid degeneration, gall-stones, etc. In 
 atrophy from pressure, the liver-cells are apt to become very much flat- 
 tened and squeezed together as they diminish in size. 
 
 DEGENERATIVE CHANGES. 
 
 Parenchymatous Degeneration {Cloudy Swelling). — In a variety of 
 acute and infectious diseases — pneumonia, typhoid and typhus fever, scar- 
 latina, variola, erysipelas, yellow fever, septicaemia, and in certain cases 
 of acute anaemia and phosphorus poisoning — the liver is somewhat 
 swollen and, on section, of a dull yellowish-gray color, looking somewhat 
 as if it had been boiled. It contains less blood than usual, and the out- 
 lines of the lobules are indistinct. Microscopical examination shows the 
 lesion to consist of a swelling of the liver-cells and an accumulation in 
 them of moderately refractile, finer and coarser albuminous granules. 
 These granules may disappear and the cells return to their normal condi- 
 tion, or, as is frequently the case, they may pass into a condition of fatty 
 degeneration. Very frequently fatty and parenchymatous degenerations 
 are associated together. 
 
 Fatty InMtration. — In the normal human liver, there is usually a cer- 
 
THE LITER. 
 
 339 
 
 tain amount of fat in the liver-cells, and this amount varies considerably 
 under different conditions. 
 
 The gross appearance of pathological fatty livers varies a good deal, 
 depending upon the amount and distribution of fat and its association 
 with other changes. If the lesion is uncomplicated and considerable, 
 the organ is increased in size, the edges rounded, the consistence firm, 
 the color yellowish, and the cut surface greasy. The lobules are en- 
 larged and their outlines usually indistinct, and the blood content 
 diminished. The liver is increased in weight. If the amount of infil- 
 tration be moderate, the outlines of the lobules may be more distinct 
 than usual, and the centres appear unusually red. This is due to the fact 
 that the accumulation of fat usually commences in the periphery of the 
 lobules and progresses towards the centres, so that the centre appears 
 darker by contrast with the fatty periphery. The lesion may be uniform 
 throughout the organ, or it may occur in patches. In the latter case the 
 liver has a mottled appearance, irregular yellowish patches alternating 
 with the brownish-red unaffected portions. 
 
 Eatty infiltration is often associated with chronic congestion {nutmeg 
 
 Fig. 117. — Fatty Infiltration of Liver-Cells, x 700. 
 
 liver), with cirrhosis and amyloid degeneration; the picture may then 
 present considerable complexity. Fatty livers may be stained brown or 
 greenish with bile pigment. 
 
 Microscopically the liver-cells are seen to contain larger and smaller 
 droplets of fat (Pig. HI'), and frequently large drops of fat occupy nearly 
 the entire volume of the cell, so that the protoplasm may be visible only 
 as a narrow nucleated crescent at one side; or it may disappear altogether. 
 The microscopical appearances of course vary, depending upon the degree 
 of infiltration and the association with other lesions. 
 
 Fatty infiltration of the liver may occur as a result of excessive in- 
 gestion of oleaginous food, in chronic alcohol, phosphorus, and arsenic 
 poisoning; in certain exhausting diseases accompanied by malnutrition, 
 as in pulmonary phthisis, chronic dysentery, etc., and under a variety of 
 condition which we do not understand. 
 
 Fatty Degeneration. — In this condition, which in many cases cannot 
 
340 
 
 THE LrVEE. 
 
 be morphologically distinguished from fatty infiltration, the fat is 
 believed to be formed by a transformation of the protoplasm of the liver- 
 cells. The fat-droplets are, for the most part, very small and 
 abundant, though this is not constant. Patty degeneration of the liver- 
 cells frequently follows, and is associated with cloudy swelling, under the 
 varying conditions in which this occurs, or it may appear in profound 
 anaemia. 
 
 Amyloid Degeneration (Waxy Liver). — In the liver, amyloid degene- 
 ration may be general or local ; so extensive as to give the organ very 
 characteristic appearances, or so slight as to be unrecognizable without 
 the aid of the microscope. It may be associated with other lesions. 
 When the change is extensive and general, the liver is enlarged some- 
 times to more than twice its normal size ; the edges are thickened and 
 rounded; the surface smooth; the tissue tough, firm, inelastic, more or 
 less translucent, and of a brownish-yellow color. The lobular structure 
 may be more or less indistinct, or it may become very evident by an 
 associated fatty degeneration of the peripheral or central cells of the 
 lobules. The translucency and peculiar appearance of the tissue may be 
 best seen by slicing off a thin section, and holding it up to the light. 
 When the lesion is less considerable, the liver may be of the usual size. 
 
 
 Eig. 118.— Amyloid Degeneration of Livek Capillaries, X about 100. 
 
 and may feel harder than normal, and here and there a translucent 
 mottling may be evident, or the degeneration may be apparent only on 
 the addition on staining agents (see p. 62). When, as is frequently the 
 case, it is associated with cirrhosis, the liver may be small and nodular, 
 and the appearance of the cut surface will vary greatly, depending upon 
 the character of the cirrhotic change and the presence or absence of fat. 
 This degeneration usually commences in the walls of the intralobular 
 blood-vessels, causing them to become thickened and translucent. The 
 liver-cells are squeezed by the thickening of the vessels and may become 
 
THE LIVEE. 341 
 
 atrophied, sometimes completely so (Fig. 118). It is stated by some ob- 
 servers that the liver-cells may also become waxy, but we have been unable 
 to find them unmistakably thus changed. The liver-cells not infrequently 
 undergo fatty metamorphosis. Amyloid degeneration may also involve 
 the interlobular vessels, and in advanced stages larger and smaller areas 
 of liver-tissue may be nearly or completely converted into the dense 
 refractile substance, which in its arrangement but obscurely represents 
 the grouping and structure of the affected lobules. Not infrequently atro- 
 phic or fatty liver-cells are seen scattered singly or in clusters through 
 the amyloid masses. In the affected regions the blood content of the 
 liver is considerably diminished, or it may be nearly entirely absent. 
 
 Amyloid degeneration of the liver is usually associated with a similar 
 lesion of other organs, such as spleen, kidneys, intestines, etc., although 
 it may occur in this organ alone. It usually occurs in cachectic condi- 
 tions, as in chronic phthisis, in chronic suppurations especially of the 
 bones, in syphilis, and sometimes in malarial poisoning. It occasionally 
 occurs unassociated with any of these conditions. 
 
 PIGMENTATION OV THE LIVEit. 
 
 As a result of severe malarial poisoning, a variable amount of brown, 
 black, or reddish pigment is often found in the blood. This is usually 
 mostly taken up by the leucocytes and deposited in various parts of the 
 body, chiefly in the liver, spleen, and marrow of the bones. In the liver it 
 is usually found inclosed in variously shaped cells, especially in the blood- 
 vessels, but sometimes in the tissue between them. The liver-cells fre- 
 quently contain bile-pigment, but usually are free from the melanotic 
 pigment characteristic of this condition. As the result of this accumu- 
 lation of pigment, the liver may have a dark reddish-brown, an olive- 
 brown or black color (sometimes called bronze liver). This condition 
 may be associated with various other lesions of the liver, depending upon 
 the nature and extent of which the organ will present a great variety of 
 appearances. Thus there may be fatty or waxy degeneration, cirrhosis, 
 chronic congestion, etc. 
 
 Pigment may be found in the connective tissue along the portal ves- 
 sels similar in character to that which occurs in the lungs from the inha- 
 lation of coal-dust. This inhaled pigment, according to the researches 
 of Weigert, doubtless finds access to the blood (see j). 57), and is depos- 
 ited in the liver as it is in the spleen and hepatic lymph-glands. 
 
 Pigmentation of the liver-cells, which is to a certain extent normal, 
 may be greatly increased as a result of atrojDhy, localized hemorrhage, 
 and of destructive jaundice.' 
 
 ' The distribution and amount of the pigment may be well seen by stainmg 
 thin sections with eosin and mounting in eosin glycerin or balsam. 
 
342 THE LITEE. 
 
 ACUTE YELLOW ATROPHY OE THE LIVER. 
 
 This disease is characterized anatomically by a rapid diminution in 
 the size of the lirer as the result of a granular and fatty degeneration 
 and disintegration of the liver-cells. The liver, sometimes within a few 
 days, may be reduced to one-half its normal size. On opening the abdo- 
 minal cavity, the organ may be found lying concealed by the diaphragm, 
 close against the vertebral column. The amount of diminution and the 
 general appearance of the affected organ depend to a considerable extent 
 upon its previous condition, i. e., whether or not it was the seat of other 
 lesions, as well as upon the degree of degenerative change. In general, 
 if the lesion is well marked, the liver is small, flabby^sometimes almost 
 fluctuating — and the capsule wrinkled. On section, the cut surface may 
 show but little trace of lobular structure, but presents an irregular mot- 
 tling with gray, ochre-yellow, or red; sometimes one, sometimer another 
 color preponderating. 
 
 Microscopical examination shows varying degrees of degeneration 
 and destruction of the liver-cells. Most evidently in those parts which 
 have a grayish apjjearance, the outlines of the cells are preserved and the 
 protoplasm is filled with larger and smaller granules. In the yellow por- 
 tions the outlines of the liver cells may be preserved, and they may 
 contain varying quantities of larger and smaller fat-droplets and granules 
 of yellow pigment. Or the cells may be completely disintegrated, and in 
 their place irregular collections of fat-droplets, pigment-granules, red and 
 yellow crystals, and detritus; only the connective tissue and blood-vessels 
 of the original liver-tissue remaining. The red areas may show nearly 
 complete absence of liver-cells and cell-detritus, and sometimes irregular 
 rows of cells which are variously interpreted as being new-formed gall- 
 ducts or proliferated liver-cells. In these areas it appears to be, in part 
 at least, the blood contained in the vessels which imparts the red color. 
 Sometimes the interstitial tissue is infiltrated with small spheroidal cells 
 resembling leucocytes. Crystals of leucin and tyrosin are sometimes 
 found intermingled with the cell-detritus. In some cases the liver is not 
 diminished in size. 
 
 These lesions of the liver are frequently associated with enlargement 
 of the spleen and parenchymatous degeneration of the kidney and of the 
 heart-muscle. Multiple hemorrhages may occur in the gastro-intestinal 
 canal, kidneys, bladder, and lungs. There is usually marked jaundice. 
 Rod-shaped bacteria and micrococci have been found in the liver, but 
 their significance is doubtful; we have not been able to find them in the 
 cases which we have examined. The cause of the disease is unknown, 
 and it is doubtful whether it is a disease primarily of the liver, or a gen- 
 eral disease with local lesions. 
 
THE LIVEE. 343 
 
 INFLAMMATION OF THE LITER. 
 
 Acute Hepatitis (Purulent Hepatitis, Abscess of the Liver). — Puru- 
 lent inflammation of the liver may be the result of injury: it may be 
 secondary to inflammation of the gall-ducts, or the branches of the portal 
 vein. It may occur as the result of the presence of tumors, parasites, 
 .or from propagation of an inflammatory process from without, as in ulcer 
 of the stomach with adhesions to the liver and secondary involvement of 
 the latter. It may be due to the introduction into the organ, through 
 the blood-vessels, of septic material, bacteria, etc., or it may be due to un- 
 known causes. Purulent inflammation in the liver almost always results 
 in abscess. 
 
 Large abscesses of the liver may be traumatic, but are, for the most 
 part, due to unknown causes. They are not infrequently associated with 
 dysentery, and may then be due to the conveyance through the veins of 
 septic material from the intestinal ulcers. They occur most frequently 
 in tropical climates, but are not very uncommon in the temperate zones. 
 They are usually single, but there may be several of them. They are 
 sometimes so large as to occupy a large part of a lobe. They are most 
 frequent in the right lobe, but may occur in any part of the organ. 
 They tend to enlarge, and as they do so, they approach the surface of the 
 liver. Here the contents of the abscess may be discharged into the peri- 
 toneal cavity. More frequently, however, as they approach the surface, 
 a localized adhesive peritonitis ensues, so that the liver becomes bound to 
 adjacent parts, and thus the abscess may open into the pleural cavity, 
 or, owing to a secondary pleurisy with adhesions, into the lung- tissue. 
 They may open into the pericardium. They may open externally 
 through the abdominal wall; into the stomach, duodenum, colon, or pel- 
 vis of the right kidney; into the hepatic veins, portal vein, vena cava, or 
 gall-bladder or gall-ducts. 
 
 The early stages in the formation of large abscesses of the liver are but 
 little known. It is probable, however, that in many cases they are the 
 result of the confluence of smaller abscesses. Their contents, usually 
 bad smelling, may be thick and yellow, like ordinary pus; but more com- 
 monly it is thin, reddish-brown, or greenish in color, from admixture with 
 the pus of blood, gall-pigment, and broken-down liver tissue. Micro- 
 scopical examination shows the contents to consist of fluid with pus-cells, 
 more or less degenerated blood, degenerated liver-cells, fragments of 
 blood-vessels, and pigment granules and crystals. The walls of the 
 abscess are usually ragged, shreds of necrotic liver-tissue hanging from 
 the sides. Microscopical examination of the liver-tissue near the ab- 
 scess shows infiltration with pus, flattening of the liver-cells from pres- 
 sure, cloudy swelling, and necrosis of those lying along the cavity. 
 
 After the discharge of the contents of the abscess, or without this if it 
 
844 THE LIVEE. 
 
 be not very large, granulation tissue may form in the wall of the cavity, 
 and a fibrous cajDsule be produced, inclosing the contents, which become 
 thickened and often calcareous, and in this condition may remain for a, 
 long time. Or, the connective-tissue walls may approach one another 
 and join, forming a fibrous cicatrix at the seat of the abscess. 
 
 Abscesses of the liver, accompanying infiammation of the portal vein 
 and gall-ducts, are considered elsewhere in this section. 
 
 Small multiple metastatic abscesses are not infrequent in jiyjemia, and 
 are called pywmic abscesses. In these abscesses we can readily study the 
 various stages of formation. Suppurative processes in any joart of the body 
 — in the head, upper and lower extremities, etc. — may favor the production 
 of the noxious materials, which lu many cases are associated with bacteria, or 
 are bacteria themselves. These, entering the circulation, may pass the heart 
 and pulmonary capillaries, with or without inducing lesions in the lungs, 
 and lodging in the vessels of the liver, induce circumscribed necrosis of 
 the liver-tissue and suppurative inflammation. Under these conditions, 
 we may find on a section of the liver larger and smaller, yellowish or 
 grayish spots, the larger of which may be soft and present the usual 
 characters of abscesses. The smaller, which may not be larger than a pin's 
 head, may present the usual consistence of liver-tissue with the lobular 
 structure still evident; others may be softer, more yellow, and surrounded 
 by a zone of hypersemic liver-tissue. Microscopiical examination of the 
 earlier stages often shows the blood-vessels filled with micrococci, scat- 
 tered, and in zoogloea colonies. Around these, the liver-cells are found 
 in various stages of necrosis; in many the nuclei do not stain, and the 
 bodies are very granular; or, the entire cell is broken down into a mass 
 of detritus. About these necrotic islets of liver-cells, pus-cells collect 
 and often form a zone of dense infiltration. Thus, by the increase of 
 pus-cells and the necrosis of liver-tissue, small abscesses are formed, 
 whose contents are intermingled with greater or less quantities of bacteria 
 which seem to increase in number as the process goes on. By the con- 
 fluence of small abscesses, larger ones may be formed. Death usually 
 ensues, however, before the abscesses attain a very large size. 
 
 Chronic Interstitial HejxUitis {Cirrhosis).- — The primary result of 
 chronic interstitial hepatitis is the formation of new connective tissue 
 in the liver. The character, amount, and distribution of the new tissue 
 vary greatly in different cases. Secondarily there are usually marked 
 changes in the liver-cells and in tlie blood-vessels and gall-ducts. The 
 new tissue is most commonly formed and most abundant, in the peri- 
 phery of the lobules along the so-called capsule of Glisson, but it may 
 extend into the lobules between the liver-cells. It may surround single 
 . lobules, or more frequently larger and smaller groups of lobules (Fig. 119). 
 It may occur in broad or narrow irregular streaks or bands. It is fre- 
 quently more abundantin one part of the liver than in another. The 
 
THE LIVEB. 
 
 345 
 
 ne-w-formed tissue tends to contract, and thus compromise by pressure 
 the inclosed islets of liver-tissue, causing them to project, in larger and 
 smaller nodules, from the surface of the organ. The liver-cells may be 
 flattened or atrophied from pressure; or from interference with the portal 
 circulation they may atrophy or become fatty; or they mjiy become 
 
 
 
 
 
 
 -1 ~,^Jt^ 
 ^ " 'if- 
 
 - /, rr 
 
 
 Fig 119 — Chronic Interstitial Hepatitis X about 20 
 
 a, New-formed connective tissue; b, dilated blood-vessels in the new tissue; c, gall-ducts; 
 
 d, parenchyma of liver. 
 
 colored with bile pigment. The varied appearances which cirrhotic livers 
 present to the naked eye depend largely upon the amount and distribu- 
 tion of the new connective tissue, and upon the secondary changes in the 
 liver-cells. 
 
 In some cases the liver is enlarged, sometimes so much so as to weigh 
 nine or ten pounds, the surface smooth, or slightly roughened; in other 
 cases it may be finely or coarsely nodular on the surface. It may be 
 smaller than normal, sometimes very small indeed, so as to weigh only 
 one or two pounds. The surface may then be very rough and uneven 
 from the projection of larger and smaller nodules of liver-tissue, or it 
 may be quite smooth ; or the organ may be greatly distorted by the con- 
 traction of large bands or masses of new connective tissue. In sections 
 
346 
 
 THE LIVEE. 
 
 tlirougli cirrhotic livers, the new tissue may not be visible to the naked 
 eye, or it may appear as grayish irregular streaks, or bands, or patches, 
 often sharply outlined against the dark-red, or brown, or yellow, or 
 greenish-yellow parenchyma. 
 
 On microscopical examination, the new connective tissue (Fig. 130) is 
 
 Fig. 120.— Chronic Interstitial Hepatitis. 
 The same specimen as Fig. 119, but more highly magnifled. u. Portions of liver-lobules; 6, new- 
 formed connective tissue; c, gall-ducts, apparently newly formed; d, blood-vessels in the new 
 tissue. 
 
 found in some cases loose in texture, and containing many variously-shaped 
 cells; or it may be dense and contain comparatively few cells; it is usually 
 quite vascular. Not infrequently, when occurring largely between the 
 lobules, it will be found to have encroached more or less upon their 
 peripheral portions. Very frequently there are found in the new con- 
 nective tissue cylindrical ducts lined with cuboidal cells, and resembling 
 gall- ducts (Fig. I20c); or irregular rows of more or less cuboidal or polyhe- 
 dral cells, which look somewhat like the lining-cells of the medium-sized 
 gall-ducts, or like altered liver-cells. The branches of the hepatic and portal 
 veins, joarticularly the latter, often become obliterated by pressure from 
 the new connective tissue, or from chronic thickening of their walls, so 
 as to seriously interfere with the function and nutrition of the liver- 
 cells. The bile-ducts also may become obliterated, or there may be 
 catarrhal inflammation, especially of the larger trunks. The branches 
 of the hepatic artery are much less liable to alterations than the other 
 vessels. The capsule of the liver is usually thickened either uniformly 
 
THE LIVEE. 34:7 
 
 or in in-egular patches ; or its surface may be roughened by larger and 
 smaller papillary projections. The liver is frequently bound to the 
 diaphragm or other adjacent organs by connective-tissue adhesions. 
 Amyloid and fatty degeneration may be associated with cirrhosis. Cir- 
 rhotic livers frequently show an unusual number of leucocytes in the 
 blood-vessels. 
 
 The obstruction to the portal circulation induced by cirrhosis 
 usually gives rise to a number of secondary lesions, since collateral cir- 
 culation is rarely established in sufficient degree to afford much relief. 
 The hemorrhoidal and vesical veins may be greatly enlarged, and also 
 veins of communication between Glisson's capsule and the diaphrag- 
 matic veins. 
 
 In rare cases, a very peculiar dilatation of the cutaneous veins about 
 the umbilicus is observed. The enlarged veins form a circular network 
 around the umbilicus, or a pyramidal tumor alongside of it, or all the 
 veins of the abdominal wall, from the epigastrium to the inguinal region, 
 are dilated. This condition is said to be produced by the congenital 
 non-closure and subsequent dilatation of the umbilical vein and its anas- 
 tomoses with the internal mammary, epigastric, and cutaneous veins. 
 According to Sappey, it is not the umbilical vein which is dilated, but 
 a vein which accompanies the ligamentum teres. 
 
 There is very frequently also a dilatation of the veins of the abdomi- 
 nal wall, which has a different cause. It is produced by the pressure 
 of the fluid of ascites on the vena cava, and is found with ascites from 
 any cause and with abdominal tumors. 
 
 Ascites is the most common secondary lesion of cirrhosis. It usually 
 begins at an early stage of the disease, and increases constantly. It 
 usually precedes oedema of the feet, but both may appear at the same 
 time. This fluid is of a clear yellow or brown, green or red ; it is some- 
 times mixed with shreds of fibrin, and more rarely with blood. The 
 peritoneum remains normal, or becomes opaque and thick, or there may 
 be adhesions between the viscera. 
 
 The spleen is very frequently enlarged, and the enlargement may 
 be very considerable. When it is not increased in size, this seems 
 usually due to previous atrophy of the organ, or to fibrous thickening of 
 its capsule, or to hemorrhages from the stomach and bowels, occurring 
 just before death. 
 
 The stomach and intestines are often secondarily affected by the 
 obstruction to the portal circulation. Profuse hemorrhage from the 
 stomach and intestines may occur, and sometimes cause sudden death. 
 The mucous membrane is then found pale, or congested, or with hem- 
 orrhagic erosions. Sometimes the blood is infiltrated in the coats of the 
 stomach and intestines. The mucous membrane of the stomach, and of 
 the entire length of the intestines, is frequently the seat of chronic catar- 
 
348 THE LIVEE. 
 
 rhal inflammation, and is sometimes uniformly and intensely congested, 
 and coated with mucus. In other cases both the mucous and muscular 
 coats are jiale, but very markedly thickened. 
 
 Cirrhosis of the liver is not infrequently accompanied by chronic dif- 
 fLise nephritis. 
 
 The causes of cirrhosis are imperfectly understood. It is a disease 
 of adult life, but exceptionally occurs in children. In adults, it seems 
 in many cases to be directly dependent upon the continued ingestion 
 of large quantities of strong alcoholic liquors. It very rarely occurs as a 
 result of beer- drinking. There are many cases of cirrhosis for which 
 no cause can be discovered. 
 
 Sypliilitic Hepatitis. — Chronic interstitial inflammation of the liver 
 very frequently results from syphilitic infection, either congenitally, or 
 in the later stages of the acquired form. It may occur in a diffuse 
 manner, new connective tissue being formed either between the lobules. 
 
 /o 
 
 ' , 
 
 
 \ 
 
 If- 
 
 1 ' - \' 
 
 
 k_ c 
 
 r "" 
 
 1 
 
 f 
 
 
 A- 
 
 C) 
 
 
 1 rfn f-^ V 
 
 Fig. 121,— a Very Small Syphilitic Tumor, X 850 and reduced. 
 Formed of small polygonal cells developed around the blood-vessels, from a child with 
 congenital syphilis. 
 
 or within them, between the rows of liver-cells. The new tissue may be 
 rich in cells, or dense and firm. This form is frequently seen in chil- 
 dren, and cannot be distinguished, either macroscopically or microscopi- 
 cally, from similar forms of interstitial hepatitis from other causes. 
 
THE LITEE. 
 
 349 
 
 In other cases, particularly in children, there may be numerous small 
 gummata scattered through the liver, together with more or less new con- 
 nective-tissue (Fig. 131). In adults, gummata are usually lai'ger, varying 
 in size from that of a pea to a hen's egg, and may be surrounded by larger 
 
 
 
 a, Cheesy centre 
 liver-lobules. 
 
 Fig. 122. — GtJMMA of Livee, X about 10. 
 6, fibrous periphery ; c, small-celled peripheral infiltration ; d, portions o£ 
 
 and smaller irregular zones of ordinary connective tissue (Fig. 123). In 
 still other cases in adults, we find larger and smaller dense irregular bands 
 or masses of connective tissue running through the liver, drawing in the 
 capsule, and often causing great deformity of the organ. These bands and 
 masses of new tissue may or may not inclose gummata, either large or 
 small. These deforming cicatrices, either with or without gummata, are 
 very characteristic of syphilitic inflammation of the liver. 
 
 This, like the simple interstitial inflammation of the liver, may be 
 associated with fatty and waxy degeneration, and with atrophy of the 
 parenchyma from pressure. 
 
 Tulercular Hepatitis. — This lesion, which is usually secondary to 
 tubercular inflammation in some other part of the body, or a part of 
 •acute general miliary tuberculosis, is most frequently characterized by 
 the formation of larger and smaller miliary tubercles which may be 
 either within or between the liver-lobnles, or in the walls of the bile- 
 ducts. Many of the tubercles are too small to be seen with the naked 
 eye; others may be just visible as grayish jooints; still others may be from 
 one to three mm. in diameter, with distinct yellowish-white centres. 
 Microscopical examination shows considerable variation in the structure 
 ■of the tubercles in different cases, as well as in the same liver. Some of 
 
350 THE LIVEE. 
 
 them, usually the smaller ones, consist simply of more or less circum- 
 scribed collections of small spheroidal cells, which are not morphologi- 
 cally distinguishable, so far as the form and arrangement of the cells are 
 concerned, from simple inflammatory foci, or from the diffuse masses of 
 lymphatic tissue ■which occur normally in the liver. 
 
 In other forms we find a well-marked reticulum with larger and 
 smaller spheroidal and polyhedal cells, with or without giant-cells. In still 
 other forms, there is more or less extensive cheesy degeneration. The larger 
 forms are conglomerate, being composed of several tubercle granula 
 joined together to form a single nodular mass. The liver-cells at the 
 seat of the tubercle are destroyed, and the interstitial tissue and blood- 
 vessels either destroyed or merged into the tubercle-tissue. In the peri- 
 phery of the tubercles the liver-cells may be in a condition of coagulation 
 necrosis and the tissue round about may be infiltrated with small sphe- 
 roidal cells. There is in some cases a new formation of gall-ducts or of 
 structures which resemble these, and which in transverse sections look 
 considerably like giant-cells. Tubercle bacilli, frequently in small num- 
 bers, but often in great abundance, may be found within the tubercles. 
 
 Tuberculosis of the liver may be associated with cirrhosis, waxy and 
 fatty degeneration. 
 
 Much more rarely than the above form, there are found in the liver 
 more or less numerous scattered tubercular masses from the size of a pea 
 to that of a walnut or larger, with cheesy centres and usually a new 
 growth of connective tissue in the periphery. These so-called solitary 
 tubercles of the liver may be softened at the centres. Tubercular inflam- 
 mation of the gall-ducts may give rise to numerous scattered cheesy 
 nodules, as large as a pea or larger, which may be softened at the centre 
 and stained yellow with bile. This lesion is rare and seems to be more 
 frequent in children than in adults. 
 
 Perihepatitis. — Acute inflammation of the serous covering of the 
 liver with the formation of fibrin may occur as a part of acute general or 
 localized peritonitis, and over the surface of abscesses, tumors, hydatids, 
 etc., of the organ, when these lie near or approach the surface; or it may 
 be secondary to acute pleurisy. 
 
 Chronic perihepatitis, resulting in the thickening of and formation of 
 new connective tissue in and beneath the capsule of the liver, may be 
 secondary to an acute inflammation of the capsule, or it may be chronic 
 from the beginning and associated with chronic pleurisy, chronic peri- 
 tonitis, and cirrhosis. In this way, more or less extensive adhesions of 
 the liver to adjacent structures may be formed; or by contraction of the 
 new-formed connective tissue, considerable deformity of the liver may be 
 produced. The capsule is sometimes uniformly thickened, sometimes the 
 new tissue occurs in more or less sharply circumscribed patches. The sur- 
 face is sometimes roughened from little irregular projecting masses of con- 
 
THE LIVEE. 351 
 
 nective tissue. Microscopically the new-formed tissue is usually dense 
 and firm, but it may be loose in texture and contain many cells. Not 
 infrequently bands or masses of connective tissue run inwards from the 
 thickened capsule between the superficial lobules, causing localized 
 atrophy of the parenchyma. 
 
 Hyperplasia of Lymphatic Tissue in the Liver. — In some forms of 
 leukaemia and pseudo-leuksemia, the liver is not infrequently enlarged and 
 soft and besprinkled with small white spots, or streaked with narrow 
 whitish irregular bands, or of a diffuse grayish color. Microscopical ex- 
 amination shows this change to be due to an accumulation of cells re- 
 sembling leucocytes, either along the portal vein, or diffusely through 
 the liver-tissue, or in small circumscribed masses. The amount of accu- 
 mulation of these small cells varies much, but is sometimes so great as to 
 seriously comi^romise the liver-cells. The origin of these new cells is not 
 .yet definitely known. They may be, and doubtless in part are, brought 
 to the organ through the portal vein, but they may, in part at least, be 
 formed in the liver itself. 
 
 In typhoid fever, small-pox, scarlatina, diphtheria, and measles, 
 small circumscribed masses of cells resembling leucocytes are sometimes 
 found in the liver, lying in the meshes of a delicate reticular tissue. 
 These are sometimes called miliary lymphomata, but it should be re- 
 membered (see p. 291) that small masses of lymphatic tissue normally 
 occur in the liver, and that, as under the above conditions, an hyperplasia 
 of the lymph-glands and spleen is wont to occur; these so-called lympho- 
 mata are very probably normal structures, which have become altered 
 and more prominent under the conditions of disease. 
 
 TUMORS OF THE LITER. 
 
 Tumors of tbe liver may be primary or secondary; the latter are most 
 common. 
 
 Cavernous Angiomata. — These tumors, usually small, from five to 
 fifteen mm. in diameter, are most common in elderly persons and are of 
 no practical significance. They may be situated at the surface or em- 
 bedded in the organ, and are of a dark-red color; sometimes sharply 
 circumscribed by a connective-tissue capsule, sometimes merging imper- 
 ceptibly into the adjacent liver-tissue. Microscopically they consist of a 
 congeries of irregular cavities (Fig. 44, p. 139) filled with blood and fre- 
 quently communicating freely with one another. The walls of the cavi- 
 ties consist of connective tissue, often containing small blood-vessels, and 
 are sometimes thick, sometimes thin. They are believed to be formed by 
 dilatation of the liver capillaries with subsequent thickening of their walls 
 and atrophy of the adjacent liver- cells. 
 
 ^maW fibromata and lipomata have been described, as also fibre neuro- 
 mata of tlie sympathetic. 
 
352 THE LITEE. 
 
 Adenomata of the liver are of not infrequent occurrence. They are 
 sometimes small and circumscribed, sometimes very large and multiple. 
 They present two tolerably distinct types of structure. In one form the 
 tissue presents essentially the same structure as normal liver-tissue, ex- 
 cept that the arrangement of the cells is less uniform and the cells are 
 apt to be larger. They look like little islets of liver-tissue, sometimes 
 encapsulated and sometimes not, lying in the liver-parenchyma. In the 
 other form, the cells are less like liver-cells, are frequently cylindrical, and 
 are arranged in the form of irregular masses of tubular structures with 
 more or less well-defined lumina. These tumors are sometimes large 
 and multiple, and, in one case described by Greenfield, there were meta- 
 static tumors in the lungs. These tubular adenomata are in some cases 
 so closely similar to some of the carcinomata as to be scarcely dis- 
 tinguishable from them and seem indeed to merge into them. 
 
 Carcinomata are the most common and important of the liver tumors, 
 and may be primary or secondary. Primary carcinomata of the liver are 
 probably developed from the epithelium of the gall-ducts, and in some 
 cases are arranged along the larger trunks. Their cells are usually poly- 
 hedral, sometimes cylindrical, and may be arranged irregularly in alveoli, 
 or form more or less well-defined tubular structures. 
 
 Secondary carcinomata of the liver, which are by far the most common, 
 are most frequently due to the dissemination in the organ of tumor-cells, 
 from carcinomata of the stomach, intestines, pancreas, or gall-bladder. 
 But they may be the result of metastases from the mamma, cesophagus, 
 uterus, and various other parts of the body. In secondary carcinomata 
 the cells resemble more or less closely the tyjpe of those forming the 
 primary tumor. 
 
 The form in which the carcinomatous nodules in the liver present 
 themselves is subject to considerable variation. Sometimes they are 
 single, but more often multiple; they maybe very large, or so small as 
 to be scarcely visible to the naked eye ; very frequently numerous small 
 nodules are grouped in the periphery of a larger cancerous mass. They 
 are sometimes deeply embedded in the liver, sometimes they project 
 from the surface. The liver is frequently enlarged, sometimes enor- 
 mously so. The nodules are usually whitish or yellowish, or pink in 
 color, but they are often the seat of hemorrhages, and may become soft- 
 ened at the centre, forming cysts filled with degenerated tumor-tissue, 
 which is often mixed with blood. The nodules are sometimes hard, 
 sometimes soft, and almost diffluent. Fatty degeneration is frequent, 
 and may be evident to the naked eye in the form of yellowish streaks or 
 patches on the cut surfaces. Owing to the degeneration and partial 
 absorption of the central portions of the tumors, the nodules on the 
 surface frequently present a shallow depression at the centre. The 
 tumors may be sharply outlined against the adjacent liver-tissue, or may 
 
THE LIVEE. 353 
 
 merge imperceptibly into it. Tliey may be so large or numerous as to 
 occupy the greater part of the enlarged organ. The liver-tissue in their 
 vicinity shows flattening and atrophy of the liver-cells from pressure, and 
 there may be infiltration with small spheroidal cells. The tumors may 
 press upon the portal vein or its branches, or upon the gall-ducts, and 
 thus seriously interfere with the functions of the organ. Sometimes, 
 however, the tumors are very large and abundant without causing any 
 apparent detriment to the liver functions. They are not infrequently 
 stained with bile. Melanotic carcinomata sometimes occur in the liver, 
 most frequently as secondary tumors. 
 
 In some cases, instead of forming separate distinct nodules, the can- 
 cerous growth develops in the form of a diffuse infiltration of the 
 organ, so that the often greatly enlarged liver is irregularly mottled with 
 white and reddish-brown masses, and may then somewliat resemble some 
 forms of chronic interstitial hepatitis. 
 
 Sarcomata. — Spindle-celled, melanotic, and telangiectatic sarcomata 
 may occur in the liver as secondary tumors. Secondary myxomata and 
 clionclromata have also been described, but they are very rare. 
 
 Oavernous lymphangiomata have been described in a few cases. 
 Cysts, usually of small size, may occur by dilatation of the bile-ducts. 
 They may be multiple and contain serum, mucus, and degenerated 
 epithelium. Single cysts, apparently unconnected with the gall-ducts, 
 are occasionally found in the connective tissue of the liver. They may 
 be lined with ciliated epithelium. 
 
 The liver is sometimes the seat of larger and smaller multiple cysts, 
 varying from microscopical size up to that of a pea, and sometimes larger. 
 They do not appear to communicate with the gall-ducts. They are 
 sometimes associated with multiple cysts of the kidney. Their origin 
 and nature is not understood.' 
 
 PARASITES. 
 
 Ecliinococcus. — This parasite is the most common and important of 
 those which occur in the human liver. It forms the so-called hydatids 
 of the liver. These represent one of the developmental stages of the 
 small tape-worm of the dog tmnia ecJiinococcus (see p. 68). The cysts 
 in the liver may be very small and multiple, but they may be as large as a 
 man's head or larger. The liver may be greatly increased in size, and 
 the tissue about the cysts atrophied. The liver itself furnishes a connec- 
 tive-tissue capsule, within which is the translucent lamellated membrane 
 furnished by the parasite. On the inside of this we may find a layer of 
 cells, granular matter, and a vascular and muscular system belonging to 
 the parasite. Projecting from this inner capsule are the brood-capsules 
 
 ' Consul Pye-Smith : " Cystic disease of liver and both kidneys." Trans. 
 London Patli. Soc, Vol. xixii., p. 113, 1881. 
 23 
 
35:1: _ THE LIVER. 
 
 and heads or scolices of the immature tape-worm. The scolices may 
 become detached from the wall and lie free in the cavity which is filled 
 with a transparent or turbid fluid. Not infrequently the cysts are 
 sterile, and are then simply filled with clear or turbid fluid ; or the 
 embryos may have died and disintegrated, and their detritus, including 
 the booklets, may be intermingled with the fluid contents of the cysts. 
 The contents of the cysts may be mixed with fat, cholestearin crystals, 
 pus, bile, or blood; or form a grumous mass in which we may or may not 
 be able to find the booklets of the scolices, or fragments of the lamellated 
 wall. The connective tissue of the walls of the cysts may be greatly 
 thickened, or they may be calcified. 
 
 In other countries the lesion is much more common and frequently 
 more formidable than in the United States. The cysts reach an enorm- 
 ous size, the veins of the liver may be compressed and filled with thrombi, 
 the bile-ducts compressed and ulcerated. So much of the liver-tissue 
 may be replaced by the hydatids, that the patient may die from 
 this cause alone. Very frequently there is local peritonitis, and adhe- 
 sions are formed between the liver and the surrounding parts. In 
 some cases the cysts rupture, and their contents are emptied into 
 the peritoneal cavity, the stomach, the intestines, the pleural cavity, 
 or the lung-tissue. Sometimes the cysts perforate the bile-ducts, the 
 vena cava, or some of the branches of the portal or hepatic veins. 
 Sometimes the abdominal wall is perforated and a fistula formed 
 between the cavity in the liver and the surface. 
 
 lu cases in which we do not find the scolices entire, a careful examina- 
 tion of the inner cyst-wall, or of its contents, will frequently establish 
 the diagnosis by revealing single booklets (see Fig. 6, p. 70) or fragments 
 of the characteristically lamellated wall (see Fig. 4, p. 69). 
 
 Ecldnococcus inuUilocularis, which is apparently an abortive form 
 of the above species (see p. 70), is very rare indeed in the United States. 
 The writer (T.M.P.), has examined a specimen sent to him by Dr. 
 Edward J. Ill, of ISTewark, IST. J., and which is now in the museum of 
 the College of Physicians and Surgeons, New York. The patient was 
 a male, age thirty-one, German, single, farmer. He had been in the 
 United States five years. For a year previous to his death he had been 
 out of health and jaundiced, and somewhat emaciated. A large indis- 
 tinctly fluctuating tumor was evident in the right lumbar and umbilical 
 regions, and apparently connected with the liver. Aspiration of the 
 tumor gave a milky fluid believed to be pus. An opening Avas made in. 
 to the tumor by one of the surgeons attending the case, and death oc- 
 curred after ten hours, from hemorrhage. 
 
 The liver was found adherent to the abdominal walls and about one- 
 fourth of the right lobe of the liver was occupied by an irregular cavity, 
 with very rough ragged walls. These walls were in some places from one 
 
THE I.IVEE. 
 
 355 
 
 to two inches in thickness, and appeared to the naked eye to consist of 
 dense connective tissue in irregular bands and fascicles which inclosed 
 very irregular, mostly small cavites. Microscopical examination showed 
 that the cavities were lined with the delicate lamellated outicula charac- 
 teristic of the echinococcus cysts. No hooklets were found. Fig. 133 is 
 a drawing from this specimen. 
 
 Fig. 123. — EcaiNOCOCCUs multilocularis op Liver, x 50 and reduced. 
 
 Distovia liepaticioni; D. sitiensej D. lanceolatum, may occur in the 
 gall-ducts and gall-bladder. D. sinense occurs especially in the East, 
 
 and has been found in great numbers in the bodies of Chinamen. 
 
 V. 
 
 hmmatobium is very common in Egypt and Abyssinia, occurring in the 
 blood-vessels of the liver. 
 
 Pentastoma denticulahim is the undeveloped form of Pentastoma 
 tsenioides, a parasite which inhabits the nasal cavity of dogs and some 
 other animals. In the liver of man, it usually occurs in the form of 
 small rounded calcified cysts. The cysts may contain fat, calcareous 
 matter, and the remains of the dead parasite among which the hooklets 
 may be found. 
 
 Ascaris lumbricoides sometimes finds its way from the intestines into 
 the bile-ducts. It may cause no disturbance here, but in some cases the 
 worms have been present in large numbers, and caused occlusion, dilata- 
 tion, and ulceration of the biliary passages, and have led to the formation 
 of abscess of the liver. 
 
 PsorospermicB, the very common parasite in the rabbit's liver, has 
 been found a few times in the liver of man. 
 
356 THE LIVEE. 
 
 THE BILIARY PASSAGES. 
 
 Catarrhal inflammation most frequently attacks the lower portion of 
 tlie common duct and the gall-bladder. In the acute form, it usually 
 leaves but few changes appreciable after death. An abnormal coating of 
 mucus and sometimes congestion of the blood-vessels, are almost the 
 only post-mortem lesions. Owing to the swelling of the mucous mem- 
 brane and the accumulation of mucus in the lumen, the ducts may be 
 temporarily occluded; but this occlusion may not be evident after death, 
 If, however, the inflammation becomes chronic, the walls of the bile- 
 ducts may become thickened, and their lumina more or less permanently 
 obstructed. In consequence of this, dilatation or ulceration of the bile- 
 ducts may ensue. Temporary obstruction of the bile-ducts may produce 
 marked pigmentation of the liver, owing to the accumulation of pigment 
 granules in the liver-cells, particularly in the vicinity of the capsule of 
 G-lisson, and jaundice of the entire body. 
 
 The gall-bladder may be inflamed by itself, or in connection with in- 
 flammation of the biliary passages. If the disease is chronic, the wall of 
 the bladder may be thickened, polypoid growths may occur in the 
 mucosa; the duct may be occluded; dilatation, ulceration, the formation 
 of gall-stones, calcification and atrophy may ensue. 
 
 Inflammation of the stomach and duodenum, hyperaemia and inflam- 
 mation of the liver, concretions, and parasites, are the usual causes of 
 catarrhal inflammation of the biliary passages, but it may occur without 
 these. 
 
 Suppurative and Oroi/pons Inflammation may attack the biliary pas- 
 sages and produce infiltration of pus in their walls, and purulent fluid in 
 their cavities; or flakes and tubular casts of flbrin on their walls; or in- 
 filtration of their walls with fibrin, and consequent ulceration. These 
 lesions occur most frequently in connection with obstruction of the bile- 
 duct'd, and in typhoid and typhus fever, pysemia, cholera, or they may 
 be due to the extension of inflammatory processes from without. They 
 also occur under unknown conditions. Purulent inflammation may pro- 
 duce perforations of the ducts or bladder, with escape of bile and peri- 
 tonitis; or fistulous openings between the gall-bladder and the duodenum, 
 colon, and stomach, or through the abdominal wall. Or the inflamma- 
 tion may extend to the liver-tissue and produce abscesses. Under the 
 latter conditions, we may find a series of small abscesses arranged along 
 the walls of the suppurating gall-ducts. In more advanced stages, the 
 abscesses may become large and communicate with one another, so that 
 a considerable portion of the liver may be occupied by a series of com- 
 municating cavities with ragged walls, containing pus and detritus of 
 liver-tissue, more or less tinged with bile. These abscesses are apt to con- 
 tain various forms of bacteria. They may become more or less com- 
 
THE LIVEE. 357 
 
 pletely inclosed by connective-tissue walls. Or, the portal vein may be 
 inflamed and even perforations may be formed between it and the bile- 
 ducts. Constrictions of the biliary passages may also be produced by the 
 same causes. 
 
 Oonsiriction and occlusion may be produced by inflammation of the 
 ducts themselves, by new growths in their walls, by calculi or parasites in 
 their lumina, by changes in the hepatic tissue in chronic and acute 
 hepatitis, by aneurisms, or by pressure on the duct from without, as by 
 tumors in the head of the pancreas, etc. 
 
 The obliteration of the smaller bile-ducts produces no marked lesions. 
 When the ductus communis, or the hepatic duct, is obstructed, the 
 ducts throughout the liver are frequently dilated and the liver-tissue 
 bile-stained. The liver may undergo atrophy and the whole body be 
 intensely jaundiced. When the cystic duct is obstructed, the gall- 
 bladder is dilated. 
 
 Dilatation of the bile-ducts is usually produced by strictures in the 
 ways just mentioned, or by calculi. When calculi have produced the 
 dilatation, this condition may sometimes continue after they have found 
 their way into the intestines. Sometimes, however, we meet with very 
 marked dilatation of the bile-ducts without being able to make out any 
 present or past obstruction. The dilatation may affect only the common 
 and hepatic ducts, or it may extend to the smaller ducts in the liver, 
 which are then dilated uniformly, or sacculated. They may contain 
 bile, mucus, or calculi. The liver is at first enlarged, but may after- 
 ward atrophy. The gall-bladder may be dilated in consequence of 
 obstruction of the common or the cystic ducts. In the latter case, it 
 may reach an immense size, and form a large tumor in the abdominal 
 cavity. The dilatation is generally uniform, the bladder retaining its 
 normal shape; sometimes, however, there are diverticula, which are usu- 
 ally produced by calculi. If the obstruction to the hepatic duct is incom- 
 plete or movable, the gall-bladder may contain bile, and often calculi. 
 If the obstruction is complete, the contained fluid may gradually lose its 
 biliary character, and become a serous or mucous fluid of a light yellow 
 <io\o\-— hydrops cystidis felloi. The walls of the bladder may be of nor- 
 mal thickness, or thinned, or thickened, or calcified. If the obstruction 
 is due to a calculus, this may pass into the intestine and the gall-bladder 
 be suddenly emptied. Usually "the bladder fills again, owing to its loss 
 •of contractile power. 
 
 'Biliary Calculi.— These bodies are of common occurrence. They 
 are found usually in the gall-bladder, sometimes in the hepatic, cystic, 
 and common ducts; less frequently in the small ducts of the liver. In 
 the gall-bladder from 1 to 7,800 calculi have been counted. They vary 
 in size from that of a pin's head to tliat of a hen's egg, or they may be 
 
358 THE LITER. 
 
 larger. Single gall-stones are usually spheroidal or ovoidal; when mul- 
 tiple, they are usually flattened at the sides or facetted. 
 They may be composed: 
 
 1. Principally of cAoZesiJearm, and may be of a pure white color, or 
 tinged with various shades of yellow, or brown, by bile-pigment. The 
 fractured surface shows a radiating crystalline structure. 
 
 2. Of cholestearin, lile-plgment, and salts of calcium and magnesium. 
 These are usually dark-colored, brown, reddish-black, or green, and may 
 be spheroidal or facetted, smooth or rough on the surface; the fractured 
 surface is usually radiating crystalline. This is the most common form. 
 
 3. Principally of bile-pigment. — Such calculi are rare, usually small, 
 very dark-colored, and not numerous. 
 
 4. Of calcium carbonate. — These are rare, have a nodular surface, 
 and a clear crystalline not radiating fracture. 
 
 Most calculi are formed around a central mass, sometimes called the 
 nucleus, which may consist of cholestearin, bile-pigment, mucus, or 
 
 
 / 
 
 
 :?r^'-'; 
 
 
 
 ' 
 
 
 
 
 
 
 
 ^';'0 
 
 
 
 
 
 ■■'M 
 
 
 
 it 
 
 
 
 
 
 
 
 
 riG.124. — Primary Carcinoma of the common bile-duct, X 300 and reduced. 
 
 epithelium, or more rarely of some foreign body. Thus a dead parasite, 
 a needle, and fruit seeds may serve as nuclei. The body of the cal- 
 culus may be homogeneous, or lamellated, or crystalline. 
 
 Biliary calculi in the gall-bladder may produce no symptoms and only 
 
THE LIVEE. 359 
 
 be discovered after death. In the hepatic and common ducts they may 
 obstruct the flow of bile and produce fatal jaundice; or they may pass 
 from time to time into the intestine producing biliary colic. If they are 
 impacted in the cystic duct, they may produce dilatation of the gall-blad- 
 der. They may get into the duodenum by ulceration through the walls 
 of the ducts or gall-bladder, or in the same way into the peritoneal cav- 
 ity. Gall-stones which get into the intestinal cavity usually pass off 
 without doing any further injury, but very large calculi may cause occlu- 
 sion of the gut, with fatal rejsults. 
 
 TUMORS OF THE GALL-BLADDER AND LARGER GALL-DUCTS. ' 
 
 Small fibromata have been described in the gall-bladder and in the 
 common duct, but they are very rare. The most common tumors are 
 carcinomata. These may be primary or secondary, and present the usual 
 structural variations. The cells may be cylindrical, polyhedral, or they 
 may present the characteristics of colloid cancer. Primary carcinomata 
 of the gall-bladder and larger ducts (Fig. 134) are not very common. 
 Not infrequently the pancreatic and common ducts are both involved 
 and it is difficult to say whether the tumor is primary in the head of the 
 pancreas or in the gall-duct. The bladder and ducts may also be secon- 
 darily involved in carcinomata of the stomach, liver, and duodenum. 
 
THE SPLEEK 
 
 In studying the alterations produced in the spleen in disease, it is 
 important to bear in mind the peculiar relations in which this organ 
 stands to the blood-vessels and to the circalation. After passing through 
 the various branches of the splenic artery and the limited systems of 
 capillaries wliich are associated with it, the blood is not received at once 
 into venous trunks, as in other parts of the body, but is poured directly 
 into the pulp tissue. In this it circulates, under conditions which ren- 
 der it liable to stagnation and undue accumulation, before it is taken 
 again into well-defined vessels, through the open walls of the cavernous 
 veins. Moreover, these conditions, naturally unfavorable to undisturbed 
 and vigorous circulation, are reinforced by the association of the splenic 
 with the sluggish and often interrupted portal circulation. Bearing 
 these considerations in mind, it will be in a measure plain why, as is in 
 fact the case, the spleen should be more liable to alterations in size tlian 
 any other organ in the body, and why, serving as it does as a sort of blood 
 filter, it should be especially susceptible to the influence of deleterious ma- 
 terials of various kinds which in one way or another gain access to the 
 blood. In this respect the relations of the spleen to the blood, and of 
 the lymph-glands to the lymph, present suggestive analogies. 
 
 "VVOUITDS, RUPTUBE, AKD HEMORRHAGE. 
 
 Wouv.ds of the spleen are usually accompanied by extensive hemor- 
 rhage, and are commonly fatal. Death usually occurs as the result of 
 this hemorrhage^ but it may be due to secondary inflammatory changes. 
 Healing and recovery may, however, occur. 
 
 Rupture of the spleen may be traumatic or spontaneous. In the for- 
 mer case it may be due to direct violence in the region of the organ or to 
 injury to the thorax, falls, etc. In certain diseased conditions, the spleen 
 is more liable to rupture than when it is normal. The rupture usually 
 involves not only the capsule, but a more or less considerable portion of 
 the parenchyma, and of course leads to hemorrhage. Spontaneous rup- 
 ture is rare, but may occur as the result of excessive enlargement of the 
 
THE SPLEEN.' 361 
 
 organ, as in tyj^lioid fever, malaria, etc. — see below — or as the result of 
 abscess. 
 
 He^nori'Iiage. —Aside from the extensive hemorrhages from injury 
 and rupture, the spleen may be the seat of small circumscribed hemor- 
 rhages in various infectious diseases, although, owing to the peculiar dis- 
 tribution of the blood, it is often very difficult to distinguish between a 
 moderate interstitial hemorrhage and hyperemia. 
 
 DISTURBANCES 01? THE CIECULATION. 
 
 Ancemia. — This may be associated with general anemia, but it is not 
 always present iu this condition. When marked and unassociated with 
 other lesions, the spleen is apt to be diminished in size, the capsule more 
 or less wrinkled, the cut surface dry and lighter in color than normal, 
 the trabecule unduly prominent. 
 
 In this as in other alterations simply of the blood content of the 
 spleen, neither the gross nor microscopical appearances are constant, be- 
 cause of the redistribution of blood which is apt to occur in the viscera 
 after death. 
 
 Hyperwmia. — This may be passive, occurring when some obstruction 
 to the portal circulation exists, most frequently in cirrhosis of the 
 liver, but also with certain valvular lesions of the heart, emphysema, etc. 
 The spleen is enlarged, but usually only to a moderate degree. The 
 capsule is apt to be tense, and on section, the pulp is dark-red and may . 
 be soft or firm. Usually, when the lesion has existed for some time, 
 there is a thickening of the trabeculse and reticular framework of the 
 spleen, so that they are prominent on section. In other words, there is 
 a chronic interstitial splenitis following the chronic congestion. 
 
 Active congestion of the spleen, which in most cases is scarcely to be 
 differentiated from some forms of acute inflammation, and probably in 
 many cases is associated with it, very frequently occurs in a great variety 
 of acute and infectious diseases, such as typhoid fever, pneumonia, 
 diphtheria, pyaemia, the exanthemata, etc. The spleen is enlarged, the 
 capsule tense; on section, the pulp is soft, dark-red in color, often swell- 
 ing out from the cut surfacej and concealing the glomeruli and trabec- 
 ule. Under these conditions, we may find the cavernous veins distended 
 with blood, and the interstices of the pulp infiltrated with a variable, 
 sometimes large quantity of red and white blood-cells. Or we may find, 
 in addition to this, an increase in cells, which characterizes acute inflam- 
 mation or hyperplasia of the spleen (see p. 362). 
 
 Infarctions of the Spleen. — Embolic infarctions of the spleen are of 
 frequent occurrence. They may be single or multiple, small or .very 
 large, sometimes occupying half of the organ. They are in general 
 approximately wedge-shaped, corresponding to the area of tissue supplied 
 by the occluded artery. They may be hemorrhagic, i.e. red, or they may 
 
362 THE SPLEEN. 
 
 be white (see p. 53). Infarctions, originally red, may become white after 
 a time from changes in the blood-pigment. They may usually be seen 
 as dark-red, reddish-white, or white, hard, sometimes slightly pro- 
 jecting areas on the surface of the organ. Not infrequently, the 
 centre of the infarction is light in color, while the periplieral zone is 
 dark-red. A layer of fresh fibrin is sometimes seen over the surface of 
 tlie infarction. The general, as well as the microscopical appearances 
 which they present, depend largely upon the age of the infarction. In 
 the earlier stages the hemorrhagic infarctions present little more under 
 the microscope than a compact mass of red blood-cells, among which 
 may be seen the compressed necrotic parenchyma. The white infarction 
 may show at first in a general way the usual splenic structure, but the 
 entire tissue is in a condition of coagulation necrosis. The tissue may 
 disintegrate and soften, and be more or less completely absorbed, with or 
 without fatty degeneration. A zone of inflammatory tissue may appear 
 around the infarction and ujjon the capsule, and this tissue, becoming 
 denser, assumes the characters of cicatricial tissue, and contracts around 
 the unabsorbed remnant of the infarction, so that finally nothing may be 
 left but a dense mass of fibrous tissue which frequently draws in the 
 surface, causing more or less distortion of the organ. This cicatrix may 
 be pigmented or white. 
 
 If the embolus be of an infectious irritating nature, in addition to its 
 mechanical effects, there may be suppuration, gangrene, and the forma- 
 tion of abscess. There may be perforation of the capsule and fatal peri- 
 tonitis. 
 
 INELAMMATIOK. 
 
 Acute Hyi^erplastic Splenitis (Acute splenic tumor). — The condi- 
 tions under which acute inflammation of the spleen occurs have already 
 been mentioned under active hypersemia, with which it is usually asso- 
 ciated. It is a frequent, though not a constant accompaniment of the 
 acute infectious diseases, and seems in all cases to be a secondary lesion. 
 The spleen is enlarged, sometimes to two or three times its normal size. 
 On section the pulp is soft, often almost diffluent, and projects upon the 
 cut surface. The color is sometimes dark-red, sometimes grayish-red, or 
 mottled red and gray. The trabeculee and glomeruli are usually con- 
 cealed by the swollen and softened pulp, but the glomeruli are some- 
 times unusually prominent. 
 
 ilicroscopical examination shows the marked increase in size to be 
 due in part to the hyperemia; in part to a swelling and increase in the 
 number of cells, sometimes of the pulp, sometimes of the glomeruli, or 
 of both. We find large multinucleated cells ; cells resembling the ovoidal 
 and polyhedral cells of the pulp, but larger and with evident division of 
 the nuclei. Cells resembling leucocytes may be present in large num- 
 
THE SPLEEN. 363 
 
 bers. and larger and smaller cells in a condition of fatty degeneration or 
 containing pigment, are often seen. The elongated cells lining the cav- 
 ernous veins may be swollen or increased in number. ISIot infrequently 
 larger and smaller cells are found ■which contain structures looking some- 
 what like red blood-cells. In some cases, particularly in scarlatina, 
 hyperplasia of the glomeruli is a prominent feature. In some cases, par- 
 ticularly in typhus and recurrent fevers, the cells of the glomeruli 
 undergo marked degenerative changes, so that they may form small, soft- 
 ened areas looking like little abscesses. Small necrotic areas, often asso- 
 ciated with localized suppuration, are sometimes found in typhus and 
 typhoid fever, scarlatina, etc., and may be due to infectious emboli. As 
 the primary disease runs its course, the swelling of the spleen subsides, 
 the capsule appears wrinkled, the color becomes lighter, and sometimes 
 the organ remains for a long time, or permanently, small and soft. 
 
 The cause of these marked changes in the spleen in infectious diseases 
 is not understood . It seems probable that they are due to the lodg- 
 ment in the organ of some deleterious materials -which have found access 
 to the blood. Whether these materials are bacteria, or joroducts of the 
 life processes of bacteria, or something entirely apart from these, we do 
 not know. Bacteria have, indeed, in many cases been found in the 
 organ under these conditions, but by no means with the frequency and 
 abundance wjiich the commonness and prominence of the lesion would 
 lead us to expect, if it were in all cases due to their presence. 
 
 Suppurative Splenitis (Splenic Abscess). — Small abscesses may 
 be found in the spleen as the result of minute infectious emboli, and 
 these may coalesce to form larger abscesses ; bat larger and smaller 
 abscesses may form in the spleen without evidence of their embolic 
 origin. Sometimes the entire parenchyma is converted into a soft necro- 
 tic purulent mass surrounded by the capsule. It is rare for simple infarc- 
 tions to result in abscess, but it does occasionally occur. Abscess 
 of the spleen may occur from the propagation of a suppurative inflam- 
 mation to the organ from adjacent parts ; from perinephritic abscesses, 
 ulcer and carcinoma of the stomach, etc. Abscesses of the splean may 
 open into the peritoneal cavity, inducing fatal peritonitis, or, owing to 
 an adhesive inflammation, the opening may occur into the post-perito- 
 neal tissue, into the pleural cavity, lung, stomach, intestines, or it may 
 open on the surface. On the other hand, the contents of the abscess 
 may dry, shrink, and become encapsulated and calcified. Abscesses may 
 occur in ulcerative endocarditis, pyaemia, typhoid fever, and more rarely 
 in intermittent fever, and under a variety of other conditions whose 
 nature is unknown to us. 
 
 Chronic Indurative Splenitis (Chronic Splenic Tumor). — ^There 
 may be, as we have already seen, a new-formation of connective tissue in 
 the spleen as a result of chronic congestion, or infarctions, or about 
 
364 THE SPLEEN. 
 
 abscesses. But there is a more diffuse formation of connective tissue, 
 usually in the nature of an hyperplasia, Avhich occurs under a variety of 
 conditions, and is now marked and extensive, and again comparatively 
 ill-defined. It is always associated with more or less extensive changes 
 in the parenchyma. In its most marlted form it is found in chronic 
 malarial poisoning, and under these conditions it may be found not only 
 in persons who have suffered from repeated attacks of intermittent fever, 
 but also in those who have not thus suffered, but have resided in mala- 
 rial regions. The enlarged spleen is often called '■' ague cake." Simi- 
 lar conditions, though usually less marked, may occur in congenital 
 and acquired syphilis, from prolonged typhoid fever, and as a result of 
 acute hyperplastic splenitis from various causes, and also in leuksemia 
 and psendo-leuksemia. 
 
 The gross appearance of the spleen in chronic indurative splenitis 
 varies greatly, both in the size of the organ and in the appearance of the 
 section. The spleen may be enormously enlarged or it may be of about 
 normal size. It is usually, however, enlarged. The capsule is usually more 
 or less thickened, frequently unevenly so. The consistency is usually con- 
 siderably increased, but this is not always the case. The color and appear- 
 ance of the cut surface present mucli variation. It may be nearly normal 
 or it may be grayish or dark-brown or nearly black. The color may be 
 uniform or the surface may be mottled. The glomeruli may be scarcely 
 visible or very prominent; the trabecules are in some cases nearly eon- 
 cealed by the pulp, in others they are large, prominent, and abundant; so 
 that the surface is crossed in all directions by an interlacing network of 
 broader and narrower irregular bands, between which the red or brown or 
 blackish pulp lies. 
 
 ]^ot less varied are the microscopical appearances of the spleen under 
 these conditions. In one class of cases, there is more or less uniform 
 hyperplasia of both pulp and interstitial tissue. The parenchyma cells 
 are increased in size and number; there may be swelling of the lining cells 
 of the cavernous veins. The reticulum of the pulp, as well as that of the 
 glomeruli, and also the trabeculas, are thickened. In another class of 
 cases, the thickening of the reticular and trabecular tissue, either uni- 
 formly or in patches, is the prominent feature, while the changes in the 
 l^ulp are rather secondary and atrophic. In both forms, irregular pigmen- 
 tation is frequent, the pigment particles being deposited either in the cells 
 of the pulp or glomeruli, or in the new-formed interstitial tissue. Fi- 
 nally, there are all intermediate forms of induration between those 
 described, and the changes are by no means uniform in the same organ. 
 When those spleens are large, they are liable to dis2ilacement. 
 
 Siipldlitic Splenitis. — This lesion may present itself as an indurative 
 process due to the formation of new connective tissue, and present no 
 distinct morphological characteristics. In rare cases, however, gummata 
 
THE SPLEEN. 365 
 
 may be present, in connection with the new fibrous tissue; then the 
 nature of the lesion becomes evident. 
 
 Tiihercular Splenitis. — This lesion is secondary, either to tubercular in- 
 flammation in some other part of the body; or is the result of the general 
 infection in acute general miliary tuberculosis. The tubercles may be 
 very numerous and still invisible to the naked eye, or they may be just vis- 
 ible, or as large as a pin's head or thereabouts, and very thickly strewn 
 through the organ, or sparsely scattered. In other cases, the tubercles 
 are larger, sometimes as large as a pea, and they are then usually not very 
 numerous. Microscopically, they present the usual variety of structure: 
 sometimes as simple tubercle granula, sometimes as conglomerate tuber- 
 cles, they may consist simply of a collection of small spheroidal cells; or 
 there may be larger polyhedral cells and giant-cells, with a well-defined 
 reticulum. Cheesy degeneration occurs under the usual conditions. 
 Tubercle bacilli are usually present,, particularly in the more acute forms, 
 sometimes in small, sometimes in enormous numbers. They seem to be 
 especially abundant in acute general miliary tuberculosis of children. 
 These tubercles may be formed in the glomeruli, in the walls of the smaller 
 arteries, in the pulp tissue, and in the trabeculse and capsule. Owing 
 to the peculiar character of the spleen tissue, the eai-lier stages are not 
 readily recognized, since simple collections of small spheroidal cells are 
 not distinctly outlined against the normal tissue. There is frequently 
 a moderate swelling of the spleen, owing to hypersemia and hyperplasia 
 of the parenchyma. 
 
 Perisplenitis. — Acute inflaniviation of the capsule of the spleen may 
 occur as a part of a general or localized peritonitis, or as a result of lesions 
 of the spleen itself, such as infarctions, abscesses, and acute hyperplastic 
 inflammation. Under these conditions, a fibrinous pellicle, with more 
 or less pus, may be formed on the surface of the organ. Chronic pi&i'i- 
 splenitis, resulting in the production of new connective tissue, either in 
 patches, or as a more or less general thickening of the capsule, is of frequent 
 occurrence. It may follow acute inflammation of the capsule, or be a part 
 of general or localized chronic peritonitis. It is common in connection 
 with chronic indurative splenitis, and it may occur from unknown causes. 
 Sometimes the capsule is three or four mm. in thickness over a consider- 
 able area; sometimes vei-y small nodular thickenings or i^apillary projec- 
 tions occur. As a result of this process, adhesions, sometimes very ex- 
 tensive, may form between the spleen and adjacent parts. The thickened 
 capsule is sometimes more or less extensively calcified. 
 
 Alterations of the Spleen in Leukceniia and Pseudo-Leuhmmia. — The 
 lesions of the spleen are essentially the same under both of these condi- 
 tions. They consist, in general, of an hyperplasia, sometimes most 
 marked in one, sometimes in another of the structural elements of 
 the organ, but usually they all participate in the alterations. The 
 
366 THE SPLEEN. 
 
 changes which occur in the earlier stages are but little known. The 
 gross appearances of the spleen as we find them in persons dying of either 
 of the above diseases, present considerable variation. Tlioy are usually 
 enlarged, and sometimes are ten or fifteen times the normal size. They 
 are usually hard, bat are sometimes of the ordinary consistency, or 
 softer. The capsule is usually thickened and rough. The section of the 
 spleen may be of a uniform dark-red color, but it is more frequently 
 mottled red and gray. Sometimes the glomeruli are inconspicuous, but 
 they are very often enlarged and prominent. Tliey may be 2 to 4 mm. 
 in diameter, and owing to an infiltration of the arterial sheaths with 
 lymph-cells, may appear to the naked eye as grayish, round or elongated 
 bodies, arranged along branching interrupted grayish streaks. The tra- 
 becula may be greatly thickened, as also the reticulum of the pulp, so as 
 to be evident to the naked eye. Brown or black pigment may be col- 
 lected around the glomeruli or in the pulp. Hemorrhagic infarctions or 
 circumscribed extravasations of blood may further complicate the picture. 
 Microscopically, the appearances are essentially the same as those 
 above described in acute hyperplasia and in chronic interstitial splenitis, 
 depending upon the stage and variety of the disease. Owing to the great 
 size which some of these spleens attain, they are liable to displacement, 
 and they may interfere by pressure with the function of neighboring- 
 organs. 
 
 DEGENERATIVE CHANGES IN THE SPLEEN. 
 
 Atrophy. — The spleen may become atrophied in old age ; as a result 
 of prolonged cachexife, and in connection with profound and persistent 
 ansemia ; or more rarely from unknown causes. The capsule may be 
 wrinkled and thickened, the color pale, the trabecula prominent, the 
 consistency increased. The change is largely in the pulp, whose paren- 
 chyma-cells are decreased in number. 
 
 Amyloid Degeneration. — This degeneration may affect the glomeruli 
 or the pulp-tissue, or both together. When confined to the glomeruli, 
 the spleen may or may not be enlarged, and the cut surface is more or 
 less abundantly sprinkled with round or elongated translucent bodies 
 resembling considerably in general appearance, the grains of boiled sago. 
 These are the Avaxy glomeruli. Such spleens are often called "sago 
 spleens." Microscopical examination shows that the degeneration is con- 
 fined to the walls of the arteries, capillaries, and reticulum of the glomer- 
 uli with atrophy and disappearance of the lymphoid cells. 
 
 In other cases, either with or without involvement of the glomeruli, 
 there is waxy degeneration of the blood-vessels and reticulum of the 
 pulp, which may occur in patches or be general and more or less exces- 
 sive. If the alteration is general and considerable, the spleen is enlarged, 
 its edges rounded, its consistence increased. On section it appears trans- 
 
THE SPLEEN. 36T 
 
 lucent and the distribution of the degenerated areas may be readily seen 
 by holding a thin slice np to the light. , The spleen maybe alone affected, 
 or there may be similar degenerations in other organs.. The general con- 
 ditions under which tliis lesion occurs and the methods of staining and 
 studying are given on p. 63. 
 
 Pigmentation of the spleen may occur as the result of the decomposi- 
 tion of haemoglobin in the organ under a great variety of conditions, thus 
 after hemorrhagic infarctions, small multiple hemorrhages, acute hyper- 
 plastic splenitis, etc. Or the pigment may be anthracotic and be brought 
 to the organs from the lungs or bronchial glands (see p. 65). Bile pig- 
 ment may also be deposited in the spleen in jaundice. The pigment may 
 lie in the walls of the smaller arteries, in the cells and reticulum of the 
 pulp, or free in the latter tissue, or in the follicles. It is usually quite 
 unevenly distributed. The pigment may be red, brown, or black. Ac- 
 cording to Weigert, anthracotic pigment may be sometimes seen with 
 the naked eye in the periphery of the glomeruli, as dark crescents. 
 
 TUMORS. 
 
 Primary tumors of tlie spleen are rare. Small fibromata, sarcomata, 
 ■and cavernous angiomata sometimes occur. Sarcomata and carcinomata 
 may occur in the spleen secondarily either as metastatic tumors, or 
 by extension from some adjacent part, as the stomach. Dermoid cysts 
 are described, but are rare. Other larger and smaller cysts, whose mode 
 •of origin is in most cases obscure, not infrequently occur. 
 
 PARASITES. 
 
 Pentastomum denticulatum is not infrequently found in the spleen, 
 usually encapsulated and calcified. Oysticercus is rare. Echinococcus 
 is occasionally found, and if the cysts are large or numerous, may cause 
 more or less extensive atrophy of the organ. 
 
 Various forms of bacteria have been found in the spleen. Micrococci 
 have been found in pyaemia, small-pox, ulcerative endocarditis, and 
 under other conditions. The Bacillus anthracis occurs here in anthrax; 
 the B. tuberculosis in tubercular inflammation, and bacilli have been de- 
 scribed in typhoid fever. Spirochcete Obermeieri may be found in relaps- 
 ing fever. 
 
 MALFORMATIOMS AND DISPLACEMENTS. 
 
 The spleen may be absent in acephalous monsters, and with defective 
 development of other abdominal viscera. Very rarely it is absent in per- 
 sons who are otherwise perfectly developed. Small accessory spleens from 
 the size of a hazel-nut to that of a walnut are not infrequent. They 
 usually lie close to the spleen, but may be considerably removed from it ; 
 thus they have been found embedded in the head of the pancreas. Two 
 spleens of about equal size have been observed. The form of the spleen 
 
368 THE SPLEEN. 
 
 is subject to considerable variation. The spleen may be displaced con- 
 genitiilly or as the result of disease. It may be on the right side in trans- 
 position of the viscera. As the result of congenital defects in the dia- 
 phragm, the spleen maybe found in the thorax; or in deficient closure of 
 the abdominal wall, it may, together with other abdominal viscera, be 
 found outside of the body. 
 
 The spleen may be pressed downward by any increase in the contents 
 of the thorax. It may be fastened by adhesions to the concave surface 
 of the diaphragm, so that its long axis is nearly horizontal, instead of 
 vertical. It may be displaced by changes in the contents of the abdomi- 
 nal cavity. If the organ is increased in size, it frequently becomes tilted, 
 so that its lower border reaches the right iliac region. If the ligaments 
 are too long congenitally, or if they are lengthened by traction, and if the 
 organ is at the same time increased in weight, it may become very mov- 
 able. It may sink downward, with its hilus turned upward; or it may be 
 rotated on its axis, and owing to torsion of the vessels thus produced, 
 the organ may atrophy. Or, 'the pressure of the ligament and vessels 
 across the duodenum may cause occlusion of the gut. 
 
THE PANCREAS. 
 
 The diseases of the pancreas are, so far as we know, with a few excep- 
 tions, of no great practical importance; that is, they do not often give rise 
 to symptoms of disease, or cause death, but the lesions are found in the 
 bodies of persons dead from other diseases. It is probable, however, 
 that in many cases their /Apparent insignificance is due to our lack of 
 ■ knowledge of the interference with functions which lesions of the glan^ 
 induce. Hemorrhage into the substance of the organ may occur as the 
 result of injury; in the hemorrhagic diathesis; in connection with val- 
 vular diseases of the heart, or interference with the portal circulation; 
 or in connection with extensive fatty degeneration of the organ. A few 
 cases of sudden death are recorded, in which the only discoverable lesiou 
 was an extensive hemorrhage into the substance of the gland and the tis- 
 sue about it. In these cases it has been assumed that death was caused 
 by interference with the heart's action, through pressure on the solar 
 plexus and semilunar ganglion, but it may be due other causes (see below, 
 fat necrosis). 
 
 INFLAMMATION. 
 
 In some cases of typhoid fever, pysemia, yellow fever, and other acute 
 infections diseases, the pancreas is red, swollen, and oedematous. Micro- 
 scopically the most prominent lesion is a swelling and undue granulation 
 of the glandular epithelium and hypersemia. This condition is known 
 as parenchymatous pancreaiitis. 
 
 Suppurative pancreatitis is not very common, and may be primary or 
 due to the extension of a suppurative inflammation from adjacent parts) 
 There may be a difl'use infiltration of the organ with pus-cells or larger 
 and smaller abscess. The causes of primary suppurative pancreatitis are 
 obscure. 
 
 Chronic interstitial pancreatitis (cirrhosis of the pancreas). — This 
 lesion consists in an increase of interstitial connective tissue which may 
 be general or confined to some particular portion of the gland. The 
 24 
 
370 THE PAJfCEEAS. 
 
 organ is sometimes enlarged, sometimes 'smaller than normal. It is 
 usually dense and hard; secondary atrophy of the parenchyma regularly 
 occurs. It may be due to chronic inflammatory processes in the vicinity 
 of the organ. 
 
 Syphilitic inflammation. — Chronic interstitial pancreatitis is fre- 
 quently found in congenital syphilis of the new-born, and the gross and 
 naicroscopical lesions are similar to those above described. It is not defi- 
 nitely established whether or not a similar lesion may be caused by 
 acquired syphilis. Gummata are very rare in the pancreas, but have 
 been described in congenital syphilis in very young children. 
 
 Tubercular Inflammation. — Larger and smaller tubercles and. tuber- 
 cular cheesy nodules are occasionally found in the pancreas in connection 
 with acute general miliary tuberculosis or with tubercular inflammation 
 in some other organ, particularly with that of adjacent lymph-glands, 
 the lungs and the intestine. 
 
 DEGENERATIVE CHANGES IN" TmE PANCREAS. 
 
 Atrophy of the pancreas may occur in old age, and as a result of 
 pressure from tumors or other adjacent structures. Marked atrophy of 
 the pancreas is found in a certain proportion of cases of diabetes mellitus, 
 but it is not constant. 
 
 Fatty degeneration of the parenchyma cells may occur, and in some 
 cases is so extensive as to lead to nearly com|)lete destruction of their 
 protoplasm. 
 
 Fatty infiltration, which should be distinguished from fatty degene- 
 ration, consists in the accumulation of fat in the interstitial tissue of the 
 gland. This may be so excessive as to cause nearly entire destruction of 
 the gland structures. Under these conditions, the outline of the organ 
 may be preserved, the fat being inclosed by the capsule. 
 
 Amyloid Degeneration. — This usually occurs in connection with sim- 
 ilar degeneration in other organs, and is confined to the walls of the blood- 
 vessels and the interstitial tissue. 
 
 Fat 7iecrosis. — A very peculiar lesion of the fat-tissue, most frequently 
 seen in the fat-tissue about the pancreas or between its lobules, but some- 
 times in fat tissue in other parts of the body, has been a few times de- 
 scribed and caWeA fat necrosis. White or yellowish nodules, varying from 
 the size uf a pin's head to that of a pea or larger, are seen embedded in 
 the fat, the central portion being often soft and grumous and readily 
 squeezed out. They are sometimes calcified and sometimes surrounded 
 by a connective-tissue capsule. Microscopical examination shows degen- 
 eration and disintegration of the fat tissue. They are most frequently 
 found in marasmatic persons. When the lesion is extensive, according to 
 Balser, it may cause death either directly, or by inducing hemorrhage. 
 
THE BANCEEAS. 371 
 
 Some of the extensive hemorrhages about the pancreas, above mentioned, 
 may be caused in this way.' 
 
 TUMORS. 
 
 Garcinoniata are the most common and important of the tumors of 
 the pancreas. They may be primary or secondary. Primary carcino- 
 mata are most frequently found in the head of the organ, but may occur 
 in other parts. The hard or scirrhous form is most common, but occa- 
 sionally soft and succulent, and colloid forms are found. They are liable 
 to involve adjacent parts by continuous growth, and may form metasta- 
 ses in the liver, adjacent lymph-glands, etc. Secondary carcinoma in 
 the pancreas may occur in carcinoma of the stomach, duodenum, and 
 the gall-ducts and gall-bladder. As a result of carcinoma of the pancreas, 
 aside from the extension of the growth, there may be pressure on the 
 ductus choledochus with jaundice; or on the pancreatic duct with cys- 
 tic dilatation; or pressure on the duodenum with stenosis of the gut; or 
 pressure on the vena cava or portal vein, or superior mesenteric vein, etc., 
 with disturbances of the circulation. 
 
 Concretions of carbonate and phosphate of lime are frequently found 
 in the pancreatic ducts. They are usually multiple, small, whitish, 
 smoothjOr of rough and irregular shape. Sometimes, however, they reach a 
 diameter of more than an inch. They consist chiefly of calcium phos- 
 phate and carbonate. Besides these free concretions, the walls of the 
 ducts are sometimes incrusted with salts of lime. Such concretions may 
 produce dilatation of the pancreatic ducts and large cysts, or more rarely 
 
 Foreign Bodies. — G-all-stones sometimes find their way into the pan- 
 creatic duct. Ascarides have been found in the ducts in a considerable 
 number of cases. 
 
 Dilatation of the pancreatic ducts, and the formation of cysts, take 
 place in several different ways. 
 
 (1) The entire duct may undergo a uniform, cylindrical dilatation. 
 With this cylindrical dilatation we sometimes find associated small sac- 
 culi. 
 
 (2) There may be sacculated dilatations at some point in the ducts. 
 These dilatations form cysts of large size, as large even as a child's head. 
 Their walls frequently undergo degeneration and calcification. These 
 cysts often become filled with blood, and may then be mistaken for aneu- 
 risms. 
 
 (3) The small branches of the pancreatic duct may be dilated so as 
 to form a number of small cysts. These cysts are filled with serum, mu- 
 cus, pus, or a thick cheesy material. 
 
 ' Consult Balser: "Ueber Fettnekrose," Virch. Archiv, Bd. 90, 1883, p. 530, 
 and Chiari, Prager Wochenschrift, 1883, Nos. 30 and 31. 
 
372 THE PASrOEEAS. 
 
 MALFORMATIONS AND DISPLACEMENTS. 
 
 The pancreas may be entirely absent in anencephalous and double 
 monsters, and in congenital umbilical hernise. The pancreatic duct may 
 be double; it may open into the duodenum at some distance from the 
 biliary duct, or into the stomach. The head of the pancreas may beun- 
 duly developed, and 'sometimes even completely separated from the rest 
 of the organ, opening into the duodenum with a duct of its own. Occa- 
 sionally there is small accessory pancreas situated beneath the serosa of 
 the duodenum or stomach. 
 
 The pancreas is so iirmly bound down that its position is not often 
 changed. Sometimes, however, it is found pressed downward by tight 
 lacing, displaced by aneurisms, or contained in umbilical and diaphrag- 
 matic herniffi. ' 
 
THE SALIVARY GLANDS. 
 
 THE PAROTID, SUBMAXILLAEY, AND SUBLINGUAL. 
 
 Inflammation. — This condition is most; frequent and important in the 
 parotid. The epidemic disease known as mumps is most frequently con- 
 fined to the parotid gland of one side, but tlie submaxillary and sublin- 
 gual may be at the same time involved. The gland is swollen and there 
 is often oedema of the mucous membrane of the mouth and pharynx. 
 Very little is known of the actual minute changes which the gland 
 undergoes in this disease. 
 
 Acute parotiditis occasionally occurs as a secondary lesion in a variety 
 of diseases, as in typhoid and scarlet fever, pyaemia, pneumonia, etc., and 
 by propagation of inflammation from the mouth. Under these condi- 
 tions the inflammation is usually suppurative, and frequently results in 
 abscess or sloughing. The interstitial tissue of the gland is more or 
 less densely infiltrated -with pus-cells, and the parenchyma cells may 
 undergo fatty degeneration and disintegration. The inflammation may 
 be confined to the gland or it may spread to adjacent parts, sometimes 
 causing much destruction of tissue, and may give rise to inflammation 
 of the brain, or of the inner ear, or even to metastatic pysemic abscesses in 
 different parts of the body. Healing may occur with the formation of 
 salivary fistulffi. 
 
 The submaxillary gland may be involved with the parotid in the sup- 
 purative inflammation. 
 
 Acute suppurative inflammation of the connective tissue about the 
 submaxillary gland is sometimes of serious import. Sloughing and gan- 
 grene may occur, and are apt to spread to adjacent parts. Septicsemia, 
 ■oedema of the glottis, or pneumonia may complicate the process and 
 cause death. 
 
 The sublingual gland is not often the seat of inflammation. 
 
 Chronic inflammation, leading to the formation of dense interstitial 
 tissue, sometimes occurs in the salivary glands. This may occur by it- 
 self or follow an acute inflammation. 
 
 The Excretory Ducts of the salivary glands may become inflamed from 
 
374 THE SALIVABT GLANDS. 
 
 the presence of foreign bodies or of concretions formed in them. They 
 may become occluded, from the presence of calculi or as the result of 
 inflammation, and may thus become widely dilated both in the main 
 branches and in the finer ramifications. The dilatation of Wharton's 
 duct to form larger and smaller cysts containing salivary fluid, sometimes 
 gives rise to very large and troublesome tumors which constitute one of 
 the forms of ranula. 
 
 TUMORS. 
 
 Fibromata are of occasional occurrence in the parotid. Chondromata, 
 sarcomata and Jiiro-sarcomata, and myxomata, or more frequently mixed 
 tumors, formed of varied combinations of these, are of frequent occur- 
 rence in the parotid, and of occasional occurrence in the submaxillary 
 gland. These complex or mixed tumors are of more frequent occurrence 
 in these glands than in any other part of the body, except possibly the 
 ovary. They are sometimes rendered still more complicated in structure 
 by a partially atypical glandular growth lending them an adenomatous 
 character, and by the formation of cysts. Or they may present in parts 
 a distinctly carcinomatous character. 
 
 Fibrosarcoma and melano-sarcoma have been described. Primary 
 Carcinoma of these glands is very rare. 
 
 One case of rliabdomyoma of the parotid gland with evidences of 
 atypical development of portions of the gland, has been described by the 
 writer.' 
 
 PARASITES. 
 
 Ecliinococcus has been observed in the parotid gland. 
 
 ' Prudden: " Ehabdomyoma of the Parotid Gland." American Journal of the 
 Medical Sciences, April, 1883. 
 
THE THYEOID GLAND. 
 
 Hypermmia of the thyroid gland, often accompanied by considerable 
 enlargement of the organ, may be the result of valvular disease of the 
 heart ; it occurs in Basedow's disease ; it may be temporary or permanent ; 
 and in the latter case may give rise to the formation of new connective 
 tissue. Hemorrhages may occur, causing pigmentation of the organ. 
 
 Inflammation of the thyroid gland is not very common, and may 
 occur from a variety of causes. It may result in the formation of larger 
 and smaller abscesses, or in the production of new connective tissue. 
 Tubercular inflammation with the formation of miliary tubercles is of 
 infrequent occurrence. Sypliilitic inflammation with the formation of 
 gummata has been described, but is rare. 
 
 Degeneration. — Colloid degeneration of the epithelial cells of the 
 gland and the filling of the alveoli with colloid material is of common 
 occurrence, and when occurring. in moderate degree may be regarded as 
 a normal event, since a certain amount of this change is found in many, 
 otherwise apparently normal glands. It may occur, however, to such an 
 extent as to constitute a lesion. See below. 
 
 Amyloid degeneration, particularly of the blood-vessels, is of infre- 
 quent occurrence. 
 
 TUMORS. 
 
 Among the most important of the lesions of the thyroid is the enlarge- 
 ment of the organ commonly known as the goitre or struma. The 
 enlargement of the gland may occur in several different ways, and in only 
 a part of the cases is to be considered as a tumor. Thus, a simple hypere- 
 mia may, as above stated, cause considerable enlargement of the organ, 
 and this is sometimes called Struma hyperwmica. The true goitre, how- 
 ever, consists in the enlargement of the old and the formation of new 
 gland alveoli, while with these changes there is very frequently asso- 
 ciated a greater or less amount of colloid degeneration. When there is 
 new formation of gland-tissue, the growth has the character of an ade- 
 }ioma. The hyperplasia may occur diffusely, so that the whole gland is 
 more or less enlarged; or it may occur in the form of circumscribed 
 
376 THE THTEUID GLAUD. 
 
 nodules. When the colloid degeneration is prominent so that the tumor 
 has a gelatinous look, it is called colloid struma. Accumulations of fluid, 
 blood, colloid, etc., in the old or new formed alveoli may cause dilatation 
 and atrophy of the walls of the alveoli so that cysts, sometimes of large 
 size, are formed. Thus occurs the cystic struma. Again, the blood- 
 vessels may undergo marked dilatation so that we may have a telangiec- 
 tatic struma ; or cavernous angiomata may form within them. Very 
 frequently all of these varieties of lesion are present in the same goitre. 
 The appearances may be rendered still more complex by the occurrence 
 of hemorrhages and pigmentation, calcification, purulent or indurative 
 inflammation, and by the not very infrequent association with carcinoma 
 and sarcoma. The cause of goitre is not well understood. The growth 
 is, as rule, slow, but occasionally a very rapid enlargement occurs as the 
 result of a sudden increase of the colloid degeneration. In many cases 
 even very large goitres give rise to but moderate inconvenience, but they 
 may assume great significance by encroaching upon neighboring parts. 
 Thus death may be caused by pressure on the trachea, CESophagus, or on 
 the large vessels. 
 
 Sarcoma, either spheroidal or spindle-celled, may occur as primary 
 tumors in the thyroid, either in otherwise normal glands or in connection 
 with struma. J/«Z«?^o-sffrco??^« has been observed. Secondary sarcomata 
 are rare. 
 
 Primary Carcinoma, both glandular and scirrhous, occur in the thy- 
 roid, and particularly the softer forms may spread to adjacent parts, 
 and occasionally form distant metastases. 
 
 PARASITES. 
 
 Echinococcus cysts have been found in the thyroid. 
 
THE SUPEA-EEI^AL CAPSULES. 
 
 MALFORMATIONS. 
 
 In aceplialic and other monsters the supra-renal capsules may be atro- 
 phied or entirely absent. Sometimes in well-formed adults these organs 
 cannot be discovered. 
 
 There may be little rounded nodules loosely attached to the surface of 
 the capsules and having the same structure. 
 
 If one of the kidneys is absent, or in an abnormal ]Dosition, its capsule 
 usually retains its proper position. 
 
 HBMOEKHAGB. 
 
 In children, soon after birth, it is not very infrequent to find large 
 hemorrhages in one of the capsules, converting it into a cyst filled with 
 blood. Tlie same lesion has been observed in a few cases in adults. 
 
 THROMBOSIS. 
 
 Klebs describes a case of capillary thrombosis of the cortex in botli 
 capsules in a woman after excision of the knee-joint. 
 
 INFLAMMATION". 
 
 The most frequent lesion of the supra-renal capsules is tulercular iji- 
 ■flammation. They are usually increased in size, their surfaces are smooth 
 or nodular. The normal structure of the gland is lost, and is replaced 
 by tubercle tissue, connective tissue, and cheesy matter. 
 
 Suppurative inflammation with the formation of abscesses has been 
 seen in a few cases. 
 
 DEGENERATION. 
 
 Fatty Degeneration of the cortical portion of the capsules is the rule 
 in the adult. In children under five years of age, it is a pathological 
 condition. 
 
 Amyloid Degeneration may involve both the cortical and medullary 
 portions. In the cortex, it usually involves only the walls of the blood- 
 
378 THE SUPEA-EENAL CAPSTJLES. 
 
 vessels; in the medulla, both the blood-vessels and the cells of the paren- 
 chyma may iindergo this degeneration. The capsules are usually firm 
 and of a grayish, semi- translucent color. 
 
 TUMOHS. 
 
 Carcinoma of the supra-renal capsules is not common. It may be 
 primary, but is much more frequently secondary. Either one or both of 
 the capsules may be the seat of the new growth. 
 
 Sarcoma occurs as a primary and secondary growth. Probably many 
 of the older cases described as cancers were really sarcomata. 
 
 Gylindroma. — Klebs describes a growth of this character in one of the 
 capsules, secondary to a tumor of the same kind in the supra-orbital 
 region. He gives to such tumors the name of lymphangioma caver- 
 nosum. The exact character of these growths is still obscure. They 
 consist of irregular follicles and cavities, lined with epithelium, and con- 
 taining peculiar hyalin, structureless bodies. 
 
 Gysts ai-e found both single and multiple. They are usually situated 
 in the cortex. 
 
 Neuroma. — A ganglionic neuroma has been described by Weichsel- 
 baum.' 
 
 ' Virch, Archiv, Bd. 85, p. 554. 
 
THE UEII^AEY APPARATUS. 
 
 THE KIDNEYS. 
 MALFOBMATIONS. 
 
 Entire absence of both kidneys is sometimes associated with great mal- 
 formation of the entire body. Such foetuses are not viable. 
 
 Absence of one kidney is not uncommon; the left kidney being more 
 frequently absent than the right. The absence of the kidney may be 
 complete, the ureter being also absent; or there may be a little mass of 
 connective tissue and fat to represent the kidney, and a ureter running 
 down to the bladder. The single kidney which is present is usually 
 much enlarged. It may be in its natural position or displaced down- 
 wards. 
 
 Since the extirpation of the kidney has been practised by surgeons, it 
 has been found that absence of one kidney is more common than was 
 formerly believed. 
 
 When botli kidneys are present, one of them may be much larger than 
 the other. 
 
 Sometimes one kidney will have two pelves or two ureters. 
 
 A rather frequent malformation is the so-called horse-shoe kidney. 
 The lower ends of the kidneys are Joined together by a commissure. 
 The commissure is usually composed of kidney tissue, but sometimes of 
 connective tissue. The two kidneys may be normal, except for the com- 
 missure; or their shape, the arrangement of the vessels and ureters, and 
 tlie position, may be unnatural. 
 
 The two kidneys may be united throughout so as to look like a single 
 misshapen kidney with two or more pelves, and irregular blood-veasels. 
 The united kidneys may be both situated on one side of the vertebral 
 column or in the pelvis. 
 
 CHAN'GES Ilf POSITION. 
 
 The kidneys may be placed in an abnormal situation, in which they 
 are either fixed or movable. 
 
380 THE UEINAET APPAEATUS. 
 
 The change in position is either lateral or downward. When dis- 
 placed downwards, the kidney may be over the sacrum, or below this in 
 the cavity of the pelvis. The vessels also have an irregular origin and 
 distribution. The kidney is firmly attached in its abnormal position. 
 
 Movable or wandering kidneys are found in adult life as a result of 
 tight lacing, of pregnancy, of over-exertion, and of unknown causes. 
 They are more frequent in females than in males. The right kidney is 
 the one more frequently affected. Qlie blood-vessels become lengthened 
 and the attachments of the kidney longer and looser. 
 
 height's disease. 
 
 This name is given to a grouj) of kidney diseases which are charac- 
 terized by changes in the urine and by certain clinical symptoms. The 
 clinical relationship of these diseases is so marked jthat it seems probable 
 that they will always be grouped together, although anatomically they 
 are quite distinct. If, then, we divide the cases of Bright's disease ana- 
 tomically, we must distinguish: 
 
 1. Congestion of the kiduey. 
 
 2. Acute parenchymatous nephritis. 
 
 3. Chronic parenchymatous nephritis. 
 
 4. Acute diffuse nephritis. 
 
 5. Chronic diflluse nephritis. 
 
 6. Acute interstitial nephritis. 
 
 7. Chronic interstitial nephritis. 
 
 1. Congestion of the Kidney. 
 
 This condition of the kidney is produced by any mechanical cause 
 which increases the amount of blood in the renal veins. Valvular dis- 
 •ease of the heart, dilatation of the heart, aneurism of the aorta, emphy- 
 sema of the lungs, hydro-pneumothorax, pericarditis, tumors, and thrombi 
 in the veins, are all capable of producing venous congestion of the kid- 
 ney. 
 
 If the congestion has not existed for a long time, the kidneys are 
 increased in size and heavy. They are of a stony hardness; the capsules 
 are not adherent, and the surface of the kidney is smooth. Both the 
 pyramidal and cortical portions contain too much venous blood, which 
 gives them a dark-red color. There are no structural changes in the 
 Malpighian bodies, tubes,,- or stroma, except that the epithelium of the 
 convoluted tubes may be somewhat swollen. 
 
 If the congestion has lasted for a long time, the kidneys may con- 
 tinue to be large, or they may be somewhat diminished in size, the con- 
 sistence remaining hard and the color dark-red. The capsules are now 
 adherent, and the surface of the kidney is finely nodular. In the cortex 
 are patches of new connective tissue inclosing atrojDhied tubules, or a more 
 
THE UEINAEY APPAEATUS. 
 
 381 
 
 diffuse growth of connective tissue separating the tubules. In the convo- 
 luted tubules the epithelial cells are swollen and coarsely granular, or 
 very much swollen, or flattened against the walls of the tubules. The 
 tubules contain cast matter and detached and broken epithelial cells. 
 The capsules of the Malpighian bodies are a little thickened and the cap- 
 sular endothelium is swollen. In the pyramids, the epithelium of the 
 straight tubules is granular and detached, and there may be cast matter 
 both in the straight and looped tubules. 
 
 The same mechanical conditions which cause congestion of the kidr 
 ney may also cause a peculiar form of chronic difEuse nephritis, which 
 will be described later. 
 
 2. Acute Parencliymatous Nephritis. 
 
 This form of nephritis occurs both as a secondary and an idiopathic 
 lesion. As a secondary lesion, it is of very frequent occurrence, espe- 
 cially with the infectious diseases. 
 
 The morbid changes are confined to the epithelium of the tubules and 
 the endothelium of the Malpighian capsules, and vary much in the degree 
 of their development. 
 
 4^7^"^^ 
 
 ^ 1^ V ^, 
 
 Fig. 125.— Acute Parenchymatods Nephritis, X TOO and reduced. 
 From a case of yellow fever, i., The swoUen and granular epithelium is peeling off and disin- 
 tegrating; 6, hyalin casts in the lumen of the convoluted tubule. 
 
 There is a corresponding variety in the gross appearance of the kid- 
 
382 THE UEII^AET APPAEATUS. 
 
 neys. Some of them can hardly be distinguished by the naked eye from 
 a normal kidney. In others, the cortex is swollen and pale, and the en- 
 tire kidney increased in size. The capsules always strip off readily, 
 leaving the surface of the organ smooth. 
 
 In the milder cases, only the cells of the convoluted tubes are swollen 
 and granular. 
 
 In more severe cases, the epithelium of both the convoluted and 
 straight tubes and the endothelium of the Malpighian capsules are swollen 
 and granular, and there is cast matter in the tubes (Fig. 125). 
 
 In the most severe cases, the changes in the epithelium of all the 
 tubes are very marked. They are very much swollen, granular, broken- 
 down, and detached from the walls of the tubes. Oast matter and blood 
 are found in the tubes. 
 
 It is often a matter of very great difficulty to decide as to the jDresence 
 or absence of the lesser grades of parenchymatous nephritis. The mor- 
 bid process consists simply in a change in the composition and appearance 
 of the epithelial cells — a change which is closely simulated by decomposi- 
 tion. And yet such kidneys may give, during the patient's life, albu- 
 min, casts, and blood in the urine, and other symptoms. 
 
 There is also a very marked discrepancy in different cases between 
 the development of the kidney lesion and the degree of the renal symp- 
 toms during life. Especially in children who have scarlatina or diph- 
 theria, there may be marked renal symptoms with but very slight anatomi- 
 cal changes in the kidney. 
 
 3. Chronic Parenchymatous Nephritis. 
 
 This name should properly be applied only to those case in which the 
 lesions are confined the epithelium of the tubes and the endothelium of 
 the Malphighian bodies. A good deal of confusion has arisen from 
 applying the name to kidneys with more complicated lesions. 
 
 This form of nephritis is really not a very common one, and its clini- 
 cal history resembles very closely that of chronic diffuse nephritis. 
 
 The kidneys are increased, in size, and weigh together from sixteen to 
 twenty ounces. The capsules are not adherent, tlie surface of the kidney 
 is smooth. The cortical portion is thick and white, the pyramids are large 
 and red. Such kidneys are often called " large white kidneys," but 
 the same name is even more frequently applied to some of the forms of 
 acute and chronic diffuse nephritis. 
 
 The epithelium of tlie tubes, especially of the convoluted tubes, is 
 swollen, granular, and often broken down. The endothelial cells of the 
 Malpighian capsules are also swollen, and there is cast matter in the 
 tubes. The stroma and the blood-vessels are unchanged. 
 
THE UEINART APPARATUS. 
 
 383 
 
 4. Acute Diffuse Nephritis. 
 This form of nephritis occurs as an idiopathic disease, and as a com- 
 plication of scarlatina and of acute phthisis. 
 
 The kidneys are considerably increased in size, the capsules are not 
 adherent, the surfaces are smooth. The entire kidney with the mucous 
 membrane of the pelvis may be intensely congested ; or the cortex is of 
 an opaque white color, mottled with red spots, while the pyramids are 
 red. The tissue of the kidney is moist and succulent. 
 
 In most of the tubes, both in the cortex and pyramids, the epithelial 
 cells are swollen, granular, broken down, and detached from the walls of 
 the tubes. Cast matter and blood -globules are found in the tubes in 
 
 Fig. 126. — Acute Diffuse Nepgritis, X 350 and reduced. 
 Case of scarlatina, a, Swollen endothelium of the capsule of the glomerulus; h, proliferation 
 of lining ceUs of glomerulus; c, compressed vascular tuft; d, swollen stroma infiltrated with cells; 
 e, dilated convoluted tubule; fir, swollen epithelium peeling off; ft, hyaline casts. 
 
 considerable quantities. The endothelial cells of the Malpighian capsules 
 are swollen, or they are increased in number, sometimes to such an ex- 
 tent as to compress the tuft of vessels (Fig. 126). The stroma of the 
 kidney is infiltrated v/ith serum, pus-cells, and blood to a greater or less 
 degree. 
 
 5. Chronic Diffuse Nephritis. 
 This is the most common and the most important form of kidney 
 disease. 
 
 Although the lesions are essentially the same in all the cases of chronic 
 
384 THE UEIKAET APPAEATUS. 
 
 diflEuse nephritis, yet there is a variety in the degree of development of 
 the lesions and in the gross appearance of the kidneys. 
 
 There is also very frequently a discrepancy between the severity of 
 the clinical symptoms and the extent of the lesions in the kidney. This 
 discrepancy is so great as to lead us to look for the causes of the symp- 
 toms in other morbid conditions which co-exist with the disease of the 
 kidneys. 
 
 The most common form of chronic diffuse nephritis is that which is 
 often called " the atrophied kidney," or "interstitial nephritis." Many 
 of these kidneys are much diminished in size, but some are of normal 
 size and some increased in size. The capsules are more or less adherent, 
 and when they are stripped off, portions of the kidney adhere to them. 
 The surface of the kidney is finely or coarsely nodular. The cortical por- 
 tion of the kidney is of its natural thickness, or increased, or thinned ; 
 it is of a red or grayish color, the normal striations are obscured. The 
 pyramids are of normal size or- small, sometimes studded with little 
 white concretions of urate of soda. There are often cysts both in the 
 cortex and pyramids. 
 
 Another common form is that in which the kidney is hardly changed 
 at all in its size, color, or gross appearance. Except for the adherence 
 of the capsule, it resembles a normal kidney. 
 
 Another variety is "the large white kidney." The kidneys which 
 have the gross appearance of the large, white kidney are not, however, 
 all examples of chronic diffuse nepliritis ; some are in the condition of 
 jjarenchymatous nephritis. These kidneys are considerably increased in 
 size. The capsules are not adherent, or but slightly so, the surfaces 
 are smooth. The cortex is thickened, of an opaque white color, or 
 mottled with yellow, red, or gray. The pyramids are large and red. 
 
 There are other kidneys which resemble the large white kidneys in 
 their color and general appearance, but are diminished in size, with 
 atrophy of the cortex and adherence of the capsules. 
 
 A peculiar form of chronic diffuse nephritis may be produced by car- 
 diac lesions in the place of the ordinary chronic congestion. The .kid- 
 neys are increased in size, the capsules are not adherent, the surfaces are 
 smooth. The cortex is thickened, and of a peculiar pinkish-white color, 
 the pyramids are red. The whole coloring is different from that of 
 chronic congestion, and the texture is not of the same stony hardness. 
 
 There are still other kidneys which look as if they had passed from 
 the condition of chronic congestion into that of chronic diffuse nephritis. 
 They retain the color and hardness of chronic congestion, but the cap- 
 sules are adherent and the surfaces nodular. 
 
 In all these different varieties of chronic diffuse nephritis, there are 
 morbid changes in the tubes, the Malpighian bodies, the stroma and the 
 arteries. 
 
THE UEINAET APPARATUS. 
 
 385 
 
 In the tubes the epithelium is changed, especially in the tubes of the 
 cortex. The cells are swollen, finely or coarsely granular, or fatty, or 
 completely broken down, or the seat of hyalin degeneration. They may 
 remain in place on the walls of the tube, or be flattened, or detached. 
 The tubes may also contain cast matter, blood, pus-cells, and small, flat, 
 nucleated cells. 
 
 The calibre of the tubes is often changed. They are dilated either 
 in the cylindrical or sacculated form, sometimes so as to form cysts of 
 considerable size. Such dilatations regularly affect groups of tubes, as 
 if they were due to obstruction of the large tubes in the pyramids. In 
 other cases, the tubes are denuded of epithelium, are small, fall together. 
 
 Fio. 127.— Waxy Degeneration of Blood-Vessels of GLOMBauLus, X 350 and reduced. 
 a. The tuft is completely transformed into a waxy mass; b, portions of vascular loops waxy; c, 
 vascular loops in normal condition; d, convoluted tubules with swollen, degenerating, and peeling 
 ephitelium. 
 
 and so may come to resemble connective tissue. The walls of the tubes 
 may be thickened, or they may be the seat of waxy infiltration. 
 
 The Malpighian bodies are changed, and from the alterations in the 
 surrounding tissue may be unnaturally close together. The capsules 
 may be dilated, or thickened and contracted. Their endothelial cells are 
 swollen and sometimes increased in number. The capillary tuft of ves- 
 sels may be the seat of a fibrous thickening of its walls, which may go on 
 to complete obliteration of the vessels; or of waxy infiltration (Fig. 127). 
 
 In the stroma there is a new growth of connective tissue (Pig. 128). 
 25 
 
386 
 
 THE TTEINAET APPARATUS. 
 
 This is usually found ia patches surrounding tlie Malpighian bodies, 
 and the blood-vessels in the cortex. Less frequently it is diffuse, follow- 
 ing the distribution of the capillary veins between the tubes. 
 
 j , kin ).A^x', 
 
 •?^ 4*f^Vo 
 
 ''!?'-'■%»■ 
 i^^ 
 
 Fig. 128.— Chronic Diffuse Nephritis, Atrophied Kidney, X 350 and reduced. 
 Showing small patch of new connective tissue with atrophy of inclosed tubules, tt. New con- 
 nective tissue; b, atrophied tubule containing hyalin casts; c, tubule with epithelium peeling off; 
 d, thickened capsule of glomerulus. 
 
 The walls of the arteries are thickened. This thickening seems to be 
 a uniform and symmetrial hypertrophy of all the coats of the vessel. 
 
 In the atrophied kidneys the changes ia the stroma, the Malpighian 
 bodies and the arteries, and the dilatation of the tubes are especially de- 
 veloped. 
 
 In the large white kidneys waxy infiltration of the tufts of the Mal- 
 pighian bodies and of the small arteries are especially common. 
 
 When chronic diffuse nephritis occurs in gouty persons, the kidneys 
 are usually atrophied and there are deposits of urate of soda in the tubes. 
 
 G. Acute Interstitial JVephritis. 
 
 This is a rare form of nephritis of which the clinical history is still 
 incomplete. One of its most noticeable features is that the patients 
 may have marked dropsy and other renal symptoms without albumen in 
 the nrine. 
 
 The kidneys are very large and succulent, the capsules are not adhe- 
 rent, the surfaces are smooth, the cortex is thick and whitish. 
 
THE UEINAKT APPAEATUS. 387 
 
 The most marked change is the accumulation of white blood-cells in 
 the capillary veins, and in the stroma between the tubes, while the 
 
 
 
 
 
 &-«5> 
 
 
 Fig. 129.— Acute Interstitial Nephritis, X 850 and reduced. 
 
 epithelium of the tubes is but little altered (Fig. 129). 
 
 7. Chronic Interstitial Nephritis. 
 
 I think that there can be no question that there exists a true inter- 
 stitial nephritis — a condition like that of cirrhosis of the liver, in which 
 the primary changes are in the stroma of the kidney, with secondary de- 
 generation of the epithelium. 
 
 The proper recognition of this form of nephritis has been much de- 
 layed by the attempt to bring into it all the atrophied kidneys. The 
 larger number of the atrophied kidneys belong to the class of chronic 
 diffuse nejDhritis, although probably some of them are examples of true 
 interstitial nephritis. 
 
 The best marked examples of chronic interstitial nephritis are those 
 in which the kidney is large and nodular. The growth of interstitial 
 connective tissue is very considerable both in the cortex and pyramids. 
 It is a diffuse growth, but more marked in some places than in others. 
 Not only is there a thickening of the stroma, but also of the walls of the 
 
388 THE UEHSTAEY APPARATUS. 
 
 tubes^ the Malpighian capsules, and the arteries. The arteries may also 
 be the seat of obliterating endarteritis. 
 
 The epithelium of the tubes is more or less degenerated and broken 
 down. 
 
 Fatty Infiltration. 
 
 In chronic alcoholism, chronic phthisis, and the fatty diathesis there 
 may be developed a condition of the kidneys analogous to fatty infiltra- 
 tion of the liver. The kidneys are increased in size, the capsules are not 
 adherent, the surfaces are smooth. The cortical portion is thickened 
 and of yellowish color. The epithelium of the tubes of the cortex is 
 infiltrated with fat-globules. 
 
 Suppurative Nephritis and Pyelo- Nephritis. 
 
 Suppurative inflammation of the kidney may be produced by injuries, 
 by emboli, by cystitis, and may occur without discoverable cause. 
 
 (1) Suppurative nephritis from injury. Gun-shot wounds, incised 
 or punctured wounds, falls, blows, and kicks are the ordinary traumatic 
 causes. If the injury is a very severe one, it usually causes the death of 
 the patient in a short time; if it is less severe, suppurative inflammation is 
 developed. The inflammatory process may be diffuse so that nearly the 
 whole of one or of both kidneys is converted into a soft mass composed 
 of pus, blood, and broken-down tissue; or it is circumscribed and one or 
 more abscesses are formed in the kidney. 
 
 (3) Embolic Abscesses. In pyaemia and in malignant endocarditis, 
 small infectious emboli find tlieir way into the arteries of the kidneys 
 and produce necrosis of small areas of tissue with surrounding zones of 
 suppurative inflammation. The entire kidney is enlarged and congested, 
 and is dotted witli little white foci surrounded by red zones. The foci are 
 formed by an infiltration of pus-cells between the tubes with more or less 
 degeneration of kidney tissue. Colonies of micrococci are sometimes, but 
 not always, found in the Malpighian tufts and in the abscesses (see Fig. 
 14, p. 86). 
 
 (3) Idiopathic abscesses. Sometimes abscesses of one or both kidneys 
 are met with, which have existed for a long time, and for which no cause 
 can be discovered. After death tlie kidney is found changed into a sac 
 full of pus and surrounded by fibrous tissue. The pelvis and calyces are 
 dilated, and their walls are thickened. The connective tissue around the 
 kidney, and its capsule are also thickened. Suppurating sinuses may ex- 
 tend from the kidney into the surrounding soft parts. 
 
 (4) Suppurative pyelo-nephritis with cystitis. Both kidneys are 
 usually affected. The mucous membrane of the pelvis is congested, 
 thickened, and coated with jjus or with patches of fibrin. Scattered 
 through the kidneys are abscesses and foci of pus of different sizes. The 
 
THE UEINAEY APPARATUS. 389 
 
 smallest are hardly visible to the naked eye, but with the microscope we 
 find small collections of pus-cells between the tubes, with swelling and 
 degeneration of the renal epithelium. The larger purulent foci look like 
 white streaks or wedges parallel to the tubes and surrounded by zones of 
 congestion. The larger abscesses replace considerable portions of the 
 kidney tissue. 
 
 The ureters are sometimes inflamed, their walls are thickened, their 
 nner surfaces are coated with pus or fibrin. 
 
 The bladder is always inflamed, and this is the primary lesion to 
 which the kidney lesion is secondary. It may present any of the lesions 
 of acute or chronic cystitis. 
 
 Chronic Pyelo-Neplmtis. 
 
 Chronic cystitis or calculi in the pelvis of the kidney may set up a 
 chronic inflammation which involves both the pelvis and calyces, and the 
 kidney tissue. The mucous membrane of the pelvis and calyces is thick- 
 ened, the epithelial layer is changed, there is a growth of granulation 
 tissue beneath the epithelium, and there may be little polypoid out- 
 growths. The surface of the mucous membrane is coated with pus or 
 fibrin, or the cavity of the pelvis is dilated and distended with purulent 
 serum. 
 
 The kidney itself is the seat of a chronic interstitial inflammation 
 with the production of new connective tissue, and sometimes of pus with 
 obliteration of the renal tubules. 
 
 Nephro -Phtli is is . 
 
 The kidney may become the seat of a peculiar form of chronic inflam- 
 mation which is called tubercular, or scrofulous, or cheesy nephritis, or 
 nephro-phthisis. The kidney lesion, however, is not isolated; it is asso- 
 ciated with similar lesions in other parts of the genito-urinary tract. 
 The ureters, the bladder, the seminal vessels, the prostate, the testicles, 
 the uterus, and the ovaries are involved in the same species of inflamma- 
 tion, although not all of them in each case. 
 
 The lesion is usually unilateral, involving the kidney and other por- 
 tions of the genito-urinary tract on one side of the body, most frequently 
 the left side. In different cases, either the kidney or some other part of 
 the tract is first inflamed, and the other parts later. 
 
 The other kidney is apt to become the seat of chronic diffuse nephritis 
 with Avaxy infiltration of the walls of tlie arteries. 
 
 The lesion seems to begin in the mucous membrane of the pelvis and 
 calyces, and extend from thence first to tlie pyramidal and afterwards to the 
 cortical portion of the kidneys. In the mucous membrane of the pelvis 
 and calyces, there is a growth of granulation tissue studded with tubercle 
 granula in the stroma, while the epithelial cells jDroliferate, become de- 
 
390 THE TJEINAEY APPABATCS. 
 
 formed, and desquamate. This process is often rapidly succeeded by 
 clieesy degeneration of all the inflammatory products. 
 
 In the kidney, there is the same production of granulation tissue and 
 tubercle grannla, which soon undergo cheesy degeneration, the degenera- 
 tion involving the adjacent kidney tissue. In addition to this, there is 
 in the i-est of the kidney chronic interstitial or suppurative inflammation. 
 So the entire kidney is enlarged, portions are in the condition of cheesy 
 degeneration, or have sloughed away, while the rest of the kidney is 
 dense and hard. Or if suppuration takes place, the kidney is hollowed 
 out into cavities filled with cheesy matter and pus. 
 
 Sometimes the process comes to a standstill, and then the cheesy 
 portions are infiltrated with the salts of lime. 
 
 Embolism and Thrombosis. 
 
 Acute and chronic endocarditis affecting the left side of the heart, 
 and chronic endarteritis of the aorta, frequently result in the formation 
 of vegetations, portions of which become detached, and lodged as em- 
 boli in the branches of the renal artery. 
 
 The occlusion of an artery in this way produces in the kidneys wedge- 
 shaped infarctions, varying in their size with the size of the obstructed 
 artery. The infarction loses the natural red color of the kidney, and 
 becomes first yellow and then white. Tlie renal epithelium degenerates 
 and disappears, the tubes become collapsed and shrunken, around the in- 
 farction is a zone of congestion and of infiltration with pus-cells. After 
 this the infarction becomes shrunken, dense, and changed into connective 
 tissue. The kidney is then left deformed by the cicatricial depressions 
 and contractions. It is possible, however, for the infarction to become 
 gangrenous, or to be surrounded by a zone of purulent infiltration, 
 and break down so as to form an abscess. Karely the infarctions are of 
 the hemorrhagic variety. 
 
 Embolism of the trunk of the renal artery produces complete necrosis 
 of the kidney. 
 
 Infectious emboli are small and produce little pui'ulent foci, see above. 
 
 Thrombosis of the renal vein and its branches may occur in patients 
 suffering from chronic Bright's disease.' It can also be produced by 
 tumors pressing on the veins, by thrombi of the vena cava; and occurs 
 as a iirimary lesion dependent on the general condition of the patient. 
 
 Hydronephrosis. 
 
 Dilatation of the pelvis and calyces of the kidneyis found as a con- 
 genital condition. In some cases, other malformations such as club foot, 
 hare-lips, imperforate anus are also present. The pelves and calyces of 
 
 » Moxon, Trans. Lond. Path. Society, 1870, p. 248. 
 
 s 
 
THE UEINAR-y APPAJRATTJS. 391 
 
 both kidneys, and the ureters are distended with urine, the bladder is 
 also distended and its wall may be hypertrophied. The urethra may be 
 ■closed, or no obstruction can be demonstrated. In these latter cases it is 
 supposed that there does exist some membranous obstruction which is 
 broken by the probe or catheter used to explore the urethra. 
 
 In adult life, hydronephrosis is produced by mechanical obstruction of 
 the urethra or ureters, due to inflammation, tumors, or calculi. Accord- 
 ing to the position of the obstruction, either one or both kidneys are in- 
 volved. 
 
 The pelvis and calyces are dilated, sometimes enormously, and filled 
 with urine alone, or urine mixed with pus. The kidney tissue is flattened 
 and thinned over the distended cavities. Its texture may remain un- 
 changed, or there may be developed suppurative pyelo-nephritis, or 
 chronic diffuse nephritis. 
 
 Tlie Cystic Kidney. 
 
 Cysts are formed in the kidneys, both during intra-uterine and extra- 
 uterine life. 
 
 The congenital cystic kidney is a very remarkable pathological con- 
 dition. Either one or both kidneys are enormously enlarged and con- 
 verted into a mass of cysts. The cysts are of all sizes and are separated 
 from each other by fibrous septa or compressed kidney tissue. They con- 
 tain a clear, yellow, acid fluid, holding in solution the urinary salts. Or 
 the fluid is turbid and brown, and contains blood, uric acid crystals, and 
 cholestearin. The cysts are lined with a single layer of flat polygonal 
 ■cells. They seem to be formed by a dilatation of the tubules, and of the 
 capsules of the Malpighian bodies. As causes for such dilatations are 
 found, obliteration of the tubes in the papillse, and stenosis of the pelvis 
 ureters, bladder, or urethra. Other congenital malformations are often 
 associated with this one.' 
 
 In adult life we find three varieties of cystic kidney. 
 
 (1) In kidneys which are otherwise normal, there are one or more 
 cysts filled with clear or brown serum, or colloid matter. These cysts 
 do not {ippear to interfere at all with the function of the kidneys. 
 
 (2) In chronic diffuse nephritis, especially in the atrophic form, 
 groups of tubes are dilated. Apparently one or more of the larger tubes 
 in the pyramids is obstructed, and this causes dilatation of a correspond- 
 ing group of tubes. Such a dilatation may be moderate in size, or it may 
 form cysts visible to the naked eye. 
 
 (3) Both kidneys are very much enlarged and converted into a mass 
 of cysts containing clear or colored serum, or colloid matter. The na- 
 ture of these cysts is uncertain. It is possible that they are congenital. 
 
 ' Viroh., Ges. Abhandl. ' 
 
392 THE UBINAET APPAEATTJS. 
 
 They are sometimes associated with similar cysts in the liver. They 
 seem to produce no renal symptoms until shortly before the patient's 
 death, unless chronic nephritis also exists, and then there are the ordinary 
 symptoms of chronic Bright's disease. 
 
 PeiHnephritis. 
 
 The loose connective tissue which is situated around and beneath the 
 kidney may become the seat of suppurative inflammation, and in this 
 way abscesses of considerable size are formed. 
 
 Such a perinei^hritis may be either secondary or primary. The sec- 
 ondary cases arc due to extension of the inflammation from abscesses in the 
 vicinity, such as are formed with caries of the spine, pelvic cellulitis, pu- 
 erperal parametritis, perityphlitis, and suppurative nephritis. 
 
 The primary cases occur after exposure to cold, after contusions over 
 the lumbar region, and after great muscular exertion; or no cause can be 
 discovered. 
 
 Complicating cases occur in the course of typhus and typhoid fevers 
 and of small-pox. 
 
 Most of the reported cases have been in persons between the ages of 
 twenty and forty years. Less frequently children and older persons are 
 affected. 
 
 In the idiopathic cases, the connective tissue behind the kidney seems 
 to be the point of origin of the inflammatory process, and it is here that 
 the pus first collects. After the abscess has formed, the suppuration ex- 
 tends and the pus burrows in different directions; backward through the 
 muscles, downward into the iliac fossa, the perineum, the bladder, the 
 scrotum, or the vagina; forward into the peritoneal cavity or the colon, 
 upward through the diaphragm. 
 
 The kidney itself is simply compressed by the abscess, or its tissue be- 
 comes involved in the suppurative inflammation. 
 
 Renal Calculi. 
 
 In the kidneys of new-born children, from the first to the fourteenth 
 day after birth, the large tubes of the pyramids often contain small, 
 brownish, rounded bodies composed of the urates of ammonium and 
 sodium. Similar masses may also be jiresent in the calyces and pelves. 
 In still-born children these masses are usually absent. The carbonate 
 and phosp)hate of lime may be deposited in the tubes of the pyramids in 
 the form of white linear masses in the kidneys of old persons and of those 
 who have suffered from destructive diseases of tlie bones. 
 
 Urate of soda in the form of acicular crystals is deposited both in the 
 tubes and stroma of the kidneys of gouty iiersons. 
 
 Concretions of the urinary salts are often formed in the pelves of the 
 kidneys. They may remain there as rounded masses, or they may at- 
 
THE UKINAEY APPARATUS. 393 
 
 tain a large size and be moulded into the shape of the pelvis and calyces. 
 Smaller calculi pass into the ureter and either become impacted there or 
 pass through it into the bladder. The most common form of calculus is 
 that composed of uric acid. But they may also be formed of uric acid 
 with a shell of oxalate of lime, or of oxalate of lime alone, or of the 
 phosphates, or of cystin. 
 
 The most serious result of the presence of these calculi is the occlu- 
 sion of the ureters, or the production of pyelo-nephritis. 
 
 Tumors. 
 
 Fibroma. — Small, hard, white fibrous nodules are frequently found in 
 the pyramids. They are of no special importance. They may be mista- 
 ken for miliary tubercles. Large fibromata are very rare.' 
 
 Lipoma. — Small fatty tumors are found in the cortex of the kidney 
 just beneath the capsule. They are composed of fully developed fat- 
 tissue. The fat is developed in the stroma so as to replace the kidney 
 • tissue." 
 
 Papilloma. — Villous tumors formed of tufts of connective tissue cov- 
 ered with epithelium may grow from the mucous membrane of the pel- 
 vis.' A peculiar form of papillary and cystic growth of the ureter is 
 described.* 
 
 Myxo-Sarcoma. — Large tumors may grow from the pelvis of the 
 kidney. They are not simple myxomata, but are composed of mucous 
 tissue, fat, and sarcomatous tissue. 
 
 Myoma. — ^Small tumors composed of smooth muscular fibres and of 
 round cells arc found in the cortex close to the capsule. 
 
 A tumor composed of striated muscle and round cells is described by 
 Cohnheim.^ 
 
 A tumor composed partly of smooth muscle, partly of striped muscle, 
 and partly of sarcomatous tissue, is described by Eberth." 
 
 Angioma cavernosum occurs in the form of small nodules situated in 
 the cortex. 
 
 Lymphoma. — Small white tumors composed of tissue like that of the 
 lymjjhatic glands are found in cases of leukaemia and pseudo-leukeemia. 
 Less frequently they are found with typhoid fever, scarlet fever, and 
 diphtheria. 
 
 Adenoma.— Th\a form of tumor is situated in the cortex of the kid- 
 ney, and may invade the pyramidal portion also. Usually there is only 
 
 1 Wilks, Trans. Lond, Path. See, xx. 
 
 ' Virchow: Krank. Geschvviilste, Bd. i., p. 385. 
 
 3 Trans. Lond. Path. Soc, 1870, p. 339. 
 
 ^Vh-ch. Arch., Bd. 66, p. 139. 
 
 5 Virch. Arch., Bd. 65, p. 64. 
 
 liViroh. Arch., Bd. 55, p. 518. 
 
394 THE UEINABY APPAEATUS. 
 
 a single tumor, but sometimes two or more, or tliey may even occur in 
 both kidneys. They vary in size, some are not larger than a pea, others 
 are large as a hen's egg. They are of rounded form, of whitish color, 
 and separated by a capsule from the kidney tissue. The tumors are most 
 frequent in persons over forty years of age. 
 
 There are two principal varieties of these tumors : the papillary and 
 the alveolar. 
 
 (1) The papillary Adenoma. There are cavities of different sizes, 
 from the walls of which spring branching tufts covered with cylindrical 
 or cuboidal epithelium. These tufts nearly fill the cavities. 
 
 (2) The alveolar Adenoma. There is a connective-tissue framework, 
 inclosing small, round, oval or tubular alveoli, lined or filled with cells. 
 The cells are large, polygonal, nucleated bodies. 
 
 The adenomata frequently undergo fatty degeneration, which may be 
 so complete that they look like fatty tumors. 
 
 Or there may be an excessive development of the stroma, with atro- 
 phy of the epithelial cells. 
 
 There may be an excessive development and dilatation of the capilla- 
 ries and veins in the stroma. 
 
 Cysts of considerable size may be formed by dilatation of the cavities 
 or alveoli. ' 
 
 There are larger tumors involving the whole of the kidney and accom- 
 panied with metastatic growths in other parts of the body, which have 
 the same structure as the papillary adenomata. 
 
 A congenital adenoma is described by Weigert.' 
 
 Carcinoma. — Besides secondary carcinoma of the kidney, there is also 
 a primary form. Our knowledge of this has been much obscured by con- 
 founding with it adenomata and sarcomata. 
 
 There seems to be, however, a real epithelial growth originating in 
 the kidney tubules, which forms tumors of large size and malignant 
 character. 
 
 Sarcoma. — Tumors formed of connective- tissue cells may originate 
 either in the pelvis of the kidney or in the kidney itself. They form 
 tumors of large size and malignant character. Those which grow from 
 the pelvis arc usually myxo-sarcomata. Those which originate in the kid- 
 ney tissue reach a large size, and are soft and hemorrhagic. Their 
 stroma forms irregular alveoli filled with small round cells. 
 
 PAEASITES. 
 
 Ecliinococcus in its ordinary form of mother and daughter cysts, is 
 
 ' Medizinisoh. Jahrb., 1883, p. 213. Virch. Arch., Bd. 98, p. 39. 
 = Virch. Arch., Bd. 67, p. 492, 
 
THE TJEINAEY APPAEATUB. 395 
 
 sometimes found in the kidney. The cysts may open into the pelvis of 
 the kidney, into the pleura, or through the wall of the abdomen. 
 
 Cysticercus cellulosce is of very rare occurrence. 
 
 Pentastomitm. deniiculatuni has been seen once by E. Wagner. 
 
 Filaria sanguinis liominis is found in the arteries, veins, lymphatics, 
 and stroma. 
 
 Strongylus gigas has been found several times in the pelvis of the 
 kidney. 
 
 THE URINARY BLA.DDER. 
 
 MALFORMATIONS. 
 
 Extroversion of the bladder is one of the most frequent malforma- 
 tions, and may occur in either sex. It presents several varieties: 
 
 (1) The umbilicus is lower down than usual, the pubic bones are not 
 united at the symphysis, the pelvis is wider and shallower than it should 
 be. Between the umbilicus and pubes the abdominal wall is wanting. 
 In its place is a projecting ovoid mass of mucous membrane, in which may 
 be seen the openings of the ureters. The penis is usually rudimentary; 
 the urethra is an open fissure (epispadia); the clitoris may be separated 
 into two halves. The ureters usually open normally; sometimes their 
 openings are displaced, or are multiple. They may be dilated. 
 
 (^) There may be a fissure in the abdominal wall filled up by the 
 perfectly-formed bladder. 
 
 (3) The umbilicus may be well formed, and there is a portion of ab- 
 dominal wall between it and the extrophied bladder. 
 
 (4) The external genitals and urethra may be well formed, and the 
 symphysis pubis united, while only the bladder is fissured. 
 
 (5) The genitals, uretbra, and symphysis may be well formed^ the 
 bladder closed, except at the upper part of its anterior wall. The blad- 
 der is entirely or in part inverted and pushed through the opening in the 
 abdominal wall. 
 
 The Urachus normally remains as a very small canal, five to seven 
 centim. long, with a small opening into the bladder, or entirely closed at 
 that point. If there is a congenital obstruction to the flow of urine 
 through the urethra, the urachus may remain open, and the urine pass 
 through it. 
 
 Absence of the bladder is of rare occurrence. The bladder may be very 
 small, the urine passing almost directly into the urethra. The bladder 
 may be separated into an upper and a lower portion by a circular con- 
 striction. It may be completely divided by a vertical septum into two 
 lateral portions. Diverticula of the wall of the bladder are sometimes 
 found in new-born children. Partial or complete closure of the neck of 
 the bladder may occur. This may lead to hydro-nephrosis, or the urine 
 may be discharged through the open urachus. 
 
396 THE TJEINAET APPARATUS. 
 
 CHANGES IN SIZE AND POSITION. 
 
 Dilatation. — This may he general or partial, leading to the formation 
 of diverticula. 
 
 General dilatation of the bladder is produced by the accumulation 
 of urine in consequence of some mechanical obstacle to its escape, or of 
 paralysis of the muscular walls , of the organ. The dilatation is usually 
 uniform, and may be very great, so that the bladder may reach to the 
 umbilicus. If the walls of the bladder are paralyzed or the obstruction 
 occurs suddenly, or is complete, the wall of the bladder is thinned. 
 When an incomplete obstruction exists for some time, the walls of the 
 bladder are apt to hypertrophy, so that, although the bladder is larger 
 than normal, the walls may not only be of the usual thickness, but even 
 very much thicker. In tlie foetus, dilatation of the bladder may reach 
 such a size as to interfere with delivery. 
 
 The retained nrine in dilated bladders is liable to decomposition, 
 leading to inflammation or gangrene of the mucous membrane. 
 
 Diverticula of the bladder may be produced by the pouching out of 
 circumscribed portions of the wall of the bladder; the wall of the pouch 
 containing all the layers of the bladder-wall. More frequently, however, 
 they are produced by a protrusion of the mucous membrane between 
 hypertrophied bundles of muscle fibres. They may be very small, or 
 they may be as large as a child's head. They may communicate with 
 the bladder by a large or a small opening. The decomposition of stag- 
 nant urine in diverticula is apt to induce inflammation. Calculi may be 
 formed in them or may slip into them from the bladder. 
 
 Hyjjertropliy of the muscular coat of the bladder is usually produced 
 by mechanical obstructions to the outflow of urine, such as stricture of 
 of the urethra, enlarged prostate, calculi, new growths, etc. The mus- 
 cular coat is thickened uniformly, or assumes a trabeculated appearance. 
 The organ retains its normal capacity, or is dilated, or becomes smaller. 
 The mucous membrane is frequently the seat of chronic or acute inflam- 
 mation. Dilatation of the ureters and hydronephrosis frequently accom- 
 pany this condition. 
 
 Herniw of the bladder sometimes accompany intestinal hernije through 
 the inguinal and crural canals, and the foramen ovale. The changes in 
 position of the bladder, produced by displacements of the vagina and 
 uterus, will be mentioned with the lesions of those organs. 
 
 In the female, the base of the bladder may press downward, causing 
 jorotrusion of the vaginal wall [vaginal cystocele); or there may be inver- 
 sion and prolapse of bladder through the dilated urethra. 
 
 KUPTUEE. — PEEEORATION. 
 
 Penetrating wounds of the bladder may permit escape of urine into 
 the abdominal cavity, or infiltration into the surrounding connective tis- 
 
THE XJEllirAET APPAEATUS. 397 
 
 sue, 01' permanent fistulee. Such wounds are always serious and frequently 
 fatal, owing chiefly to the severe and often gangrenous inflammation, which 
 decomposing urine sets up in the connective tissue, or to the peritonitis 
 induced by the same cause. 
 
 Eupture of the bladder may be produced by severe blows and falls 
 when the bladder contains urine. More rarely, rupture takes place from 
 over-distention. Death may occur from rupture of the bladder with 
 €scape of urine into the peritoneal cavity without evidences of peritonitis. 
 
 Perforations of the bladder are produced by ulceration and gangreue, 
 by abscesses from without, and by cancerous ulceration from the adjoining 
 organs. Fractures of the pelvic bones may produce laceration of the 
 bladder. Perforations of the bladder may lead to the establishment of 
 fistulse, communicating with the rectum, vagina, uterus, or opening ex- 
 ternally. 
 
 DISTURBANCES OF CIRCULATION". 
 
 Hypermmia.- — Aside from active hypersemiaof the mucous membrane 
 in acute inflammation, the bladder is not infrequently the seat of chronic 
 congestion from obstruction to tlie venous circulation. Under these con- 
 ditions, there may be chronic catarrhal inflammation; or a marked dila- 
 tation of the veins (vesical hemorrhoids), which may give rise to hemor- 
 rhage, or to obstruction of the opening of the ureters. 
 
 Hemorrhage. — Extensive hemorrhages into the bladder are commonly 
 due to injury or to the presence of calculi or tumors. Small hemorrhages 
 into the substance of the mucous membrane may accompany inflamma- 
 tion, the hemorrhagic diathesis, scurvy, purpura, small-pox, etc. If the 
 hemorrhage is considerable, and occurs rapidly in an empty bladder, a 
 clot is apt to form; but when the blood mixes with urine as it is extrava- 
 sated, it more commonly remains liquid, and is discharged as a reddish- 
 ibrown fluid. 
 
 INELAMilATION. 
 
 Acute GatarrhaJ Cystitis. — ^This may be incited by the presence of 
 urine which has decomposed under the influence of bacteria; by can- 
 tharides or other drugs; by the presence of foreign bodies and calculi; or 
 it may be due to an extension of gonoi-rhoeal urethritis or vaginitis; or it 
 may occur without assignable cause. The mucous membrane is swollen 
 aud congested, although these alterations may not be very evident after 
 death. The surfaces may be coated with mucus containing red blood- 
 cells and pus. The epithelium is apt to be loosened and in some jDlaces 
 peeled off, so that superficial or deep ulceration may occur. We may 
 find mixed with the urine in the organ, shreds of mucus, pus-cells, 
 ■epithelial cells of various shapes, usually more or less swollen and granu- 
 lar, or fragments of such cells; red blood-cells and bacteria. Of the 
 .bacteria the most common forms are Bacterium termo and Micrococcus 
 
398 THE UBINAET APPAEATUS. 
 
 iirese (see pp. 80 and 81). Kesolution may occur from acute catarrhal 
 cystitis, but it very frequently assumes a chronic character. 
 
 Chronic Cystitis. — In tliis form tlie mucous membrane may be swol- 
 len, succulent, grayish, or mottled with spots of congestion or extravasa- 
 tion, and covered with a layer of mucus and pus. Microscopically the 
 membrane may be more or less infiltrated with pus-cells, and pus may be 
 constantly produced and thrown ofE into the urine. Later the mucous 
 membrane may become thickened either diffusely or in the form of tufts 
 or polypi. In somes cases it becomes atrophied. Owing to decomposi- 
 tion of the hasmoglobin in the estravasated blood, the mucosa may become 
 pigmented, brown or slate-colored. The mucous membrane frequently 
 becomes eroded, especially on the most elevated portions, or deep ulcera- 
 tions may occur. The muscular coats may become paralyzed and the 
 bladder dilated; or the submucosaor the muscularis, or both, may become 
 hypertrophied. The mucous membrane may become incrusted with 
 urinary salts. 
 
 In another class of cases the inflammation assumes a more intense 
 and necrotic character. Larger and smaller shreds and patches of the 
 mucosa die, become brown or gray in color, and loosen or peel off, and 
 become mixed with the urine and exudations. The gangrenous process 
 may extend to all the coats of the bladder so that perforation and fatal peri- 
 tonitis may occur. The gangrenous form of cystitis is most apt to occur 
 in paralytics. In still another class of cases, the inflammation assumes 
 a suppurative character. The submucosa, the intermuscluar connective 
 tissue, and the adjacent parts become infiltrated with pus, either diffusely 
 or in the form of larger and smaller abscesses, which may open externally, 
 or internally, forming dee|) ulcers. In all these cases the inflammation 
 may extend to the ureters and kidneys; it may skip the ureters and in- 
 volve the kidneys. 
 
 Croupous Inflammation. — In connection with any of above lesions, the 
 mucous membrane of the bladder may be covered in patches or some- 
 times over a considerable portion of its surface with a layer of fibrin, 
 either granular or fibrillar, inclosing pus and epithelial cells and bac- 
 teria. The mucosa may be infiltrated with fibrin. 
 
 This form of inflammation may occur in connection with severe in- 
 fectious diseases — measles, diphtheria, scarlatina, typhoid fever; in con- 
 nection with similar inflammation of the external genitals, in puerperal 
 fever, noma, and sometimes in the presence of foreign bodies. It is 
 rarely an idiopathic disease. 
 
 Tiibercular Inflammation. — This disease commences by the formation 
 of miliary tubercles in the mucous membrane of the bladder. By the 
 coalescence of the tubercles and the degeneration of tissue about them, 
 ulcers are formed, and it is most frequently in the ulcerative stage that 
 the lesion is seen. The ulcers, which may be large or small, are usually 
 
THE UEINAET APPAEATITS. 399 
 
 most abundant at the base of the organ. Their edges may be cheesy, 
 and miliary tubercles in greater or smaller numbers are usually found in 
 the mucosa about them. Not infrequently large shreds of tissue are 
 loosened and cast off. The mucosa about the ulcers is apt to be infil- 
 trated with small spheroidal cells. Tubercle bacilli are present in many of 
 the tubercles, and in the edges and base of the ulcers. They may also 
 be found in the urine, and are then of diagnostic significance. Catar- 
 rhal inflammation is a very constant accompaniment of this lesion. 
 Tubercular cystitis may occur in connection with tubercular inflam- 
 mation of the lungs, intestines, or of the kidney, uterus, prostate, etc. 
 
 TUMORS. 
 
 Fibromata have been described, occurring as small nodular tumors in 
 the submucosa, but they are rare. 
 
 Aside from the polypoid thickenings of the mucosa occurring in 
 chronic cystitis, soft vascular jjapillomafa are of frequent occurrence. 
 These tumors vary in size from that of a pea to that of a pigeon's egg 
 or larger. They consist of a fibrous, often very vascular stroma, and are 
 covered on the surface with numerous small, closely-set, villous projec- 
 tions, over which are irregular layers of elongated or cylindrical cells. 
 These tumors are very liable to bleed; are often accompanied by vesical ca- 
 tarrh, and may be covered by a precipitate of urinary salts. The^epithe- 
 lium is liable to peel of£ from the surface of the villi and appear in the 
 urine. Sarcoma of the bladder has been described. 
 
 Carcinoma. — Carcinoma of the bladder is most frequently secondary 
 and is then rarely due to metastasis, but usually to an extension of the 
 growth from neighboring parts, as the uterus, vagina, or rectum. 
 
 Primary carcinoma of the bladder may occur: 
 
 (1) As a diffuse scirrhous infiltration of the entire wall of the blad- 
 der, usually with ulcerations of its inner surface. 
 
 (2) As a circumscribed nodule which grows inward and outward, ul- 
 cerating on its inner surface, and sometimes producing perforations. 
 
 (3) As villous o\ 2>(ipillomatous growth. The tumor grows from one 
 or more points of the inner surface of the bladder. It is formed of tu- 
 bular follicles, lined with cylindrical epithelium, and on its inner free 
 surface, of tufts covered with cylindrical epithelium. The new growth 
 may involve the entire thickness of the wall of the bladder. 
 
 (4) A few cases of carcinoma have been described in which the stroma 
 contained a varying quantity of smooth muscle-tissue.' 
 
 Cysts. — Dermoid cysts of the wall of the bladder have been described, 
 but are rare.- Small cysts with serous contents sometimes occur in the 
 
 " The literature of tumors of the bladder maybe found in Stein's " Study of the 
 Tumors of the Bladder," 1881, 
 
400 THE TTEmAET APPAEATTTS. 
 
 mucous membrane. A part of them at least are believed to be due to 
 faulty embryonal development. 
 
 PARASITES, ETC. 
 
 Among the animal parasites occasionally found in the bladder may 
 be mentioned — Ecliinococcus, Distoma liematobium, Filarial satiffuitiis, 
 Ascarides and Oxyurides. 
 
 Bacteria of various forms not infrequently occur in the bladder, par- 
 ticularly in connection with chronic cystitis. B. termo, Micrococcus 
 urincB, and Sarcina may be mentioned as of most frequent occurrence. 
 
 A great variety of foreign bodies may be found in the bladder, par- 
 ticularly in the female. If their stay is long, they are apt to become in- 
 crusted with urinary salts. 
 
 CALCULI. 
 
 Vesical calculi may occur singly or in great numbers, and vary greatly 
 in size, ranging from small, sand-like particles, up to masses four or five 
 inches in diameter, but the usual range is from the size of a pea to that 
 of a hen's egg. They are usually oval, spheroidal, or elongated; or 
 when several are present, they are apt to be facetted. The surface 
 may be smooth or rough. They are usually more or less dis- 
 tinctly lamellated, and are frequently formed around a central body 
 called a nucleus, which may either be formed of urinary salts or some 
 foreign body. Their most common constiineuis axe pliosphates, uric acid 
 and urates, and calcium oxalate, or various combinations of these. 
 
 Uric Acid Calculi. — These are the most common of vesical calculi. 
 In the forrii of small brownish-red crystalline aggregations, they may be 
 passed as ' gravel.' The larger uric acid calculi are notcommonly of very 
 great size, are frequently finely nodulated on the surface, but may be 
 smooth. The color varies from light-yellow to dark reddish-brown; they 
 are usually dense and lamellated. 
 
 Oalculi formed of urates. — Calculi composed of pure urates are rare, 
 these salts being more commonly combined with nric acid, and the phos- 
 phates to form the complex calculi. Sodium urate, in the form of small, 
 spined, more or less globular crystalline masses, forms one of the forms 
 of 'gravel.' 
 
 Phospliatic calculi. — Pure calcium phosphate calculi are rarely found, 
 as whitish, usually smooth and small lamellated concretions. 
 
 Mixed or triple pliosphate calculi are common, and frequently attain 
 large size. These calculi are sometimes pure, but the deposit is more 
 frequently associated with other salts, either as incrusting or intercalated 
 lamella;. Triple phosphate calculi are usually rough on the surface, of 
 grayish- white color, lamellated, and frequently very friable. 
 
 Small gray or white hard and usually smooth calculi of pure calcium 
 
THE UEINAET APPARATUS. 401 
 
 carlonate occur rarely. Calcium carbonate, is sometimes passed as gravel 
 in the form of minute spheroidal bodies, either singly or in clusters. 
 
 Calcium oxalate calculi (mulberry calculi) are comparatively common, 
 either pure or in combination with uric acid or the phosphates. Calcium 
 oxalate may occur in the form of very small, hard, smooth concretions, 
 or as larger, heavy, hard, finely or coarsely nodulated brown or blackish 
 lamellated masses. The nucleus or some of the lamella, or both, are 
 often composed of uric acid. 
 
 Cystin calculi are usually ovoidal in shape, of waxy consistency, 
 of clear or brownish or greenish-yellow color, with mamillated surface 
 and crystalline fracture. Cystin may be associated in a variety of ways 
 with other calculi. 
 
 JTanthin calculi, which are very rare, are usually of moderate size, 
 smooth, of a cinnamon or cinnabar-red color, lamellated, and oval or 
 flattened in shape. 
 
 Solid masses of fibrin and blood sometimes occur in the bladder, and 
 may exist as independent structures, or form nuclei for the deposit of 
 urinary salts. 
 
 Por a detailed account of calculi, the conditions under which they 
 form, modes of analysis, etc., we refer to special works on this subject. 
 
 THE URETHRA. 
 
 COifGEN'ITAL MALrOEltATIONS. 
 
 Some of the malformations of the urethra are described with those of 
 the penis. 
 
 The urethra may be impervious, or may open at the root of the penis. 
 More commonly there is partial obliteration or stricture of some part of 
 the canal. 
 
 The entire urethra may be dilated into a sac full of urine. 
 
 There may be a canal on the dorsum of the penis, formed by the fu- 
 sion of the spermatic cords, and opening in the glans above the urethra. 
 
 There may be two or more openings of the urethra. 
 
 The canal may be dislocated so as to open in the inguinal region. 
 
 A number of cases have been reported in which a valve in the urethra 
 has produced hypertrophy of the bladder, dilatation of the ureters, and 
 hydronephrosis.' 
 
 Owing to its narrowness, greater length, and peculiar connections 
 with the internal generative organs, the male urethrals much more liable 
 to disease than the female. 
 
 CHANGES IN SIZE AND POSITION. 
 
 Dilatation of the urethra may be produced by strictures, or by calculi 
 
 ' Virch. Arch., Bd. 49, p. 348. 
 26 
 
402 THE UEINAEY APPARATUS. 
 
 or other bodies fixed in its lumen. The dilatations are fusiform or sac- 
 culated in shape, and may reach the size of an orange or be even larger. 
 
 Strictures of the urethra are usually produced by inflammation of its 
 walls. 
 
 The stricture may be temporarxj, produced by a diffuse inflammatory 
 swelling of the mucous membrane, or by the raising of the relaxed mem- 
 brane into a fold or pocket. 
 
 Permanent strictures are produced by structural changes in the walls 
 of the urethra. 
 
 (1) The mucous membrane and submucous tissue is left hard and 
 unyielding by the preceding inflammation. Subsequently, the new 
 fibrous tissue contracts and narrows the canal. 
 
 (2) Ulceration of the mucous membrane leaves cicatricial tissue, which 
 contracts, and also produces adhesions and bands of fibrous tissue. 
 
 (3) There is fibrous induration of the corpus spongiosum, and conse- 
 quent constriction of the urethra. 
 
 The most frequent position of strictures is at the junction of the 
 membranous and spongy portions of the urethra, or close to this point. 
 They also occur at the fossa navicularis and the meatus, but frequently 
 in the prostatic portion. There may be one stricture or several. The 
 consequences of stricture are dilatation of the urethra, the bladder, the 
 ureters, and hydronephrosis; inflammation and ulceration of the urethra 
 behind the stricture, with perforation, infiltration of urine, or the forma- 
 tion of fistulse.' 
 
 The urethra may also be obstructed by folds of the mucous membrane; 
 by muscular valves at the neck of the bladder; by wounds; by polypi and 
 swollen glands; by new growths; by changes in the prostate and perineum; 
 by calculi, mucus, blood, and echinococci coming from the bladder; by 
 foreign bodies introduced from without. 
 
 Prolapse and inversion of the mucous membrane is seen in young 
 girls and women in rare cases. There is a bluish-red swelling, from the 
 size of a pea to that of a walnut, at the meatus. In the male, invagina- 
 tion of the mucous membrane of the urethra has been seen after injuries 
 of the perineum. 
 
 WOUNDS, RUPTURE, PERFORATION. 
 
 Wounds of the urethra are produced in many ways, but most com- 
 monly by catheters and bougies. The wounds may cicatrize, or there 
 may be infiltration of urine, or the formation of fistulse or false passages. 
 
 Kuptures of the urethra are produced by severe contusions and by 
 
 ' For literature of stricture of urethra and plates illustrating several forms, see 
 article by Dittel, in Pitha and Billroth's " Handbuoh der allg. Chirurgie," Bd. 3, 
 Abth. 3. 
 
THE UEINAET APPARATUS. 403 
 
 fracture of the pelvic bones. Extrayasations of blood and urine, and 
 gangrenous inflammation of the surrounding soft parts, are the ordinary 
 results. 
 
 Ulceration and perforation of the urethra may lead to the formation 
 of fistulsB, which open in various directions through the skin. 
 
 INFLAMMATIOiq". 
 
 Catarrhal Urethritis may be simple and due to the action of chemical 
 irritants; to the extension to the urethra of inflammation from other 
 parts, and to unknown causes; but it is most frequently due to the action 
 the gonorrhceal poison. In its acute form, it involves either a portion or 
 the whole of the urethra. The mucous membrane is red, swollen, and 
 covei-ed with muco-pus. The inflammation may extend to the fibrous 
 wall of the urethra, the corpora spongiosa and cavernosa. This may 
 result in the formation of new connective tissue, or of abscesses, especially 
 near the fossa navicularis. The inflammation may also extend to the 
 bladder, the glands of Cowp^r, the prostate, the spermatic cord, and the 
 testicles. The inguinal glands also may be swollen and inflamed, and 
 the lymphatic vessels on the dorsum of the penis may be involved in the 
 same process. 
 
 Chronic inflammation of the urethra may exist for a long time with 
 the production of a muco-purulent exudation, but without the occurrence 
 of marked structural lesions. In other cases it leads to ulceration, 
 to fibrous induration of the wall of the canal, to induration and swelling 
 of the mucous follicles, to polyjioid thickenings of the mucous mem- 
 brane. 
 
 The exudation in gonorrhceal inflammation of the mucous membranes 
 not only of the urethra, but also of the vagina and of the eye, constantly 
 contains, in greater or less numbers, a form of micrococcus, which is said 
 by some observers — although this is denied by others — to present charac- 
 teristic morphological characters. 
 
 The micrococcus — called gonococcus— which is spheroidal or ovoidal in 
 shape, usually occurs in pairs or in groups of four or more, and may be con- 
 tained in the pus-cells, or lie on their su.rfaces or free in the fluid. The 
 pus-cells sometimes contain very large numbers of the micrococci. While 
 the very constant presence of these micrococci justify the conjecture that 
 they may stand in an etiological relation to the gonorrheal inflammation, 
 the exjoeriments thus far recorded upon their purification by culture and 
 inoculation have not led to such definite results as to justify us in assign- 
 ing to them a definite role in the disease. The conclusions of investiga- 
 tors are in many respects at variance; the results of animal inoculations 
 are usually negative; and the inoculations thus far practised on the 
 human subject have not been sufiiciently extensive and exact. 
 
404 THE TJEmAEY APPAEATUS. 
 
 The gonococcus may be stained by drying the exudation on a cover 
 glass and using fuchsin or methylin blue.' 
 
 Croiqjous inflammation is sometimes seen in children. Fibrinous 
 casts of a small or large portion of the canal may be formed. 
 
 Syphilitic ulcers may be situated at the meatus^ or as far back as the 
 fossa navicLilaris. They are apt to produce strictures. 
 
 Tubercular inflammation rarely occurs in the mucous membrane of 
 the urethra in connection with tubercular inflammation of the bladder, 
 prostate or testicles. 
 
 TUMORS. 
 
 Aside from the polypoid outgrowths from the mucous membrane of 
 the urethra as the result of chronic inflammation, fibrous polyps may 
 occur congenitally, or polyps containing glandular structures or cysts 
 rarely occur. Carcinoma may occur as a result of local extension from 
 adjacent organs or metastasis from the bladder. Cysts may occur in the 
 mucous membrane as a result of the dilatation of the mucous glands. 
 Circumscribed masses of dilated veins occasionally occur in the urethra, 
 forming the so-caUed tirefJiral liemorrlioids. 
 
 The sinus pocularis may be dilated in children by the retention of its 
 secretion, so as to form a tumor which may obstruct the exit of urine, 
 cause hypertrophy of the bladder, and dilatation of the ureters. 
 
 ' The bibliography of the so-called Oonococcus may be for the most part found 
 in journal articles by Neisser, " Die Mikrokokken der Gonorrhoea," Deutsch. med. 
 Wochenschrift, May 13th, 1882, Bd. viii., No. 20, p. 279, and by Keyser, "Is Gonor- 
 rhoea a Bacteria disease?" Maryland Med. Jour., Feb. 15th, 1883, Vol. ix., No. xx. 
 p. 481; or in Magnin and Sternberg's "Bacteria," 1884. 
 
THE ORGANS OF GEITERATIOK 
 
 FEMALE. 
 THE VULVA. 
 
 MALrOBMATIONS. 
 
 TJie external genitals may be entirely absent or imperfectly developed. 
 The fissure between the labia may be unformed, or the labia may grow- 
 together, with or without obstruction of the urethra. The clitoris and 
 nymphee may be abnormally large, or the nymphsB may be increased in 
 number. The clitoris may be abnormally long, resembling a penis; at 
 the same time the vagina is narrow, the uterus small and undeveloped or 
 malformed, the ovaries small, sometimes 'situated in the labia, the 
 mammje small, and the body of a masculine character. Such cases 
 are sometimes called pseudo-hermaphrodites. The clitoris may be per- 
 forated by the urethra, or may be cleft and apparently double. 
 
 The hymen frequently exhibits various anomalies. It may bo en- 
 tirely absent. The opening may be very large, or in unusual places; 
 there may be several openings; the free edge may be beset with 
 papillary projections; there may be no opening at all.' 
 
 HEMORRHAGE, HYPEREMIA, ETC. 
 
 Hemorrhage may take place from wounds or ulcers of the vulva, but 
 the most important form of hemorrhage is that which occurs in the con- 
 nective tissue of the labia majora. This is produced during labor, or 
 from external injury. One of the labia may be swollen and distended by 
 the extravasated blood, until it is as large as a child's liead. The blood 
 may be gradually absorbed, or it may decompose, with suppuration or 
 gangrene of the surrounding tissue. The purulent matter may escape 
 through the skin, and the patient recover; or the suppuration may ex- 
 tend into the pelvis and cause death. 
 
 ' For description and illustrations of anomalies of the hymen, which may be 
 useful for medico-legal purposes, see Courty's "Diseases of Uterus, Ovai-ies, Fal- 
 lopian Tubes," Trans, by McLaren, 1883, p. 90. 
 
406 THE OEGANS OF GENEEATIOIT. 
 
 A varicose condition of the veins of the labia is not infrequent. 
 (Edema may occur in acute form in pregnant and puerperal women, and 
 may terminate in suppuration or gangrene. (Edema of the labia majora, 
 frequently accompanies disturbances of the venous circulation, as in cer- 
 tain heart and lung diseases, or it may occur in chronic diffuse nephritis 
 or other wasting diseases, or as a result of thrombosis or other disturban- 
 ces of circulation in the uterine or peri-vaginal venous plexuses. This 
 may be excessive, leading to the transudation of fluid through the skin, 
 to the formation of vesicles, to superficial erosion, or even to gangrene. 
 
 INFLAMMATION. 
 
 The skin, mucous membrane, connective tissue, and glands of the 
 vulva may be the seat of inflammation. Acute catarrh of the mucous 
 membrane may be caused by a variety of irritating influences, but is most 
 frequently due to gonorrhoeal infection. The mucous membrane is 
 swollen and red, and covered with a muco-purulent exudation. The labia 
 may bp swollen and the glands are liable to be involved, and abscesses 
 of the labia may be developed. Chronic catarrhal inflammation may 
 lead to superficial or deep ulceration of the mucous membrane, or to pap- 
 illary outgrowths, or to thickening of the labia. Suppurative inflamma- 
 tion of the tissue of the labia may occur in connection with a similar pro- 
 cess in neighboring parts. Erysipelatous inflammation of the skin of the 
 vulva is frequent in young children, and may cause death. In adults it 
 is less common. Inflammation of the vulvo-vaginal glands may be acute 
 and produce abscesses; or chronic and produce induration of the gland. 
 
 Gangrene may follow erysipelatous inflammation, may occur after 
 parturition, may accompany severe exhausting and infectious diseases, or 
 may occur as an epidemic disease, especially among children. It may be 
 the result of braises or other injuries. In some forms, such as those 
 known as noma and liospital gangrene, the destruction of tissue proceeds 
 with extreme rapidity. 
 
 Herpes, eczema, lichen, prurigo, etc., may be found on the skin of the 
 vulva. 
 
 Syphilitic inflammation and ulceration is of frequent occurrence on 
 the vulva, particularly on the mucous surfaces, and frequently lead ta 
 considerable destruction of tissue and cicatricial contractions. 
 
 Croupous inflammation may occur with or without diphtheria and a 
 similar lesion of the fauces, and is frequently associated with gangrene. 
 
 Liopus.- — This form of inflammation, usually with more or less de- 
 structive ulceration, occasionally occurs in the vulva. 
 
 TUMORS. 
 
 Fibroma.- — Circumscribed fibrous tumors are found in the connective 
 tissue of the labia, mons veneris, perineum, clitoris, and entrance to the 
 
THE OKGANS OF GENEEATION. 407 
 
 vagina. They may attain a large size, and, attached only by a pedicle, 
 may hang far down between the legs. The skin is usually movable over 
 the surface of these tumors. 
 
 Fibroma diffusum (elephantasis). — This usually involves the clitoris 
 or the labia, or both, and may extend to surrounding parts of the skin. 
 It consists essentially of a diffuse hypertrophy of the skin and subcu- 
 taneous tissue, with or without involvement of the papillae and epi- 
 dermis. The surface may be smooth or rough. Sometimes when the 
 new growth is circumscribed, rough or smooth polypoid growths, often 
 of large size, are formed. When the papillse and epidermis are much 
 involved, larger and smaller cauliflower-like excrescences may cover the 
 hypertrophied parts, and the surface be very rough and scaly. 
 
 Papillomata. — These growths consist of hypertrophied papillee covered 
 with thick layers of epithelium. They vary in size from that of a pea to 
 that of an apple, and have a cauliflower appearance. 
 
 SypMlUic Condylomata. — In one form, the so-called mucous patch, 
 there is an infiltration of the papillary layers of the skin or mucous mem- 
 brane with variously shaped cells and fluid, so that the tissue has a gela- 
 tinous appearance. In others cases, tliere is an hypertrophy of the papillse, 
 so that larger and smaller wart-like excrescences are formed. This is 
 called the jjointed condyloma. Lipomata, fibro-myomata, and fibro-sarco- 
 mata are of occasional occurrence of the vulva. Chondroma of the clitoris 
 has been described. Carcinoma of the vulva may be primary, usually in 
 the form of epithelioma of the clitoris or labia, or it may be secondary to 
 cancer of the uterus, vagina, etc. * 
 
 Cysts are found in the connective tissue of the labia majora and 
 .minora. They are from the size of a pea to that of a child's head. 
 They may contain serum, colloid material, purulent or bloody fluid, or 
 they may have the characters of dermoid cysts or. atheroma cysts. Their 
 origin is in many cases obscure. In some cases they are doubtless due 
 to dilatation of lymph-vessels. Cysts may be formed by a stoppage and 
 filling with fluid of the canal of ISTuck, or by a dilatation of the ducts or 
 acini of the vulvo-vaginal glands. 
 
 THE VAGINA. 
 
 MALFORMATIONS. 
 
 The vagina may be entirely absent, and the internal organs of genera- 
 tion also absent, or imperfectly developed. 
 
 Either the upper or the lower portion of the canal may be absent 
 while the remaining portion is present. 
 
 The vagina may be closed by an imperforate hymen or by fibrous 
 septa at any part of its canal. The canal may be abnormally small with- 
 out being occluded. 
 
408 THE ORGANS OF GENEEATION. 
 
 The vagina may be double, in connection witli a double uteras; or, 
 while the uterus is normal, the vagina may be incompletely divided by a 
 longitudinal septum. 
 
 CHANGES IN SIZE AND POSITION. 
 
 Dilatation of the vagina is produced by tumors, by the prolapsed 
 uterus, and by the accumulation of blood and mucus behind constric- 
 tions or obliterations of the canal. Lengtliening of the vagina is pro- 
 duced by any cause which draws the uterus upward. Narrowing of the 
 vagina is found as a senile change; is produced by tumors and by ulcera- 
 tion of the wall of the canal. Extensive ulcers may even cause entire 
 obliteration of the canal. 
 
 Prolapse of the vagina occurs by itself, usually as a result of thicken- 
 ing or laxity of its walls, or in connection with prolapse of the uterus. 
 As an idioj)athic ijrocess, it usually takes jilace soon after parturition. 
 A larger or smaller portion of the canal is inverted, and projects through 
 the vulva. The entire circumference of the canal may be inverted and 
 prolapsed, or only the anterior or posterior wall. The prolapse is 
 at first small, but may afterwards gradually increase in size, and may 
 drag down the uterus with it. In other cases, prolapse of the uterus is 
 the primary lesion, and the vagina is inverted by the descent of that 
 organ, or the body of the uterus may retain its normal position, while an 
 hypertrophy and lengthening of the cervix alone drags down the vagina. 
 
 Hernia vesico-vaginalis — cystocele — may be either the cause or effect 
 of a pirolapse of the vagina and uterus. If the cystocele is the primary 
 lesion, it begins as a small projection of the wall of the bladder into the 
 anterior part of the vagina. As the urine accumulates in this sac, it 
 increases in size, projects through the vulva, draws down the vagina and 
 the anterior lip of the cervix, and finally the entire uterus. If the cysto- 
 cele is the secondary lesion, it is simply jiroduced by the dragging down 
 of the posterior wall of the bladder by the inverted vagina. 
 
 Hernia intestino-vaginalis.- — A portion of the intestines may become 
 fixed in Douglas' cul-de-sac between the rectum and uterus. This por- 
 tion of intestine gradually becomes larger, pushes forward the posterior 
 wall of the vagina, inverts and fills up that canal, and finally projects 
 through the vulva. It may drag with it the posterior wall of the vagina 
 and the uterus. 
 
 Rectocele vaginalis. — A sac is formed by the projection of the ante- 
 rior wall of the rectum and the posterior wall of the vagina. This 
 lesion is of rare occurrence, and does not reach a large size. 
 
 When the vagina is pi elapsed, there is usually an inflammatory con- 
 dition of the lining membrane or a thickening of the epidermis. 
 
 WOUNDS. PERFOKATIONS. 
 
 Wounds of the vagina are made by penetrating instruments, by for- 
 
THE ORGANS OF GENEEATION". 409 
 
 ceps and other obstetrical weapons, and by the foetus during delivery. 
 Such wounds may heal, may give rise to large hemorrhages, may suppu- 
 rate, may produce abscesses in the surrounding tissues, may leave fistii- 
 lous openings into the vagina, or may cause constriction or obliteration of 
 its canal. 
 
 Vesico-vaginal fistulm are usually produced by injuries from instru- 
 ments or from the fcetus during delivery ; less frequently by ulceration 
 of the vagina, bladder, or adjacent connective 'tissue, or by abscess in the 
 surrounding parts. The fistulas form an opening between either the 
 bladder or the urethra and the vagina. They allow the urine to pass into 
 the vagina. Spontaneous cure does not take place. 
 
 Recto -vag inal fistulcB are formed in the same way as the last-mentioned. 
 They allow the passage of gas or f^ces into the vagina. They sometimes 
 heal spontaneously. 
 
 INJFLAMSXATIOlf. 
 
 Catarrhal Inflammation of the vaginal mucous membrane may be 
 acute or chronic. It is most frequently caused by gouorrhoeal infection, 
 but may be due to local irritation or depend upon general causes. It 
 not infrequently occurs in the new-born. In tlie acute form, the mucous 
 membrane is swollen and frequently covered with a muco-purulent or a 
 purulent exudation. In the chronic form, the mucous membrane may 
 be swollen, covered with a purulent exudation ; there may be an exfolia- 
 tion of epithelium, shallow or deep erosions, or ulcers. In other cases, 
 the mucous membrane is thickened, dense, and sometimes pigmented, 
 or it may be roughened, covered with papillae, or it may be relaxed and 
 prolapsed. 
 
 Oroupoics Inflammation maj occur after parturition, in dysentery, in 
 typhus and typhoid fever, diphtheria, scarlatina, measles, and other in- 
 fectious diseases. The mucous membraue is swollen and covered with a 
 grayish layer of fibrin and pus. 'Clie mucosa and sub-mucosa may be 
 infiltrated with fibrin and pus. The infiltrated jiortions of the mucosa 
 and submucosa may die and become gangrenous, and thus deep and ex- 
 tensive ulcers be formed. 
 
 Suppurative Inflammation of the fibro-muscular coat of the vagina 
 may occur after injuries or in pregnant and puerperal women. Abscesses 
 may be formed which penetrate into the labia or into the pelvic connective 
 tissue. In other cases, the intense phlegmonous inflammation may lead 
 to the death and casting off of portions of the vaginal wall, or even of 
 the entire wall. 
 
 Gangrene of the vagina may occur as a result of croupous or intense 
 suppurative or syphilitic inflammation, or from unknown causes. In the 
 form of noma it may be very extensive and rapidly destructive. 
 
 Tuiercular and Syphilitic Inflammation, usually leading to more or 
 
410 THE ORGANS OF GENERATION. 
 
 less extensive ulceration, may occur in any part of the vagina. Tubercu- 
 lar inflammation is secondary to tuberculosis of other parts. Syphilitic 
 ulcers may heal, sometimes leaving marked cicatrices, and sometimes not. 
 
 TUMORS. 
 
 Fibroma, fibro-myoma, sarco7na, myoma Imvicellulare, are of occasional 
 occurrence in the vagina. Myoma striocellitlare is of rare occurrence. 
 
 Papillojiiaia are of frequent occurrence as a result of chronic inflam- 
 mation. Carcmoma of the vagina is usually secondary to cancer of the 
 uterus. It may be primary as a circumscribed nodular tumor, or more 
 frequently it occurs in a papillary and ulcerating form and often spreads 
 to neighboring parts. 
 
 Cysts. — These ai'e not very common and may be small or as large as 
 a lien's egg. They may be lined with flattened epithelium, and contain 
 serous or viscid, dark-colored or transparent fluid. 
 
 PARASITES. 
 
 Among the animal parasites Oxyuris and Tricliomonas vaginalis are of 
 occasional occurrence. Among the vegetable forms Oidium albicans, 
 Leptotlirix are occasionally seen, while micrococci and various other 
 forms of bacteria are common. The pathogenic significance of the bac- 
 teria in the vagina is not yet established. 
 
 THE UTERUS. 
 MALFORMATIONS. 
 
 The uterus, up to the third month of intra-uterine life, consists of 
 two large cornua, which by the fusion of their lower ends form the 
 uterus. 
 
 The uterus, tubes, and vagina may be entirely absent, with or without 
 absence of the external genitals. Or the uterus alone, or the upper part 
 of the vagina also, may be absent. 
 
 The uterus may be only rudimentary, while the vagina is normal. It 
 then api^ears as a. flattened solid body with solid cornua. Or there are 
 two cornua joined at their lower extremities so as to form a small double 
 uterus. Or the uterus is represented by a small sac, whicli may or may 
 not communicate with the vagina. Or there is a very small uterus, with 
 thin muscular walls and two large cornua. 
 
 Only one of the cornua which should form the uterus may be devel- 
 oped, while the other is arrested in its growth. The uterus is then a 
 long cylindrical body, terminating above in one tube. On the side where 
 the other horn should have been developed, there is no tube, or only a 
 rudimentary one. Both ovaries are usually present. 
 
 The two cornua may be fully developed, but their lower ends remain 
 
THE OEGANS 01' GENERATION. 411 
 
 separated, and form a double uterus. An entire separation into two dis- 
 tinct uteri and vagina is very rare. More frequently, the uterus consists 
 of one body, divided by a septum into two cavities. There are then two 
 cervical portions of the uterus projecting into a single vagina, or each into 
 a separate vagina. Or there is only a single cervix. The septum in the 
 uterus may be complete, or only partial. 
 
 We also find abnormal size of the uterus, abnormal flexions ; the cer- 
 vix may be solid, or may be closed by the vaginal mucous m.embrane. 
 Or the cervix may have an abnormal form with a small opening or 
 canal. ' 
 
 CHANGES IN SIZE. 
 
 In the new-born infant, the utei'us is small, the body flattened, the 
 cervix disproportionately large. During childhood, the organ increases 
 in size, but the body remains small in proportion to the cervix. At pu- 
 berty the shape changes, and the body becomes larger. 
 
 At every menstruation the uterus is somewhat swollen and congested. 
 After pregnancy it does not return to its virgin size, but remains some- 
 what larger. In old age, it gradually becomes smaller ; its walls are 
 harder and more fibrous. 
 
 Alnormal Sniallness of the uterus is sometimes found as an arrest of 
 development. The uterus in adult life retains the size and shape of that 
 of the infant. It may result, however, from chronic endometritis, from 
 repeated pregnancies, from old age, or from chronic exhausting diseases. 
 Its cavity may be smaller than normal, or distended with mucus. Large 
 myomata sometimes cause marked atrophy of the uterine wall. Atrophy 
 of the vaginal portion of the uterus is sometimes observed after repeated 
 pregnancies, sometimes without known cause. Narrowing and oblitera- 
 tion of the cavity of the uterus and of the cervix are usually produced by 
 chronic inflammation. 
 
 Enlargement of the Utenis may be due to too early development. It 
 is accompanied by abnormally early development of all the sexual organs 
 and functions. The uterus may be enlarged in connection with heart 
 disease, prolapse and abnormal flexions and versions, chronic inflamma- 
 tions, repeated pregnancies, myomata, and accumulations of blood or 
 mucus in the uterine cavity. Enlargement of the vaginal portion may 
 be produced by the above causes, and is also found without known cause. 
 One or both lips of the cervix may be uniformly increased in size, or they 
 may be lobulated. 
 
 Dilatation of the uterus is produced by accumulations of blood, 
 mucus, or pus, in consequence of narrowing or obliteration of the cervix 
 
 ' Illustrations of various forms of malformations of the cervix may be found 
 in the translation by McLaren of Courty's " Diseases of the Uterus, Ovaries, 
 etc.," 1883. 
 
412 THE OEGAKS OF GENEEATION. 
 
 or vagina. The uterine walls may retain their normal thickness, be thick- 
 ened or thinned. The most frequent position of the stenosis is the os 
 internum. The retained contents after a time change in character, 
 forminga thin serous fluid — liydrometra — or they may be mixed with blood. 
 The dilated uterus is not usually larger than an apple, but it sometimes 
 reaches enormous dimensions. If both os internum and os externum are 
 closed, the cervical cavity may be also dilated, and the utertis have an hour- 
 glass shape. If the obstruction is in the vagina, the uterus and vagina 
 may form a large flask-shaped body, and the line of demarcation between 
 cervix and vagina be lost. In some cases the dilatation is confined to 
 the cervix. If the obstruction is not complete, the retained fluid may 
 escape into the vagina and afterward accumulate again. 
 
 Accumulations of menstrual blood in the cavity of the uterus — hema- 
 tomdra — ^is usually produced by congenital stenosis of the cervix or 
 vagina. The dilated uterus may reach an enormous size. If the fluid is 
 not evacuated by surgical interference, there may be either rupture or 
 ulcerative perforation of the uterus. The blood may escape into the 
 abdominal cavity or be shut in by adhesions, or perforate into the bladder 
 or intestines. Sometimes the blood passes into the Fallopian tubes, 
 dilates them, and escapes through their abdominal ends. 
 
 CHANGES IN" POSITION". 
 
 The body of the uterus may become fixed in an abnormal position; 
 while the situation of the cervix is unchanged. The body may be 
 bent forward — anteflexion; backward — retroflexion; or sideways — -lateral 
 ■flexion. The flexion may be slight, or so great that the neck and body 
 form an acute angle. Anteflexion is the most common variety, and that 
 in which the flexion is greatest. Peritoneal adhesions, flaccidity of the 
 uterine walls particularly after delivery, atrophy of the walls, ovarian 
 and other tumors, etc., are the usual causes of flexions. 
 
 The Versions of the uterus consist in an abnormal inclination of the 
 long axis of the organ to that of the vagina. The uterus may be inclined 
 backward, forward, or to one side. 
 
 Retroversion is very much the most common. The fundus uteri is 
 directed backward and downward; the cervix, forward and upward. This 
 condition is found in various degrees; in the highest, the fundus lies in 
 Douglas' cul de sac with the cervix upward, so that the axis of the uterus is 
 parallel to that of the vagina, but in a direction nearly opposite to the 
 normal one. Abnormal looseness of the uterine ligaments, abnormally 
 large capacity of the pelvis, hypertrophy or tumors of the uterus, and 
 pregnancy during the first four months, are some of the more common 
 conditions under which tliis lesion occurs. 
 
 Anteversion. — Inclination of the fundus forward and downward, and 
 of the cervix backward and upward is not common, and seldom reaches a 
 
THE OEGAIfS OF GENEEATION. 413 
 
 high degree. It occurs under the same general external conditions as 
 anteflexion. 
 
 Lateroversion is not very common as a simple lesion, but is not 
 infrequently combined with other displacements. It may be produced 
 by congenital shbrtening of one of the broad ligaments, by adhesions, or 
 by the pressure of tumors. 
 
 The greater degrees of version may produce very grave lesions. The 
 urethra and rectum may be compressed. Cystitis, perforation of the 
 bladder, dilatation of the ureters and hydronephrosis, and fatal obstruc- 
 tion of the bowels may follow. If pregnancy exists, abortion may take 
 place, or the inverted uterus may be forced through the peritoneum and 
 posterior wall of the vagina and project through the vulva. In the non- 
 pregnant uterus, pressure on the veins, and consequent chronic inflam- 
 mation of the organ may follow. 
 
 Prolapsus uteri consists of a descent of the uterus into the vagina. 
 The uterus may be only slightly lowered or it may project at the vulva. 
 In complete prolapse we find a tumor projecting through the vulva, 
 partly covered by the distended vagina, and presenting the opening of 
 the OS externum near its centre. The bladder and rectum may be drawn 
 down with the vagina or may remain in place. The exposed cervix and 
 vagina usually become inflamed and sometimes ulcerated, or the mucous 
 membrane may become thickened. The lesion is frequently complicated 
 by hypertrophy of the cervix. 
 
 Gradual prolapse, which is most frequent, may be due to an increased 
 weight of the uterus, as in j^regnancy, inflammatory enlargement, the 
 presence of tumors, etc.; or to some abnormal condition of the uterine 
 supports. It is frequently caused by a vaginal cystocele or rectocele. 
 Sudden prolapse is most apt to occur in an enlarged uterus or one unduly 
 heavy by reason of tumors connected with it. It is most common in sub- 
 volution after parturition. 
 
 Elevation of the uterus is produced by mechanical causes crowding or 
 dragging it upward, as adhesions, tumors, etc. The vagina is drawn up 
 and lengthened, and the vaginal portion of the cervix may be oblit- 
 erated. 
 
 Inversion of the uterus consists of an invagination of the fundus. 
 The fundus may be invaginated in the body; the fundus and body in the 
 cervix; or the entire organ in the vagina. It usually occurs when the 
 uterine walls are relaxed, and is very frequently due to traction on the 
 placenta during parturition. It may take place spontaneously after partu- 
 rition. It may be produced by intra-uterine tumors. The mucous 
 membrane of the inverted organ is frequently inflamed, particularly 
 when the inversion is complete. 
 
 EernicB of the uterus are rare. Ventral Jiernim may occur during 
 the latter months of pregnancy; the peritoneum, aponeuroses, and skin 
 
414 THE OEGANS OF GENEEATION. 
 
 being forced outward to form a sac in which the uterus lies. Crural 
 hernice are produced by the drawing down of the uterus and ovaries into 
 the sac of an intestinal hernise. Inguinal hernia may be produced in 
 the same way or be congenital. Ischiadic hernia has been seen. Preg- 
 nancy may occur in the uterus while situated in a crural or inguinal 
 hernia. 
 
 EUPTURB AND PERFORATION. 
 
 Rupture of the unimpregnated uterus is rare. It may, however, 
 occur when the uterine cavity is distended with blood or serum, or in 
 connection with large myomata of the uterine walls. 
 
 In the gravid uterus, ruptures have been seen in nearly every mouth 
 of pregnancy, but most frequently toward the end. The rupture may be 
 produced by thinning of the uterine wall by tumors, or by violent con- 
 tusions. 
 
 The act of parturition is the most frequent cause. Malpositions of 
 the foetus, narrowing of the pelvis, protracted labor, thinning of the 
 uterine wall from tumors, forcible use of the forceps and other instru- 
 ments are the ordinary causes. The rupture may be in the body of the 
 uterus or the cervix; it may be large or small; it may extend completely 
 or only partly through the uterine wall. The consequences of partial 
 rupture are hemorrhage, gangrenous inflammation of the edges of the 
 rupture, peritonitis, and usually death. In rare cases, the rupture cica- 
 trizes, and the patient recovers. Complete rupture usually causes death 
 in a short time. The foetus escapes partly or completely into the abdo- 
 minal cavity. If the patient survives the immediate shock, fatal peri- 
 tonitis soon ensues. In rare cases, the foetus is shut in by adhesions, and 
 the patient survives. 
 
 Perforations of the uterus may be produced by carcinoma, by abscesses 
 in its neighborhood, and by ovarian cysts. 
 
 htpertBmia, uterine and peri-uterine hemorrhage. 
 
 Jlyperceviia. — Aside from the active menstrual hypersemia, the uterus 
 may be hyperffimic in acute and chronic inflammation, as a result of dis- 
 placement of the organ, and in certain forms of heart disease. The organ 
 is usually enlarged, the mucous membrane swollen, and the veins more 
 or less evidently dilated. 
 
 Hemorrhage. — EfEusion of blood into the cavity of the uterus occurs 
 normally at the menstrual periods. For the abnormalities to which this 
 function is subject we refer to works on gynaecology. Effusions of blood 
 at other than the menstrual periods may be caused by mechanical hyper- 
 semia, by hemorrhoids, by acute hyperajmia, by intra-uterine polypi and 
 other tumors, by acute and chronic inflammation, by typhus fever, scurvy, 
 etc., by ulcerating carcinoma, by abortions and miscarriages. 
 
THE OEGANS OF GENERATION. 415 
 
 A peculiar form of hemorrhage is the polypoid haematoma, or fibrin- 
 ous polypus of the uterus. lb occurs after parturition and after abor- 
 tions. The portion of the uterine wall where the placenta was attached, 
 with or without a portion of retained placenta, forms the point of attach- 
 ment of the pedicle of the polypus. "We find a large, polypoid, bloody 
 mass, firmly attached by a pedicle to tiie uterine wall. The uterus 
 enlarges with the growth of the polypus; the cervix is dilated, and the 
 thrombus projects into and may even fill up the vagina. The formation 
 of such a thrombus is accompanied by repeated hemorrhages. 
 
 Hemorrhage in the substance of the uterus occurs in old age. The 
 mucous membrane and uterine wall are infiltrated with blood, and there 
 is some blood in the uterine cavity. 
 
 Peri-uterine or Retro- Uterine Hcematocele consists in an accumula- 
 tion of blood around the uterus or in. Douglas' cul de-sac. It may con- 
 sist of blood extravasated into the abdominal cavity, which settles into 
 the pelvis; or, in consequence of local hypersemia, there may be repeated 
 extravasations of blood. In the latter case, the local peritonitis may 
 produce false membranes, between the layers of which hemorhages take 
 place. A similar condition rarely occurs in the male. The hemorrhagic 
 mass may become encapsulated, or may soften or suppurate, and perfo- 
 rate into the rectum or vagina, or may be absorbed. A form of extra- 
 peritoneal hematocele is described in which the blood lies between the 
 folds of the broad ligament. The extravasation may proceed from hem- 
 orrhage of any of the abdominal viscera or rupture of aneurisms; from vas- 
 cular new-formed, false membranes; from rupture of the varicose 
 veins of the broad ligaments; from rupture of hemorrhagic cysts of the 
 ovaries; from the Fallopian tubes in tubal pregnancy, or in hemato- 
 metra, or from general causes, such as scurvy, purpura, etc. In some 
 cases the extravasation begins at a menstrual period, and increases at the 
 succeeding periods. 
 
 Ante-uterine luematocele is of occasional occurrence, either in connec- 
 tion with the retro-uterine form, or when the posterior cul-de-sac is ob- 
 literated. 
 
 INFLAMMATION. 
 1. OF THE UNIMPEEGNATED UTERUS. 
 
 Acute Catarrhal Endometritis. — In this disease, which in its lighter 
 grades may leave but little alteration after death, the mucous membrane 
 is swollen, hyperaemic, and sometimes the seat of punctate hemorrhages. 
 The epithelium may desquamate, and the mucosa contain an undue 
 quantity of small S23heroidal cells. The surface is more or less thickly 
 covered with muco-puruleut exudation. In severe cases, shreds of mu- 
 cous membrane may be exfoliated. The lesion is usually most marked 
 
il6 THE OEGANS OF GENEEATION. 
 
 in the mucous membrane of the body, but may also afEect the cervix, or 
 the cervix alone. The body of the uterus may be swollen and hyperse- 
 niic. Acute catarrhal inflammation may be due to injury, exposure dur- 
 ing menstruation, the gonorrhoeal infection; or it may accompany acute 
 infectious diseases. 
 
 Chronic Catarrhal Endometritis. — This may be a continuation of an 
 acute inflammation, or begin as a chronic disease. In some of the lesser 
 degrees of inflammation, we find but slight changes after death. The 
 •mucous membrane, on the other hand, may be swollen, hypersemic, and 
 covered with muco-purnlent exudation. In other cases, there is more 
 or less well-marked thickening of the mucous membrane, which may 
 present a smooth or a rough papillary surface. Owing to the decompo- 
 sition of extravasated blood in the mucous membrane, the latter may be 
 mottled with brown or black. The glandular elements of the mucosa 
 may be partially or almost entirely destroyed. The papillae of the cervix 
 may be hypertrophied, the mucous follicles swollen, and their outlets ob- 
 structed, leading to the formation of the so-called ovula Nabothi. The 
 uterine wall becomes flaccid and atrophied, or it may be hypertrophied, 
 especially in the cervical portion. Ulceration of the mucous membrane, 
 especially of the cervix, may occur. Contraction or obliteration of the 
 cervical canal may occur. The inflammation may extend to the Eallo- 
 pian tubes, or to the vagina. 
 
 Chronic endometritis may exist at any age, but is most common after 
 puberty, and is produced by a great variety of causes. It may occur in 
 ill-nourished persons, or in those sufl;ering from exhausting diseases. It 
 may be due to displacements and tumors of the uterus, subinvolution, 
 injuries, etc. 
 
 Croupous Endometritis. — This form of inflammation is not very com- 
 mon. It occasionally occurs in the puerperal uterus, in acute infectious 
 diseases, cholera, typhoid fever, the exanthemata, etc. The disease 
 sometimes involves the vagina and Fallopian tubes. It may co-exist with 
 croupous inflammation of the colon. 
 
 Tubercular Endometritis. — This usually occurs as part of a tubercular 
 inflammation of the genito-urinary tract. We find a part or the whole of 
 the cavity of the uterus lined with a rough yellowish or gray cheesy mass, 
 which may deeply involve the muscular walls of the organ. At the edges 
 of the ulcerating cheesy areas we may find well-defined miliary tubercles, 
 or we may find tubercles scattered through the otherwise intact mucosa. 
 The lesions resemble those of nephro-phthisis. 
 
 Syjphilitic endometritis. — The results of this infection are usually con- 
 fined to the cervical jDortion, and consist of shallow or deej) ulcerations 
 and condylomata of the mucous membrane; or there may be a diffuse 
 thickening of the mucosa. 
 
 Acute metritis is usually the result of acute catarrhal endometritis. The 
 
THE ORGANS OF GENEEATION. 417 
 
 organ is swollen, succulent, congested; the mucous membrane covered 
 with muco-pus; the peritoneal coat congested. There may be small ex- 
 travasations of blood in the wall or cavity of the uterus. The inflamma- 
 tion, in rare cases, becomes suppurative, and abscesses are formed in the 
 uterine wall. These may perforate into the peritoneal cavity or into the 
 rectum. 
 
 Chronic metritis is the result of an acute metritis, or accompanies 
 acute or chronic endometritis, and is dependent upon the same conditions : 
 subinvolution, displacements, tumors, active irritants, etc. The uterus 
 is enlarged, the wall congested, thickened, and soft; or, owing to the 
 new-formation of connective tissue, hard and dense. The lesion may be 
 most marked in the body or in the cervical portion. 
 
 Perimetritis. — The peritoneal coat of the uterus may be inflamed 
 with the production of membranous adhesions or of pus. The adhesions 
 may be small or very extensive, and owing to their contractions may 
 cause various distortions and displacements of the pelvic organs. The 
 inflammation is usually an accompaniment of chronic metritis and endo- 
 metritis. In prostitutes such adhesions are of very common occurrence. 
 
 Parametritis. — The connective tissue about the uterus, between that 
 organ and the reflexions of the peritoneum, may be the seat of suppura- 
 tive inflammation. It most frequently causes the death of the patient, 
 but may result in the formation of dense connective tissue about the 
 uterus. 
 
 II. OF THE PREGNANT UTERUS. 
 
 The same forms of inflammation which have just been described may 
 attack the pregnant uterus. Catarrhal endometritis may produce eifu- 
 sion of serum, extravasations of blood, and abortions. Metritis may 
 lead to softening of the uterine wall, so that ruptures take place during 
 labor. Perimetritis and parametritis produce adhesions and abscesses 
 about the uterus. 
 
 PUERPERAL INFLAMMATION. 
 
 For a week or more after delivery, we flnd the inner surface of tne 
 still dilated uterus rough, especially at the insertion of the placenta, and 
 covered with blackened, gangrenous-looking shreds of blood, mucous 
 membrane, and placenta. This condition is not to be mistaken for in- 
 flammation. 
 
 As a result of some injury to the uterus during or after delivery, or of 
 the action of some infectious material which may gain access to the tis- 
 sues, the puerperal uterus is liable to become the seat of a series of severe 
 and often destructive inflammatory and necrotic changes. These may 
 be confined to the uterus; they may induce serious alterations in sur- 
 rounding parts; they may lead to an involvement of the peritoneum, or 
 27 
 
418 THE ORGANS OF GENEEiTION. 
 
 to pyaemia and its accompanying lesions in the most distant parts of the 
 body. In one series of cases a more or less extensive gangrenous inflam- 
 mation of the mucous membrane and the underlying parts may lead to 
 the casting off of larger and small shreds of necrotic tissue, and the for- 
 mation of deep and spreading ulcers, which may be accompanied by 
 severe parametritis and fatal peritonitis. This condition may be due to 
 injury or to the presence of decomposing portions of retained placenta. 
 In other cases the inflammation has a croupous character which may af- 
 fect the vagina and lead to necrosis and -gangrene, ulceration, and peri- 
 tonitis. In connection with either of the above forms of inflammation, 
 or without them, there may be thrombosis of the uterine sinuses, purulent 
 inflammation of the veins, suppuration and abscess in the uterine wall, 
 and, owing to the generalization of the infectious material, to metastatic 
 abscesses in the lungs, spleen, kidneys, etc. Or, acute pleurisy, ulcerative 
 endocarditis, purulent inflammation of the joints, hyperplastic swelling 
 of the spleen and lymph-glands, may furnish characteristic features of 
 the presence of an acute infectious disease. In some cases which rapidly 
 pass to a fatal termination, the local lesions may be but slightly marked, 
 and general alterations characteristic of pyaemia, such as metastatic ab- 
 scesses, etc., be entirely wanting. 
 
 Bacteria, in the form of micrococci, are very constantly present in the 
 exudation, in the lymph-vessels and inflamed tissue of the uterus; often 
 in enormous quantities in the peritoneal exudation and in the metastatic 
 inflammatory foci. There is a good reason for believing, although it has 
 not yet been absolutely proven, that the destructive local processes are due 
 to the presence and action of micrococci, and that the general infection 
 in this, as in other forms of septicsmia and pyaemia, is dependent upon 
 the same cause (see Septicsemia). 
 
 ULCERATION" AND DEGENERATION. 
 
 Catarrhal, tuhercular, and sy2]liilitic ulceration have been mentioned 
 above. 
 
 Phageclmnic or corroding ulcer. — This rare form of ulceration 
 usually occurs in old age without assignable cause. It begins in the cer- 
 vix and gradually extends until it may destroy the greater part of the 
 uterus or even invade the bladder and rectum. The ulcer is of irregular 
 form, its base is rough and blackish, its walls indurated. It should not 
 be confounded with carcinomatous ulcer which it considerably resem- 
 bles. 
 
 Fatty Degeneration. — This may occur in connection with inflam- 
 matory changes; in acute infectious diseases, and in phosphorus poison- 
 ing. 
 
 Amyloid Degeneration in the uterus is of rare occurrence. It may 
 affect the muscle-fibres or the walls of the blood-vessels. 
 
THE 0EGAN8 OF GENERATION. 419 
 
 TUMORS. 
 
 Fibromata. — Dense nodular fibromata of the uterus are exceedingly 
 rare, the so-called fibromata being in most cases niyomata or fibro- 
 myomata. Fibroma papillare, on the other hand, is a common form of 
 growth from the mucous membrane. It consists of a more or less 
 Tascular connective-tissue stroma covered with epithelium. The surface 
 may be smooth or villous. It may contain very numerous gland-folli- 
 cles, and then approaches the type of adenoma or even carcinoma. The 
 stroma may be loose and succulent and resemble mucous tissue, forming 
 the so-called mucous polypi; and these again may contain glandular 
 structures. In any of these forms the blood-vessels may be abundant 
 and dilated, forming telangiectatic or cavernous polypi. The adenomat- 
 ous polypi may become cystic from the dilatation of the gland-follicles. 
 
 Polypi of the uterus may be multiple or single, small or large. 
 Numerous smaller and larger papillary outgrowths from the mucous 
 membrane may occur in chronic endometritis. Single polypi may grow 
 from the mucosa of the body of the uterus or from the cervix, and hang 
 by a long pedicle down into the vagina. 
 
 Syphilitic papillary growths in the form of pointed condylomata may 
 form finely papillary wart-like excrescences of variable size, particularly 
 on the cervix. 
 
 Myomata. — These tumors, whose characteristic structural elements 
 are smooth muscle-cells, are the most common of uterine tumors and 
 are frequently of no special practical importance, but are sometimes 
 of very serious import. They are especially common in negroes. 
 They are most frequently composed of both muscular and fibrous 
 tissue — fibro-myomata — but the relative amount of the two kinds of 
 tissue is subject to great variation. They are most apt to occur 
 after puberty and usually in advanced life. They may be single 
 or multiple, small or of enormous size; are usually sharply circum- 
 scribed, whitish or pink, dense and hard, or sometimes soft, and present 
 on section interlacing bands or irregular masses of glistening tissue. 
 Their favorite situation is in connection with the body of the uterus, but 
 they may occur in the cervix, or in the folds of the broad ligaments. Ac- 
 cording to their position, we may distinguish subserous, submucous, and 
 intraparietal forms. The subserous myomata grow from the outer 
 muscular layers of the uterus in the form of little nodules. As they 
 increase in size they may become separated from th'e uterine wall and 
 remain attached only by a narrow pedicle or by a little connective tissue. 
 They may work their way between the folds of the broad ligament 
 until they are at some distance from their point of origin. Some 
 authors mention cases in which the tumors became entirely detached 
 from the uterus and were free in the abdominal cavity. In some cases. 
 
420 THE ORGANS OF GENERATION. 
 
 the tumors excite inflammation of the adjacent peritoneum, leading to 
 the formation of adhesions or of collections of pus. Oases are recorded 
 in which, owing to the atrophy of the pedicle, subserous myomata have 
 become completely detached from the uterus and were held in place and 
 nourished by peritoneal adhesions. In other cases, the tumor i-eaches a 
 large size, but remains firmly attached to the uterus. This organ may 
 then be drawn upward, the cervix and vagina being elongated and nar- 
 rowed. The traction may be so great that the body of the uterus is entirely 
 separated from the cervix. The bladder may also be drawn upward, 
 producing incontinence of urine and cystitis. Subserous myomata are 
 very often multiple and frequently attain great size. 
 
 The submucous myomata grow from the inner muscular layers of the 
 uterine wall. They commence as rounded nodules which lift up the 
 mucous membrane. Their usual position is the fundus uteri. They 
 rarely occur in the cervix. As the tumors increase in size, they project 
 into the uterine cavity. They then remain continuous with the uterine 
 wall over a large area, or are attached by a large or small pedicle. They 
 are usually well supplied with vessels. The uterus dilates with the 
 growth of the tumor, arid its walls may be also thickened. The tumor 
 may reach such a size as to entirely fill the cavity of the dilated uterus 
 and project through the cervix into the vagina. 
 
 The submucous myomata are usually single, although there may be 
 at the same time subserous and iutraparietal tumors. They are fre- 
 quently soft. If they are of large size and polypoid in form, they may 
 project through the cervix, and drag down the fundus of the uterus, pro- 
 ducing inversion. The mucous membrane covering them may be atro- 
 phied or hyperaemic, with dilated blood-vessels, and may thus give 
 rise to severe and repeated hemorrhages. Hemorrhage may occur in the 
 substance of these tumors. Inflammation, suppuration, and gangrene 
 may also occur. The surface may be ulcerated. In some cases the pedi- 
 cle of the tumor is destroyed, and it is spontaneously expelled. 
 
 The intraparietal myomata grow in the substance of the uterine 
 wall, but, if they attain a large size, project beneath the serous or the 
 mucous coat. They are found i)i every part of the uterus, but are most 
 frequent in the posterior wall. 
 
 The shape of the uterus is altered in a great variety of ways by the pres- 
 ence of these tumors; its cavity is narrowed, dilated, or misshapen; it 
 undergoes flexion and version in every direction. The tumors may sink 
 downwards, and become attached to the posterior wall of the vagina, 
 looking as if they grew from it. They may, without the formation of a 
 pedicle, project into the cavity of the uterus, fill it up, and project 
 through the cervix. The uterus is dilated, its wall hypertrojphied or 
 atrophied. 
 
 The tumors themselves may undergo a variety of secondary altera- 
 
THE OEGAHS OF GENERATION. 421 
 
 tions. The muscle-fibres may undergo fatty degeneration, and the 
 tumor diminish in size, or even undergo, it is said, entire destruction 
 and atrophy. Calcification may occur, converting a part or the whole 
 of the tumor into a stony mass. The intraparietal and submucous 
 myomata may give rise to profuse hemorrhages; they may suppurate, 
 and become gangrenous. 
 
 Sometimes the tumors or circumscribed portions of them are very 
 vascular, Gonstituting the telangiectatic or cavernotis variety. These 
 tumors, which possess some of the characters of erectile tissue, may sud- 
 denly change in size from a variation in the amount of blood which they 
 contain. 
 
 A very important change, which is sometimes found in these tumors, 
 is the development of cysts in their interior (fibro-cystic tumors). This 
 sometimes takes place in those tumors which grow outward beneath the 
 peritoneal coat. "We find one or more cavities communicating with each 
 other, with rough, trabeculated walls. The appearance is more that of 
 cavities than of cysts. There may be a number of smaller cavities, or 
 they may fuse to form one large one. The fluid contained in the cavi- 
 ties is like synovia, or is mixed with blood. These cystic myomata may 
 reach an immense size, and fill the abdominal cavity. The diagnosis 
 between them and ovarian cysts is very difficult, and they have fre- 
 quently been the subjects of fatal operations. 
 
 In the cervix uteri, myomata are rare. They may grow as polypi 
 beneath the mucous coat, or produce enlargement of the anterior or pos- 
 terior lips, or may grow outward into the abdominal cavity. 
 
 Combinations of myoma and sarcoma sometimes occur — myosarcoma. 
 
 Sarcoma may occur as a primary tumor in the mucous membrane of 
 the uterus, either in the form of a diffuse infiltration or as a circumscribed 
 nodular or polypoid mass. They frequently involve the muscular wall, 
 are liable to hemorrhage and gangrene, aud>, particularly in the diffuse 
 form, are liable to recur after removal. They may consist largely of 
 spindle or spheroidal cells or both. It is said that sarcoma of the 
 uterus is more liable to occur at an advanced age than at an early period, 
 as is the rule with sarcomata of other organs. 
 
 Angioma. — A small, cavernous angioma of the wall of the uterus has 
 been described. 
 
 Carcinoma.— The carcinomata of the uterus commence most fre- 
 quently in the cervix and portio vaginalis, and the most common form is 
 the epithelioma. The growth of epitheliomata of the cervix uteri pro- 
 ceeds under three tolerably distinct forms, which, however, frequently 
 merge into one another. 
 
 (1^ The flat ulcerating epithelioma.— This form of cancer commences 
 as a somewhat elevated, flat induration of the superficial layers of the 
 cervix, sometimes circumscribed, sometimes diffuse. This induration is 
 
422 THE OEGANS OF GENEEATIOJST. 
 
 due to the growth of plugs and Irregular masses of epithelial cells into the 
 nnderlying tissue. Ulceration usually commences early, and may pro- 
 ceed slowly or rapidly. The edges of the ulcer are irregular, indurated, 
 and somewhat elevated. The ulceration of the new-formed cancerous 
 tissue at the edges is usually progressive, so that the vaginal portion of 
 the cervix, the cervical canal, the vagina, and even the bladder and rec- 
 tum may be involved. More or less extensive hemorrhages and necrosis 
 of the base of the ulcer are liable to occur. The entire cervix may be 
 destroyed. 
 
 (2) In another class of cases, the carcinomatous growth develops 
 under the form of papillary or fungous excrescences, which may form 
 larger or smaller masses composed of epitheliomatous tissue. Hand in 
 hand with this projecting growth, there may occur an epithelial infiltra- 
 tion of the underlying tissue of the cervix. These growths are often 
 quite vascular, and may give rise to severe hemorrhages. They may 
 ulcerate, and thus produce great destruction of tissue. 
 
 (3) In still another class of cases, there is a more or less deep infil- 
 tration of the submucous tissue, either diffuse or in circumscribed 
 nodules, with epithelial cell masses. We find at first, in the vaginal 
 portion of the cervix, in the submucous connective tissue, either nodules, 
 or a genera] infiltration of a whitish new growth. The cervix then 
 appears large and hard. Very soon the mucous membrane over the new 
 growth degenerates and falls ofl; the superficial layers of the new growth 
 undergo the same changes. After this, the formation of the new growth 
 and its ulceration go on simultaneously, producing first an infiltration and 
 then destruction of the cervix, and often of a part of the body of the 
 uterus. The growth frequently extends to the vagina, the bladder, and 
 rectum with the same destructive character, so that we often find the 
 cervix and upper part of the vagina destroyed, and in their place a large 
 cavity with ragged, gangrenous, cancerous walls. Less frequently the 
 pelvic bones are invaded in the same way. Not infrequently the ureters 
 are suri'ounded and compressed by the new growth, so that tliey become 
 dilated. The dilatation may extend to the pelves and calyces of the kid- 
 neys. The new growth may begin in the cervix, and extend uniformly 
 over the internal surface of the cervix and of the body of the uterus. 
 The entire uterus is converted into a large sac, of which the walls arc 
 infiltrated with the new growth, while the internal surface is ulcerating 
 and gangrenous. In some cases there is a considerable formation of 
 new, dense connective tissue, so that tlie growth has a scirrhous form. 
 
 In rare cases, the growth begins in the upper part of the cervix or in 
 the body of the uterus, while the lower part of the cervix is not involved. 
 In all of these cases the epithelial cells of the new growth follow more or 
 less closely the type of the epithelial cells of the part from which they 
 spring. 
 
THE OEGANS OF GENERATION. 423 
 
 In still another class of cases, in which the new growth may be in the 
 form of nodules or diffuse infiltrations, or polypoid masses, or may pre- 
 sent more or less extensive alterations, the cells are irregular, polyhedral 
 in shape, the tumor belonging to the class of glandular or medullary 
 <;arcinomata. These also usually commence in the cervix and, according 
 to the views of many writers, probably in the mucous glands. 
 
 In rare cases the entire wall of the uterus is inliltrated with the new 
 growth, and the organ is much enlarged. Colloid carcinoma sometimes 
 occurs, but is rare. 
 
 While we may for convenience recognize the above types of carcinoma 
 of the uterus, it should be borne in mind, as above stated, that they are 
 not apt to be perfectly distinct, and some of them may merge- into one 
 another, or exist simultaneously. 
 
 As a result of the ulceration of these various forms of carcinoma, recto- 
 vaginal fistulse may be formed; the lumbar glands may be involved, and 
 metastases in distant organs are occasionally, though not frequently 
 formed. Frequent and profuse hemorrhages, gangrenous destruction of 
 tissue, the absorption of deleterious materials, etc., are apt to lead to 
 the development of a more or less profound anaemia and cachexia. 
 
 PARASITES AND CYSTS. 
 
 Various forms of lacteria are of frequent occurrence. EccMnococciis 
 has been found in the body and neck of the uterus, and may rupture into 
 the peritoneal cavity or into the vagina. 
 
 Cysts. — Aside from the cysts which develop in tumors of the uterus, 
 in the cervix uteri the mucous follicles are frequently so dilated as to 
 form cysts filled with a gelatinous material, and more or less epithelium. 
 These cysts may be large or small, and are frequently called ov^da Nalo- 
 ■tlii. Sometimes there is an inflammatory growth of new connective 
 tissue about these cysts. In other cases the cysts may project from the 
 mucous membrane in the form of polypi. Similar changes are infre- 
 ■quently found in the body of the uterus from the dilatation of occluded 
 uterine glands. Dermoid cysts are rarely found in the walls of the 
 uterus. 
 
 THE OVARIES. 
 
 MALFOEltATIONS. 
 
 One or both ovaries may be absent, the other organs of generation 
 being also absent or undeveloped. Or the ovaries may be only partially 
 •developed. Absence or arrest of development of one ovary is sometimes 
 met with in otherwise well-formed individuals. It is sometimes accom- 
 panied by a low position of the kidney on the same side. The ovaries 
 may pass into the inguinal canal or into the labia majora, and remam 
 
424 THE OEGAUS OF GENERATION. 
 
 fixed there through life. Less frequently they are found in the crural 
 canal or the foramen ovale. 
 
 CHANGES IN" SIZE. 
 
 The ovaries may become larger than normal by chronic inflammation, 
 by the formation of cysts and tumors. They may become atrophied in 
 old age, the Graafian follicles disappearing, and the organ shrivelling into 
 a small irregular fibrous body. Atroj^hy may be produced by ascites, by 
 chronic inflammation, or from unknown causes. As the result of the 
 maturing and rupture of the G-raafian follicles with and without preg- 
 nancy, the surface of the ovary which before puberty is smooth may be- 
 come roughened by irregular cicatricial depressions. 
 
 CHANGES IN POSITION. 
 
 In adult life, the ovaries may pass as hernise into the inguinal or cru- 
 ral canal, the foramen ovale, or the umbilicus. 
 
 The position of the ovaries in the abdomen may be changed by the 
 pressure of tumors, the traction of false membranes, etc. It may occur 
 in enlarged ovaries or in those of normal size, and by the compression of 
 the veins may lead to congestion and chronic inflammation of the organ. 
 
 HYPEEiEMIA AND HEMOKRHAGE. 
 
 Aside from the normal hyperemia of the ovaries during menstruation, 
 the vessels may be congested in inflammation, in displacements with inter- 
 ference with the venous circulation, in certain diseases of the heart, etc., 
 and may then be followed by chronic inflammation. 
 
 The menstrual periods are accompanied by the effusion of blood into 
 a Graafian follicle. Normally, the amount of blood is small, becomes 
 solid, is decolorized, and then gradually absorbed. Sometimes the effu- 
 sion of blood is much greater; the follicle filled with blood is as large as. 
 a pigeon's egg. The blood may remain in the follicle and be absorbed, 
 and replaced by a serous fluid, or it may rupture it and escape into the 
 peritoneal cavity. Death may ensue from the hemorrhage, or the blood 
 may collect in Douglas' cul-de-sac, and be inclosed in false membranes. 
 Hemorrhages also occur in follicles which have become cystic. 
 
 INFLAMMATION (OOPHORITIS). 
 
 Inflammation of the ovaries occurs most frequently in the puerperal 
 condition, either as part of a general peritonitis, or as a primary affection. 
 
 With puerperal peritonitis, both ovaries are usually inflamed ; they 
 are swollen, congested, soft, infiltrated with serum or pus, or gangrenous. 
 The inflammation may attack principally the capsule, the stroma, or the 
 follicles. Inflammation of the capsule results in adhesions and collec- 
 tions of pus, shut in by false membranes; of the stroma, in abscesses and 
 
THE ORGANS OF GENEEATION. 425 
 
 fibrous induration ; of the follicles, in their containing purulent serum. 
 If the inflammation of the ovary is the primary lesion, it is usually con- 
 fined to one organ. The stroma of the ovary is infiltrated with serum 
 and pus, and may contain abscesses of large size. In other cases the 
 ovary itself is but little changed, but is surrounded by a mass of fibrinous 
 and purulent exudation. Such idiopathic forms of inflammation may 
 terminate in recovery; or the abscesses may perforate into the rectum 
 and vagina; or the ovary is left indurated and bound down by adhesions; 
 or the patient dies from the violence of the disease. 
 
 Inflammation of the ovaries unconnected with the puerperal condi- 
 tion is not common, but it may occur in connection with acute or chronic 
 peritonitis or perimetritis. It is usually confined to one ovary. Either 
 the follicles, stroma, or capsule, or all together, may be involved. The 
 inflamed follicles are enlarged, their walls thickened ; they may contain 
 bloody or purulent fluid. The stroma becomes infiltrated with serum or 
 pus; and later we may find abscesses or fibrous induration of the organ. 
 The inflammation of the capsule may lead to the formation of membra- 
 nous adhesions between the ovary, Fallopian tube, and surrounding 
 parts. 
 
 As a result of chronic interstitial oophoritis the organ may be increased 
 in size, owing to the formation of loose cellular, or dense firm connective 
 tissue, with many blood-vessels; or it maybe small, dense, and atrophied. 
 
 Tubercular Infiammation of the ovaries is rare, and may accompany 
 tubercular inflammation of other organs, particularly the peritoneum and 
 Fallopian tubes. It usually results in the production of cheesy nodules 
 of considerable size. 
 
 Syphilitic Inflammation in the form of gummata is uncommon. 
 
 TUMORS. 
 
 Filromata. — These tumors are not very common, nor usually of great 
 importance. They may be very small or of great size. They are usually 
 dense in texture, and in a considerable number of cases seem to originate 
 in the tissue formed in the closure of the ruptured Graafian follicle. 
 They may contain cysts or be accompanied by cysts of the surrounding 
 stroma. Papillary fibromata of the surface of the ovary is sometimes 
 seen. 
 
 Leiomyomata containing more or less fibrous tissue are of occasional 
 
 occurence. 
 
 Sarcoma of the ovaries is 'not common. It is usually primary, but 
 may be metastatic. It is usually of the spindle-celled variety, but may 
 contain areas of spheroidal-celled tissue or more or less fibrous tissue. 
 The tumors may be hard or soft, and are apt to involve both ovaries. 
 
 Chondroma of the ovaries is described, but is rare; cartilage not in- 
 frequently occurs, however, in dermoid cysts. 
 
426 
 
 THE ORGANS OF GENEEATION". 
 
 Carcinoma, "usually of the* glandular variety, may occur as a primary 
 tumor of the ovary. It may be due to a continuous infection from 
 neighboring organs, or more rarely it is of metastatic origin. Albhough 
 the glandular medullary carcinoniata are the most common, scirrhous, 
 melanotic and colloid cancer sometimes occur. Some forms of carcinoma 
 stand in very close relation with certain of the cystic adenomata — see be- 
 low. 
 
 Adenomata. — {Cystic Adenomata — Compound Ovarian Cysts. — These 
 growths, which may occur in one or both ovaries, form one of the most 
 common and important classes of ovarian tumors. Some of their most 
 noteworthy and important features depend upon their tendency to the 
 formation of cysts. It should be remembered, however, that the pri- 
 mary lesion is a true new-formation of glandular tissue, and not, as in 
 the case of most cysts, a transformation, by retention or otherwise, of pre- 
 existing structures. 
 
 The growth primarily consists of a fibrous stroma, in which are tubu- 
 lar follicles lined with cylindrical epithelium. Or, in some cases, it con- 
 sists of the above follicular or glandular structures associated with papil- 
 lary outgrowths from a fibrous stroma, which are covered with cylindri- 
 
 ^"3^ 
 
 'Z' 
 
 
 
 f^SBrm^ 
 
 
 
 
 Fig. 130.— Cystic Adekoma of Ovary (Papillary Form), X 330 and reduced. 
 
 cal epithelium. Sometimes one, sometimes the other, form of growth — 
 the glandular or the papillary — predominates (Fig. 130). There is, as above 
 stated, a marked tendency, particularly in the glandular form of adenoma, 
 to a, dilatation of the follicles by a semi-fluid material, and the formation 
 of cysts. There may be a number of follicles equally dilated, so as to form 
 a number of cysts of moderate size; or only a few follicles are enormously 
 
THE ORGANS OF GENEEATION. 427 
 
 dilated to form a large multilecular cyst, with but few compartmeats. 
 The walls of the cysts may fuse together, and bo absorbed so as to form 
 ■ one large cyst divided by incomplete septa— «?u7oc««Zffr cysts. The stroma 
 in which the follicles and cysts are embedded may be largely developed 
 or very scanty. 
 
 The walls of the larger cysts are composed of fibrous tissue which is 
 dense in the outer layers, more cellular in the inner, upon which the epi- 
 thelium is placed. They may may be thin and membranous; or we find 
 developed on their internal surfaces an intra-cystic growth composed of 
 a fibrous stroma and tubular follicles. These secondary follicles may also 
 be filled with fluid and form larger and smaller cysts. The intracystic 
 growths may be so large as to fill up the original cysts. Sometimes the 
 intra-cystic growth presents very little dilatation of its follicles, so that 
 the entire tumor has more the character of a solid growth than of a 
 cyst. 
 
 In many of the cysts in which the formation of follicles and their di- 
 latation is well shown, the growth of the papillomatoas projections is 
 also seen, so that the cyst cavity may be more or less filled with cauli- 
 flower-like tufts. 
 
 The cylindrical epithelium lining the cysts, usually forms a single 
 layer, but, owing to the accumulation of fluid, the cells may become flat- 
 tened and atrophied, or they may be fatty or desquamated. The con- 
 tents of the cysts differ considerably in different cases, and even in dif- 
 ferent cysts in the same case. It may be tough and ropy, or gelatinous, 
 or seroas; transparent and colorless, or yellow or reddish, or reddish- 
 brown; or it may be turbid and colorless, or variously colored, red, brown 
 or chocolate. 
 
 Chemically the cyst contents, when thick and ropy, contain mucin or 
 paralbumin, and perhaps other less well-known compounds belonging to 
 the same class. It is believed that the peculiar ropy character which 
 the fluid often possesses is due to the paralbumin, but the chemical na- 
 ture and relations of this substance are still matters of dispute. It is 
 probable that the contents of these cysts are, so far as the mucin and 
 paralbumin are concerned, pi'oduced by a metamorphosis of the proto- 
 plasm of the lining cells, similar to that by which the mucin is produced 
 in the mucous glands and in mucous membranes. We frequently find 
 the cylindrical cells presenting the form of the so-called "beaker cells," 
 and in some cases the mucous contents of the cysts are seen to be con- 
 tinuous with the similar contents of the beaker cells. It is probable that 
 much of the fluid contents of the cysts comes from simple transudation. 
 
 Microscopically the contents of these cysts present also considerable 
 variation. We may find almost no structural elements; or there may be 
 red blood-cells in variable quantity, and pus-cells in various stages of 
 granular or fatty degeneration or of disintegration, so that variously 
 
428 THE OBGANS OF GENERATION. 
 
 shaped fragments of the cells appear. Thea we may find cylindrical, or 
 flattened, or polyhedral cells, either well preserved, swollen, or in a state 
 of fatty degeneration (Fig. 131), or we may find fragments of these cells. It 
 is these various forms of cells, often more or less swollen and in acondition 
 of more or less well-marked granular and fatty degeneration, which have 
 been considered characteristic of the ovarian cysts and are sometimes 
 called Drysdale's corpuscles. While, however, they are of frequent occur- 
 rence under these conditions, they are by no means pathognomonic, since 
 we find them in the contents of various kinds of cysts and cavities where 
 the cells are undergoing degeneration. In addition to the above struc- 
 tural elements, we may find free fat droplets, cholestearin crystals, pig- 
 ment granules, and more or less granular detritus. The material filling 
 these cysts is sometimes called colloid, and the cysts are frequently called 
 colloid cysts; but we believe that the above view of their nature is the 
 correct one. 
 
 Fig. 131.— Cells from Ovarian Cyst in a Condition of Fatty Degeneration, X VOO and reduced. 
 
 Numerous secondary changes are liable to occur in these cysts. The 
 cells may become fatty, and peel off so that we may find in some parts 
 only a connective-tissue wall. The walls may atrophy, may become in- 
 filtrated with salts of lime, or contain concentrically lamellated lime con- 
 cretions. Inflammatory changes may occur in them. There may be a 
 su|)purative inflammation of the walls leading to the formation of ab- 
 scesses, or pus may be mingled with the cyst contents; the epithelium 
 may be exfoliated, and granulation tissue may form in the walls. 
 Chronic inflammation may lead to considerable thickening of the walls, 
 and to adhesions with neighboring parts. Hemorrhages, sometimes very 
 extensive, may occur in inflammation, or as the result of other disturb- 
 ances of the circulation, so that some of the cysts may be filled with 
 blood. Inflammatory softening, gangrene, etc., of the walls, may lead to 
 perforation; so that the contents of the cysts may be discharged into the 
 peritoneal cavity, or, in virtue of adhesions, into the bladder, vagina, or 
 rectum. Perforation may be caused by the piercing of the walls by 
 the papillomatous growth. Carcinoma may be developed from the epi- 
 thelium of the cysts. Since these cysts sometimes reach a very large 
 size, they may ])roduce the greatest variety of disturbances in the ab- 
 dominal cavity, which need not be enumerated here. 
 
THE ORGANS OP GENEEATION. 429 
 
 They -probably originate in the glandular epithelium of the' ovary 
 either before or after the formation of the Graafian follicles.' 
 
 Follicular cysts of the ovary. — The Graafian follicles may be dilated 
 so as to form cysts. This may occur in one or both ovaries, and the 
 cysts may be small or large, single or multiple. They are usually found 
 after middle life, but may occur during youth, childhood, or even in 
 the foetus. The follicles dilate from the accumulation of fluid within 
 them; the ovum is destroyed; the epithelium flattened. The contents 
 are usually serous and colorless, but may be viscid, turbid, purulent, or 
 variously colored, red, yellow, or brown. The ovary may be crowded 
 with numerous cysts of moderate size, whose adjacent walls may coalesce 
 and atrophy, forming communications between them. 
 
 A variety of this form of cyst is formed by the dilatation of a follicle 
 containing a corpus luteum. Such cysts may communicate with a Fal- 
 lopian tube. 
 
 Dermoid cysts.- — These cysts may be uni- or multilocular, are usually of 
 moderate size, but sometimes becomes as large as a man's head or larger- 
 Their fibrous walls may be thick or thin, and portions of the internal sur- 
 face may present more or less completely developed cuticular structures, 
 such as corium, papillse, epidermis, hairs, and hair-follicles, sebaceous 
 glands, etc. The cavity may contain a thick greasy material composed 
 of flattened epithelium, fat, or cholestearin crystals. Or, the cavity or 
 walls may contain masses of irregularly formed hair, teeth, bone, carti- 
 lage, striated muscle, and nerve-fibres and cells. Such growths, which 
 are doubtless of embryonal origin, may exist for many years without 
 ■causing inconvenience; but inflammatory changes may occur in them 
 leading to adhesions and perforations into adjacent organs. They may 
 form the nidus for the development of carcinoma, or they may calcify. 
 
 In addition to the above-described adenoid, dermoid, and simple 
 follicular cysts, there are a number of composite forms, of not infrequent 
 ■occurrence. Thus, in connection with dermoid cysts or separately, we 
 find larger and smaller cysts lined with ciliated epithelium. Then there 
 Are several cases described of cysts which partake of the characters of 
 both adenoid and dermoid cysts. Such cysts may be multilocular and 
 be lined with flattened, cylindrical, or ciliated epithelium, and may con- 
 tain epidermal cells, cholestearin, or mucin, etc." 
 
 Small cysts, sometimes pediculated, sometimes not, of doubtful origin 
 
 ' For more extended descriptions of the cyst-adenomata of the ovaries, see Wal- 
 deyer: " Die epithelialen Eierstocksgesoliwiilste,'' Archiv fiir Grynakologie, Bd. 
 I., Heft 3, p. 252-316, 1870. Also Klebs: " Handbuch der pathologischen Ana- 
 tomie," vierte Lieferung, p. 796, 1873. 
 
 * A tolerably full bibliography of the tumors of the ovaries may be found in 
 Lawson Tait's " Pathology and Treatment of Diseases of the Ovaries,'' 4th ed., 
 Wm. Wood & Co., p. 131. 
 
430 THE ORGANS OF GEN'EEATION. 
 
 and of no special significance, are frequently found growing from the 
 broad ligament near the ovary. Tlie walls are usually very thin, lined 
 with flattened epithelial cells; and the contents serous. 
 
 Cysts of the parovarium, lying between the peritoneal layers of the 
 broad ligament, are usually small, but may be as large as a man's head. 
 They are usually lined with ciliated epithelium, but sometimes by flat- 
 tened non-ciliated cells. The contents may be serous or may be thick, 
 and contain mucin and paralbumin. 
 
 THE FALLOPIAN TUBES. 
 ITALFOKMATIONS. 
 
 Absence of both tubes occurs with absence of the nterus. One tube 
 may be absent, with arrested development of the corresponding side of 
 the uterus. Both tubes may be imperfectly developed, either of their 
 ends may be closed, they may be inserted into the uterus at an abnormal 
 place, they may terminate in two or three abdominal ostia. 
 
 CHANGES IN POSITION AND SIZE. 
 
 The Fallopian tubes may participate in the various malpositions of the 
 uterus and ovaries; but they are most frequently displaced by the con- 
 traction of adhesions, formed in perimetritic and periovarial inflamma- 
 tions. 
 
 The lumen of the tube may be partially or completely closed as the 
 result of inflammation of the mucous membrane; of peritonitis about the 
 fimbriated extremity; of tumors or inflammation of the uterus; or by 
 pressure from without, as by adhesions, tumors, etc. It may become 
 stopped by plugs of mucus or pus. 
 
 Dilatation of the tubes may be produced by an accumulation of 
 catarrhal or other exudation, when there is partial or complete stenosis 
 at some portion of the tube. The dilatation may be moderate, convert- 
 ing the tube into a tortuous sacculated canal containing mucous or serous 
 fluid; or, more rarely, large cysts may form containing several pounds of 
 serous fluid — hydro-salpi7ix. As the fluid collects, the epithelium may be- 
 come flattened or fatty, or may desquamate. As a result of an inflamma- 
 tion iQ the walls of the dilated tube, the contents may be mixed with pus 
 or blood. Eupture of a dilated tube sometimes occurs; or severe and 
 even fatal hemorrhage may take place into its cavity. Papillary growths 
 are sometimes found springing from the inner wall of the cysts. 
 
 HEMORRHAGE. 
 
 Hemorrhage into the tube may occur in puerperal women with retro- 
 version of the nterus, with abortions; hematometra and tubal pregnancy; 
 in acute infectious diseases. The blood may undergo degenerative 
 
THE ORGANS OF GENERATION. 431 
 
 changes and be largely absorbed, or it may escape into the peritoneal 
 cavity and cause peritonitis. 
 
 INFLAMMATION (SALPINGITIS). 
 
 Catarrhal inflammation of the mucous membrane of the Fallopian 
 tubes commonly occurs in connection with endometritis, frequently in 
 the puerperal condition. In the acute stage, the mucous membrane is 
 hypersemic and swollen, and covered with a muco-purulent exudation. 
 The inflammation may subside, leaving no lesions, but it more frequently 
 becomes chronic and may then result in peritoneal adhesions, obliteration 
 of the tubes, and dilatation. 
 
 Suppurative Salpingitis. — The inflammation of the mucous mem- 
 brane may assume a suppurative character, particularly in connection 
 with puerperal metritis and peritonitis, but sometimes as a result of 
 gonorrhceal inflammation. 
 
 Under these conditions, the wall of the tube may be involved, and pus 
 may exude from the abdominal ends. It is difficult, in many cases of 
 suppurative salpingitis associated with peritonitis, to say which is the 
 primary lesion. 
 
 In some cases, there is a considerable collection of pus in the tubes, 
 causing dilatation — pyo-salpinx. These collections may rupture into the 
 peritoneal cavity, or the pus may escape into a cavity shut in by adhe- 
 sions, or may perforate into the intestine or bladder. Or it may dry, and 
 finally become calcified. 
 
 Tubercular Inflammation. — This form of inflammation in the tubes 
 is most frequently seen in its later stages, when the mucous membrane is 
 partially or entirely converted into a thick, cheesy, often ulcerating 
 layer. The lumen of the tubes may be dilated, the walls thickened from 
 chronic inflammation. This lesion may occur by itself, or may be associ- 
 ated with tubercular inflammation of the lungs, or of the other genito-uri- 
 nary organs, or the peritoneum. The lesion usually commences at the 
 abdominal ends of the tubes, and both tubes are apt to be involved. 
 
 Syphilitic Inflammation in the form of a diffuse thickening of the 
 wall by gummatous tissue has been described. 
 
 TUMOES. 
 
 Small flbromata and fihro-myomata sometimes occur in the wall of 
 the tubes or in the fimbrise. Small lipomata have been seen between 
 the folds of the broad ligament in close connection with the tubes. 
 
 Carcinoma of the tubes is usually, if not always, secondary to cancer 
 of the uterus or ovaries. 
 
 Cysts, usually of small size, sometimes pediculated and with thin 
 walls, are fi'equently seen in the peritoneal covering of the tubes or in the 
 fimbrise. They are believed to be of embryonal origin. 
 
432 THE OEGAJSrS OF GENEEATION". 
 
 EXTRA-UTERINE PREGNANCY. 
 
 Tuial Pregnancy. — The impregnated ovum is in some way hindered 
 from passing into the uterus, becomes fixed in the tube, and is there 
 develofied. The villi of the chorion grow into the mucous membrane of 
 the tube, forming an incomplete placenta, Eare cases are recorded in 
 which the placenta was situated in the uterus, while the foetus was devel- 
 oped in the tube. The embryo and its membranes are developed until 
 they reach such a size that the tube surrounding them ruptures. This 
 may occur in the first month or not until much later. In rare cases, 
 when the wall of the tube was extensively involved in the forma-tion of 
 the placenta, the development has gone on until term. The ovum may 
 remain in the tube after the rupture; or may escape into the peritoneal 
 cavity still enveloped in its membranes; or the membranes may be rup- 
 tured and left in the tube. The rnpture is generally attended with fatal 
 hemorrhage. In some cases, death is caused by the rupture of a dilated 
 vein, while the tube is still intact. Hemorrhage into the sac may occur 
 before its rupture. 
 
 In rare cases, death does not take place, and the fcBtus is shut in by 
 adhesions and false membranes. The embryo soon dies. In favorable 
 cases, there is a slow absorption of the soft parts of the foetus, the bones 
 are separated and left embedded in a mass of fibrous tissue, fat, choles- 
 tearin, and pigment. Or the foetus retains its shape and becomes mum- 
 mified, and may then be iucrusted with the salts of lime. 
 
 In unfavorable cases, degeneration and gangrene of the foetus take 
 place rapidly, with inflammation and suppuration of the surrounding 
 tissues. There may be perforation and escape of the broken-down foetus 
 through the rectum, vagina, bladder, or abdominal wall. The patient 
 may die from peritonitis or exhaustion, or may recover after the escape 
 of the foetus. 
 
 In some cases, the foetus may escape through a rupture of the tube 
 into the space between the folds of the broad ligament. 
 
 Tubo-Abdomi7ial Pregnancy is produced by the development of the 
 ovum in the fimbriated extremity of the Fallopian tube. Adhesions are 
 formed, so that the foetus is partly in the end of the tube and partly in 
 the abdomen. 
 
 Interstitial Pregnancy. — The ovum in these cases is arrested and 
 developed in the portion of the tube which passes through the wall of the 
 uterus. 
 
 Abdominal Pregnancy. — The ovum, after escaping from the ovary, 
 does not enter the Fallopian tube, but becomes fixed to the peritoneum, 
 usually at some part near the ovary. It is surrounded by thickened peri- 
 toneum and develops in that position. 
 
 Ovarian Pregnancy. — The existence of this form of pregnancy is 
 
THE ORGANS OF GENEEATION. 433 
 
 doubtful and difBcult to prove, but there are some cases in which it 
 seoms probable that the ovum develops in its Graafian follicle. The pla- 
 centa may be attached to the tube or to the abdominal. wall. 
 
 In all forms of extra-uterine pregnancy, the uterus becomes enlarged, 
 and a sort of decidua is formed on its internal surface. 
 
 LESIONS OB THE PLACENTA. 
 
 Aside from the variations from the normal in size, shape, and position, 
 for a description of which we refer to the works on obstetrics, we may 
 briefly mention here some of the more important structural changes which 
 the placenta may undergo. 
 
 Hemorrhage. — This may occur either on the maternal surface 
 in t^he decidua; or between the foetal surface and the membranes; 
 or in the substance of the placenta. The latter form of hemor- 
 rhage constitutes the true placental apoplexy. This may occur as the 
 result of rupture of a placental sinus. The placental tissue is crowded 
 apart, and a blood-clot, often infiltrating the parenchyma, is formed. This 
 may lead to abortion, or the blood may undergo disintegration and 
 absorption, and its place be occupied by a cicatrix. The placental tissue 
 in its vicinity may undergo fatty degeneration. Under other conditions, 
 without evidence of rupture of the vessels, the placental tissue may 
 become infiltrated with blood in the form of an infarction. In this, degen- 
 erative changes, similar to the above, may occur, leading to fibrous 
 induration of the placenta. 
 
 INFLAMMATION (PLACENTITIS). 
 
 Suppurative Inflammation of the placenta with the formation of 
 abscesses is of rare occurrence as the result of injury. 
 
 Chronic Indurative Inflammation of the placenta may result in the 
 formation of circumscribed masses of cellular and loose, or dense and 
 cicatricial connective tissue; or in a diffuse formation of connective tissue, 
 which may interfere with the nutrition of the foetus and cause abortion. 
 The new-formed connective tissue may undergo fatty degeneration or 
 calcification. 
 
 In another class of cases, the new connective tissue is formed mainly 
 in the walls of the vessels, particularly the arteries. This may occur in 
 circumscribed portions of the vessels, leading to nodular growths 
 around the arteries, or it may occur extensively along the various ramifi- 
 cations of the vessels, converting them into thick fibrous cords. The 
 change is primarily in the adventitia, but all the coats of the vessel may 
 become involved, leading to more or less complete obliteration of the 
 lumen. 
 
 Various proliferative and indurative changes in the placenta may 
 occur as the result of syphilitic infection. 
 28 
 
4:34 . THE OEGANS OF GENERATION. 
 
 DEGENERATIONS. 
 
 Patty and amyloid degeneration and calcification of the placental tis- 
 sue are of not infrequent occurrence. 
 
 Cysts of the placenta are of occasional occurrence, their origin is in 
 most cases obscure.' 
 
 MALE. 
 
 THE PENIS. 
 
 MALFORMATIONS. 
 
 Entire absence of the penis is met with in connection with great de- 
 fects of development of the rest of the body. 
 
 Absence of the penis with proper development of the other organs of 
 generation is rare. The urethra then usually opens into the rectum. 
 
 An abnormally small penis is found with absence or arrested develop- 
 ment of the testicles. 
 
 Absence or a rudimentary form of the prepuce has been observed in 
 a number of cases. Congenital phimosis is also not infrequent. 
 
 HyposojMclia consists in an arrest of development of the penis and 
 scrotum. In its highest degrees, the penis is one-half to one inch long, 
 the glans penis small and resembling a clitoris. On the lower side of 
 the penis is a deep cleft, lined with mucous membrane. Into this cleft 
 the urethra opens at the root of the penis. The scrotum remains sepa- 
 rated into two halves, resembling labia majora. The testes descend into 
 their proper position on each side, or remain in the abdomen. If the 
 testicles continue to develop normally, the individual has the appearance 
 and capacities of a man; if their develoiiment is arrested, the individual 
 is small and has a womanish appearance. 
 
 In lesser grades of the same malformation, the two halves of the scro- 
 tum are joined and the penis is larger, but a part of the urethra remains 
 open as a cleft, at any point of the jienis. 
 
 Epispadia is an opening of the urethra on the upper side of the penis. 
 It presents various gi-ades and forms. 
 
 Hermapliroditism. — This is a union of two sexes in the same person, 
 the test of which is the presence of the secreting organs, the ovaries and 
 testicles. True hermaphroditism is rare, but it does occur, while most of 
 the conditions called hermaphroditism are in reality due to varying mal- 
 formations of the external generative organs. 
 
 Pseudo-hermapJirodiiism. — This malformation consists in an abnormal 
 change in the transition from the festal condition of the parts to their 
 fully developed form. In the male, normally, the greater part of Miil- 
 
 'See Ahlfeldfc, Arch, ftir Gynakologie, Bd. ii., p. 397. Fenomenodes, ibid., 
 Bd. 15, p. 343. 
 
Tns OEGANS OF GENERATION. 435 
 
 ler's canal disappears, and its lower end forms the vesicula prostatica. 
 In this malformation Miiller's canal is changed, as it is in the female, into 
 Fallopian tubes, uterus, and vagina, while at the same time the 
 testes, epididymes, vesicnlse seminales, and spermatic cord are formed 
 as usual. In the lesser degrees of this malformation, we find, in the 
 place of the vesicula prostatica, a pear-shaped sac, as large as pigeon's 
 egg, with muscular walls, and an epithelial lining. This sac may be 
 incompletely divided into a uterus and vagina, and it opens into the 
 urethra. In the higher grades, we find a well-formed vagina and ute- 
 rus. The uterus may or may not have Fallopian tubes. The testicles 
 are usually retained in the abdomen or inguinal canals, and are small. 
 The spermatic ducts run on the sides of the uterus and open into the 
 urethra, or are closed. The penis and scrotum aj^pear as in hypospadia, 
 or are well formed. The appearance of the individual varies with the 
 development of the testicles. 
 
 True hermaphroditism may be lateral. In this condition there is 
 hypospadia; a vagina and uterus and a Fallopian tube and ovary on one 
 side, and a testicle and spermatic cord on the other. 
 
 In certain cases, Avhich may be called iilatcrul liermaphroditism, there 
 is a testicle on one side, and an ovary on the other.' 
 
 Enlargement of tlie penis is sometimes caused by venous congestion 
 from heart disease; by long-continued masturbation, as a result of which 
 the corpus cavernosum may lose its contractility; and in rare cases, 
 by hypertrophy of the stroma of the corpus cavernosum. 
 
 Injury and Hemorrhage. — Injuries to the penis are liable to give 
 rise to severe hemorrhage on account of its peculiar vascular character; 
 supjjurative inflammation, gangrene, infiltration with urine, and its con- 
 sequences are also liable to occur. The contractions of the cicatricial 
 tissue by which wounds are healed, frequently give rise to various distor- 
 tions of the organ and not infrequently prevent subsequent erections. 
 
 INFLAMJIATION. 
 
 Balanitis, inflammation of the prepuce, is usually produced by 
 gonorrhoea, or by accumulations of smegma. The skin is red and swol- 
 len, and may ulcerate. Condylomata may be formed, and adhesions 
 between the prepuce and glans. The glans may ulcerate and the prepuce 
 may be much thickened. If the prepuce is long, there is an inflam- 
 matory phimosis, and the products of inflammation accumulate within 
 the swollen prepuce. In some cases, the prepuce becomes gangrenous. 
 
 Paraphimosis is produced by the retraction of a narrow prepuce 
 
 ' For a detailed consideration of the malformations of the male and female 
 generative organs, consult Klebs: " Handbuch der Pathologischen Anatomie," 
 and more recent cases of hermaphroditism by Heppner, Arch, f . Anat. u. Phy- 
 siol., 1870, and by Hofraann, Wien..Med. Jahrb., 1877. 
 
436 THE ORGANS OF GENERATION. 
 
 behind the glaus, with consequent stricture, inflammation, and sometimes 
 gangrene. 
 
 Inflammation of the Corpora Cavernosa is produced by gonorrhoea, 
 injuries, fistulse, typhus fever, measles, and occurs in connection with 
 inflammation of tlie connective tissue of the pelvis. It results in fibrous 
 induration of portions of the corpora cavernosa; in rare cases, in abscesses 
 or diffuse purulent infiltration; sometimes in gangrene. 
 
 Syphilitic Ulcers frequently occur on the glans penis and prepuce. 
 The indurated chancre is formed either from an excoriation in which a 
 pustule is formed, or from a little nodule. The pustule breaks and its 
 walls are infiltrated with small round cells. The nodule softens, breaks 
 down, and forms an ulcer, of which the walls are infiltrated with cells in 
 the same way. 
 
 Syphilitic condylomata are of frequent occurrence on the glans. 
 
 Phagedaenic ulcers occur, and may destroy a considerable part of the 
 penis. Herpes of the prepuce occurs in the form of small vesicles, which 
 may later become ulcers. Erysipelatous and furuncular inflammation 
 sometimes involve the skin of the penis. 
 
 TUMORS. 
 
 Papilloma is found on the prepuce and glans penis. It occurs in the 
 form of little warty growths, or of composite, cauliflower masses, even 
 as large as a fist. In either case, the structure is the same, hypertrophied 
 papillae covered with epithelium. Sometimes the eiDithelial layers be- 
 come thick and horny, forming large dense projections. 
 
 Fibroma diffusxtvi, or elephantiasis of the prepuce, may occur, leading 
 to immense thickening of the structure. It consists in a diffuse growth 
 of the deep fibrous tissue of the cutis. Lipomata; angiomata; circum- 
 scribed fibromata, and sebaceous cysts may occur in the penis. Carcinoma 
 of the penis usually occurs in the form of epitheliomata. These are 
 most frequent in the prepuce and glans penis. They may have the form 
 of flat ulcers ; or of infiltrating ulcerating nodules, or very frequently 
 assume the form of papillary outgrowths, which may attain great size, 
 ulcerate, or undergo a variety of inflammatory changes. These growths 
 may involve the entire skin of the penis; they may invade deeper parts. 
 The inguinal glands may be invaded. Distant metastases may occur, but 
 are not frequent. 
 
 Glandular carcinoma of the ^Denis is not common. It may be secon- 
 dary to carcinoma in some other part of the body. 
 
 Calcification and Ossification of the connective tissue of the corpora 
 cavernosa sometimes occurs. Large and small preputial calculi are 
 occasionally found between the prepuce and the glans. These may be 
 formed in situ, may come from the bladder, or from without, and may 
 later increase in size. 
 
THE ORGANS OF GENERATION. 437 
 
 THE SCROTUM. 
 
 The skin of the scrotum is subject to the Tarious forms of lesions 
 which may occur in any part of the integument. 
 
 Elephantiasis of the scrotum consists in the main, of a development 
 or new connective tissue from the cutis, which is sometimes accompanied 
 by dilatation of the lymph-vessels. The thickened scrotum sometimes 
 forms very large tumors, of ten rough upon the surface, which may entirely 
 cover in the penis. Lipomata, fibromata, atheromatous or seiaceotis cysts, 
 and dermoid cysts containing hair, bone, cartilage, etc., are sometimes 
 found. Occasionally the skin of the scrotum is beset with numerous 
 larger and smaller sebaceous cysts, which raise the surface of the skin in- 
 to little wart-like projections. Epitheliomata, in the form of flat or papil- 
 lary ulcerating tumors are of frequent occurrence among chimney 
 sweepers, and may lead to extensive ulcerations of the adjacent parts 
 and involvement of neighboring lymph-glands. 
 
 In very rare cases, tumors containing a considerable portion of a foetal 
 skeleton have been found in the scrotum. 
 
 THE TESTICLES. 
 MALFORMATIONS. 
 
 Absence of both testicles, either with or without absence of the epi- 
 didymes, spermatic cord, and vesiculse seminales, occurs in rare cases. 
 The scrotum is only indicated, or may contain the epididymes. The 
 penis is small, and the individuals are small and poorly developed. 
 
 Instead of being entirely wanting, the testes may be imperfectly 
 developed. The individuals are weakly and effeminate. Absence of 
 one testicle, with healthy development of the other, is more frequent. 
 The corresponding epididymis and cord may be absent or present. 
 
 The spermatic cords and vesiculse seminales may be absent or im- 
 perfectly developed on one or both sides, while the testes are normal. 
 
 Either one or both testicles may remain permanently in their foetal 
 position, or may not descend into the scrotum for several years after 
 birth {cryptorchismus). Their descent may even be delayed until the 
 thirtieth year of life. This condition may depend on an arrest of de- 
 velopment in the testes, or the gubernaculum testis; on adhesions pro- 
 duced by intra-uterine peritonitis; on narrowing of the inguinal canal; 
 on narrowing or shortening of the vaginal process of the peritoneum; or 
 on abnormal size or position of the testicle. Usually the malformation 
 is confined to one testicle, and then is more frequent on the left side. 
 The testicle is usually found in the abdomen close to the mouth of the 
 inguinal canal or in the inguinal canal, just below the external ring; but 
 it may be beneath the skin in the perineum; or in the crural canal with 
 
438 THE ORGANS OF GENEEATIOK". 
 
 the femoral vessels, or elsewhere. The retained testis is usually not fully 
 developed, or undergoes fatty or fibrous degeneration. The retention of 
 one or even of both testicles does not preclude the possibility of procrea- 
 tion. Eetained testicles are prone to inflammatory changes and liable to 
 become the seat of malignant tumors. 
 
 Sometimes, while the testis is retained, the epididymis and spermatic 
 cord descend into the scrotum. In rare cases, the position of the testis 
 may be changed, so that the epididymis and cord are in front. The ex- 
 istence of a supernumerary testis has been asserted in some cases, but is 
 rather doubtful. 
 
 Atrophy of the testicle may occur in old age or in persons who are in 
 a condition of premature senility; or as the result of pressure from 
 hernise, hydrocele, or inflammatory joroducts. 
 
 HTDBOCELE. 
 
 Hydrocele of the tunica vaginalis consists in an accumulation of serum 
 in the cavity of this membrane. It is usually confined to one side. It is 
 caused by acute or chronic inflammation of the tunica vaginalis, by vari- 
 cocele, or by general dropsy. The serum is found in small or in large 
 quantities; it is usually transparent, may contain cholestearin, or be 
 purulent, or be mixed with blood. The tunica vaginalis remains un- 
 changed, or is thickened, or contains plates of bone, or is covered with 
 polypoid fibrous bodies, which fall ofl:, and are found free in the cavity 
 of the sac. There may be adhesions between the layers of the tunica 
 vaginalis, and in this way the fluid becomes sacculated. The testis is 
 pushed downward and backward; it remains unchanged, or is atrophied. 
 
 Hydrocele of the processus vaginalis consists in an accumulation of 
 serum in the cavity of the vaginal process of the peritoneum, which re- 
 mains open after the descent of the testicle. There are several difEerent 
 varieties. 
 
 (a) The vaginal process is entirely open, and there is a free communi- 
 cation with the peritoneal cavity. The serum may originate in the 
 cavity of the peritoneum, or of the vaginal process, and passes freely from 
 one to the other, 
 
 (5) The processus vaginalis is closed in the inguinal canal, while its 
 lower portion is filled with serum. 
 
 (c) The processus vaginalis is closed about the testis, and the vis- 
 ceral layer of the tunica vaginalis is formed. The serum accumulates in 
 the upper part of the vaginal jirocess, which communicates with the 
 peritoneal cavity. 
 
 (f?) The vaginal process is closed in the inguinal canal and over the 
 testis; the serum accumulates so as to form one or more sacs between 
 these two points. Inguinal hernia may complicate this form of hydro- 
 cele. 
 
THE ORGANS OF GENEEATION. 439 
 
 Hydrocele of the spermatic cord consists in a general oedema of the 
 connective tissue of the cord, or in the development of circumscribed 
 cysts in this connective tissue. 
 
 A peculiar form of hydrocele is produced by the accumulation of 
 serum in the sac of an inguinal hernia, from which the intestine has he- 
 come retracted. 
 
 SPERMATOCELE. 
 
 Cysts containing spermatic fluid not infrequently arise from the epi- 
 didymis or from the rete testis. These sometimes acquire a large size and 
 crowd the tunica vaginalis before them, so that they simulate a collec- 
 tion of fluid in the cavity of the latter. The wall of the cyst may be 
 lined with ciliated or with flattened epithelium. The contents are some- 
 times simply serous, but more frequently opalescent, and contain great 
 numbers of spermatozoa. 
 
 H.EMATOCELE. 
 
 Hsematocele of the tunica vaginalis consists in an efEasion of blood 
 into the cavity of this sac. It may be produced by injury; in scurvy, or 
 the hemorrhagic diathesis; or it may complicate a pre-existing hydrocele. 
 The efEused blood usually soon degenerates, and we find the sac filled 
 with a brownish fluid, or a thick grumous mass. The tunica vaginalis 
 may be thickened. The testis remains normal or is atrophied. 
 
 Effusion of blood into the loose connective tissue of the scrotum is 
 often called extravaginal hmmatocele. 
 
 Hsematocele of the spermatic cord occurs in rare cases as a diffused 
 infiltration of blood in the connective tissue of the cord. Or blood may 
 be efEused into a hydrocele of the cord. 
 
 IN'FLAMJIATION". 
 
 Inflammation of the testicles may be caused by injuries, exposure to 
 cold, inflammation of the urethra, syphilis; or it may occur in parotitis. 
 The testes, epididymis, or tunica albuginea may be principally involved. 
 Usfially only one testicle is inflamed, sometimes both. The inflammation 
 may extend to the vas deferens. The inflammation may be acute or 
 chronic. 
 
 Acute Orcldtis is more frequent in the epididymis and tunica albugi- 
 nea. When the testis is involved, the organ is congested and infiltrated 
 with serum or pus. From this condition it may return to the normal 
 state, or small abscesses may form. These abscesses may increase in size 
 so as to involve nearly the entire organ. Tliey may perforate externally 
 and then liealing may occur by means of granulation tissue; or extensive 
 gangrenous destruction of the scrotum may occur. They may become 
 inclosed in a flbrous capsule and the contents dry and become cheesy or 
 
440 THE OEGAKS OF GENEEATION. 
 
 calcified, and so persist for a long time. Tlae acute inflammation may- 
 pass over into the chronic form. Acute epididymitis is frequently the 
 result of gonorrhoeal infection, and may or may not be associated with 
 inflammation of the testis. 
 
 Chronic Orchitis occurs as a sequel of acute inflammation or as an 
 original condition. It may affect the testis, the epididymis, or the sper- 
 matic cord. The seminiferous tubules may be filled with desquamated 
 and degenerated epithelium ; they may be atrophied, or their walls may 
 be greatly thickened so that they are converted into dense fibrous cords 
 with almost or quite complete obliteration of their lumina. There is 
 usually a marked increase in the interstitial tissue which causes atrophy of 
 the tubules. Thealbuginea may be greatly thickened. In some cases the 
 testis is converted into a mass of dense connective tissue, in which but- 
 little trace of the original structure can be made out. The new-formed 
 connective tissue may become calcified. A peri-orchitis may lead to thick- 
 ening and union of the layers of the tunica vaginalis testis. Abscesses 
 are not infrequent in connection with chronic orchitis. 
 
 Tubercular Orchitis may occur in connection with tuberculosis of the 
 other gen i to-urinary organs or the lungs, in acute general miliary tuber- 
 culosis; or by itself. It usually begins in the epididymis, and may extend 
 from there to the testis ; or it may commence in the testis itself. The 
 appearances which the testicles present when the seat of this form of 
 inflammation are exceedingly varied and diSicult of interpretation. This 
 is partly due to the complex structure of the organ, partly to the varied 
 complicating simple inflammatory changes which the diilerent parts of 
 the organ undergo in connection with the special tubercular inflammation, 
 and the impossibility of making any definite morphological distinction 
 between them. Further researches are urgently needed in this direction, 
 and it seems probable that in the presence or absence of the tubercle- 
 bacillus we shall find the needed differentiating factor between various 
 inflammatory processes which are at present grouped under the general 
 heading of tuberculosis testis. 
 
 We may find in the testicle small circumscribed masses of cells, visible 
 to the naked eye as whitish spots, which are sometimes composed of small 
 spheroidal cells, or of larger polyhedral or fusiform or round cells. 
 These occur in the walls of seminiferous tubules and blood-vessels, and in, 
 the interstitial tissue. Sometimes associated with these smaller nodules 
 and sometimes not, we find larger, irregular yellowish or gray cheesy 
 masses, which are believed by many to be formed by the confluence and 
 degeneration of the smaller nodules. The cheesy masses may break 
 down and open externally, giving rise to fistulse, gangrenous inflamma- 
 tion, etc. Hand in hand with this nodular formation of tissue, -which is 
 disposed to degenerative changes, there are various more or less diffuse- 
 alterations of the parenchyma and interstitial tissue of the organ, which. 
 
THE ORGANS OF GENERATION. 441 
 
 must not be overlooked, and which often constitute a most prominent 
 and important factor in the lesion. The interstitial tissue may be more 
 or less densely and diffusely infiltrated with small spheroidal cells. The 
 arteries are often the seat of obliterating endarteritis. The walls of the 
 seminiferous tubules may be very much thickened, so that the lumen may 
 be entirely obliterated. The epithelium lining the tubules maybe fatty, 
 disintegrated, and peeled off; or it may have largely disappeared, or the 
 lumen of the tubules may be filled with a granular, nucleated mass which 
 in transverse sections looks like a giant-cell. The thickened walls of the 
 tubules may be infiltrated with small spheroidal cells, so that the under- 
 lying stroma is scarcely visible. When this occurs in connection with a 
 similar infiltration of the interstitial tissue and the formation of giant- 
 cells in the lumina, we have structures which present the greatest resem- 
 blance to some forms of tubercle granula. This resemblance is especially 
 striking when, as is not infrequently the case, the infiltrated tissue under- 
 goes cheesy degeneration. 
 
 Tubercular inflammation may extend from the testis to the vas defe- 
 rens, vesiculffl seminales, and prostate.' 
 
 Syphilitic orchitis. — This may occur in the form of a diffuse new 
 formation of connective tissue, which may occur in some particular part 
 of the organ or be widely distributed through it, and by reason of which 
 the organ becomes dense and firm. Morphologically, there is no differ- 
 ence between this form of orcliitis and chronic indurative orchitis 
 from other causes. It may occur in children affected with congenital 
 syphilis. 
 
 Gummata may form in connection with the interstitial induration. 
 These may disappear, leaving irregular cicatrices. 
 
 TUMORS. 
 
 Fibroma occurs in the form of small dendritic or polypoid growths 
 of the visceral layer of the tunica vaginalis. These sometimes become 
 free, and are found in the sac, usually in connection with hydrocele. 
 Small nodular fibromata occasionally occur in the albuginea and in the 
 spermatic cord. 
 
 Lipomafa, either pure or in combination with myxoma and sarcoma, 
 may arise from the connective tissue of the spermatic cord, or from the 
 tunica albuginea. 
 
 Chondroma, sometimes in a pure form, but more frequently combined 
 with myxoma and sarcoma, occur in the testicles, and may attain a large 
 size. Osteoma has been described. 
 
 I For the literature of Tuberculosis of the Testicle, consult Waldstein : "Zur 
 Kenntniss der tuberculosen Erkrankungen des Hodens." Viroh. Archiv, Bd. 85, 
 p. 397, 1881. 
 
442 THE OEG-ANS OF GENEEATION. 
 
 Sarcomata occar in the testes and epididymis, most frequently in tlie 
 former. Tliey present the greatest variety in structure. They may be 
 composed of spheroidal or spindle-shaped cells; they may be soft or con- 
 tain much fibrous tissue; they are very frequently combined with myxoma, 
 chondroma, lipoma, etc. Owing to the occlusion of the seminiferous 
 tubules, cysts may be formed in these sarcomata. In these cysts poly- 
 poid growths of sarcomatous tissue may occur in the form of intracana- 
 licular growths. Thus the so-called cysto-sarcomata of the testicle are 
 formed. The walls of these cysts may coalesce, so that large irregular 
 cavities may be formed. When the cysts are not filled by polypoid out- 
 growths from their walls, they may contain a mucous, serous, or bloody 
 fluid, or masses of flattened cells, fat, and cholestearin. The cysts maybe 
 lined with cylindrical, ciliated, or flattened cells. 
 
 Rlutbclomyomata have been several times observed, frequently in com- 
 bination with cysts. 
 
 Adenoma is occasionally found, usually in combination with sarcoma, 
 ■or carcinoma, or with cyst-formation. 
 
 Carcinoma of the testicle is commonly of the soft medullary form, 
 •of rapid growth, and usually primary. It may commence in the testis 
 or epididymis. Usually only one testicle is involved. Frequently the 
 entire glandular portion of the organs is replaced by the new growth. 
 The albugiuea expands with the growth of the tumor, and may continue 
 to inclose it even when of large size. The tissues are often very vascular, 
 tmd hemorrhages, areas of softening, fatty and mucous degeneration are 
 frequent. The inguinal and lumbar glands are apt to become involved, 
 and distant metastasis may occur. Rarely the growth assumes a scirrhous 
 form. 
 
 Cysts. — Aside from the above-mentioned cysts which occur in con- 
 nection with tumors and spermatocele, cysts may be formed from per- 
 sistent remnants of Miiller's canal in the epididymis, or from obstruction 
 of the seminiferous tubules or ducts by inflammatory products or tissue. 
 
 Dermoid cysts of various kinds are of infrequent occurrence, and are 
 sometimes quite complex in character. They may be embedded in the 
 substance of the gland. Probably some of the above-mentioned cystic 
 rhabdomyomata belong here. 
 
 PARASITES. 
 
 EchinococcHS may occur in the testis or e|)ididymis. 
 
 THE SEMINAL VESICLES. 
 
 The seminal vesicles may be the seat of acute or chronic inflamma- 
 tion, which are most frequently connected with inflammatory changes in 
 adjacent parts, prostate, urethra, etc. As a result of chronic inflamma- 
 
THE OEGANS OF GENERATION. 443 
 
 tion, the vesicles may be atrophied, or they may be greatly dilated as a 
 result of constriction of the ducts. 
 
 Tubercular inflammation is usually secondary. Carcinoma of the 
 rectum or other genito-urinary organs may secondarily involve the semi- 
 nal vesicles. Small concretions, sometimes containing masses of sperma- 
 tozoa, are occasionally found in the seminal vesicles. 
 
 THE PROSTATE. 
 
 Hypertrophy of the prostate is a frequeut senile change; it is geueral 
 or partial. 
 
 In general hypertrophy, the entire organ is enlarged, and may reach 
 the size of a man's fist. The enlargement is symmetrical, or is most 
 marked in one-half or in the so-called middle lobe. The organ is hard 
 and dense, or soft, or alveolar, containing numerous small openings, from 
 which a turbid fluid exudes. These different appearances depend upon 
 the character of the hypertrophy. The muscular and fibrous tissue alone 
 may be increased, which is most common, or at the same time the glan- 
 dular tissue, or the glandular tissue alone. In the latter case, the lesion 
 is more properly an adenoma. The increase of muscular tissue properly 
 constitutes a myoma. 
 
 In partial hypertrophy, we find circumscribed nodules of musclar tis- 
 sue, or of muscular and glandular tissue. They are usually situated at 
 the periphery of the organ, and project into the bladder. They may 
 become detached from the prostate, and are found as small movable tu- 
 mors beneath the mucous membrane of the bladder. 
 
 Both forms of hypertrophy frequently produce, by pressure, reten- 
 tion of urine and changes in the bladder. 
 
 Atrophy of the prostate is sometimes seen in connection with atrophy 
 of the testicles, with castration, and as a result of inflammation. Some- 
 times the ducts of the glandular portion are enlarged, or there may be 
 fibrous degeneration of the organ. 
 
 INFLAMMATION. 
 
 Inflammation of the prostate is caused by gonorrhoea, by injuries, or, 
 more rarely, is idiopathic. It may run an acute or chronic course. The 
 gland may after a time return to its normal condition, or is gradually 
 converted into a mass of fibrous tissue filled with abscesses. The ab- 
 scesses may perforate into the bladder, urethra, vesiculffi seminales, rec- 
 tum, or peritoneum. Or the inflammation may extend to the connec- 
 tive tissue of the scrotum, or beneath the pelvic peritoneum. The pus 
 may become thickened and cheesy, or even calcified. 
 
 Tubercular Inflammation of the prostate usually accompanies a simi- 
 lar lesion of some of the other genito-urinary organs, and is rarely of 
 
444: THE OEGAJSrS OF GENERATION. 
 
 primary occurrence. Large cheesy masses are often formed, which may 
 break down and open into the bladder or rectum. 
 
 TUMOES. 
 
 Adenoma of tlie prostate occurs in one of tlie forms of hypertrophy 
 of the gland, either with or without an increase in the fibro-muscular in- 
 terstitial tissue. 
 
 Oarcinoma is of occasional occurrence and may be primary or secon- 
 dary. 
 
 Cysts of the prostate are sometimes found either as a result of occlu- 
 sion of the ducts by hypertrophy of the interstitial tissue, tumors, etc., 
 or as a result of faulty development. 
 
 PARASITES. 
 
 Bchinococcus of the prostate has been described, but is rare. 
 
 CONCRETIONS. 
 
 Small ovoidal or spheroidal bodies having the characters of corpora 
 amylacea are of very frequent occurrence in the alveoli of the prostate, 
 particularly in old persons. We find a certain number of them in the 
 prostate of nearly all old men, but they are sometimes present in great 
 numbers. Larger irregular concretions, apparently formed by the co- 
 alescence or growth of the smaller ones, are less frequently found, and 
 may be incrusted with lime salts. These concretions may give rise to 
 ulceration of the ducts of the gland or to interference with the passage 
 of urine, but in a majority of cases they seem to be of little or no practi- 
 cal importance. 
 
 THE MAMMA. 
 MALFORMATIONS. 
 
 Absence of both mammEe is only found in connection with other 
 marked malformations. 
 
 Absence of one mamma has been observed in a few cases, with and 
 without defective development of the corresponding half of the thorax. 
 
 Absence of one or of both nipples is more common. 
 
 Arrest of development of the mammae is found in connection with 
 arrest of development of the organs of generation, and, to a less degree, 
 alone. 
 
 Supei'numerary mammse and nipples have been observed in a number 
 of cases. The glands may all secrete milk during lactation. 
 
 Too early development of the mammae is sometimes found in young 
 children in connection with abnormal development of the organs of 
 generation. 
 
THE OEGANS, OF GENERATION. 445 
 
 HEMORRHAGE. 
 
 In young women who suJBEer from amenorrhoea or dysmenorrhoea, 
 small hemorrhages sometimes occur in the mammse at the time of men- 
 struation. The blood may find its way into the milk-ducts, and exude 
 in small quantities at the nipple. 
 
 Contusions of the breast may produce extravasations of blood in the 
 mammary gland or the surrounding connective tissue. Tliis may be- 
 come absorbed, or may remain and be surrounded by fibrous tissue, or be 
 converted into cysts. 
 
 INFLAMMATION. 
 
 During lactation, the nipple is liable to become inflamed in three 
 ways, which may occur separately or be combined together. 
 
 (1) The epidermis is rubbed off by nursing, the cutis becomes in- 
 flamed and converted into granulation tissue; in this way small or large 
 ulcers may be formed. 
 
 (3) Fissures are formed at the base of the nipple, which extend com- 
 pletely through the skin, and of which the fl.oors are composed of gran- 
 ulation tissue. 
 
 (3) There is a diffuse inflammation of the whole nijople, which does 
 not, however, go on to suppuration. The nipple is conical, red, swollen, 
 and very painful. 
 
 Acute inflamniatio7i of the mamma— mastitis — occurs most frequently 
 ■during lactation; it also occurs during pregnancy, and occasionally in 
 women who are neither pregnant nor nursing. 
 
 The inflammation may involve the subcutaneous connective tissue, 
 the gland itself, or the connective tissue between the gland and the wall 
 of the thorax. The inflamed tissues are at first congested, swollen, hard, 
 -and painful. The inflammation may stop at this point and resolution 
 take place; but more frequently it is succeeded by suppuration. If the 
 inflammation involves the subcutaneous connective tissue, the abscess is 
 superficial, and soon opens through the skin. If the gland is involved, 
 one lobule after another may become inflamed, so that successive ab- 
 scesses are formed in different parts of the gland. If the connective 
 tissue beneath the gland is inflamed, a deep abscess of large size is 
 formed, which usually perforates through the skin, but sometimes into 
 the pleural cavity. In both these latter forms of abscess, there is apt to 
 be necrosis of large portions of tissue. These abscesses may cicatrize, or 
 they pass into a chronic condition, and remain as suppurating, fistulous 
 tracts for a long time. 
 
 In new-born children, there is often a painful swelling of the breasts, 
 •which usually subsides in a few days, but may go on to suppuration. 
 
 Epidemic parotitis is sometimes complicated by mastitis. 
 
 Chronic inflammation of the interstitial connective tissue of the 
 
M6 
 
 THE OEGANS OF GENEEATION". 
 
 mammary gland may result in the formation of dense connective tissue 
 (Fjg. 132), with or without cystic dilatation of the milk-ducts, or there 
 may be added to this the gradual development of abscesses. 
 
 Fig, 133.— Chronic Inflammation of Mammary Gland, X 350 and reduced. 
 New formation of connective tissue witli compression of acini. 
 
 Eczema sometimes affects the skin of the nipple. Attention has 
 lately been drawn to the relationship between this inflammation and car- 
 cinoma of the nipple, for the two are frequently associated. It is possi- 
 ble that the eczema may lead to the subsequent development of the 
 carcinoma. 
 
 Syphilitic ulcers may occur in the nipple, either as primary chancres 
 or as mucous patches. Gummy tumors have been observed in the 
 mamma. 
 
 TUMOES. 
 
 There may be a general hypertrophy of one or both breasts. This is 
 usually found in young, unmarried women, but sometimes in advanced 
 life. There is an increase in all" the elements of the gland, both the 
 glandular and the connective tissue. 
 
 Cysts of the mamma seem to be for the most part retention cysts, 
 formed by the dilatation of the glandular ducts or acini. During lacta- 
 tion, such retention cysts are sometimes formed, and then contain milk. 
 They may reach an enormous size. At other times, retention cysts are 
 formed containing serous, or viscid brownish fluid, which often exudes 
 through the nipple. These cysts may be large or small, single or multi- 
 ple. There is usually at the same time some growth and induration of 
 the connective tissue of the gland. In some cases there are polypoid 
 outgrowths of connective tissue from the wall of the cyst. These cysts 
 are not to be confounded with the cysts which are develoiJed with the 
 intracanalicular tumors, of which we shall speak below. 
 
THE ORGANS OF GENEEATION. 
 
 Wi 
 
 Fibroma.—C'ncnrascvihed tumors composed of connective tissue are 
 sometimes found in the breast. They are dense and hard, and may in- 
 close in them some of the gland ducts and acini. 
 
 Intracanalicular Fibro)7ia.— These tumors are formed by a diffuse 
 growth of connective tissue, a dilatation of the milk ducts, and a growth 
 of polyijoid fibrous tumors from the walls of the ducts into their cavities. 
 
 /4 
 
 'jLLyU 
 
 Fig. 133. — Intra-canalicular Fibroma of the Mamma, X 170 and reduced. 
 Cross section of a milk duct with polypoid ingrowths. 
 
 The glandular acini may be atrophied, or enlarged, or cystic. A section 
 of such a tumor looks like a solid mass of fibrous tissue, divided by clefts 
 and fissures lined with cylindrical or cuboidal epithelium (Fig. 133), or 
 containing cysts into which project polypoid fibrous outgrowths. These 
 tumors grow slowly, but if left to themselves may reach an enormous size. 
 The skin over them may ulcerate, and the tumor project through the 
 opening in fungous masses. 
 
 Myxoma. — -This form of tumor may occur as a circumscribed growth 
 
448 THE OEGANS OF GENERATION. 
 
 replacing part of the mamma; or it may be developed in the same way as 
 the intracaualicular fibromata. It is not uncommon in these intraeanali- 
 cular tumors to find a combination of fibrous, mucous, and sarcomatous 
 tissue in tlie same tumor. 
 
 Chondroma is a very rare form of tumor in the mamma. A few cases 
 have been described in which it was combined with carcinoma. 
 
 Adenoma. — Tumors composed of glandular acini, and ducts sur- 
 rounded by connective tissue, are of frequent occurrence in the mamma 
 (Fig. 45, p. 143). They are either single or multiple, or several may be 
 developed successively in the same breast. They grow at first slowly, 
 afterwards more rapidly. Their structure may be further complicated 
 by the dilatation of one or more of the ducts which compose the tumor 
 into cysts, and the ingrowth of connective tissue from the walls of these 
 cysts. 
 
 Sarcoma. — This form of growth may be developed as a circumscribed 
 tumor of small or large size. Its basement substance is that of connective 
 or of mucous tissue, and may be scanty or abundant. The cells are 
 spheroidal, fusiform, branched, or polygonal. These tumors may simply 
 replace the gland; or glandular acini and ducts may be inclosed within 
 them; or these ducts and acini may be dilated so as to form cysts; or 
 there may be a new growth of the gland-tissue so as to form an adeno- 
 sarcoma. 
 
 In other cases the sarcoma takes the intracaualicular form. There is 
 a diffuse growth of sarcomatous tissue, a dilatation of milk-ducts and au 
 outgrowth of sarcomatous tissue from the walls of the dilated ducts into 
 their cavities. These tumors often reach an enormous size, and there is 
 apt to be ulceration of the skin over them. 
 
 Garcinovia of the mamma is most common in women between the 
 ages of thirty-five and fifty-five, but it sometimes occurs in women not 
 over twenty years old, and sometimes in old persons. It occurs in either 
 breast, in the right rather more frequently than in the left, but some- 
 times in both. The growth begins more frequently at the periphery of 
 the gland than at its centre, and more frequently in the upper edge of 
 the gland than in any other place. 
 
 The growth most frequently begins as a small circumscribed nodule 
 which enlarges and involves more and more of the breast; sometimes, 
 however, it is diffuse from the first, and sometimes it begins in the nip- 
 ple. 
 
 It may infiltrate the adjacent tissues, and the axillary and cervical 
 glands, and form metastatic tumors in different parts of the body. 
 
 There are several different anatomical forms of the growth. 
 
 (1) There is a connective-tissue stroma, in which are tubular or ir- 
 regular spaces filled with small polygonal cells, or with larger cells of 
 irregular shape. 
 
THE ORGANS OF GENERATION". 449 
 
 (3) The connective-tissue stroma is very abundant and dense, while 
 the epithelial cells are scanty (see Pig. 54, p. 150). It is said that with 
 these tumors secondary infiltrations of the bones are especially common. 
 
 (3) The connective-tissue stroma is comparatively scanty, while the 
 cells are very numerous. The cells arc small and polygonal or large and 
 of irregular shape, they are arranged in irregular spaces, or in spaces re- 
 sembling the shape of the glandular acini. 
 
 (4) The new growth follows the normal distribution of the gland 
 ducts and acini. These are enlarged, their epithelial cells are increased 
 in size and number, and there are infiltrations of similar cells in the 
 stroma. 
 
 (5) Colloid cancer is of rare occurrence. 
 
 (6) The basement substance may resemble mucous tissue. 
 
 In any of these forms of cancer there may be cystic dilatations of the 
 ducts and acini. 
 
 Besides the primary cancers of the mamma, secondary cancers are 
 met with in rare cases. 
 
 THE MALE MAMMA. 
 
 There may be an abnormal number of mammae. In boys, at about the 
 time of puberty, the mamm^ may be swollen and inflamed; or they may 
 secrete milk. Oases are recorded in which adult males possessed large 
 mammae which secreted milk. The breasts may be enlarged from an 
 increase of fat or of connective tissue. 
 
 Cysts of the male breast are not very infrequent. Fibromata, sarco- 
 mata, cysto-sarcomata, myxomata, and various forms of carcinomata are 
 recorded.' 
 
 ' For literature of tumor of male mamma, see Gross : " Tumors of the Mam- 
 mary Gland," p. 237. 
 39 
 
THE BONES. 
 
 DISTUEBANCES OF CIRCULATION". 
 
 HyjMrcBviia.- — The evidences of this condition are most marked to 
 the naked eye in the periosteum and marrow, particularly the latter. It 
 should be remembered that the color of the marrow varies consider- 
 ably under normal conditions, depending upon age and situation. In 
 the bones of the foetus and new-born, and near the areas of ossifica- 
 tion in the young, the marrow is normally red in color. In adults, the 
 marrow of the sternum, vertebrae, and to a certain degree that of the 
 ribs, pelvic and cranial bones, and the cancellated tissue of the ends of 
 the long bones, is red or reddish in color. But most of the marrow, par- 
 ticularly in long bones of the extremities, is of a yellowish color from 
 the presence of fat-cells. In old age the marrow of all the bones is apt 
 to become pale, and to assume a more or less translucent or gelatinous 
 appearance. 
 
 Hyporsemia usually occurs as an accompaniment of inflammatory pro- 
 cesses in the bone, and when marked, the j)eriosteum is swollen and red; 
 the compact bone-tissue may appear of a pink color, while the marrow, 
 either by an increase in the amount of blood, or absorption of its fat, or 
 both, may be of a uniform dark-red color, or mottled with red and red- 
 dish-yellow. 
 
 Hemorrhage. — This may be due to wounds and injuries; to in- 
 flammatory and necrotic processes, and small hemorrhages often accom- 
 pany scurvy, jDurpura, hemorrhagic diathesis, and leukfemia. Hem- 
 orrhages of considerable size between the periosteum and bone may lead 
 to serious consequences, by cutting off the blood-supply to the superficial 
 layers of bone, and thus inducing necrosis; but when not in contact with 
 the air, they are not usually of serious import, since they are readily ab- 
 sorbed. The smaller hemorrhages of the medulla are not usually of 
 much importance. The decomposition of the extravasated blood may 
 lead to extensive pigmentation of the marrow. 
 
THE BONES. 45 X 
 
 WOUNDS, ERA.CTURES, AND DISLOCATIONS. 
 
 For details of the yaried alterations produced under these conditions, 
 and the secondary changes involved in the healing process, we refer to 
 the works on surgery. It may be stated here, however, that the healing 
 of fractures occurs by the formation of granulation tissue in greater or 
 less amonnt about the seat of fracture, and the direct formation of bone 
 under the influence of osteoblasts, or by a preliminary formation of car- 
 tilage or fibrous tissue, and the gradual conversion of this into bone by 
 metaplasia. 
 
 INFLAMMATION. 
 
 The periosteum, bone-tissue, and marrow are so intimately connected, 
 that in most cases they all share to a greater or less degree in the patho- 
 logical alterations of the bones. But as sometimes one, sometimes 
 another, is most markedly involved, it is convenient to consider separately 
 here the inflammatory changes by which they are respectively affected. 
 
 PERIOSTITIS. 
 
 We may distinguish several varieties: 
 
 (1) Simple Acute Periostitis. — This form is apt to occur in children 
 and ill-nourished persons from comparatively slight injuries, or from 
 unknown causes. The periosteum is thickened, succulent, congested, 
 and more or less abundantly infiltrated with leucocytes, while the con- 
 nective-tissue fibres are swollen. The periosteum becomes less firmly 
 adherent to the bone, and the cells of the inner layers are increased in 
 number. This variety of inflammation may terminate in the disappear- 
 ance of the new elements, and complete resolution ; or it may represent 
 a preliminary stage of one of the other varieties of inflammation. 
 
 (2) Suppurative Periostitis may begin as a simple or as a purulent 
 inflammation. The pus is formed in the inner layers of the periosteum, 
 and between it and the bone. The outer layers of the periosteum may 
 resist for a long time the suppurative f)rocess. The accumulation of pus 
 may dissect up the membrane from the bone, and leave the latter bare. 
 The pus thus formed may remain in this position for a long time, may 
 be absorbed, may become dry and cheesy, or may burst through the peri- 
 osteum, and form abscesses in the soft jjarts. The bone, if separated 
 from its nutrient membrane, may remain unchanged, but more frequently 
 necrosis, or inflammation of the bone itself, is set up. Such a periostitis 
 may run an acute or a chronic course. 
 
 Sometimes suppurative loeriostitis takes on a very malignant charac- 
 ter. Pus is developed not only beneath, but in the periosteum, forming 
 abscesses fllled with foul pus. The periosteum breaks down into a gan- 
 grenous, foul-smelling mass, and the same change may affect the neigh- 
 boring soft parts. The medulla may take part in the process, and break 
 
452 the' bones. 
 
 down into a puruleiib, gangrenous mass. Hemorrhages may complicate 
 the process. The lymphatic glands are enlarged and swollen ; abscesses 
 may form in different parts of the body, and the patient may die with 
 the symptoms of septicaemia. Micrococci may be found under these 
 conditions in the exudations of the periosteum as well as in the metastatic 
 abscesses. 
 
 (3) Fibrous Periostitis . — This is a slow, chronic form of inflammation, 
 resulting in the formation of new connective tissue in the periosteum, 
 which becomes thickened and dense, and unusually adherent to the bone. 
 It may be the result of necrosis, chronic arthritis, chronic ulcers of adja- 
 cent soft parts, etc. It may follow a simple acute periostitis. 
 
 (4) Ossifying Periostitis results in the formation of new bone from 
 the inner layers of the periosteum. The masses of new-formed bone, 
 called osteophytes, are of variable shape. They may form a thin, velvet- 
 like, villous layer; or they are little spiculse; or they form larger, rounded 
 masses, or a thick, uniform layer, extending over a large part of a bone. 
 They may be at first very loosely connected with the bone. The new 
 bone has at first a loose, spongy character. It is formed of thin plates of 
 bone inclosing large cavities filled with marrow. Layers of compact 
 bone-tissue are formed from the medulla on the sides of the original 
 plates, and thus the medullary cavities are gradually filled up' witli bone. 
 The new bone may thus become as compact, or even denser than normal 
 bone. The hyperostoses and exostoses thus formed may remain indefi- 
 nitely, or they may gradually become smaller, and finally disappear by 
 absorption. 
 
 The formation of new bone in the form of osteophytes, or in dense 
 masses beneath and in the periosteum, occurs as a result of the same 
 process by which bone-tissue is normally formed. Certain rather large 
 colls, called osteoblasts, which are formed along the blood-vessels, possess 
 the power of depositing osseous basement substance about themselves, and 
 so forming bone. Pathological new formation of bone differs from the 
 normal mainly in the conditions under which it occurs. The blood-ves- 
 sels around which the pathological bone develops which grow out of from 
 the old vessels, as in the formation of granulation tissue, are irregularly 
 arranged and subject to a variety of abnormal nutritive and mechanical 
 conditions, so that tire new bone is not usually formed in a series of defi- 
 nite systems of lamellse, but, as above described, in a series of irregular 
 spiculse or masses. Moreover, as will be seen farther on, the conditions 
 under which it is formed being liable to change, and itself serving no 
 definite purpose in the economy, as does normal bone, pathological new 
 bone is often an evanescent structure. The details of its disappearance 
 will be considered below. 
 
 (5) Syphilitic Periostitis. — Syphilitic poisoning may give rise to 
 simple, purulent, fibrous, and ossifying periostitis. Or, in addition to 
 
THE BONES. 453 
 
 these, gummy tumors may be developed in the periosteum. The bone 
 tissue is usually more or less involved. Tlie giimmatii may be absorbed 
 or undergo cheesy degeneration, or be converted into fibrous tissue, or 
 they may supjourate. 
 
 (6) Tubercular Periostitis.— In badly nourished persons, particularly 
 in children suffering from the so-called scrofulous diathesis (see p. 288), 
 a chronic purulent periostitis is frequently associated with the formation 
 of miliary tubercles. Abscesses are apt to form in and about the perios- 
 teum, and when these are evacuated, granulation tissue may develop, in 
 which miliary tubercles are formed. In these tubercles the Bacillus tu- 
 berculosis may be found. The bone is apt to be involved to a greater or 
 less extent, in the form of inflammatory changes, or caries. 
 
 - OSTEITIS. 
 
 Inflammation in bone-tissue is dependent upon the same general con- 
 ditions and presents essentially the same series of phenomena as inflam- 
 mation in other kinds of connective tissue. But it is variously modified 
 in detail, by the peculiar, dense, and unyielding character of the base- 
 ment substance, and by certain peculiarities of the blood-supply and the 
 nutritive conditions under whicli the cells are placed. In simple exuda- 
 tive inflammation, the same series of phenomena occur in connection with 
 the blood-vessels, resulting in the production of serum, fibrin, and pus, as 
 in other tissues ; but the extent to which these changes can occur is 
 limited, and constantly associated with striking alterations in the base- 
 ment substance. It is these secondary alterations in the basement sub- 
 stance which lend to inflammations of the bone their most peculiar 
 characters, and in the prominence which these assume the fundamental 
 alterations are often overlooked. The most common of these secondary 
 alterations are the absorption of the hard basement substance of the bone 
 and its replacement by or conversion into young cellular forms of flbrillar 
 connective tissue or marrow tissue, and the new formation, in more or 
 less atypical manner, of new bone. As a result of these changes, the 
 bones in simple inflammation undergo alterations either in the direction 
 of greater vascularity and increase of the spaces filled with granulation 
 or marrow tissue, and so become more porous and less compact at the 
 expense of the dense basement substance ; or, they undergo alterations 
 in the direction of an increase in density at the expense of new-formed 
 or pre-existing marrow spaces. Or, as is frequently the case, both series 
 of changes occur either simultaneously, in different regions, or follow one 
 another, or are variously associated together. Very frequently one or the 
 other of the opposing forms of alteration predominate, or one may occur 
 to the exclusion of the other, and we thus have two prominent forms of 
 inflammation which are called rarefying osteitis or osteoporosis and con- 
 densing osteitis or osteosclerosis. The exact nature of the conditions under 
 
454 
 
 THE BONES. 
 
 which in one case the bones become more, in another less dense, we do 
 not understand. . 
 
 In addition to these phases of inflammation in bone and in frequent 
 and varied association with them, there are alterations leading to death 
 and destruction of bone-tissue in greater or less amount, which we call 
 cariex and necrosis, and also inflammatory changes, more or less charac- 
 teristic, due to the influence of peculiar specific agencies, such as the 
 syphilitic and tuberculous infection, and we thus recognize tuberciclar 
 and syphilitic osteitis. Again, the production of pus is so prominent a 
 feature in some cases as to represent a pimdent phase of the inflamma- 
 tory process. Finally, any of these forms, and commonly several of them 
 at once, are variously associated with more or less marked inflammatory 
 or degenerative alterations of the periosteum on the one hand, or the 
 marrow tissue on the other, or of both combined. 
 
 Rarefying Osteitis consists essentially in the formatioii in the marrow 
 spaces, Haversian canals, or beneatli the periosteum, of new, very cellular 
 and vascular tissue, resembling granulation or young marrow tissue, in 
 connection with which, or under whose influence, the basement substance 
 of the bone is absorbed. The absorption of the bone occurs chiefly in 
 the same way in which the bone is absorbed in normal growth, namely 
 under the influence of certain large cells called osteoclasts, which ai'e 
 
 6 — - ^ "^^ "U. * " 
 
 
 Fig. 134.— "Rarefving Osteitis, Ulna of Child, x about 7.50 and reduced, 
 a, Isolated bone fragments witli roughened edges; &, marrow tissue; c, Howship's lacuua3 with 
 osteoclasts. 
 
 grouped around the blood-vessels. If we examine a thin section of bone 
 which is undergoing absorption (Fig. 134), we find the edges of the bone^ 
 which border on the vascular surfaces, irregularly indented by deep or 
 shallow depressions, sometimes simple, sometimes quite complex. These 
 
THE BONES. 455 
 
 are called HowsJiip's lacunm and are usually filled or lined by larger aiid 
 smaller granular, frequently multinuclear cells — the so-called osteoclasts. 
 In the larger lacunae, there may be granulation tissue with loops of blood- 
 vessels, with or without cells which have tlie morphological characters of 
 osteoclasts. Under the influence of these peculiar cells, or of the new 
 vascular tissue, the bone is gradually absorbed. In other cases, we find 
 irregular branching channels through the bone across the lamellse, which 
 appear to be due to the enlargement and coalescence of the lacunae and 
 canaliculi without the direct influence of blood-vessels or other cells than 
 the fixed cells of the bone. The tissue which replaces the absorbed bone 
 may be very rich in small spheroidal cells, or it may be more or less 
 fibrillar. As a result of this process, irregular islets of bone -tissue may 
 be entirely separated from adjacent bone and surrounded by a more or less 
 fibrillar vascular tissue; this is most apt to occur in the cancellous tissue. 
 Or the originally compact bone may become traversed by a series of larger 
 And smaller irregular branching, communicating channels with ragged 
 walls. These progressive alterations may cease and be succeeded by a 
 new formation of bone along the edges of the channels or cavities; it may 
 result in necrotic changes; the vascular changes may become prominent, 
 and suppuration ensue. 
 
 Rarefying osteitis may occur as an idiopathic disease from unknown 
 causes; it is often associated with the scrofulous diathesis, with diseases 
 of the joints, with fractures or other injuries to the bone; it often forms 
 a predominant feature in tubercular inflammation of the bones, etc. It is 
 ohiefly by a rarefying osteitis that bone-tissue is eroded and destroyed in 
 the vicinity of tumors, aneurisms, etc., which exert pressure on the bones. 
 By the same process, the sharp ends of fractured bones may be rounded 
 off as healing proceeds. 
 
 "When this form of inflammation occurs in cancellous bone-tissue, the 
 marrow is red or gelatinous, and the bony septa may disappear alto- 
 gether, so that, in extreme cases, we may have, instead of cancellous bone, 
 a mass of granulation tissue. When the disease occurs in the articular 
 extremity of a bone, the granulating medulla may send little offshoots 
 throuo-h the articular cartilage. These may -become fused together, and 
 inflanrmation of the joint follow. The walls of the shafts of the long 
 bones may be converted into spongy tissue. If, as is sometimes the case, 
 an ossifying periostitis occurs at the same time, the bone is thickened but 
 spongy; or, sometimes, there are concentric layers of compact bone-tissue 
 separated by rarefied bone. 
 
 Condensing Osteitis (osteo-sclerosis).— This lesion is characterized by 
 the new formation of bone in the walls of the marrow cavities or Haver- 
 sian canals. The bone is formed under the influence of the blood-vessels 
 and osteoblasts, as in normal bone formation, but with less regularity. 
 It may result in the conversion of cancellous tissue into compact bone. 
 
456 
 
 THE BONES. 
 
 in the filling np of the medullary cavity of long bones with moreor less- 
 dense bone-tissue. The compact bone, owing to the filling of its 
 Haversian canals, may become very dense and ivory-like. When tlie 
 medullary cavities of long bones are involved, the yellow marrow is con- 
 verted into red marrow by the absorption of fat and increased vascularity. 
 It is frequently associated with ossifying periostitis. 
 
 It very frequently follows rarefying osteitis, and under the microscope 
 ■we can then often see the Howship's lacunae resulting from the original 
 
 
 ',m^^^^. 
 
 Fig. 135. — Condensing Osteitis or Osteo-Sclerosis op Ulna of Child, X about TOO and reduced. 
 fl, Fragment of the old bone with roughened sinuous edges; b, old Howship's lacunse coveretJ 
 with more recently formed bone lamellse ; d, marrow tissue. 
 
 absorption process filled and covered in with new bone lamellse (Fig. 135). 
 It is apt to occur in connection with necrosis or some chronic inflamma- 
 tion of adjacent soft parts, but it is sometimes idiopathic or occurs under 
 unknown conditions. 
 
 Stippurafive osteitis {abscess of bone). — This process occurs usually in 
 the ends of the long bones. It begins with a rarefying osteitis. The 
 medulla undergoes actual supj)uration, the bone-tissue is destroyed, and 
 a circumscribed cavity is formed in the bone, filled with pus, and lined! 
 with granulation tissue. 
 
 Less frequently, abscesses are formed in the shaft of a long bone, by a 
 cii'cumscribed suppuration of the medulla. These abscesses usually occur 
 in old people. They last for many years, have little tendency to perfora- 
 tion, may gradually enlarge, and be accompanied by an ossifying peri- 
 ostitis, so that the bone is expanded. Very rarely acute suppurative 
 osteitis, with rapid formation of an abscess, and perforation has been 
 observed. 
 
THE BONES. 457 
 
 In some cases, instead of abscess, there may be a diffuse infiltration 
 with pus of the Haversian canals, or the spaces formed by rarefying 
 osteitis. 
 
 TtCbercular Osteitis is essentially a rarefying osteitis associated with the 
 formation of tubercle tissue and cheesy degeneration. The tubercles are 
 sometimes small, scattered, and miliary in form; sometimes they unite to 
 form larger and smaller masses. There may be extensive involvement of 
 the medulla. There may be much simple granulation tissue or the 
 formation of abscess associated with the process. Condensing osteitis 
 and necrosis are not infrequently present. Tubercular osteitis is often 
 associated with tubercular inflammation of the joints. It is most apt to 
 occur in cancellous bone-tissue and is most common in the bodies of the 
 Yertebrse and in the carpal and tarsal bones. Tubercle bacilli may be 
 found in the tubercular masses, sometimes in considerable numbers. 
 
 SypMUtic Osteitis. — The syphilitic jDoison may induce one of the 
 above-mentioned varieties of osteitis, or it may produce gummy tumors. 
 The gummatous osteitis usually commences in the periosteum, which 
 becomes thickened and infiltrated with cells, so that there may be a cir- 
 cumscribed thickening of the periosteum with or without distinct gum- 
 mata. The vessels which extend from the periosteum into the bone 
 become surrounded by new cellular tissue, which causes an enlargement 
 of the canals. At this stage, if we strip off the periosteum, we drag with 
 it the vessels surrounded by the new cell-growth, leaving the bones 
 beneath with numerous small perforations extending inwards. As the 
 disease progresses, the gummatous tissue around the vessels continues to 
 increase, and the channels in the bone enlarge by a rarefying osteitis, and 
 coalesce, forming large irregular defects filled with gummatous tissue. 
 In these masses of new tissue cheesy degeneration and the formation of 
 fibrous tissue occur, giving them the characteristic appearance. In the 
 vicinity of these gumma-filled sf)aces, a condensing osteitis may occur, 
 both in the substance of the bone and on the surface in the form of oste- 
 ophytes, so that the opening in the bone may be surrounded by an ele- 
 vated irregular ring of bone-tissue. All this may occur beneath the 
 uninvolved skin, or the skin may participate by a suppurative inflamma- 
 tion, resulting in ulceration. These processes may be circumscribed or 
 involve a large part of a bone. It is not infrequently associated with 
 necrosis of larger and smaller portions of bone. The gummatous tissue 
 may be absorbed and its place be more or less filled with fibrous tissue. 
 Syphilitic osteitis is most frequent in the cranial bones, but may occur 
 elsewhere, as in the sternum, clavicle, tibia and fibula, the ribs, etc. 
 
 Congenital Syphilis.— The bones of young children in this condition 
 may occasionally show increased density or evidences of periostitis, or 
 irregular thickenings, particularly of the skull. The researches of Weg- 
 
458 THE BONES. 
 
 iiei'j' which have been frequently confirmed by other observers, have 
 shown that exceedingly characteristic changes very uniformly occur in 
 the long bones in still-born or young children who are the victims of 
 hereditary syphilis. These changes are found for the most part along the 
 border zone between the epiphysis and diaphysis. It will be remembered 
 that in normal ossification of the long bones, the border line between the 
 calcification and ossification zones is narrow, sharply defined, and straight, 
 or gently and evenly curved. In the syphilitic bones, on the contrary, 
 this line is broader, uneven, and presents various modifications depending 
 upon the stage of the disease. "Wegner distinguishes three prominent 
 stages, which, however, merge into one another, so that all intermediate 
 forms may be seen. In the first stage, there may be seen between the 
 cartilage and the new-formed spongy bone, a white or reddish- white zone 
 about two mm. in breadth, with very irregular borders consisting of calci- 
 fied cartilage, in which the linear groups of cartilage cells are more abun- 
 dant than normal. In the second stage, the calcified zone, still contain- 
 ing an unusual number of cartilage cells, is broader and still more 
 irregular and less sharply outlined against the ossification zone. The 
 cartilage just beyond it is softer and almost gelatinous, and may contain 
 numerous blood-vessels, islets of connective tissue, or of calcification, or 
 irregular ossification. In the third stage, the bone may be pouched out 
 at the sides around the ossification and calcification zones, and the peri- 
 chondrium and periosteum thickened. The whitish irregular calcified 
 zone is hard and friable. Between this and the new-formed bone, there 
 is an irregular soft, gray or grayish-yellow zone from two to four 
 mm. in thickness, which forms a loose, readily separated connection 
 between the cartilage and the diaphysis. The white friable zone 
 consists mainly of irregular rows of degenerated and distorted carti- 
 lage cells, lying in a calcified basement substance; of irregular 
 masses of atypical bone-tissue, and of blood-vessels surrounded by vari- 
 ously shaped cells. The soft zone consists of more or less vascular tissue 
 with homogeneous basement substance, and round and spindle-sliaped 
 cells. Tliis soft zone is not sharply outlined against the adjoining new- 
 formed spongy bone, which, instead of consisting of the normal narrow 
 spaces with bony lamellae between them, is largely composed of granula- 
 tion tissue. 
 
 Different stages of this faulty development may be seen in different 
 bones in the same individual. According to Wegner, the lesion is usually 
 most advanced in the lower end of the femur, then in the lower ends of 
 the leg bones and of the forearm; then in the upper ends of the tibia, 
 femur, and fibula. 
 
 Not infrequently, there is fatty degeneration of the marrow cells and 
 
 ' Vii-chow's Ai-chiv, Vol. 50, 1870, p. 305. 
 
THE BONES. 459 
 
 blood-vessels, giving the marrow a reddish-yellow color. These alterations 
 of the bones may occur, not only in children which have gummata in 
 other parts of the body, but also in those in which other evidences of 
 syphilitic poisoning are absent. So uniform is their occurrence that their 
 presence alone suffices for the establishment of a diagnosis. 
 
 OSTEOMYELITIS. 
 
 In most of the inflammatory processes which afEect the bones, the 
 medulla has an important share, so that many conditions described as 
 osteitis are really osteomyelitis. It is customary, however, to reserve 
 the latter name for those cases in which the medulla is primarily or 
 chiefly involved. Using the word in this sense, we may distinguish an 
 idiopathic and a traumatic osteomyelitis. 
 
 Idiopathic osteomyelitis. — At the commencement of this disease, which 
 usually begins in the shaft of one of the long bones, there is hypersemia 
 and oedema of the medulla, so that if the bone be opened, the marrow is 
 soft and of a dark-red color. A diffuse suppuration now rapidly ensues, 
 and the marrow becomes streaked or mottled with gray. Occasionally, 
 though not often, larger and smaller abscesses may form in the marrow. 
 The inflammatory areas may be circumscribed and scattered; or, in the 
 more malignant cases, the entire marrow may become rapidly involved. 
 The cancellous tissue of one or both of the epiphyses usually becomes 
 involved. The disease, however, is not commonly confined to the me- 
 dullary spaces. The periosteum becomes oedematous and infiltrated with 
 pus, and the surrounding soft parts may become the seat of intense inflam- 
 matory changes. Abscesses of the periosteum or surrounding tissues are 
 apt to form. As a result of these changes, necrosis of greater or less por- 
 tions of the bone may ensue. The medullary cavity may become en- 
 larged as pus accumulates, and the wall of the bone may be broken 
 through, permitting the discharge of pus outwards. Sometimes several 
 bones may be involved at once. Secondary involvement of the joints is 
 very frequent. There maybe only a serous or pui'ulent exudation; or 
 the acute and destructive inflammatory process may extend to the joint 
 and produce extensive alterations. In young persons the epiphyses very 
 frequently become separated from the shaft by the destruction of the 
 cartilage which binds them together. 
 
 In the severer cases, which are often denominated, jxir excellence, 
 malignant osteomyelitis, the changes may be very rapid and destructive. 
 The medulla becomes broken down and gangrenous; the joints are soon 
 involved; large portions of the bone, sometimes the whole shaft, necrose; 
 the periosteum and surrounding parts become gangrenous; the veins 
 contain thrombi, and pyemic infarctions and abscesses may form in 
 various parts of the body. Micrococci have been found by several 
 observers in spontaneous osteomyelitis in the bone and iu the metastatic 
 
460 THE BONES. 
 
 abscesses, and while there is much reason for believing that some forms 
 at least of malignant osteomyelitis are due to the presence of micrococci, 
 this does not seem yet definitely established. It is moreover uncertain 
 whether the micrococci which have been observed are peculiar to this 
 disease, or whether they may not be identical with forms which are 
 fonnd in connection with other suppurative inflammations.' 
 
 In the more chronic forms of the disease there is apt to be more or 
 less ossifying periostitis, and osteo-sclerosis, and fistulse may form ia the 
 bone through which the exudations are discharged. 
 
 Traumatic Osteomyelitis. — This form of inflammation may be the 
 result of fracture, amputation, etc. It consists essentially in a more or 
 less diffuse suppurative inflammation of the marrow, variously associated, 
 depending upon the intensity and cause of the disease, with necrosis, 
 gangrene, periostitis, etc. In its more intense and destructive forms, its 
 lesions are similar to those of spontaneous osteomyelitis, and are probably 
 identical with them. Micrococci have been found in the inflammatory 
 foci. Metastatic pyaemic abscess may be formed in other parts of the 
 body. 
 
 STECEOSIS. 
 
 By necrosis we understand the death of a larger or smaller portion of 
 bone. This condition is induced by causes which deprive the bone of 
 its proper vascular supply from the periosteum and medulla. Sup- 
 purative periostitis, osteomyelitis, and osteitis, traumatic separation 
 of tlie periosteum, ulcers of neighboring soft parts, emboli, the action of 
 phosphorus vapor, and diseases like typhus, which diminish the vitality, 
 may cause necrosis. Necrosis is a pure form of gangrene,' differing from 
 gangrene of soft parts in that the dead bone has at first, and may retain 
 for a long time, the general outward characters of normal bone; while in 
 dead soft parts, the phenomena of decomposition, under the influence of 
 bacteria, rapidly ensue, inducing marked complicating appearances in 
 the dead tissue. 
 
 When a portion of bone has died, an inflammation is set up at the 
 dividing line between the dead and living bone. This inflammation has 
 the characters of a rarefying osteitis (see above), and finally separates the 
 dead from the living bone. The dead bone, or seipiestrum, may remain 
 smooth and unaltered, or it may be eroded by the influence of surrounding 
 
 ' Consult Kocher, Arch, fur klin. Chirurgie, Bd. 23, p. 101. Solmller, 
 Centralblatt ftlr Chirurgie, 1881, No. 43. Rosenbach, Centralb. fiir Chirurgie, 
 No. 5, Feb. 2d, 1884, p. 65. Becker, Deutsch. Med. Wochenschrift, Nov. 14th, 
 1883, No. 40. General bibliography and cultivation and inoculation experi- 
 ments in articles by Krause in Fortschritto derMedicin, Bd. 2, 1884, Apr. 1st, No. 
 7; April ]5th. No. 8. Consult also Rosenbach: " Mikro-Organisnien bei dea 
 Wundinfections-Krankheiten des Menschen," 1884, p. 49. 
 
THE BONES. 4gl 
 
 pus or granulation tissue, or osteoclasts. In this way it is possible for the 
 sequestrum, if it be small, to be entirely absorbed; but this does not 
 often occur. More frequently there is a production of new bone around 
 the sequestrum, either beneath the periosteum or in the substance of the 
 bone, and this becomes lined with granulation tissue, from which pus 
 may continue to be formed, bathing the sequestrum. 
 
 Necrosis may involve the superficial layers, or the entire thickness of 
 the wall of a long bone, or only the spongy tissue and inner layers of the 
 wall, or an entire bone, or a number of different portions of the same 
 bone; but it is most apt to occur in compact bone. 
 
 The death and separation of the bone is very soon followed by the 
 growth 'Of new bone to repair the loss. The periosteum, the medulla, 
 and the surrounding soft tissues may all take part in this new growth. 
 The new bone is usually irregular, rough, perforated with openings, 
 through which pus formed around the sequestrum may be discharged. 
 If the sequestrum be removed, healing may occur by the formation of 
 new bone; but the bone is usually more or less distorted by the irregular 
 new ossification. 
 
 Phosphorus Necrosis. — Under the influence of phosphorus vapor, 
 periostitis and osteitis, particularly of the jaw, are apt to occur, which 
 usually lead to more or less extensive necrosis, usually associated with 
 prolonged and often extensive suppuration. 
 
 CARIES. 
 
 Caries of bone is essentially an ulcerative osteitis, resulting in pro- 
 gressive molecular destruction of the bone-tissue. It difEers fi'om necro- 
 sis in that, in the latter, larger and smaller masses of bone die, while in 
 caries the destruction is molecular and gradual. It may occur in con- 
 nection with any form of osteitis, with periostitis, and osteomyelitis, or 
 it may be secondary to inflammatory or destructive j)rocesses in the 
 joints or adjacent soft parts. The depressed surfaces of bones in which 
 •caries is progressing are rough and more or less finely jagged, and may 
 be covered with granulations. The minute changes by which ulceration 
 and destruction of the bone are produced in caries are somewhat analo- 
 gous with those in rarefying osteitis, but there are marked degenerative 
 changes in the bone-cells, which may become fatty or converted into a 
 granular material. Moreover, the basement substance of the bone, in- 
 stead of being absorbed, may disintegrate with the formation of larger 
 ■and smaller masses of detritus. Sometimes the lime salts are removed 
 from the basement substance, which is converted into atypical fibrillar tis- 
 sue and fatty and granular detritus. Very extensive suijpurations and 
 necrosis may be associated with caries. 
 
 Long-continued caries, especially in badly-nourished individuals, is 
 •apt to become complicated with tubercular inflammation. 
 
462 THE BONES. 
 
 There is very little tendency to- spontaneous healing in caries, but it 
 may occur, and the defects produced may be more or less supplied by 
 means of new-formed bone. 
 
 RACHITIS (rickets.) 
 
 Eickets is a disease affecting the development of bone, preventing 
 its proper ossification. The disease usually occurs during the first two 
 years of life, but may be congenital, or may occur as late as the twelfth, 
 year. 
 
 The physiological growth of bones depend upon three conditions. 
 They grow in length by the production of bone in the cartilage between 
 the epiphysis anddiaphysis; in thickness, by the growth of bone from the 
 inner layers of the periosteum. At the same time, the medullary canal is 
 enlarged in proportion to the growth of the bone by the disappearance of 
 the inner layers of bone. 
 
 In rickets, these three conditions are abnormally affected. The 
 cartilaginous and subperiosteal cell-growth, which precedes ossification, 
 goes on with increased rapidity and exuberance, and in an irregular 
 manner, both between the ejDiphyses and diaphyses, and beneath the 
 periosteum, while the actual ossification is imperfect, irregular, or want- 
 ing. At the same time, the dilatation of the medullary cavity goes on 
 irregularly, and often to an excessive degree. 
 
 If we examine microscopically the region between the epiphysis and 
 diaphysis, wo find that the cartilage cells are not regularly arranged in 
 rows along a definite zone in advance of the line of ossification, as in 
 normal development, but that there is an irregular heaping up of carti- 
 lage cells, sometimes in rows, sometimes not, over an ill-defined and 
 irregalar area. The zone of calcification also, instead of being narrow, 
 regular, and sharply defined, is quite lacking in uniformity. Areas of 
 calcification may be isolated in the region of proliferating cartilage cells, 
 or calcification may be altogether absent over considerable areas. 
 
 Corresfionding to these irregularities, the ossification zone is also 
 irregular. New-formed bone and marrow cavities containing blood- 
 vessels may lie in the midst of the cartilage, or masses of cartilage may 
 lie deep in the region which should be completely ossified. In other 
 places, it seems as if the cartilage tissue were directly converted into an 
 ill-formed bone-tissue by metaplasia or direct transformation. It will 
 readily be seen from this that the medullary spaces of the new-formed 
 bone are irregular, and this abnormality is enhanced by the premature 
 intramedullary absorption of the bone. 
 
 The same sort of irregularity in the bone formation may be seen be- 
 neath the periosteum. An excessive proliferation of cells in the inner 
 layers of the periosteum, the irregular calcification which occurs about 
 them, and the absence of uniformity in the elaboration of ill-structured 
 
THE BOKES. 463 
 
 bone, conspire to produce an irregular spongy bone-tissue instead of the 
 compact lamellated tissue which is so necessary here for the solidity of 
 the structure. The increased cell-growth between the epiphyses and 
 diaphyses produces the peculiar knobby swellings which are characteris- 
 tic of rickets. At the same time, the medullary cavity increases rapidly 
 in size, and the inner layers of the bone become spongy. The medulla 
 may be congested, and fat, if it has formed, may be absorbed, and a 
 modified form of osteitis may ensue. 
 
 The result of these processes is, that the bones do not possess solidity 
 and cannot resist the traction of the muscles or outside pressure. The 
 epiphyses may be displaced or bent, especially in the ribs, less frequently 
 in the long bones. The long bones and the pelvic bones may be bent 
 into a variety of forms. Incomplete fractures are not infrequent. Com- 
 plete fractures do not usually occur until the later stages of the disease, 
 when the bones have become more solid. In the head, the cranium may 
 be unnaturally large for the size of the face; the fontanelles and sutures 
 may remain open; the bones may be soft, porous, and hypersemic; while 
 at their edges there may be rough bony projections beneath the peri- 
 cranium. Sometimes, especially in the occipital bone, there are rounded 
 defects in the bone filled only with a fibrous membrane; this constitutes 
 one of the forms of so-called craniotabes. 
 
 It does not fall within the scope of this work to describe the various 
 deformities which may occur as a result of this disease. The familiar 
 pigeon breast; the rows of knobs along the sides of the chest from bend- 
 ing and dilatation of the ribs at the point of junction of cartilage and 
 bone; the knock-knee, bow-legs, spinal curvatures, etc., may all be the 
 result of rachitic weakening of the bones. 
 
 After a time, the rachitic process may stop, and the bones take on a 
 more normal character. The porous bone-tissue becomes compact aud 
 even unnaturally dense, the swellings at the epiphyses disappear, many 
 of the deformed bones may become of a normal shape. In severe cases, 
 however, the deformities continue through life; especially is there a cessa- 
 tion of the growth of the bones in their long axis, so that the persons 
 affected are dwarfed. 
 
 The disease may have an acute or a chronic character. The acute form 
 begins usually during the first six months of life. The children suffer 
 from vomiting, diarrhcea, profuse sweating, chronic bronchitis and pneu- 
 monia, general anaemia, and wasting. They either die, or the rachitic 
 process is gradually developed. The chronic form is seen in older chil- 
 dren, and often in those apparently healthy. The changes in the bones 
 may take place without any constitutional symptoms, though there is 
 often catarrhal bronchitis, pneumonia, and anfemia. 
 
464 
 
 THE BONES. 
 
 OSTEOMALACIA. 
 
 This lesion consists in the softening of fully formed hard bone-tissue 
 by the removal of its inorganic salts. It is to be clearly distinguished 
 from rickets, whose lesions are due to a faulty development of bone, al- 
 though in certain external characters the two diseases sometimes present 
 considerable similarity. Osteomalacia usually occurs in adults, most 
 frequently in females during pregnancy and after parturition ; more 
 rarely it occurs in males, and in females uuassocialed with the above 
 conditions. Its cause is not known. 
 
 Microscopical examination shows that the decalcification occurs first 
 in the periphery of the Haversian canals and in the inner layers of the 
 walls of the marrow spaces. As the salts of lime are removed, the base- 
 ment substance at first remains as a finely fibrillated material still preserv- 
 ing the original lamellation. The bone-cells may be changed in shape 
 or degenerated. After a time the decalcified tissue may disintegrate and 
 be absorbed and its place occupied by new-formed marrow or granulation 
 tissue. As the disease goes on, the marrow tissue is congested and red, 
 the fat absorbed, and there is a great accumulation of small spheroidal 
 cells; or the marrow may assume a gelatinous appearance. The decal- 
 cification and absorption of the bone from within may proceed so far 
 that the bony substance in the cancellous tissue almost entirely dis- 
 appears and the compact bone is reduced to a thin soft decalcified tissue. 
 The disease is not always continuously progressive, but may be subject to 
 temporary cessation. 
 
 As a result of this softened conditions of the bones the weight of the 
 body and the actions of the muscles may induce a series of deformities 
 which are sometimes excessive: curvatures of the spine, complete and in- 
 complete fractures of the bones, distortions of the pelvis, sternum, etc. 
 There is a tendency in this disease to a general involvement of the bones, 
 but the changes are sometimes confined to single bones or groups of 
 bones. The cranium is rarely much afliected. 
 
 ALTERATION'S OF THE BONE-ilAKROW IN LEUKEMIA AND ANEMIA. 
 
 In certain forms of leukemia, the marrow of the bones is very mark- 
 edly altered. The change consists mainly in an accumulation in the 
 marrow-tissue of small spheroidal cells often in a condition of fatty 
 degeneration, which lie in the meshes of reticular connective tissue, 
 and in and along the walls of the blood-vessels. There may also be 
 absorption of the fat and sometimes enlargement of the marrow cavity 
 from absorption of the bone. The marrow cavity may also contain, 
 intermingled with its other elements, nucleated red blood-cells, small 
 spheroidal cells, which contain red blood-cells (Fig. 13G), and not infre- 
 
THE BONES. 
 
 465 
 
 quently considerable numbers of small octahedral crystals (called Char- 
 cot's crystals). 
 
 The degree to which this accumulation of cells occurs varies much in 
 different cases,, and the gross appearances of the marrow are consequently 
 very variable. In some cases the marrow is soft and has a uniform 
 
 Fig. 136. — Cells from the Marrow of Femur in Leukemia, X 750 and reduced, 
 a, Spheroidal and elongated cells containing small red blood-cells or fragments of red blood- 
 cells; b, small spheroidal cells in condition of fatty degeneration; c, cell similar to the last but not 
 fatty ; d, nucleated red blood-cells. 
 
 red appearance, or it is variously mottled with gray and red. Occasion- 
 ally circumscribed hemorrhages are seen. In another class of cases in 
 which the cell accumulation is more excessive, the marrow may be gray, 
 grayish-yellow, or 23uriform in appearance. 
 
 ,These changes may occur in the central marrow cavity, as well as in 
 the marrow spaces of the spongy bone. They may be present in several or 
 many of the bones. They are usually accompanied by analogous changes 
 in the spleen and lymph-glands. 
 
 In certain cases of acute and chronic anmmia, particularly in the per- 
 nicious and progressive varieties, the marrow, especially of the larger 
 long bones, may lose its yellow color from absorption of the fat, and be- 
 come red. Microscopical examination of the marrow under these con- 
 ditions shows considerable increase of small spheroidal cells, and some- 
 times an abundance of developing nucleated red blood-cells and Charcot's 
 crystals. 
 
 In many of the acute infectious diseases, typhus and typhoid fever, 
 ulcerative endocarditis, recurrent fever, etc., the bone-marrow has been 
 found hyperssmic and containing an unusual number of small spheroidal 
 cells. 
 
 All of these lesions of the ma,rrow, although our knowledge of them 
 is still very incomplete, together with what is known of the physiological 
 functions of the marrow, point to a close relationship between the mar- 
 row and the spleen and lymph-glands as blood-producing organs.' 
 
 ' The literature of the researches on the diseases of the spleen may be found 
 30 
 
466 THE BOHTES. 
 
 ATROPHY. 
 
 In old age or in senile conditions the bones may become atrophied by 
 the absorption of the hard tissue; the medullary spaces are enlarged, the 
 marrow tissue contains less fat, and is often gelatinous in appearance. 
 As the result of the lack of use or from any cause which interferes with 
 the nutrition of the bone, such as paralysis of the muscles or diseases of 
 the joints, the bones may atrophy. In connection with atrophy, there 
 may be an ossifying periostitis, which results in making the bone look even 
 larger than normal. Many of the conditions commonly called atrophy, 
 such as the erosions of bone from tumors, etc., pressing upon them, are 
 really due to a rarefying osteitis. 
 
 The bones, sometimes as the result of atrophy, and sometimes from 
 causes which we do not understand, are unusually brittle and liable to 
 fracture. This disposition is sometimes hereditary. 
 
 TUMORS. 
 
 Tumors of the bone may involve either the periosteum, the compact 
 bone, or the medulla, or, as is more frequently the case, two or more 
 of these structures are involved at once. Tumors of the bone are usually 
 accompanied by various secondary and sometimes very marked altera- 
 tions of the bone-tissue, osteoporosis, osteosclerosis, ossifying periostitis, 
 etc. The new growths are very apt to undergo calcification and ossifica- 
 tion. 
 
 Fibromata may grow either from the periosteum or medulla. Their 
 most common seat is in the periosteum of the bones of the head and face. 
 They are apt to form polypoid tumors projecting into the posterior nares, 
 pharynx, mouth, and antrum of Highmore. Central fibromata, i. e., 
 those growing from the medulla, are rare. They usually occur in the 
 lower jaw, but have been found in the ends of the long bones, the pha- 
 langes of the fingers, and the vertebrse. The fibromata may calcify or 
 ossify, contain cysts, and not infrequently occur in combination with 
 sarcoma. 
 
 Myxomata are of occasional occurrence in bone. 
 
 Oateomata. — New formations of bone, as a result of inflammatory 
 processes, are, as we have already seen, of frequent occurrence in bone, 
 and although not strictly-speaking tumors, some of their forms are very 
 closely allied to them, and they may, therefore, be conveniently mentioned 
 here. New growths of bone which arise from the surfaces are called ex- 
 ostoses or enostoses, according to their origin from the external surface or 
 interior of the bone. They may contain all the constituents of normal 
 bone: bone, medulla, vessels, periosteum, and cartilage. The new bone 
 
 in part in Orth's "Lehrbuch der speciellen pathologischen Anatomie." Berlin^ 
 1883. Erste Lieferung, p. 119 et seq. 
 
THE BONES. 467 
 
 maybe compact and like ivory, or spongy, or contain large cavities filled 
 with marrow. 
 
 The shape of exostoses varies greatly; they may be in the form of sharp, 
 narrow spiculae and processes, and occurring in connection with periostitis 
 are called osteophytes. They maybe polypoid in shape, or form rounded 
 tumors with a broad base. They may form a general enlargement of the 
 bone, with much roughening of the surface; this condition is often called 
 hyperostosis. 
 
 The bone beneath these new growths may be normal, or sclerosed, or 
 rarefied, or the medullary cavity of the bone may communicate with that 
 of the exostosis. Exostoses are usually developed from the periosteum, 
 sometimes in the insertion of tendons and ligaments. They are very fre- 
 quently multiple, and may occur at all ages, even during uterine life. 
 
 Enostoses are developed in the interior of bones from the medulla. 
 They may increase in size with absorj)tion of the surrounding bone, until 
 they project from the surface like exostoses. Their most frequent situ- 
 ation is in the bones of the cranium and face. 
 
 Ohondromata.- — These tumors may be single or multiple, and most 
 frequently grow from the interior of the bone, bait sometimes from the 
 periosteum. They are prone to form various combinations with other 
 forms of tumors, as fibroma, myxoma, sarcoma, etc. They are fre- 
 quently congenital and are most common in young people. They occur 
 most frequently in the bones of the hand and foot. 
 
 There is a form of chondroma called osteoid chondroma, which devel- 
 ops beneath the periosteum, most frequently in the femur and tibia near 
 the knee-joint, forming a club-shaped enlargement of the bone. The 
 characteristics of the tissue composing these tumors are, that it resembles 
 somewhat the immature bone-tissue which is seen beneath the periosteum 
 in developing bone. It differs from cartilage in the irregular shape of its 
 cells, in the fibrillation and density of the basement substance, and in its 
 general vascularity. On the other hand, it has not the inorganic con- 
 tents or appearance of true bone. It resembles considerably the callus 
 tissue forming about fractures of the bones. It may, however, and most 
 frequently does, become converted in some parts of the tumor into true 
 bone. On the other hand, combinations with sarcomatous tissue are of 
 frequent occurrence (see below). 
 
 Sarcoma. — This form of tumor is especially common in the bones. It 
 grows from the inner layers of the periosteum, or from the medulla, so 
 that we may distinguish a periosteal and a tnyelogenic sarcoma. Some- 
 times the tumor attacks the bone itself so early that it is impossible to 
 say whether the tumor began in the periosteum or in the medulla. There 
 is also a variety which grows close to the outside of the periosteum, and 
 becomes connected with it — parosteal sarcoma. 
 
 The periosteal sarcomata usually belong to the varieties fibro-, myxo-. 
 
468 THE BOTSTES. 
 
 cliondi'o-, and osteo-sarcoma, more rarely to the medullary variety. They 
 commence from the inner layers of the periosteum, pushing this mem- 
 brane outward. After a time the periosteum is attacked, and the tumor 
 invades the surrounding soft parts. The bone beneath may remain nor- 
 mal, or may be eroded and gradually disappear until the tumor is con- 
 tinuous with the medulla. Portions of the tumor may be calcified, or a 
 growth of new bone may accompany its growth. The new bone usually 
 takes the form of plates, or spiculse, radiating outward. The minute 
 anatomy of these tumors is very variable. The simplest — the fibro-sar- 
 comata — are composed of fusiform, round, stellate, and sometimes giant- 
 cells (myeloplaxes), in variable proportions, packed closely in a fibrous 
 stroma. In the medullary form, the stroma is diminished to a minimum, 
 and the round cells are most numerous. In the chondro- and myxo-sar- 
 coma, the basement substance may be hyalin, or mucous, and the cells 
 follow the type of cartilage and mucous tissue more or less closely. 
 There is a mixed form of tumor, called osteoid-sarcoma, which is very apb 
 to spread and to form metastases. The growth consists in part of tissue 
 corresponding to fibro-sarcoma, and round-celled sarcoma. In addition 
 to this, there occurs in greater or less quantity immature bone-tissue 
 called osteoid tissue, which may in part become calcified; the calcifica- 
 tion usually occurring in the central portions leaving a softer peripheral 
 zone. This form of tumor is most apt to occur at the ends of the long 
 bones, and may form tumors of large size. It is often called, on account 
 of its tendency to spread, and to form metastases, malignmit osteoma or 
 osteoid cancer. 
 
 Myelogenic sarcomata commence in the medulla and may grow 
 rapidly. The bone surrounding them is destroyed, and they project as 
 rounded tumors. Most frequently, new bone is formed beneath the peri- 
 osteum, so that the tumor is inclosed in a thin, bony shell; sometimes 
 there are also i^lates of bone in the tumor; sometimes the periosteum is 
 unaltered; sometimes it is perforated, and the tumor invades the sur- 
 rounding soft parts. The tumors are frequently very soft, vascular, and 
 hemorrhagic in parts, or may inclose cysts filled with tumor detritus and 
 blood. They are usually of the spindle or round-celled variety and not 
 infrequently contain giant-cells. 
 
 The par osteal sarcomata resemble the periosteal, but they appear to 
 grow from the outer layers of the periosteum. They may be as firmly 
 connected with the bone as the periosteal form. The periosteum may 
 remain intact between the tumor and the bone, or it may disappear and 
 leave them in apposition. 
 
 Angiomata and Aneurism of Bone. — A very large number of the 
 tumors which have been described under these names are really sarco- 
 mata, or other tumors which happened to be very vascular. Some 
 authors, indeed, are disposed to deny altogether the existence of real 
 
THE BONES. 469 
 
 Tascnlar tumors in bones. There are, however, reliable cases of cavern- 
 ous angiomata growing between the periosteum and bone, and intimately 
 connected with the latter. Whether myelogenic angiomata occur is 
 doubtful. There are several cases described of cavities filled with blood 
 in the interior of bones, which it is difficult to interpret. They have 
 mostly been found in the head of the tibia. They are said to have con- 
 sisted of single sacs composed of thickened periosteum lined with plates 
 of bone, and filled Avith fluid and clotted blood. N"o large vessels com- 
 municated with the sacs, but their walls were covered which a rich vas- 
 cular plexus, branches of which opened into the cavity of the sac. 
 
 Carcinomata. — Primary carcinomata are of very doubtful occurrence 
 in the bones. Most of the structures thus named have doubtless been 
 sarcomata. Secondary carcinomata, on the other hand, as a result of 
 metastases, or local extension, are of not infrequent occurrence and pre- 
 sent various structural forms. Metastatic carcinomata may occur in the 
 bones of various parts of the body at the same time, and are most .apt to 
 be secondary to carcinoma of the mamma. 
 
 Cysts. — These most frequently occur in the maxillary bones, doubtless 
 in connection with the teeth. They may be unilocular or multilocular, 
 and contain clear serum or a mucous or brown fluid, and sometimes 
 cholestearin. Tliey may be lined with ejiithelinm. They begin in the 
 interior of the bone, and, as they increase in size, expand it until they 
 may be covered with only a thin shell of bone. They may reach a large 
 size, even as large as a child's head. 
 
 Dermoid cysts are occasionally found in connection with the bones, 
 particularly of the skull. 
 
 PARASITES. 
 
 EcMnococcus and cysticercus are of rather rare occurrence in the 
 bonfis; the former is most frequently found. 
 
DISEASES OF THE JOINTS. 
 
 For a description of the dislocations, misplacements, and injuries of 
 the joints we refer to works on surgery. 
 
 INFLAMMATION. 
 
 Acute arthritis. — The earlier stages of acute inflammation of the 
 synovial membranes ai^ better known from experiments on animals than 
 from post-mortem examinations. The first changes are swelling and 
 congestion of the membrane, with increased growth and desquamation of 
 epithelium, and infiltration of the membrane with lymphoid cells. These 
 conditions are soon followed by an exudation. The exudation may be 
 a clear serum, in which epithelial cells, lymphoid cells, and sometimes 
 blood will be found. Or flocculi of fibrin may float in the serum, or the 
 fibrin may be in excess and the serum nearly absent. Or there is an 
 excessive production of lymphoid cells, and the synovial sac is filled with 
 pus. 
 
 In serous arthritis, the accumulation of serum within the synovial sac 
 is the most prominent lesion. The disease may terminate in recovery, 
 or become chronic, or pass into the suppurative form. It may be caused 
 by contusions, penetrating wounds, gonorrhoea, rheumatism, or it may oc- 
 cur without evident cause. 
 
 Sero-fibritious arthritis may occur under the same conditions as those 
 which lead to simple serous inflammation. The fibrin may be present 
 largely as flocculi in the serum, or it may form false membranes over 
 the surfaces of the joint. 
 
 Purulent arthritis may follow or be associated with the above forms 
 of inflammation. The synovial membrane is thickened and cloudy, and 
 there may be but a moderate amount of pus in the joint, and a slight 
 degree of infiltration of the synovial membrane with pus-cells. Under 
 these conditions resolution may readily occur. 
 
 In other cases, the accumulation of pus in the cavity may be great, 
 the synovial membrane and its surrounding tissue densely infiltrated with 
 pus-cells. Under these conditions, granulation tissue is apt to be found, 
 
DISEASES OE THE JOINTS. 471 
 
 and the cartilages of the joints are apt to become involved. There is 
 swelling and proliferation or degeneration of the cartilage cells; the 
 basement substance becomes disintegrated, ulcerates, and exposes the 
 bone, in which osteitis, caries, rarefaction, etc., may occur. The new- 
 formed granulation tissue may penetrate the cartilage, absorbing the base- 
 ment substance, and by metaplasia the cartilage tissue may be converted 
 into embryonal or granulation tissue. The pus may brealc through the 
 capsule of the joint and form large abscesses in the adjacent soft parts. 
 Sometimes the inflammation is not only suppurative, but gangrenous, 
 and runs a rapidly fatal course. The synovial membrane, arbioular car- 
 tilages, and ends of the bone, all undergo a rapid suppuration and gan- 
 grene. Pyaemia and septiceemia, small-pox, measles, scarlet fever, 
 diphtheria, mumps, typhus fever, glanders, the puerperal condition, 
 exposure to cold, penetrating wounds, and injuries may all give rise to 
 purulent synovitis. 
 
 Chronic arthritis may begin as such, or it may be the result of 
 previous acute inflammation. There is an increase of fluid in the joint. 
 This fluid is thin and serous, or is thickened with flocculi of fibrin 
 and epithelial and lymphoid cells, or is thick, syrupy, or even gelatinous. 
 The synovial membrane is at first congested, its tufts prominent. Later 
 it becomes thickened, sclerosed, and ansemic; the epithelium is de- 
 stroyed, and the tufts become large and projecting. From the distention 
 of the capsule there may be subluxations or luxations of the joint; or the 
 capsule may be ruptured. 
 
 Chronic rheumatic arthritis is most common in elderly persons, 
 usually affecting several joints and advancing slowly and steadily. There 
 is a chronic thickening of the synovial membrane, and the fibrous tissue 
 adjacent to it. Fluid accumulations are not common. The articular 
 cartilages are apt to degenerate or ossify, or become softened and fibril- 
 latcd, and they may disappear. The contracting synovial membranes 
 and fibrous tissue render the joints stiff, and may cause considerable de- 
 formity. Kot infrequently fibrous and bony anchyloses are formed between 
 the ends of the bones. 
 
 Arthritis deformans. — This name has been applied to a variety of 
 chronic inflammation of the joints which, combined with degeneration 
 of parts of the joint and the new formation of bone, may result in marked 
 deformities of the part. 
 
 It usually occurs in elderly persons, and is apt to involve several joints, 
 most frequently the hip, knee, fingers, and feet. It may be idiopathic, 
 or due to rheumatism, to injuries, or follow an acute arthritis. The 
 capsules of the affected joints are thickened and sclerosed. The syno- 
 vial fluid is at flrst increased in quantity; later, diminished and thickened. 
 The tufts of the synovial membrane become much enlarged and vascular; 
 they may be converted into cartilage. Sometimes the capsule becomes 
 
472 DISEASES OF THE JOINTS. 
 
 ossified. The new bone grows from the edge of the cartilage within the 
 capsule. Its articular surface is covered with cartilage. The articular 
 cartilages are much changed. The basement substance splits into tufts, 
 while the cartilage cells are increased in number. Or the basement sub- 
 stance becomes fibrous; or it is split into lamellse and the cartilage-cells 
 are multiplied; or there is fatty degeneration and atrophy. 
 
 As a result of these changes, larger or smaller portions of the cartilage 
 are destroyed, and the bone beneath is laid bare. The exposed bone may 
 become compact and of an ivory smoothness. The ends of the bones are 
 much deformed. They are flattened and made broader by irregular new 
 growths of bono, while at the same time they atrophy. The new growth 
 of bone starts from the articular cartilages. The cartilage-cells increase 
 in number, and the basement substance in quantity. This growth is 
 most excessive at the edge of the cartilage, so that a projecting rim is 
 formed there. This projecting rim may ossify next the bone, and at the 
 same time new cartilage may form on its surface, so that we may find 
 large masses of bone covered with cartilage. All these changes occur in 
 in various combinations and sequences, so that joints in this condition 
 present the greatest variety of appearances. 
 
 Arthritis uritica (Gouty Arthritis). — This disease is characterized 
 by the dejsosit of salts of uric acid in the cartilages, bones, and liga- 
 ments, and also in the cavity of joints. The deposits may be in the form 
 of stellate masses of acicular crystals in and about the cartilage-cells, or 
 in the basement substance; or they may be dejoosited in the fibrillar con- 
 nective-tissue structures of the joint in single crystals ; or in the subcu- 
 taneous tissue about the joint, as white concretions. The deposits may 
 occur in repeated attacks of the disease, and are accompanied by acute 
 inflammatory changes. They may lead to various forms of chronic 
 inflammation of the joints. 
 
 Tubercular arthritis (Chronic fungous Arthritis — Strumous Arthri- 
 tis). — This disease may commence in the joint itself, or be transmitted 
 to it from a tubercular inflammation of the bone. It is characterized 
 by the formation of granulation tissue containing tubercles, sometimes 
 in great quantity, and usually associated with secondary inflammatory 
 and degenerative changes of surrounding parts. According to the 
 prominence of one or other of these secondary alterations, several 
 forms of tubercular arthritis may be distinguished. If there is an 
 excessive growth of granulation tissue without much suppi]ration, 
 this constitutes a fungous form. Sometimes there is extensive su])~ 
 juration, so that the cavity of the joint may be filled with pus, which 
 may be discharged through openings in the skin ; or there may 
 be more or less extensive formation of abscesses or infiltration of the 
 soft parts about the joint with pus. In other eases, there is a 
 predominent tendency to breaking down of the new-formed tubercular 
 
DISEASES OF THE JOINTS. 473 
 
 tissue, and of the tissues of the jomt—ulcerative form. The cartilao-e 
 basement substance may become split into fragments and the cells deo-en- 
 erate, and thus deep and destructive ulcers of the cartilage be formed. 
 Or, the granulation tissue may work its way through the cartilage into 
 the bone beneath, by absorption of the basement substance of the carti- 
 lage, with or without proliferation of its cells. Caries and necrosis of 
 the underlying bone may lead to extensive destruction. Hand in hand 
 with these alterations, subperiosteal new formation of bone may occur, 
 or sclerosis of the adjacent bone-tissue. There may also be a great in- 
 crease of fibrous tissue about the joint. Tubercle bacilli may be found 
 in the tubercular tissue and in the exudations. 
 
 This disease is most common in children and young persons. The 
 so-called scrofulous diathesis is said to dispose to it, but local injuries are 
 frequently the exciting cause. It is most common in the large joints. It 
 may occur in connection with tubercular inflammation in other parts of 
 the body; but it is frequently quite local, and may remain so for a very 
 long time or permanently; since general infection from tubercular arthri- 
 tis is comparatively infrequent. 
 
 The disease always runs a very chronic course and may destroy the 
 patient's life. If recovery takes place before the cartilages and bones are 
 involved, the joint is preserved; but it may be stiffened, or even immova- 
 ble, from the contraction of the new fibrous tissue around it. If the 
 cartilages and bones are diseased, the joint is destroyed, and either bony 
 or fibrous anchylosis results. Sometimes from the change in the articu- 
 lating surfaces, and the contraction of the muscles and the new fibrous 
 tissue, partial or complete dislocations are produced. 
 
 Occasionally miliary tubercles occur in the synovial membranes in 
 cases of general miliary tuberculosis, with but little accompanying simple 
 inflammatory change. 
 
 TUMORS. 
 
 Secondary tumors of the joints as a result of local extension from the 
 adjacent parts are not uncommon, and the tumors may be of various 
 kinds. Primary tumors of the joints, on the contrary, are not very 
 common. 
 
 Lipoma. — A new growth of fatty tissue may begin in the other por- 
 tions of the synovial membrane, push this inward, and project into the 
 joint in a mass of tufts — lipoma arborescens. 
 
 Filroma occurs as an hypertrophy of the little tufts and fringes of the 
 synovial membrane. In this way, large polypoid and dendritic bodies are 
 formed. The pedicles of these growths may atrophy and even disappear, 
 so that the growths are left free in the cavity of the joints. 
 
 Corpora Aliena Articulorum—Looze. Cartilages in the Joints.— These 
 names are given to bodies of various structure and origin, which are 
 
474 DISEASES OF THE JOINTS. 
 
 found free, or attached by slender pedicles in the cavities of the joints. 
 They are most frequently found in the knee; next in order of frequency? 
 in the elbow, hips, ankle, shoulder, and maxillary joints. They may be 
 single, or in hundreds. Their size varies from that of a pin's head to 
 that of the patella. They are polypoid, rounded, egg-shaped, or almond- 
 shaped; their surface is smooth or facetted, or rough and mulberry-like. 
 They are composed of fibrous tissue, cartilage, and bone in various pro- 
 portions. 
 
 These bodies are formed in different ways. 
 
 (1) By hypertrophy of the synovial tufts, and production of cartilage 
 and bone in them. 
 
 (3) More frequently by a change into cartilage of portions of the 
 synovial membrane. Small, flat plates of cartilage form on the inner 
 surface of the synovial membrane, and these increase in size and their 
 outer layers ossify. They may remain fixed in the synovial membrane, 
 or they project and become detached from it, and they then appear as 
 flattened concave bodies, composed of bone covered with cartilage on one 
 side. 
 
 (3) The growth of cartilage and bone begins in the outer layers of 
 the synovial membrane, or in the periosteum, near the joint. The new 
 growth pushes the synovial membrane inward, and projects into the 
 joint as a polypoid body covered with the inner layers of the synovial 
 membrane. Later, the membrane atrophies, and the growth becomes 
 free in the joint. 
 
 (4) There may be cartilaginous outgrowths from the edges of the 
 articular cartihiges. 
 
 (5) Earely portions of the articular cartilages may be detached by 
 violence or disease ; or flbrinous and other concretions may result from 
 arthritis, or under conditions which we do not understand. 
 
MUSCLE. 
 
 LESIOKS OF VOLUKTART STRIATED MUSCLE. 
 
 HemorrJiage.—Th\s may occur as a result of mechanical injury; from 
 rupture of the fibres by convulsive contraction, as in tetaaus ; or it may 
 occur when the muscle-fibres are degenerated, as in typhoid fever ; or in 
 connection with certain general diseases, as scurvy, purpura, hemorrha- 
 gic diathesis, septicaemia, etc. The blood is usually readily absorbed. 
 
 Embolic Infarction of Muscles in connection with heart disease has 
 been described in a few cases, but it is rare. 
 
 Wounds and Rupture.— Wh^XY the muscle-fibres are severed by 
 wounds or rupture, there is more or less degeneration of the divided 
 fibres, and the wound may heal by the production of granulation tissue, 
 which gradually becomes converted into cicatricial tissue, thus binding 
 the severed parts together. In some cases there is a new formation of 
 muscle-fibres, which penetrate the cicatrix and establish muscular con- 
 nection between the parts. When the wound does not gap, so that the 
 severed ends are not much separated, there may be, it would seem, a 
 direct re-establishment of muscular continuity by new development of 
 muscle, without the formation of much new connective tissue. 
 
 The exact way in which muscle-fibres are regenerated is yet somewhat 
 uncertain. In many cases, there seems to be a proliferation of the so- 
 called muscle-corpuscles leading to the formation of elongated cells or 
 strings of cells, which are gradually converted into striated muscle. In 
 some cases the appearances would seem to indicate that connective-tissue 
 cells, and perhaps white blood-cells, may participate in the formation of 
 new muscle-fibres, but this is not certain.' 
 
 INFLAMMATION. 
 
 Suppurative Myositis. — In the early stages of this lesion we find the 
 muscle hypersemic and oedematous, and the interstitial tissue more or less 
 
 ' For literature of muscle regeneration, consult Llideking: " Untersuohungen 
 u. d. Eegeneration d. quergest. Muskelfasei'n," Strassburg, 1876 ; or Recklinghau- 
 sen: "Handbuchd. allg. Pathologie," in Billroth and Lticke's "Deutsche Chirur- 
 gie," Parts 2 and 3, p. 388, and bibliography, p. xxix. 
 
476 
 
 MtJSCLE. 
 
 infiltrated witli small splieroidal cells, doubtless the result of emigration. 
 If the inflammation becomes intense, there may be an excessive accumu- 
 tion of pus-cells, either diffusely in the interstitial tissue or in larger and 
 smaller masses. Hand in hand with this cell accumulation, occur degen- 
 erative changes in the muscle-fibres. By pressure, their nutrition is 
 interfered with," and they undergo granular, fatty, or hyalin degenera- 
 tion. They may completely disintegrate and gangrene may occur, sa 
 that larger and smaller masses of the infiltrated muscle-tissue become 
 soft, foul-smelling, and converted into a mass of detritus in which but 
 little muscle structure can be detected, and which is intermingled with 
 bacteria. In other cases there may be larger and smaller abscesses 
 formed in the muscle ; the muscle-tissue itself either degenerating and 
 disintegrating and mixing with the contents of the abscess, or being 
 pressed aside and undergoing atrophy and degeneration. In some cases 
 when the formation of pus is moderate in amount, there may be restora- 
 tion, by formation of granulation tissue between the muscle-fibres. This 
 becomes gradually dense and firm, and leads to more or less atrophy of 
 the muscle-fibres by pressure. 
 
 Acute suppurative myositis may accompany wounds ; it is very com- 
 mon in acute phlegmonous inflammations of the skin and subcutaneous 
 tissue, and often accompanies acute infectious diseases, such as pyjemia, 
 erysipelas, etc. In many cases, colonies of micrococci are present in 
 the inflammatory foci. It is not infrequently seen in the muscles adja- 
 cent to the inflamed mucous membranes in diphtheria. 
 
 Acute Parenchymatous Myositis. — A few cases of this disease have 
 been described, in which, without lesion of the nervous system, certain 
 groups of muscles, with the occurrence of fever and pain, become swol- 
 len, in some cases beset with small hemorrhages, soft, mottled with yel- 
 lowish-white i^atches. Microscopically the muscle-fibres showed granular 
 and fatty, or in some cases waxy degeneration. The cause of this lesion 
 is not known. In one case the muscles of the legs were thus affected in 
 a woman who died in the first week after delivery, with fever and pain 
 in the legs, and the lesion was conjecturally of infectious origin.' 
 
 Chronic Interstitial Myositis. — In this lesion there is a new forma- 
 tion of connective tissue between the muscle-fibres or bundles of fibres. 
 This new tissue is sometimes very cellular, resembling granulation tissue, 
 and this probably represents an early stage of the disease. In other cases 
 (Pig. 137), we find dense cicatricial tissue crowding the muscle-fibres apart, 
 inducing atrophy in them, and sometimes causing their complete destruc- 
 tion. This lesion, which is the analogue of chronic interstitial inflamma- 
 tion of the internal organs, may occur in muscles which are adjacent to 
 
 ' Consult Eisenlohr, Centralblatt fiir Nervenheilkunde, i., 1S79 ; Marchand, 
 Breslauer Aerztliche Zeitschrift, 21, 1880. 
 
MUSCLE. 4'^'j- 
 
 other parts which are the seat of chronic inflammatory processes. It may 
 occnr m muscles which are not used. The new formation of connective 
 tissue would in some cases seem to be secondary to atrophy of the muscle- 
 fibres. 
 
 Fig. 137.— Chronic Interstitial Myositis, X 350 and reduced. 
 The connective tissue is dense in texture, and tlie muscle fibres are atrophied and partially 
 destroyed. 
 
 Myositis ossificans. — Under conditions and for reasons which we do not 
 understand, there occasionally occurs, usually in young persons, anew for- 
 mation of bone-tissue in the interstitial tissue of muscles; in the tendons, 
 ligaments,, fascise, and aponeuroses. This sometimes apparently starts as 
 outgrowths from the periosteum, sometimes not. The bone-formations 
 are apt to commence about the neck and back, and may become very 
 widespread over' the body. So far as the muscles are concerned, there is 
 ■usually an increase of connective tissue between the fibres and bundles, 
 in which new bone is formed, usually in elongated, and sometimes in 
 spicula-like masses. The muscle-fibres undergo secondarily a greater or 
 less degree of atrophy or degeneration. There may be fatty infiltration 
 between the fibres, and various deformities are produced by the shorten- 
 ing and progressive immobility of the afl'ected parts.' 
 
 While the above disease is a progressive and frequently a general one, 
 there may be new formation of bone in muscle as a result of prolonged 
 
 ■ The literature of Myositis ossificans may be found, togetlaer witli a description 
 fiome interesting cases, in an article by Mays, in Virch. Archiv, Bd. 74, p. 145. 
 
478 
 
 MUSCLE. 
 
 or repeated mechanical irritation. Thus in the adductors of the thigh, 
 in persons who are constantly in the saddle, or in the deltoid muscle of 
 soldiers who strike this part with their weapons in drill, there may be a 
 formation of bone. 
 
 Gummata and occasionally tubercles occur in the connective tissue of 
 muscle. 
 
 DEGENERATIVE CHANGES IN THE MUSCLES. 
 
 Simple Atrophy. — This may occur in old age, in prolonged exhaust- 
 ing diseases, or as a result of pressure from a foreign body, tumors, etc. 
 The muscle-fibres grow narrower, the degree of narrowing frequently 
 varying considerably in different parts. They usually retain the stria- 
 tion, but these may be obscured by degenerative changes. The sarco- 
 lemma may become thickened and there may be a considerable increase 
 in connective tissue between the muscle-fibres and bundles. 
 
 Progressive Muscular Atrophy. — This lesion consists essentially in a 
 combination of simple or degenerative atrophy of the muscle-fibres with 
 chronic interstitial inflammation, and is sometimes associated with pro- 
 liferative changes in the muscle nuclei. In the earlier stages of the dis- 
 ease, the muscles may be pale and soft, but exhibit otherwise to the 
 naked eye but little alteration. Gradually, however, the muscle sub- 
 stance becomes replaced by connective tissue, so that in marked and 
 advanced cases the muscles are converted into fibrous bands or cords, 
 whose cicatricial contraction may induce great defoi'mities. 
 
 Microscopical examination shows in the early stages of the disease a. 
 proliferation of cells in the interstitial tissue, so that this may have the 
 appearance of granulation or embryonal tissue; also in some cases marked 
 proliferative changes in the muscle nuclei, leading to the formation of 
 new cells which may more or less replace the contractile substance within 
 the sarcolemma. The new interstitial tissue increases in quantity and 
 grows denser, and may crowd the muscle-fibres apart. The walls of the 
 blood-vessels may also become thickened. Hand in hand with these in- 
 terstitial alterations, the atrophy of the muscle-fibres proceeds. These 
 may simply grow narrower, retaining their striations ; or they may split 
 up into longitudinal fibrillae ; or transversely into discoid masses, and in 
 this condition disappear. In other cases a certain amount of fatty or 
 hyalin degeneration may be present. These degenerative and prolifera- 
 tive changes do not, as a rule, occur uniformly in the affected muscles, 
 but some parts are affected earlier and more markedly than others. 
 
 Progressive muscular atrophy is apt to commence in the small mus- 
 cles of the extremities, in many cases in the muscles of the ball of the 
 thumb. It may commence in the muscles of the shoulder, the arms, or 
 the back. It may have a continuous extension or it may jump single 
 
MUSCI-E. 
 
 479 
 
 muscles or groups of muscles. Death may be induced by afEection of the 
 muscles of respiration or deglutition. 
 
 The causes of this lesion are in many cases unknown, and there is 
 considerable lack of unanimity of opinion as to whether it is primarily a 
 disease of the muscles or of the central nervous system. In a considera- 
 ble proportion of cases, the muscle lesion is associated with atrophy of 
 the ganglion-cells in the anterior cornua of the spinal cord and the devel- 
 opment of connective tissue about them. In other cases, these changes 
 in the cord may apparently be absent. 
 
 It is sometimes accompanied by atrophy of the nerves which are dis- 
 tributed to the muscles, and atrophy of the anterior roots has been 
 described. 
 
 It is probable that there are several varieties of progressive muscular 
 atrophy which our present knowledge does not enable us to clearly dis- 
 tinguish. Muscular atrophy in some cases follows overstraining of 
 groups of muscles, or injuries; and may occur as one of the sequelae of 
 typhoid fever and diphtheria. 
 
 Fig. 138.-FSEDDO-HYPBETROPHY OF Gastroonemios Mdscle (Fatty Infiltration), X 350 and 
 
 reduced. 
 The specimen is from the case mentioned below, accompanying multiple neuroma. 
 
 Airophia Musculorum Lipomatosa (Pseudo-hypertrophy of the mus- 
 cles).— In some cases, hand in hand with the production of new 'connec- 
 tive tissue in the muscles and the atrophy of the muscle-fibres, or after 
 
480 MUSCLE. 
 
 these changes have made considerable progress, there occurs a develop- 
 ment of fat-tissue between the fibres (Fig. 138), which may prevent any 
 appa,rent diminution in the size of the muscles, or in some cases even give 
 them a great increase in size. This condition is of most frequent occur- 
 rence in children, and is most apt to appear in the gastrocnemii muscles. 
 In the upper extremities, the deltoid and triceps are most frequently 
 involved. The lesions may be symmetrical, affecting similar muscles on 
 both sides of the body ; or it may be unilateral. Parts oi muscle-bellies 
 may be affected. 
 
 The cause of this form of atrophy is not definitely known. Various 
 lesions of the spinal cord have been described as occurring with it; but, 
 in many cases at least, alterations of the nervous system cannot be 
 detected. The writer (T.M.P.) has described a case' in which this 
 lesion was marked in the gastrocnemii in conneccion with multij^le false 
 neuromata.'' 
 
 Fatty Degeneration with greater or less destruction of the muscles 
 may commence with a simple swelling and fine granulation of the fibres. 
 As the process goes on, smaller and larger fat-droplets appear in the con- 
 tractile substance, which loses its striatious and becomes friable, and 
 may be entirely destroyed, leaving within the sarcolemma a mass of 
 fatty detritus, which may finally be absorbed and disappear. This alte- 
 ration may occur in acute parenchymatous myositis in connection with 
 various forms of atrophy; in prolonged exhausting diseases, and in phos- 
 phorus poisoning. 
 
 Hyalin Degeneration. — Under a variety of conditions the muscle- 
 fibres undergo a peculiar series of changes, leading to their conversion 
 into a translucent, highly refractile material, somewhat resembling amy- 
 loid, but not giving its micro-chemical reactions, and apparently more 
 nearly allied to the material produced in the so-called hyalin degeneration. 
 The lesion in the muscle which we are considering is commonly called tvaxy 
 degeneration, from the peculiar appearance which the muscles jiresent. 
 When the lesion is far advanced and extensive, the muscles are brittle and 
 have a grayish-yellow translucent appearance. Microscopical examination 
 of various stages of hyalin degeneration of muscle shows that the contractile 
 substance of the fibres becomes at first swollen and granular and gradu- 
 ally converted into hyalin material, which may present the outlines of 
 the swollen fibres, but is more frequently broken into larger and smaller 
 shapeless clumps (Fig. 139) which may disintegrate and finally be 
 
 ' American Journal of Medical Sciences, July, 1880, p. 134. 
 
 ' For bi bliography of muscular atrophy consult Fi-iedreich : ' ' Ueber progressive 
 Muskelatrophie," etc., Berlin, 1873; also " Dictionnaire encyclopedique des Sci- 
 ences Medicales," 2 ser. I., X.; or Eulenberg's" Real-Enoyclopadie der gesamm- 
 ten Heilkunde," article by Pick on Muskelatrophie. 
 
MUSCLE. 
 
 481 
 
 absorbed. Hand in hand with these changes, there usually occurs an 
 increase in the inter-fibrillar connective tissue, and in certain cases there 
 may be a proliferation of the muscle nuclei and a new formation of 
 variously-shaped cells within the sarcolemma, which leads to the regen- 
 eration of the fibres. As a result of the brittleness of the degenerated 
 muscles, they are apt to rupture, and in this way hemorrhage may occur. 
 
 Fig. 139.— Htalin Deseneration (Waxy Degeneration) of Abdominal Muscle in Typhoid 
 
 Fever, x TOO and reduced. 
 
 This form of degeneration may occur in progressive muscular atrophy, 
 in variola, cerebro-spinal meningitis, trichinosis, in connection with 
 inflammation, injuries, freezing, etc. It is, however, most m'arked and 
 frequent in typhoid fever. In this disease the rectus abdominis and the 
 adductors of the thigh are most frequently affected. 
 
 Experimental investigations have shown that under certain conditions 
 very similar appearances may be produced in the muscles by post-mortem 
 changes. It is not unlikely that a variety of changes are at present 
 included under the name waxy or hyalin degeneration of the muscles.' 
 
 Hypertrophy of Muscle. — True hypertrophy of muscle as a patholog- 
 ical condition is rare, but it has been described in a few cases. It is 
 usually confined to circumscribed groups of muscles. On microscopical 
 examination, the diameter of the fibres, is increased, sometimes consider- 
 ably, though not uniformly. The transverse striation is unaltered, and 
 the muscle-nuclei are in some cases enlarged. The cause of the change 
 is unknown. 
 
 TUMORS. 
 
 The tumors of the muscles usually develop in the connective tissue. 
 Fibroma, chondroma, lipoma, myxoma, sarcoma may occur as primary 
 tumors. Garcinomata and sarcomata may occur secondarily in the 
 muscles as a result of local extension from adjacent parts. The muscle- 
 fibres are as a rule only secondarily affected by pressure, etc., in tumors 
 of the muscles; but there exist observations which point to the possibility 
 
 1 Consult Zenker: " Ueber die Veranderung der willktlrlichen Muskeln in 
 Typhus abdominalis," Leipzig, 1864; also Weihl: "Exp. Unters. u. d. wachsartige 
 Degeneration der quergestr. Muskelf." Virch. Arch., Bd. 61, p. 253, 1874. 
 31 
 
482 MUSCLE. 
 
 of a proliferation of the muscle-nuclei and the new formation from them 
 of cells which may take part in the growth of the tumor. 
 
 PARASITES. 
 
 The Tricliina spiralis is the most common parasite in the muscles 
 (see p. 73). 
 
 Gysticercus cellulosce and Ecliinococcus occasionally occur. 
 
PART IV. 
 
 THE LESIONS FOUmD 
 
 IN 
 
 THE GEl^EEAL DISEASES 
 
 iisr 
 
 POISOl^Il^G 
 
 AND IN 
 
 TIOLEI^T DEATHS. 
 
TYPHOID FEYER.' 
 
 The lesions of typhoid fever are usually well marked and constant. 
 They may conveniently be divided into two classes. 
 
 I. Those which are characteristic of the disease. To this class belong 
 the changes in the lymphatic follicles of the intestines, in the mesenteric 
 :glands, and in the spleen. 
 
 I .Those which are very frequently found with this fever, and yet 
 «,re not peculiar to it. To this class belong the changes in the parotid 
 and pancreas, the degenerations in the liver, kidneys, and voluntary 
 muscles, thrombosis of the blood-vessels, infarctions, diseases of the 
 lungs, and suppuration of the connective tissue in various places. 
 
 I. Tlie Intestines. — The lesions of the intestines consist in an inflam- 
 matory enlargement and subsequent degeneration of the solitary glands 
 and Peyer's patches. 
 
 The process appears to begin with a catarrhal inflammation of the 
 mucous membrane, accompanied or immediately followed by changes in 
 the lymphatic follicles. The lesions in the lymphatic follicles begin 
 •early ; they have been observed in persons who have died forty-seven 
 hours after the commencement of the disease. 
 
 The increase in size of the agminated and solitary follicles may be 
 rapid or gradual. The follicles may be only slightly enlarged, or may 
 project so as to fill up the cavity of the intestine. The enlargement is 
 ■usually more marked in the agminated than in the solitary follicles. 
 Usually the whole of an agminated follicle will be enlarged, but some- 
 times only a part of it. If the enlargement is gradual, the different folli- 
 cles which make up a Peyer's patch are enlarged, while the septa between 
 them remain but little changed, and give the jDatch an uneven appear- 
 ance. 
 
 The patches which are only moderately enlarged are of reddish 
 ■or reddish-gray color, are soft and spongy, and their edges blend 
 gradually with the adjoining mucous membrane. The patches which 
 
 ■ The most complete description of the lesions of typhoid fever is that given 
 by Hoffmann: "Abdominal Typhus," 1869. 
 
486 TYPHOID FEVEE. 
 
 are more intensely affected are of gray or brownish color, of firm con- 
 sistence, and rise abruptly from the surrounding mucous membrane, or 
 even overhang it like a mushroom. The largest patches are sometimes 
 moreJ,han three-eighths inch thick. 
 
 The enlargement and infiltration may spread from the patches to the 
 surrounding njucous membrane, so that the patches appear very lai'ge, 
 a number of them may become fused together, and there may be even an 
 annular infiltration entirely around the lower end of the ileum. 
 
 The infiltration of the agminated follicles may also extend outward 
 into the muscular coat, and even appear beneath and in the peritoneal 
 coat as small, gray, rounded nodules. This condition is usually found 
 only with a few patches in the lower end of the ileum ; sometimes in the 
 cfficum and appendix vermiformis. These little gray nodules usually 
 correspond to diseased patches beneath them ; sometimes they appear to 
 excite an inflammation of the peritoneum, accompanied by the production 
 of numbers of similar nodules all over that membrane. Hoffmann describes 
 a case in which the inflammation extended to the pleura with the pro- 
 duction of similar nodules there. 
 
 The solitary follicles are affected in the same way as Peyer's patches. 
 They may be hardly enlarged at all, or be quite prominent, or may be 
 affected over a larger portion of the intestine than are the patches. 
 Very rarely the solitary follicles are enlarged, while the patches are not 
 at all or but slightly affected. 
 
 The inflammation and enlargement of the agminated and solitary 
 follicles is followed by a healing process. The character of this process, 
 varies according to the intensity of the previous inflammation. 
 
 (1) If the disease was mild, and the enlargement of the follicles 
 moderate, the enlargement gradually disappears, and the follicles resume 
 their normal appearance. 
 
 (2) In moderate enlargements, the retrograde processes affect first 
 the follicles, and leave the septa between them still swollen and promi- 
 nent. This gives to the surface of a patch a reticulated appearance. 
 After a time, however, the entire patch becomes flattened and uniform. 
 
 (3) The solitary follicles, or the separate follicles of a patch soften, 
 break down, and their contents are discharged with some attendant haem- 
 orrhage. This leaves a bluish-gray pigmentation in the situation of 
 each follicle. This pigmentation may remain for years. 
 
 (4) In more severe types, of the disease, the enlargement of the folli- 
 cles ends in ulceration. This takes place in two ways : 
 
 (a) The enlarged follicles soften, break down, and discharge into the 
 intestine. In this way are formed small ulcers. These ulcers increase 
 in size by the same softening process which gradually attacks their 
 edges, and in this way ulcers of large size may be formed. The ulcers 
 
TYPHOID FEVEE. 487 
 
 may extend outward only to the peritoneal coat, or they may involve the 
 peritoneal coat also and perforate. 
 
 (5) In the severest forms of the disease, considerable portions of the 
 enlarged patches slough, are detached, and leave large ulcers with thick, 
 overhanging edges. The slough may involve only the follicles, or it may 
 involve also the muscular and peritoneal coats. These ulcers also may 
 afterward increase in size, and several of them may be joined together. 
 
 If the patient recovers, the ulcers cicatrize, their edges become flat- 
 tened, their floors are converted into connective tissue covered with cylin- 
 drical epithelium. 
 
 Both forms of ulceration sometimes end in perforation. This is 
 effected by the extension of the ulcerative process through the perito- 
 neal coat, or by the rupture of the floor of the ulcer. Peritonitis and 
 death are the usual result. In rare cases, however, the patient recovers, 
 and the perforation is closed by adhesions. 
 
 The minute changes which take place in the course of the intestinal 
 lesion are as follows: 
 
 At first the blood-vessels around the follicles are dilated and con- 
 gested, while the follicles are swollen, and the epithelium falls off. Then 
 the follicles increase largely in size from a growth of new cells. The 
 new cells are, in part, similar to the lymphoid cells, which normally 
 compose the follicles ; in part are large, rounded cells, some of which 
 contain several nuclei. Tlie production of new cells is not confined to 
 the follicles, but extends also to the adjacent mucous membrane. In 
 many cases also, little foci of the same cells are found in the muscular, 
 subserous, and serous coats. This increased number of cells compresses 
 the blood-vessels, and the parts become anaemic. Soon the cells degen- 
 erate, either by granular degeneration of individual cells, or by gangrene 
 of part of a follicle. In either case the degenerated portion is eliminated 
 into the intestine, and leaves an ulcer of which the floor and edges are 
 infiltrated with cells. After this the cell-growth goes on, and the ulcer 
 enlarges, or the cells are gradually replaced by connective tissue, and 
 cicatization follows. 
 
 The lesions we have described are found most frequently and most 
 developed in the lower part of the ileum. They are not always, however, 
 confined to this situation. Enlarged and ulcerated follicles may be found 
 over the entire length of the ileum, and even in the jejunum. They may 
 also extend downward, and be found in the colon, even as far down as 
 the rectum. The same changes may also take place in the appendix 
 vermiformis. 
 
 Besides the regular typhoid lesions of the intestines which have been 
 described, we occasionally meet with others of a more accidental charac- 
 ter. 
 
 Gangrene of the intestinal wall sometimes occurs. It most frequently 
 
488 
 
 TYPHOID FEVEE. 
 
 involves a portion of the wall corresponding to an ulcer, but may also 
 affect other portions where no ulcer exists. The process may terminate 
 in perforation or in healing. 
 
 Croupous inflmnmaiion may attack the mucous membrane of either 
 the large or small intestine. The mucous membrane between the typhoid 
 ulcers is covered and infiltrated with an exudation of fibrin and pus. 
 
 Peritonitis of a mild type is a frequent accompaniment of the intes- 
 tinal lesions. It appears to have but little influence on the course of the 
 disease. 
 
 Severe peritonitis is usually due to perforation, less frequently to 
 iTlccrs which reach the serous coat, but do not perforate. When there is 
 infiltration of the serous coat with the typhoid new growth, the perito- 
 nitis may be accompanied by a production of little gray nodules of the 
 same character throughout the peritoneum. 
 
 Infarctions of the spleen, inflammation of the ovaries, and perforation 
 of the gall-bladder are sometimes the cause of peritonitis. 
 
 Hemorrhage from the intestines is merely due to the inflammatory 
 swelling and congestion of the mucous membrane and is slight; or it is 
 due to the ulceration of the follicles and destruction of the blood-vessels, 
 and is then often profuse. 
 
 Mesenteric Glands. — The mesenteric glands undergo the same changes 
 as the follicles of the intestines, and are usually afEected in a degree corre- 
 sponding to the intensity of the intestinal lesion. 
 
 The glands are at first congested and succulent, then there is a pro- 
 duction of lymphoid cells and large cells, as in the intestinal follicles, 
 and the gland becomes enlarged. When the enlargement has reached its 
 full size, the congestion diminishes and the cells begin to degenerate. 
 The degeneration may take place slowly, and then the gland gradually re- 
 turns to its normal condition; or'more rapidly, and then little foci of soft- 
 ened purulent matter are formed. If the patient recovers, the small foci 
 are absorbed, leaving a fibrous cicatrix; the larger foci become dry, cheesy, 
 and inclosed in a fibrous capsule. The inflammation of the glands may 
 produce a local or general peritonitis. 
 
 The Spleen. — -In nearly every case of typhoid fever, the spleen is en- 
 larged. This enlargement begins soon after the commencement of the 
 disease, increases rapidly until the third week, remains stationary for a 
 few days, and then diminishes. The organ is congested, of dark-red color 
 and of firm consistence while it is increasing in size. After it has reached 
 its maximum size, its consistence becomes soft, and there is a considerable 
 deposit of brown pigment. The enlargement appears to be due to the 
 congestion, and to an increase of the normal elements of the spleen. 
 
 In rare cases, the softened spleen is ruptured witli an extravasation of 
 blood into the jjeritoneal cavity. 
 
TYPHOID FEVEE. 489 
 
 There may be infarctions of the spleen, which sometimes soften and 
 cause peritonitis. 
 
 II. The second' class of lesions comprises those which are frequently 
 found with typhoid fever, but are not peculiar to it. 
 
 The Mouth. — Anumber of changes are found about this region. The 
 follicles at the root of the tongue and the tonsils may be enlarged; the 
 muscles of the tongue may undergo waxy and granular degeneration; 
 gangrenous ulcers may attack the floor and sides of the mouth, and de- 
 stroy large areas of tissue. 
 
 The pharynx may be the seat of catarrhal or of croupous inflammation, 
 producing superficial and deep ulcers. 
 
 The parotid is, in a moderate number of cases, the seat of an inflam- ■ 
 mation which tends to suppuration. In this process, both the glandular 
 acini and the connective tissue between them are involved. Which of 
 the two has the larger share in the process is still in dispute. 
 
 A slight enlargement and induration of the parotid and submaxillary 
 glands is said by Hoflmann to be a frequent lesion, and to depend on in- 
 crease of the gland-cells and dilatation of the follicles with their secre- 
 tion. 
 
 J7ie^awcre«s undergoes changes similar to those in the salivary glands. 
 It becomes at first swollen and red, then hard and grayish, then yellow. 
 The vessels are at first congested; afterward, there is increase of the 
 gland-cells; and lastly, degeneration. 
 
 The liver may preserve its normal character, or may present changes. 
 
 In many cases, the organ will be found soft and flabby. Minute ex- 
 amination then shows that the liver-cells have undergone degeneration. 
 They are filled with fine granules and small fat-globules, and the degene- 
 ration may go on so far that the outlines of the hepatic cells are lost, 
 and nothing but a mass of granules can be seen. 
 
 Less frequently, we find in the liver very small, soft, grayish nodules 
 resembling those found in the peritoneum. They are situated along the 
 course of the small veins, and there is, at the same time, a diffuse infil- 
 tration of lymphoid cells along the small veins. The nodules consist of 
 lymphoid cells; they are often too small to be distinguished with the 
 naked eye. 
 
 The Heart.— In a considerable number of cases, the muscular tissue of 
 the heart is altered. The heart feels soft and flabby, it is of grayish or 
 brownish color, the muscular fibres are infiltrated with fine granules, and 
 sometimes with brown pigment. Or the heart is firm, but friable and 
 easily torn, its cut surface glistens, and its muscular fibres are in the con- 
 dition of hyalin degeneration. 
 
 Thrombi in the cavities of the heart and vegetations on the valves 
 are sometimes found. Detached fragments of these may be lodged as 
 emboli in the different arteries. 
 
490 
 
 TYPHOID FEVEE. 
 
 Tlie Arteries.^ — There may be an acute inflammation of the arteries, 
 especially at the commencement of convalescence. There are two varie- 
 ties: an obliterating and a parietal. In the obliterating arteritis there 
 is infiltration of all the coats of the artery, with roughening of the intima 
 and the formation of a thrombus within the vessel, and this is followed 
 by dry gangrene of the parts supplied by the artery. In the parietal vari- 
 ety the wall of the artery is infiltrated with cells, but the intima is not 
 roughened and no thrombus is formed. 
 
 Tlie Veins. — Thrombosis of the larger veins, especially of the femoral 
 vein in the third and fourth weeks of the disease, is not uncommon. 
 
 The Larynx is very frequently tiie seat of catarrhal inflammation, 
 with or without superficial erosions. Less frequently there is croupous 
 inflammation, followed in some cases by destructive ulceration. 
 
 The Lungs. — Catarrhal inflammation of the large bronchi is very com- 
 mon. Broncho-pneumonia occurs in two forms. There may be a severe 
 inflammation of most of the bronchi of both lungs, with cellular infil- 
 tration of the walls of the bronchi and zones of peribronchitic pneumo- 
 nia; or there is an intense general bronchitis, with lobules of the lung cor- 
 responding to obstructed bronchi either collapsed or inflamed, or both. 
 
 Prom the long-continued recumbent position of the patients, the pos- 
 terior portions of the lungs become congested, dense, and unaerated. 
 Sometimes, in addition to this, irregular portions of the lung become 
 liej)atized. 
 
 Less frequently there is regular lobar pneumonia. 
 
 There may be infarctions in the lungs. 
 
 Gangrene of the lungs is occasionally found, either associated with lob- 
 ular pneumonia, or w ith infarctions, or as an independent condition. 
 
 The Kidneys very frequently present the lesions of parenchymatous 
 nephritis. They may contain infarctions. 
 
 The Ovaries. — Hemorrhage and gangrenous inflammation have been 
 observed in rare cases. 
 
 The Testicles. — Orchitis has been described by Ollivier.'' It generally 
 is developed during convalescence; it is unilateral; it usually affects the 
 testicle alone, less frequently the epididymis; it terminates in suppuration 
 in nearly one-fourth of the cases. 
 
 The Brain. — Acute meningitis, thrombosis of the venous sinuses, and 
 obliterating endarteritis of the cerebral arteries occasionally are observed. 
 
 The Voluntary Muscles, especially the abdominal muscles, the adduc- 
 tors of the thigh, the pectoral muscles, the muscles of the diaphragm, 
 and of the tongue frequently undergo the hyalin degenerative changes 
 described under muscle lesions. Fig. 139. 
 
 ' Barie, Rev. de Med., Jan., Feb., 1884. Keen: Toner Lectures on the Surgical 
 Complications of tlie Continued Fevers, 1877. 
 = Rev. de Med., Nov. and Dec, 1883. 
 
TrPHOID FEVER. 49J 
 
 The /S'^iw.— Gangrenous inflammation of the skin frequently occurs 
 in the form of bed-sores, aEfecting especially the skin over the sacrum 
 and trochanters, wliere it is subjected to the constant pressure of the. 
 bed. 
 
 There may be suppurative inflammation of the connective tissue in 
 any part of the body. Perhaps the most important of these local suppu- 
 rations is that which produces retro-pharyngeal abscesses. 
 
 The presence of a species of bacillus in various parts of the body in 
 typhoid fever, in a considerable proportion of the cases examined, has 
 been well established by a number of observers. Klebs' found bacilli of 
 special form in various parts of the body, in all of the twenty-four cases 
 examined. Eberth" found bacilli in the intestines, mesenteric glands and 
 spleen in eighteen out of forty cases examined. Similar forms have been 
 seen and photographed by Koch.' Meyer' also found similar forms in 
 sixteen out of twenty cases. They have been repeatedly seen by other ob- 
 servers, the details of whose work it is not necessary to mention here. 
 
 GafEky^ has made a series of careful examinations and cultures with 
 the new technique suggested by Koch. Out of twenty-eight cases ex- 
 amined, G. found the characteristic bacilli in twenty-six. One of the 
 exceptional cases was examined in a late stage of the disease, and the 
 other showed similar bacilli in a swollen solitary follicle. The bacilli 
 were found in the mesenteric glands, spleen, liver, and kidneys. The 
 bacilli are about three times as long as broad, being about one-third as 
 long as the diameter of a red blood-cell, and are rounded at the ends. 
 Sometimes they are joined at the ends to form chains. Sometimes they 
 contain rounded spores. They are apt to occur in little heaps or masses, 
 but they may occur singly. They lie in the smaller blood-vessels or in 
 the capillaries, which they may completely fill. In the intestinal lesions 
 where ulceration or necrosis has occurred, the presence of various forms 
 of bacteria from the intestinal contents renders the identification of the 
 typhoid bacillus difficult; but forms similar to those in the organs were 
 detected in swollen follicles which had not undergone necrotic changes. 
 
 Pure cultui'cs were made by Gaffky, who found that the bacilli grew 
 readily on gelatinized bouillon which they did not render fluid, as do 
 many other bacteria. On the surface of boiled potatoes they grew most 
 luxuriantly, forming a delicate pellicle. The development is rapid both 
 on gelatin bouillon and on potatoes, reaching its height in from two to 
 
 'Klebs, Archiv f. exp. Path., Bd. 13, Heft 506, 1881. 
 
 » Eberth, Virch. Archiv, Bd. 81, p. 58, 1880; Bd. 83, p. 487, 1883. 
 
 2 Koch: "Mitth. a. d. k. Gesundheits-Amt," Bd. I., 1881. 
 
 * Meyer: " Untersuchungen ti. d. Bacillus des Abdominal Typhus." Inaug. 
 Diss. Berlin, 1881. 
 
 *Gaffky: "Mitlh. a. d. k. Gesundheits-Amt," Bd. II., p. 373, contains good bib- 
 liography. 
 
492 TYPHOID FEVEE. 
 
 four days. Specimens from the cultures show distinct movements under 
 the microscope, sometimes slow, sometimes rapid. 
 
 Inoculations into the lower animals were made by GafEky, but with 
 only negative results. These bacilli have not been found in any other 
 diseases than typhoid fever. It will be seen from the above experiments 
 and observations that, while the presence of the bacilli in the body in 
 typhoid fever is very suggestive of their causative agency, this has not 
 yet been proven. The failure to detect the bacilli in a number of cases, 
 especially by the earlier observers, should not be considered as very im- 
 portant evidence against their occurrence or significance, because the 
 technical procedures of the earlier workers were faulty; and furthermore, 
 as the organisms are apt to occur in foci, the chances of their detection 
 are unfavorable unless they are very abundant or an enormous number of 
 sections is examined. 
 
 Staining. — The parts to be examined should be well hardened in al- 
 cohol, and sections may be stained with methyl violet, gentian violet, 
 Bismarck brown, or fnchsin; which should be used in concentrated solu- 
 tions. GafEky recommends the staining of sections for twenty to twenty- 
 four hours, in a very dark-colored solution of methylen blue made fresh 
 ■each time, by adding to distilled water a sufficient quantity of a saturated 
 alcoholic solution of methylen blue to make the fluid opaque. They are 
 then washed in distilled water, dehydrated with absolute alcohol, cleared 
 up with turpentine, and mounted in balsam. In specimens thus prepared 
 the masses of bacilli may be seen with low powers, but for the recognition 
 of the minuter characters of the individuals, one-twelfth oil immersion 
 should be used, with tlie Abb6 condensor. The staining of these bacilli 
 is not as intense as that of many other species, and the blue preparations 
 are apt to fade. For permanent preparation the Bismarck brown is 
 better. They are decolorized after being stained, by nitric acid, and in 
 this way differ from the bacillus tuberculosis. 
 
 The observations and conclusions of earlier investigators concerning 
 the occurrence of micrococci in various parts of the body in typhoid fever 
 have not been confirmed. 
 
TYPHUS FEYER. 
 
 This disease has not, so far as we know, any characteristic lesion ; 
 but yet after death we may find a number of morbid conditions, such as 
 are common to the infectious diseases. 
 
 The entire body has a tendency to rapid putrefaction. 
 
 The blood is often darker and more fluid than in other diseases. 
 
 The voluntary muscles may undergo waxy and granular degeneration. 
 
 The brain and its membranes may be congested. 
 
 The mucous membrane of the pharynx and larynx may be the seat of 
 catarrhal or croupous inflammation. 
 
 In the lungs there may be bronchitis, broncho-pneumonia, or hypo- 
 static congestion. 
 
 The walls of the heart may be soft and flabby. 
 
 The agminated glands of the ileum, and the mesenteric glands, may be 
 a little swollen. 
 
 The spleen is often large and soft. 
 
 The kidneys are frequently the seat of parenchymatous nephritis. 
 
EELAPSIIfG FEYER 
 
 Synonyms. — Typhus recurrens. Famine fever. Spirillum fever. 
 
 The Skin may be jaundiced; it may be mottled by extravasations of 
 blood. 
 
 Tlie Brain and Spinal Cord are unchanged. 
 
 The Pharynx and Larynx may be the seat of catarrhal or croupous 
 inflammation. 
 
 The Lungs. — There may be bronchitis, broncho-pneumonia, lobar 
 pneumonia, hypostatic congestion, and pleurisy. 
 
 The Heart is often soft and flabby, with degeneration of its muscular 
 fibres. There may be ecchymoses in the pericardium. 
 
 The Stomach and Small Intestine may be congested, there may be 
 ecchymoses in the mucous membrane, there may be catarrhal inflamma- 
 tion. 
 
 The Colon may be the seat of catarrhal or croupous inflammation. 
 
 The Mesenteric Glands may be swollen. 
 
 Tlie Liver is often enlarged and the hepatic cells are swollen and 
 granular. 
 
 The Spleen is large and soft, like the spleen of typhoid fever. The 
 change in its consistence is so marked that the spleen may rupture spon- 
 taneously during life. The spleen may also contain infarctions of differ- 
 ent sizes ; some are red, some yellow, some necrotic. Those which are 
 necrotic may give rise to a local or general peritonitis. 
 
 The Kidneys show the lesions of parenchymatous nephritis. 
 
 The Bones. — Degenerative changes in the medulla of the bones have 
 been described by Ponfick.^ 
 
 The Blood. — In the blood is found a minute form of spirillum, 
 Spirochsete Obermeieri, first described by Obermeier, and characteristic of 
 the disease. It is in the form of a very thin, spiral thread from -^ to 
 y-^ of an inch in length (Fig. 140). It is found in large numbers in 
 the blood within the blood-vessels in all parts of the body. It is con- 
 
 ' Virch. Arch., Bd. 60, p. 153. 
 
RELAPSING FEVEE. 495 
 
 stantly present during the febrile attacks, and nearly or completely 
 disappears during the afebrile intervals (see p. 85.) 
 
 The spirilla may be seen in fresh blood with a magnifying power of 
 six hundred diameters. 
 
 Fig. 140.— Spiroch^ete Oberueieri, X about 750 and reduced. 
 ' From the blood of patient with relapsing fever. 
 
 The dried blood may be stained with aqueous solution of methyl vio- 
 let, anilin brown, or fuchsin ; the superfluous color is washed away with 
 water, and the specimen again dried and mounted in balsam. The spi- 
 rilla and the red and white blood-cells are deeply stained (Carter). 
 
EPIDEMIC OEEEBRO-SPII^AL 
 
 MENINGITIS. 
 
 This is an acute general infectious disease, characterized by an exuda- 
 tive inflammation of the pia mater of the brain and spinal cord. The 
 degree of the lesion in the meninges varies greatly, depending upon the 
 period at which death occurs. In some cases, when death occurs early 
 in the disease, there may be to the naked eye no evident change in the* 
 membranes, or a moderate serous infiltration. In these cases the micro- 
 scope may reveal a moderate degree of extravasation of leucocytes in the 
 vicinity of the vessels. In the well-marked cases the pia mater of the 
 brain and cord is more or less densely infiltrated with serum, fibrin, and 
 pus. This may occur over the convexity and base of the brain, and is 
 frequently most marked in the latter situation. In the cord, the infiltra- 
 tion may occur over the anterior and posterior surfaces ; but in many 
 cases, probably owing to the recumbent position of the patient, it is most 
 marked on the posterior surface. The ventricles of the brain and the 
 central canal of the cord may contain turbid serum mingled with pus- 
 cells, and sometimes blood-cells. The membranes and underlying nerve- 
 tissue may be hyperaemic and the seat of capillary hemorrhages. Earely 
 a small amount of pus and fibrin may be found between the pia and 
 dura mater. 
 
 In protracted cases the ventricles may be dilated with serum, and the 
 exudation in the meninges may become fatty or dense and cheesy. 
 
 While the above are the characteristic lesions of this disease, there are a 
 number of secondary changes in different parts of the body which are not 
 constant, but which occur with sufficient frequency to render their 
 observation necessary. There may be subserous punctate hemorrhages in 
 the endocardium; petechiee in the skin; hyalin and granular degenera- 
 tion in the voluntary striated muscle; occasional multiple abscesses in 
 various parts of the body; suppurative inflammation of the joints; paren- 
 chymatous degeneration of the heart, liver, and kidneys; and swelling of 
 the gastro-intestinal lymphatic apparatus. Bronchitis and pneumonia, 
 
EPIDEMIC CEEEBEO-SPINAL MENINGITIS. 497 
 
 pleurisy, pericarditis and endocarditis, suppurative inflammation of the 
 middle ear, and iritis and choroiditis are of occasional occurrence. 
 
 Of the causation of this disease we are in almost entire ignorance. 
 Its peculiar course and character justify the conjecture that it may be due 
 to some infectious agent, like bacteria; and micrococci have been 
 ■described as occurring in the exudation.' That they have any causative 
 connection with the disease has not yet been proven. 
 
 ' Consult Leyden: " Die Mikrokokken. der Cerebrospinal-Meningitis," 
 Centrbl. f. Klin. Med., Bd. 4, No. 10,1883. Also Ughetti, Giornale della Eeale 
 Societa Italiana d'Igiene, 1883, No. 10 and 11; Review in Centrbl. f. Klin. Med., 
 No. 14, April 5th, 1884, p. 223. Also Marchiafava and Celli, Gazz, degli ospitali, 
 1884; Review in Centrbl. f. Klin. Med., No. 7, 1884. 
 33 
 
DIPHTHEEIA. 
 
 The term 'diphtheria' is used to designate a disease belonging to the 
 class of general infectious diseases with characteristic local lesions. The 
 characteristic local lesion of diphtheria is a croupous inflammation of one 
 or more of the mucoUs membranes. Such a croupous inflammation in 
 diphtheria is anatomically identical with croupous inflammations due to 
 traumatic and other causes. 
 
 The mucous membranes which are the most frequently inflamed in 
 diphtheria are those of the tonsils, pharynx, soft palate, nares, larynx, 
 and trachea; less frequently, those of the mouth, gums, oesophagus, and 
 stomach. 
 
 In different cases of the disease, we find great variety as to the posi- 
 tion, extent, and severity of the inflammatory process. 
 
 The disease, as it occurs in New York, usually follows one of three 
 types: 
 
 (1) There is a general congestion of the affected mucous membrane, 
 and scattered on its surface are small patches of soft, yellow membrane. 
 
 (2) The mucous membrane is congested and covered with a continu- 
 ous layer of very thin membrane, sometimes so thin that it is hardly 
 appreciable by the naked eye. 
 
 (3) The mucous membrane is much swollen, and this swelling may 
 extend to the adjacent soft tissues. The layer of false membrane is 
 extensive, thick, and tenacious. There may be necrosis of portions of the 
 mucous membrane. 
 
 When we examine these lesions more closely, we find that they are all 
 characterized by the combination of necrotic and of inflammatory pro- 
 cesses; the extent of the necrosis and the quantity of the inflammatory 
 products varying in the different cases. 
 
 The most common form of necrosis is a coagulation necrosis of the 
 epithelium of those mucous membranes which are covered with pavement 
 epithelium. The epithelial cells are changed in appearance and shape; 
 the cell bodies have a peculiar homogeneous appearance, the nuclei dis- 
 
DIPHTHEEIA. 499 
 
 appear, the cells are shrunken and deformed into a variety of shapes, they 
 adhere closely together, sometimes looking like a network. Less fre- 
 quently the stroma of the mucous membrane also becomes necrotic. 
 
 The inflammatory products are pus and fibrin which infiltrate the 
 stroma of the mucous membrane and collect on its surface. 
 
 The false membrane, therefore, may consist of epithelium in the con- 
 dition of coagulation necrosis; or of fibrin, pus, and desquamated epithe- 
 lium; or of both the necrotic epithelium and the fibrin and pus. 
 
 The presence of various forms of bacteria, and particularly of micro- 
 cocci, in the false membrane has been demonstrated by numerous 
 observers, but as yet there is not sufficient evidence that these organisms 
 are the means by which the infection of the disease is effected. 
 
 (A full account of what is known concerning the micro-organisms of 
 diphtheria, as well as the results of his own researches, is given by 
 Loeffler : "Mitth. aus dem Kais. Gesundheits-Amte," Bd. 11., p. 421.) 
 
 Besides the characteristic lesions of the disease, certain accessory 
 lesions are often present. 
 
 The lymphatic glands near the inflamed mucous membrane are often 
 swollen and inflamed. 
 
 The parotid and submaxillary glands may be swollen and inflamed. 
 The bronchi may be the seat of either catarrhal or croupous inflamma- 
 tion. 
 
 In the lungs there may be zones of peribronchitic pneumonia, or dif- 
 fuse pneumonia with consolidation of considerable portions of the lung. 
 
 The kidneys regularly exhibit the lesions of parenchymatous neph- 
 ritis. 
 
YELLOW FEVER 
 
 Tlie Skin is of a yellow color from the presence of bile pigment, and 
 may be mottled by ecchymoses. 
 
 The Heart is of a pale or brownisli-yellow color. Its muscular fibres 
 are the seat of fatty degeneration. 
 
 The Lungs are congested. 
 
 The Stomach often contains the characteristic black fluid which is 
 vomited during life. Its mucous membrane is congested, softened, and 
 sometimes eroded. 
 
 The Intestines are dark colored, often distended with gas, and some- 
 times contain blood. 
 
 The Liver in the earlier stages of the disease may be intensely con- 
 gested. More frequently it contains but little blood, is of a light-yellow 
 color, and the hepatic cells are infiltrated with coarse granules and fat- 
 globules. The gall-bladder is contracted and contains but little bile. 
 
 Tlie Spleen shows no marked changes. 
 
 The Kidneys present the lesions of the intense form of parenchyma- 
 tous nephritis. 
 
CHOLERA. 
 
 In some cases of cholera there are no marked changes to be found 
 after death. 
 
 If death occurs during the invasion of the disease, or in the stage of 
 collapse, in the more marked cases the appearances are as follows : 
 
 The bodies remain warm for some time, and the temperature may 
 rise for a short time after death. The rigor mortis begins soon and 
 lasts for an unusually long time. The muscles sometimes exhibit a 
 peculiar spasmodic twitching before the rigor mortis sets in, especially 
 the muscles of the hand and arm. 
 
 The Skin is of a dusky gray color, the lips, eyelids, fingers, and toes 
 of a livid purple. The ends of the fingers are shrivelled, the cheeks and 
 eyes are fallen in. 
 
 The Brain. The sinuses of the dura mater are filled with dark, 
 thick blood. The pia mater may be normal, or oedematous, or ecchy- 
 mosed, or infiltrated with fibrin. The brain is usually normal, but 
 may be dry and firmer than usual. 
 
 The Lungs are retracted and anaemic, the pleura may be dry, or 
 coated with fibrin. 
 
 The Heart is normal. 
 
 The Peritoneum may be dry or coated with a layer of fibrin. 
 The Stomach is usually unchanged, but may be the seat of catarrhal 
 inflammation. 
 
 The Small Intestine. There may be ecchymoses in the mucous 
 membrane ; the mucous membrane may be soft and oedematous ; there 
 may be general congestion, or the congestion may be confined to the 
 peripheries of the solitary and agminated glands, and these glands may 
 be swollen ; or there may be croupous inflammation and superficial ne" 
 crosis. All these changes are regularly most marked at the lower end 
 of the small intestine. There is apt to be post-mortem desquamation of 
 the epithelium. The characteristic rice-water fluid may be found in the 
 intestines after death, or instead of this a dark-colored, bloody fluid. 
 
 The Large Intestine is usually normal, but in some ei^idemics croup- 
 ous inflammation occurs in a considerable number of cases. 
 
502 CHOLEEA. 
 
 The Liver and Spleen undergo but few changes; they may be ange- 
 mic and flabby. 
 
 Hie Kidneys are often increased in size, with white and thickened 
 cortex and congested pyramids. The epitheliam of the cortex tubes 
 contains coarse granules and fat-globules. The tubes contain cast mat- 
 ter and broken down epithelium. These changes may be looked upon as 
 being simply of a degenerative character, or as the results of a parenchy- 
 matous nephritis. 
 
 The Uterus and Ovaries may be congested and contain extravasated 
 blood. 
 
 If the patient does not die until the stage of reaction, the body does 
 not present the same collapsed appearance, and there are often inflam- 
 matory changes in difEerent parts of the body, especially in the larynx, 
 the lungs, the stomach, and the intestines. 
 
 According to recent researches by Koch, there are constantly pres- 
 ent in the small intestines of cholera patients during the early and active 
 stages of the disease characteristic bacteria, probably closely allied with, 
 if not belonging to the genus Sijirillum. 
 
 These bacteria are short and thick (from one-half to two-thirds as 
 long as the Bacillus tuberculosis, and considerably thicker). They are 
 curved, sometimes slightly, sometimes considerably, and are occasionally 
 seen in the form of a double curve or S. These bacteria are found in the 
 follicles of Lieberldihn, between and beneath the epithelium, and in the 
 submucous tissue. They are also present in varying abundance in the 
 dejections, particularly in very acute cases which are uncomplicated with 
 hemorrhage or putrefactive changes. They have been also found in 
 vomited matterwhen this had an intestinal character. They have not 
 been found in the blood or other organs. These bacteria are readily cul- 
 tivated in artificial media, proliferating with extraordinary rapidity, and 
 developing occasionally into long spiral forms. In fluid culture mfedia 
 they are seen to move about with great rapidity. They grow readily in 
 beef -tea, milk, blood-serum, and also on solid media, such as gelatinized 
 bouillon, agar agar, potatoes, etc. (see jj. 91). The form of growth 
 on solid culture media is said to be characteristic, and in gelatin cul- 
 ture the gelatin is liquefied in a peculiar manner by the growing colo- 
 nies. In moist earth, on damp linen, etc., they also increase with 
 extraordinary rapidity. A temperature of from 30°-40° C. is most favor- 
 able to their growth. At about 16° C. their proliferative activities cease, 
 but they are not killed by — 10° C. They are readily killed by drying, 
 and the presence of acids is very inimical to their growth. Their period 
 of life is short, and they appear to have no resting state, as under cer- 
 tain conditions do most bacilli. In this respect they resemble spiril- 
 lum. 
 
 This cholera bacterium, sometimes called, on account of the slightly 
 
CHOLEEA. 503 
 
 curved form under which ib commonly appears, the "comma bacillus/' 
 has not as yet been found except in connection with Asiatic cholera. 
 Attempts to inoculate the lower animals with the bacteria have in a 
 few cases been apparently successful. 
 
 As it is not always easy to find the cholera bacterium in the dejec- 
 tions of even genuine cases of cholera, and as the morphological charac- 
 ters alone do not, in the majority of cases, sufSce for a diagnosis, re- 
 course must be had to cultivation on gelatin, in most cases, for the evidence 
 which the growing colonies furnish. This may be very easily accom- 
 plished, according to Koch, by mixing a small fragment of intestinal 
 slime with a little gelatinized pepton bouillon (see p. 93), which 
 has been made fluid by warming. Tliis is then poured on to a sterilized 
 •glass plate, spread with a sterilized rod and cooled by placing on a jiiece of 
 ice. It is then placed under a glass bell jar, the air of which is liept 
 moist by water-soaked blotting-paper, and allowed to remain at a tem- 
 perature of about 35° 0. After the inoculation of gelatinized bouillon 
 with the intestinal contents, the colony makes its appearance in a few- 
 hours as a small, pale, irregular contoured spot, which soon becomes 
 granular. As the colony grows, the granulation becomes more marked, 
 and finally looks as if composed of strongly refractile granules, like par- 
 ticles of glass. As it continues to grow, the gelatin around the colony 
 becomes fluid, and the latter sinks beneath the surface, so that it is seen 
 as a whitish spot in the middle of a funnel-shaped depression in the 
 gelatin. The same appearances are observed when the cholera bacteria 
 from pure cultures are imjjlanted on gelatinized bouillon. 
 
 It is stained in the usual way after drying on a cover-glass (see p. 
 89) with an aqueous solution of fuchsin or methylen blue for a few sec- 
 onds, and examined with a high power oil-immersion lens and the Abbe 
 ■condenser. Sections of the intestine hardened in strong alcohol must 
 be gently warmed in the methylen-blue solution, or allowed to remain in 
 the cold solution for twenty-four hours.' 
 
 ' Consult Proceedings of the Conference for the Consideration of the Cholera, 
 Berlin, July 26th, 1884, Reported in Deutsche med. Woohenschrift, Aug. 7th and 
 11th, 1884, Nos. 32 and 32 A, for a resume of his investigations by Dr. Koch, also 
 later paper by Koch, " Ueber die Cholera-Bakterien," ibid., Nov. 6th, 1884, No. 45. 
 
TUBERCULOSIS. 
 
 In speaking and thinking of tuberculosis, there are usually present 
 in the mind two separate ideas: the idea of a morbid process of a gen- 
 eral and infectious character, and the idea of certain characteristic ana- 
 tomical lesions. 
 
 It is, therefore, convenient to consider separately tuberculosis as a 
 general constitutional condition, and tubercle as an anatomical product 
 of inflammation. 
 
 It has always been recognized that some persons are especially liable 
 to acquire either general or local tuberculosis. It has been supposed 
 that such a disposition is inherited, or acquired as the result of a pecu- 
 liar deterioration of the general health. Such a predisposition renders 
 the person in whom it exists liable to general or local tuberculosis when- 
 ever an exciting cause is added. 
 
 Opinions still differ as to what constitutes a sufficient exciting cause. 
 Some believe that any causes, such as injuries or exposures to cold, 
 which in most persons produce ordinary inflammation, in persons who 
 have the tubercular predisposition produce tubercular inflammation.. 
 Thus exposure to cold, instead of being followed by a bronchitis or a 
 pneumonia, will produce acute phthisis; a blow on the knee or on the 
 spine will be followed by a tubercular synovitis or osteitis instead of a 
 simple one; eczema of the scalp will produce, not a simple adenitis of 
 the cervical glands, but a tubercular adenitis. 
 
 Furthermore, a local tuberculosis is often followed by a development 
 of tubercular inflammation in other parts of the body as if by infection. 
 
 More recently, the discovery by Koch of the Bacillus tuberculosis in 
 the lesions of almost all cases of tuberculosis has led to the belief that in 
 persons who have the tubercular predisposition, the tubercle bacillus 
 finds a favorable soil, and that to the entrance, lodgment, and growth of 
 this bacillus are due the development of the tubercular lesions. 
 
 It has also been demonstrated that the Bacillus tuberculosis can be 
 cultivated artifically outside of the human body, and thus freed from 
 possible contaminations; can then be inoculated in animals, and that 
 
TUBEECTJLOSIS. 505 
 
 these animals will then develop tubercular lesions in which similar bacilli 
 will be found. This would seem to show that the bacillus is the real 
 cause of the development of tubercular lesions. 
 
 We may then assume that some persons have a peculiar constitutional 
 vice or diathesis— the tubercular diathesis; that this diathesis is inherited 
 or acquired; that the possessors of the diathesis, in order to develop tuber- 
 culosis, must be subjected to %ome exciting cause; that such exciting 
 causes are infection by the tubercle bacillus, exposure to cold and wet, 
 irritants, or injuries. 
 
 Tuberculosis, however, is not always manifested in the same way. 
 The patients may develop symptoms like those of a general disease with 
 lesions involving many different parts of the body; or the lesions are con- 
 fined to a circumscribed part of the body, while the symptoms are also 
 localized. "We must, therefore, distinguish: 
 
 1. Acute general tuberculosis which occurs in persons who have pre- 
 viously been well, or are already suffering from a local tuberculosis. 
 
 3. Localized tuberculosis. 
 
 3. Tuberculosis at first localized in some part of the body, and then 
 succeeded by the development of localized lesions in other parts. 
 
 (1) General Tuberculosis. — This is a morbid process of which the 
 clinical symptoms are eminently characteristic of an acute infectious dis- 
 ease. A person who has previously been in good health, or who has al- 
 ready a local tuberculosis, suddenly or gradually develops a febrile move- 
 ment, rapid emaciation, and at the end of a few days or weeks dies. After 
 death miliary tubercles are found throughout the body. 
 
 It is believed by some, however, that in these cases there is always first 
 present a local tuberculosis, especially of the pulmonary veins or of the 
 thoracic duct, and that from this local tuberculosis is derived the general 
 infection. 
 
 It is to be noted that there is no proof in the cases given that the 
 tuberculosis of the pulmonary veins or thoracic duct has preceded in its 
 development the other tubercular lesions; and also that it is just as easy 
 to suppose a person to be infected at first by a large dose of the tubercular 
 poison as by a small one. 
 
 (2) Localized Tuberculosis.— This condition gives an entirely differ- 
 ent clinical picture. The patients do not appear to suffer from a general 
 disease, but from a local inflammation. Their symptoms are in propor- 
 tion to the extent of the inflammation. If the inflammation is not too 
 extensive it runs its course and the patient recovers. 
 
 (3) Localized Tuberculosis, which extends.— Iri these cases there is 
 first a localized tuberculosis with its symptoms. Then after a time simi- 
 lar tubercular inflammations are developed in otlier jDarts of the body. 
 Tlie secondary tubercular lesions sometimes seem to be the result of in- 
 fection from the primary lesion. In other cases, the primary lesion be- 
 
506 TTJBEECULOSIS. 
 
 comes obsolete and the secondary lesion appears as if from a fresh infec- 
 tion. 
 
 The patients then for the most part do not resemble cases of general 
 tuberculosis, but are rather in the condition of persons sufEering from a 
 number of localized inflammations. But there are some of these cases 
 which it is diSicult to distinguish from those with general tuberculosis. 
 
 There are, therefore, three morbid conditions which are quite differ- 
 ent in their clinical histories, and yet it is customary to call them all 
 tubercular. 
 
 In persons who have suffered from any of these forms of tuberculosis 
 there are regularly found after death morbid lesions. It would indeed 
 seem possible that acute general tuberculosis may cause death before any 
 recognizable lesions have been developed, as is sometimes the case in 
 cerebro-spiual meningitis. Bat we have no certain knowledge on this 
 point. 
 
 The lesions which we regularly find are : 
 
 1. Miliary tubercles. 
 
 2. Diffuse inflammation of various kinds, with cheesy degeneration 
 of the inflammatory products. 
 
 3. The ordinary products of inflammation — pus, fibrin, serum, epi- 
 tlieliunl, granulation tissue, and connective tissue. 
 
 Associated with all these lesions we find the tubercle bacilli. 
 
 (1) Miliary Tubercles. There are small nodules, of irregularly sphe- 
 roidal shape, the smallest hardly visible to the naked eye, the largest as 
 large as a pea. The smaller ones are gray and semi-transparent; the 
 larger are opaque, whitish or yellow, especially at their centres. 
 
 Miliary tubercles do not all have the same structure. 
 
 Some are composed of amorphous granular matter, of degenerated 
 lung tissue, and of epithelial cells and pus. 
 
 Some are composed of a tissue resembling granulation tissue. 
 
 Some are composed of tubercle tissue, alone or associated with other 
 inflammatory products (Pigs. 89, 90, 91). 
 
 The term " tubercle tissue" is employed to designate an inflammatory 
 product which somewhat resembles granulation tissue. It is composed 
 of a basement-substance and of cells. The basement-substance is deli- 
 cate and finely granular, and contains round and oval nuclei. This base- 
 ment-substance has a reticulated arrangement, and in the spaces of the 
 reticulum are polyhedral nucleated cells. There may also be present 
 the large nucleated bodies called giant-cells. These giant-cells, although 
 apparently all formed in the same way by the fusion of a number of 
 smaller cells, yet do not always present exactly the same appearance. 
 Some of them seem to form part of and to be continuous with the base- 
 ment-substance; others are separated from the basement-substance, and 
 look like large cells contained in the meshes of the basement-substance. 
 
TUBEECULOSIS. 
 
 607 
 
 In some tubercle-tissue the basement-substance, in others the polybedral 
 cells, in others the giant cells are predominant (Figs. 20, 21, 22, 23). 
 
 Such tubercle tissue is arranged in the form of small spheroidal bodies 
 —tubercle granula, and of a difEase tissue. So that a ''tubercular" 
 miliary tubercle is composed of one or more tubercle granula and of dif- 
 fuse tubercle, to which may be added other inflammatory products. 
 
 All miliary tubercles may undergo cheesy degeneration, or more rarely, 
 be changed into connective tissue. 
 
 The miliary tubercles formed of amorphous granular matter or of in- 
 different round-celled tissue, are most common in acute general tubercu- 
 losis. The miliary tubercles formed of well-defined tubercle-tissue are 
 most completely developed in localized tuberculosis. 
 
 Tubercle-tissue infiltrates and replaces connective tissue; it fills cavi- 
 ties, and it projects from free surfaces. It contains but very few blood- 
 vessels, and when it infiltrates a tissue, the vessels of that tissue become 
 obliterated. There is often associated with it a proliferation of the en- 
 dothelial cells of the arteries or an obliterating endarteritis. 
 
 (2) Diffuse inflammation with cheesy degeneration of the inflamma- 
 tory products. This form of lesion is found in the large tubercular 
 masses in the brain, in the mucous membrane of the bronchi, in the large 
 flat tumors of the serous membranes, and in the diffuse cheesy infiltra- 
 tion of the kidneys, the ureters, bladder, prostate, testicle, and uterus. 
 The constant feature of the lesion is the development of an indifferent 
 round-celled tissue, which rapidly undergoes cheesy degeneration. Em- 
 bedded in this tissue there may be tubercle granula. When the lesion is 
 far advanced, the degenerative changes may involve all the inflammatory 
 products, so that we find no formed elements, nothing but a diffuse 
 caseous mass. In the earlier stages of the lesion, the indifferent round- 
 celled tissue and the tubercle granula are readily demonstrated. 
 
 (3) Pus, fibrin, serum, epithelial cells, connective tissue, and indif- 
 ferent tissue are all found in varying quantities, either separately or to- 
 gether in those parts of the body where the tubercular lesions have been 
 developed. 
 
 The Tubercle Bacilli are slender filamentous bacteria (Fig. 141), vary- 
 ing in length from one-fourth to one-half the diameter of a red blood-cell. 
 They may contain spores, which give them a beaded appearance, and are 
 sometimes slightly curved. It is possible, but very difficult, to see them 
 when they have not been stained. Morphologically they very closely re- 
 semble the bacilli of leprosy and some other forms of filamentous bac- 
 teria. They differ from most similarly formed bacilli in the tenacity 
 with which "they retain the color after staining, although the bacilli of 
 leprosy have this same property. It is, however, the effect of the living 
 bacilli upon the organism, when introduced into it under favorable con- 
 ditions, which furnishes the only absolute proof of their identity. 
 
508 TUBEECULOSIS. 
 
 The tubercle bacilli are present in the characteristic lesions of almost 
 all cases of local and general tuberculosis. But there are apparently ex- 
 ceptional cases of typical tuberculosis, in which the most careful exami- 
 nation fails to reveal the bacilli. Whether these cases are really excep- 
 tional, or only apparently so, owing to unknown conditions which 
 interfere with the demonstration of the bacilli by the present methods, 
 we are unable to say. 
 
 The number of bacilli which are j)resent in the lesions is subject to 
 great variations. They are most abundant in the walls and contents of 
 
 / / 
 
 ^ 
 
 
 
 Fig. 141.— Bacillus Tdberodlosis, X about 850. 
 From sputum in case of chronic phthisis stained with tuchsin. 
 
 phthisical cavities, and in tubercle tissue which is undergoing cheesy 
 degeneration and disintegration. In these situations they may be found 
 in myriads forming sometimes a large part of the disintegrated mass. 
 They are found in cells and scattered among them. Sometimes they are 
 present in considerable numbers in the giant-cells of miliary tubercles. 
 In the dense, firm, chronic miliary tubercles they are not commonly pres- 
 ent. In the acute general tuberculosis of children they are often present 
 in enormous numbers, particularly in the lungs. They may be found in 
 tubercular inflammation in any part of the body, and have been seen in 
 the blood. The bacilli are almost constantly found in the sputa of 
 phthisical f)atients, and their presence sometimes affords valuable diag- 
 nostic aid in early stages or obscure forms of the disease. 
 
 The characteristic features, then, of the lesions of persons who suffer 
 from tuberculosis are: 
 
 The formation of tubercle tissue. 
 
 The formation of an indifEerent round-celled tissue, which is apt to 
 degenerate. 
 
TUBEECULOSIS. 509 
 
 The presence of tubercle bacilli. 
 
 The other inilammatory lesions difEer in no respect from the same le- 
 gions when produced by other causes. 
 
 METHODS OF STAINING THE TUBERCLE BACILLI. 
 
 The most reliable and useful of the numerous methods which are 
 employed for staining the tubercle bacilli is Ehrlich's, or some modifica- 
 tion of this. For the examination of fluids, such as sputum, etc., the 
 material should be spread in a thin layer on a cover-glass, and dried ac- 
 cording to the directions given on p. 89. The staining fluid is prepared 
 by making, 1, a saturated solution of anilin oil in distilled water; this is 
 done by adding about five per cent of the oil, and shaking vigorously and 
 filtering through a moistened filter. To this clear filtrate should be 
 added: 2, a sufficient quantity of a saturated alcoholic solution of fuchsin 
 to give the fluid a dark, almost opalescent appearance (the exact amount 
 of the stain is not important). The prepared cover-glass is floated — 
 specimen side down — on this coloring fluid, and may remain from six to 
 twenty-four hours at the ordinary temperature. Or, if a more rapid 
 staining is desired, it may be completed in from five to ten minutes by 
 gently heating the fluid, not over 40° 0. A better result is obtained, 
 however, by allowing the specimens to remain in the staining fluid for 
 some time — about twelve hours — than by hastening the process by heat. 
 The entire specimen is thus completely stained, tubercle bacilli, tissue 
 elements, and other bacteria which may be present, all in the same way. 
 The next step is, to remove the color with acid, from all the structures 
 which may be intermingled with the tubercle bacilli; the latter, owing to 
 the tenacity with which they retain the color, being but slightly affected. 
 This is done by dipping the cover-glass into an aqueous solution of 
 twenty-five-per-cent nitric acid, and shaking it about for a few seconds. 
 The acid may be even a little more dilute than this. Under the 
 influence of the acid, the specimen on the covei'-glass loses its red 
 color, and becomes gray or colorless. It is then thoroughly rinsed in 
 pure water to remove the acid, and the red color is thereby slightly re. 
 stored. Care should be taken not to expose the specimen too long to the 
 'action of the acid, because then the bacilli may be also partially or com- 
 pletely decolorized. Koch recommends that the specimen be allowed to 
 remain but a very short time in the acid, and should then be. transferred 
 directly to sixty per cent alcohol, which will remove the remainder of 
 the superfluous color, and then dehydrated. This applies also to sections, 
 see below. A little experience will enable the experimenter to judge of 
 the proper time for the action of the acid. The specimen may now be 
 mounted directly in glycerin, or dried over a spirit lamp, and mounted 
 in balsam. Methyl-violet may be used instead of fuchsin for the staining. 
 Thin sections of tubercular tissue which has been preserved in alco- 
 
510 
 
 TUBEBCULOSIS. 
 
 hol, are stained in the same way, and after dehydration may be cleared up 
 with oil of cloves, or better, oil of cedar, and mounted in balsam. The 
 balsam nsed for mounting stained bacilli should be free from chloroform 
 which is apt to extract the color from them after a time. If it is neces- 
 sary to thin the balsam, turpentine should be used. Heating of the 
 balsam during the mounting is apt to cause fading of the color in the 
 bacilli. In specimens prepared in this way, the bacilli stand out as 
 sharply defined slender red rods or filaments on the uncolored or but 
 slightly tinted background. Other dilute acids besides nitric acid may 
 be used for decolorization, such as hydrochloric. This is sometimes 
 desirable in examining delicate tissues, since the nitric acid often causes 
 shrinkage and distortion in the specimen. A one-per-cent alcoholic 
 solution of hydrochloric acid is suitable for this purpose. 
 
 For purposes of simple recognition of the bacilli in specimens it 
 seems to the writer usually better to have no color in the preparation 
 other than that which the tubercle bacilli possess. But it is often 
 convenient to demonstrate the nuclei of the cells at the same time, 
 and this may be accomplished by staining afterwards with some color 
 which will contrast with that of the bacilli, such as Bismarck brown 
 or methyl blue. This double staining serves another jiurpose and 
 is very useful in cases of fluids in which the tubercle bacilli are liable 
 to be intermingled with other bacteria of similar form, as in the 
 examination of faeces in cases of suspected tubercular ulcers of the 
 intestine, and in many cases of sputum examination. For, although most 
 other bacteria very readily give up their color in the presence of nitric 
 acid, it still occasionally happens that other bacilli do retain a faint 
 color similar to that of the tubercle bacilli, after the action of the acid. 
 ISTow, if, after the action of the acid, we place the specimen in some 
 color which contrasts sharply with that which we- have used for staining 
 the tubercle bacilli, it is found that this will stain other bacteria which 
 may be present, its own color, and even replace whatever of the first color 
 they may have retained, while the tubercle bacilli will remain entirely 
 unchanged. In this way we have the tubercle bacilli stained with one 
 color, and other bacteria and the nuclei of the cells stained with the con- 
 trasting color. A convenient combination of colors for this pur- 
 pose is to use fuchsin for the primary color and methylin blue for the 
 secondary contrasting color. The tubercle bacilli will then appear red ; 
 the cell nuclei and other bacteria, blue. Prankel has shown' that we may 
 accomplish the decolorization and the second staining in one o[)eration 
 by using the following solution : Alcohol, 50; water, 30; nitric acid, 30; 
 mix and add powder of methylen blue to saturation. After staining in 
 the usual way with fuchsin, the specimen is placed for one to two 
 
 ' Frankel: " Ueber die Farbung des Koch'sohen Bacillus und seine Semiotische 
 Bedeutung," etc. Berlin. Klin. Wochenschr., Mar. 31st, 1884, No. 13. 
 
TUBERCULOSIS. 511 
 
 minutes in the above solution, which has been filtered, and then rinsed 
 with water or with a mixture of equal parts of alcohol and water, to 
 which one per cent of acetic acid has been added. It is then dried 
 and mounted in the usual way. Thus the whole operation of drying 
 the specimen on to the cover glass, staining, decolorizing, and staining 
 again with the contrast color, and mounting may be done, if heat is 
 used for the first staining, within ten minutes. Unless it is necessary, 
 however, to obtain a rapid staining, a longer exposure to the stain, as 
 above stated, seems to give better results. There are many other methods 
 described for staining the tubercle bacilli, but those which we have 
 given are sufficient for all cases and are of sufficiently easy application 
 for practical purposes when once the rationale and details have become 
 familiar. 
 
 Pure cultures are best obtained upon gelatinized blood-serum at a 
 temperature of about 37° C. (see p. 94). For a full description of the 
 methods of culture, characters of the colonies, etc., see Koch: "Mitt, 
 a. d. k. Gesundheitsamt," Bd. II., p. 48. 
 
 Bibliography. — Aside from the standard works on General Pathology, thereader 
 may consult, for an account of the earlier literature and investigations on tubei'- 
 culosis up to 1869, the monograph of Waldenburg, "Die Tuberculose," Berlin, 
 1869. The announcement of the discovery of the Bacillus tuberculosis by Koch 
 was made in the Berliner Klin. Wochenschrift, 1883, No. 15. A most elaborate 
 and valuable article on the same subject by Koch is contained in the " Mitthei- 
 lungen aus dem Kaiserlichen Gesundheitsamt," Vol. II. 
 
 The very voluminous literature on the subject of the tubercle bacillus which 
 has accumulated since 1883 is for the most part scattered through the German, 
 English, and French journals. Ifmay be best obtained by consulting files of the 
 Index Medicus of dates since April, 1883. 
 
PYEMIA. 
 
 It has long been known that a certain number df persons who have 
 received wounds by accident, or by the hands of the surgeon, may suffer 
 from constitutional symptoms and develop lesions. To designate the 
 condition of these patients, the terms pyaemia, septicEemia, septo-pyaemia, 
 ichorrhffimia, inflammatory fever, surgical fever, traumatic fever, suppura- 
 tive fever, and purulent infection have been used. Attempts have been 
 made to distinguish several different forms ot disease and to call one 
 pysemia, another septicemia, and so on, but these attempts have not 
 proved satisfactory, and for the present it is better to include them all 
 under the general name of pysemia. 
 
 As regards the nature of pysemia three theories have been held: 
 
 I. That pus is absorbed, circulates in the blood, and acts as a poison. 
 
 II. That a chemical poison is evolved from pus and the other matters 
 which are found in wounds, and that the system is poisoned by this. 
 
 III. That bacteria are introduced into and developed in the wound, 
 find their way into the blood and tissues, and there multiply (see p. 85). 
 
 The following are the ordinary forms of pysemia, with their lesions: 
 
 I. There are cases of wounds and injuries which are characterized by 
 the presence of a febrile movement without any other symptoms. In 
 such cases no lesions are found except extravasated blood, and portions of 
 necrotic tissue, neither of which are in the condition of putrefaction. 
 
 II. There are cases in which in some part of the body a portion of 
 tissue is not only dead, but putrefying. While the process of putre- 
 faction is going on, the patient suffers from rigors, a febrile movement, 
 great prostration, and may die. If, however, the dead tissue can be re- 
 moved, or the putrefactive process arrested, all the symptoms rapidly 
 disappear. 
 
 III. A very small wound may apparently introduce at once into the 
 body a specific poison, as in dissecting wounds. There is swelling and 
 redness about the wound, and inflammation of the lymphatic vessels 
 and glands in its neighborhood. Later, all the neighboring tissues be- 
 come involved in an unhealthy inflammation; there may be infarctions 
 
PTiEMIA. 
 
 513 
 
 in the viscera, a large soft spleen, and parenchymatous degeneration of 
 the liver and kidneys. 
 
 IV. There is a large number of cases which it is diflScult to classify. 
 They are the ordinary hospital cases of compound fractures and surgical 
 wounds. After the deaths of these patients, there is a considerable variety 
 in the post-mortem appearances. 
 
 (1) There are cases in which there are no recognizable lesions. 
 
 (2) These are cases characterized by early post-mortem decomposi- 
 tion ; post-mortem staining of the tissues ; congestion of the lungs, 
 stomach, intestines, and kidneys; extravasations of blood in the serous 
 membranes; swelling of the solitary and agminated glands in the small 
 intestine; swelling of the spleen and parenchymatous degeneration of 
 the liver and kidneys. 
 
 (3) In some cases there are localized inflammations. The joints, the 
 connective tissue around the joints, the pleura (Fig. 143), the pericardium, 
 the peritoneum, the pia mater, and the connective tissue in different 
 
 Fig. 142.-MICROOOCOI is Zooglosa Colonies in the Membrahods Exudation of Pyemic 
 
 Plbukisy, X about 760, 
 
 Following compound fracture of shoulder in child. (Specimen loaned by Dr. H. N. Heineman.) 
 
 parts of the body may be inflamed. These local inflammations are 
 of a purulent character, except in the serous membranes, where the 
 principal inflammatory product may be fibrin. 
 
 (4) There are cases in which the veins in the neighborhood of the 
 wound contain softened, puriform thrombi ; there are no infarctions in 
 the viscera, but there may be inflammation of the joints and serous 
 
 membranes. 
 
 (5) In other cases the veins contain thrombi ; there are infarctions 
 
 33 
 
514 PTiEMIA. 
 
 and abscesses in the viscera; local inflammations of the joints and serous 
 membranes may be present or absent. The thrombi are formed regularly 
 in the veins near the wound, but they may be situated in veins at a dis- 
 tance, and sometimes, although infarctions and abscesses are present, 
 no thrombus can be discovered. The veins may be distended by the 
 thrombi or only contain small coagula. Tlie different kinds of thrombi, 
 and the varieties of emboli and infarctions ■which they produce, are 
 described in the article on thrombosis, p. ^1. 
 
 V. Prolonged suppuration. There is first a wound, or a bruise, or an 
 idiopathic suppurative inflammation. This original focus of inflamma- 
 tion continues to sujipurate for a long time, then successive abscesses are 
 formed in different parts of the body, the patients lose flesh and strength, 
 and die in a condition of extreme emaciation. After death, abscesses 
 are found in different places, but not in the viscera. There are no thrombi 
 nor infarctions. There may be bronchitis or broncho-pneumonia. The 
 liver, spleen, and kidneys are often the seat of waxy degeneration. 
 
 VI. Spontaneous pysemia. Under this name we include a group of 
 cases which resemble ordinary i^y^mia in their symptoms and lesions, 
 but are of obscure etiology. There is no wound, fracture, or abscess to 
 account for them, but they present the same symptoms and the same 
 lesions as the ordinary cases of pysemia. 
 
 In a very large proportion of cases of pyaemia, micrococci, scattered 
 and in colonies, are found in various parts of the body (Figs. 14 and 142). 
 
GLAI^DERS, FARCY. 
 
 These names are given to two varieties of the same disease. The dis- 
 ease originates in the horse and occurs in men by contagion. According 
 to some authors, it may be idiopathic in the human subject. 
 
 In the horse, we find four varieties of the disease: chronic and acute 
 glanders, chronic and acute farcy. 
 
 (1) Chronic Glanders.— The disease begins in the mucous membrane 
 of the nose. Small, whitish nodules, composed of small round cells, 
 are formed in the mucous membrane. These nodules soften and ul- 
 cerate. The same nodules may be found in the larynx, trachea, and 
 bronchi. The ulcerations may remain superficial, or tliey may extend 
 and attack the subjacent cartilage and bone. Nodules of the same kind 
 may be found in the lungs. 
 
 (3) Acute Glanders. — There is the same formation of nodules, which 
 soften and ulcerate; but they are accompanied with an intense inflam- 
 mation of the nasal mucous membrane, and the disease runs a rapid 
 course. 
 
 (3) Chronic Farcy. — -The lymphatic glands and vesicles become en- 
 larged, and nodules are formed in the skin, lungs, and other viscera. 
 The glands become cheesy or soften and suppurate. The cutaneous 
 nodules soften and suppurate. 
 
 (4) Acute Farcy. — There are the same lesions of the lymphatics, and 
 nodules and abscesses are found in the skin. There are also nodules in, 
 and inflammation of the nasal mucous membrane, and the disease runs 
 an acute course. 
 
 In man, the disease occurs in an acute and a chronic form, but does 
 not exactly resemble any of the varieties of the disease in the horse. 
 
 The acute disease runs a rapid and malignant course. The skin may 
 be covered with a pustular eruption. Furuncles, carbuncles, and ab- 
 scesses are found beneath the skin and in the muscles. Nodules are found 
 in the nasal mucous membrane, the lungs, kidneys, testes, spleen, and 
 liver. The joints may be inflamed, and there may be osteomyelitis. 
 
 The disease may begin at a single point, so that it may be mistaken 
 for a carbuncle, or a gangrenous erysipelas. Graefe gives a case which 
 
616 GLAiq-DEES, FAKCY. 
 
 began as an acute exophthalmos, and the nature of the disease was not 
 ascertained until after death. In this case, there were nodules in the 
 choroid coat of the eye. 
 
 The chronic form of the disease is still more difficult of diagnosis. 
 The nodules grow very slowly, are hard, and may occur in groups, or like 
 a string of beads. The nodules may soften and form chronic ulcers. 
 
 Shiall bacilli have been found in the lesions of glanders. Pure cultures 
 of these were made by Schutz and Lofder,' and inoculation with the puri- 
 fied bacilli produced similar lesions in healthy animals. 
 
 ' Notice of Researches in Deutsche Med. Wochenschrift, No. 51, 1882. 
 
HYDROPHOBIA. 
 
 This is a disease produced by the inoculation of a specific poison, and 
 characterized during life by severe spasm of the voluntary muscles. 
 
 We should naturally look for lesions in the spinal cord, and some 
 morbid changes have been found there. These changes, however, al- 
 though they are well marked in some cases, are very slightly developed 
 in others. 
 
 These changes are most marked in the medulla oblongata, but are 
 -also present in the cord. The change consists in an accumulation of 
 round cells around the blood-vessels in the perivascular spaces. 
 
LUPUS. 
 
 This form of inflammation most frequently occurs n. the skm of tha, 
 
 face but also in the mucous membrane of the mouth, pharynx con- 
 
 unctiva vulva, and vagina. The lesion consists of small, multiple 
 
 Modules of Bew-formed tissue, somewhat resembling granulation tissue. 
 
 Fig. 143.— Lupus of Face, X 760 and reduced. 
 
 in the cutis or mucosa and submucosa. By the formation of new nodules 
 and a more diffuse cellular infiltration of the tissue between them, the 
 lesion tends to spread, and by the confluence of the infiltrated portions. 
 
LOTUS. 619 
 
 a dense and more or less extensive area of nodular infiltration may be 
 formed. There may be an excessiye production and exfoliation of epi- 
 dermis over the infiltrated area, or an ulceration of the new tissue. 
 
 Microscopical examination shows the lesion to consist in the formation 
 of tissue composed of small spheroidal cells, internningled with variable 
 numbers of larger, so-called epithelioid cells and cell masses, and, in many 
 cases, with giant cells (Fig. 143), In some cases, a well-marked reticulum 
 is present between the new cells, and these are often grouped in masses 
 around the blood-vessels. In some cases, there is, without previous ul- 
 ceration, a formation of new connective tissue in the diseased area, and 
 a well-marked cicatrization; in other cases, the cells and intercellular 
 substance undergo a disintegration which leads to ulceration. 
 
 The lesion resembles, in some respects, that of tuberculosis, although 
 the vascular character of lupus and a less marked tendency to cheesy 
 degeneration would seem to indicate differences in their nature. Bacilli 
 resembling those of tuberculosis, and also micrococci have been described 
 as occurring in the lesions of lu pus. ' 
 
 ' A part of the literature showing the results of the study of lupus in its rela- 
 tions to bacteria may be found in an article by Morison: "Lupus and its Relations 
 to Tuberculosis." The Am. Jour. Med. Sciences, April, 1884, p. 413. Consult also 
 Index Medicus. 
 
LEPEOST. 
 
 Lepra (Leprosy). — This form of inflamation is characterized by the 
 development of nodular and sometimes diffuse masses of tissue, consist- 
 ing of larger and smaller cells of various shapes — spheroidal, fusiform, 
 and branched — the whole somewhat resembling granulation tissue. The 
 new tissue is most frequently formed in the most exposed parts of the 
 skin, as the face, hands, and feet, but it may occur in the skin of any 
 part of the body. It is formed more rarely in the subcutaneous connec- 
 tive tissue, in intrafascicular connective tissue of nerves, in the viscera, 
 and in the mucous membranes. The mucous membranes most frequently 
 affected are those of the eye, nose, mouth, and larynx. The nodules may 
 be very small or as large as a walnut, and may be single or joined to- 
 gether in groups or masses. The tissue of the part in which the new 
 formation occurs may be atrophied and replaced, or may remain inter- 
 mingled with the leprous tissue, or it may be hypertrophied. The nod- 
 ules may persist for a long time without undergoing any apparent change, 
 or they may soften and break down, forming ulcers; but ulceration, ex- 
 cept in the mucous membranes, is said usually to occur as the result of 
 injury or unusual exposure. The leprous tissu.e may change without ul- 
 ceration into cicatricial tissue, or cicatrization may follow ulceration. 
 
 Various secondary lesions and disturbances of nerve-function are 
 associated with the formation of leprous tissue in the nerve and central 
 nervous system, but these we cannot consider here. 
 
 In all the primary lesions of leprosy, bacilli are said to be present, 
 mostly in the cells, and particularly in the larger spheroidal forms, but 
 sometimes free in the intercellular substance. The bacilli have been 
 found in the skin, mucous membrane of the mouth and larynx, in peri- 
 pheral nerves, in the cornea, in cartilage, in the testicles, and lymph- 
 glands. Sometimes the cells contain but few bacilli, but they are fre- 
 quently crowded with them. The writer (T.M.P.) found them in 
 enormous numbers in leprous nodules of the skin, testicles, and liver. 
 The bacilli are from 4 to 6 /( long and very slender, being usually less 
 than 1 yu in thickness. They are sometimes pointed at the ends, and 
 sometimes present spheroidal swellings, which seem to indicate the for- 
 
LEPE08T. 
 
 521 
 
 mation of spores (Fig. 144). They are capable of spontaneous movement. 
 In their comportment towards staining agents, as well as in general 
 morphological characters, they considerably resemble the Bacillus tuber- 
 culosis. They may be stained with fuchsin or gentian violet by the 
 ordinary method (see pp. 89 and 90), or by the method employed for 
 staining the tubercle bacillus. 
 
 Fig. 144. — Bacilli of Leprosy, X about 850. 
 From nodule in skin, stained with fuchsin. 
 
 The reasonable conjecture that the Bacillus leprae causes the lesions 
 of leprosy depends as yet largely ujDon the constancy of their occurrence 
 in the disease, and upon their relations to the cells of the new growth, 
 since cultivation and inoculation experiments have thus far not given 
 sufficiently definite results to enable us to declare positively their etiolog- 
 ical significance. 
 
EETSIPELAS. 
 
 Erysipelas is a diffuse inflammation of the skin and subcutaneous 
 tissue which tends to spread, and which especially involves the lymph- 
 spaces and the lymph-vessels. It is characterized locally by swelling of 
 the tissue, and a bright red color of the integument. It is regularly ac- 
 companied by constitutional disturbances, the most marked of which is 
 fever. The morphological changes at the seat of lesion, as we see them 
 after death, vary considerably in different cases and in different stages of 
 the disease. The redness of the skin usually disappears after death. But 
 the tissues may be swollen by the accumulation of serous fluid. This 
 fluid may be nearly transparent or turbid from admixture with pus-cells. 
 Pus-cells may infiltrate the tissues either sparsely or in dense masses. 
 Sometimes vesicles are found on the surface, or scabs; sometimes more or 
 less of the affected region becomes filled with abscesses or gangrenous. 
 
 Fig. 145.— Micrococci in Blood- and Ltmph-Vessels of Skin op Leg in Erysipelas, X about 750. 
 
 The pus-cells, as well as the cells of the affected tissue, may be in a 
 condition of fatty degeneration. Micrococci, scattered and in colonies, 
 are regularly present in the lymph-vessels and lymph-spaces in greater or 
 less numbers (Pig. 145), during the active stages of the disease. The tissue 
 about these colonies is frequently necrotic. The researches of Fehleisen,' 
 
 'Fehleisen: " Die Aetiologie des Erysipels," Berlin, 1883. This monograph 
 contains most of the older and recent literature, and an account of the author's 
 experiments. 
 
ERYSIPELAS. 523 
 
 Ziegler, and others, together with the general character of the disease, its 
 mode of invasion, etc., seem to indicate that it is an acute infectious dis- 
 order dependent upon the presence of micrococci. Frequently, hut not 
 always, the original seat of the infection may be evident in some wound 
 or abrasion of the skin or mucous membrane. In some cases we find, 
 aside from the local lesions, petechia in the serous miembranes, swelling 
 of the spleen, and parenchymatous degeneration of the kidneys and liver. 
 Simple inflammation of the skin, accompanied by redness, is often called 
 erysipelas. 
 
Al^THEAX. 
 
 (Synonyms. — Splenic fever; malignant pustule; charbon.) This dis- 
 ease, which is much more common in the lower animals, especially the 
 herbivora, than in man, is of infrequent occurrence in the United States. 
 It is induced in man by the accidental inoculation with the Bacillus anthra- 
 cis, which causes the disease in the lower animals. ' This may occur through 
 the agency of flies which have been feeding on animals infected with this 
 disease, by handling their carcases or hides, or in other ways. There 
 may be in man, local lesions in the skin, in the form of papules, pus- 
 tules, or a phlegmonous inflammation, with oedema and lymphangitis. 
 
 Fig. 146. — Bacillus Akthracis Growing in Blood-Vessels of Liver of Mouse, x 'toO and reduced. 
 
 The disease may remain local, or general infection may occur. In some 
 cases, there is apparently no external lesion. 
 
 'For the literature of the relations of the Bacillus anthracis to this disease, see 
 Koch, "Mitth. a. d. Kaiserlichen Gesundheitsamte," Bd. i., p. i^et seq. 
 
AjSTTHEAX. 525 
 
 When general infection occurs, the post-mortem appearances vary. 
 
 Decomposition, as is usual in acute infections, generally sets ia early. 
 The blood is frequently not much coagulated and dark in color. Hem- 
 orrhages and ecchymoses are frequently found in the serous and mucous 
 membranes and in various other parts of the body. 
 
 The lungs may show small hemorrhages and oedema; and the bronchi 
 may be deeply congested. The pleural cavities may contain serum. 
 The intestines may exhibit the lesions of the so-called intestinal mycosis 
 (see p. 321). Tlie bronchial and other lymphatic glands may be swollen. 
 The spleen may be swollen, very dark in color, and soft, sometimes al- 
 most diffluent. The characteristic bacilli (Fig. 146) are found in various 
 parts of the body (see p. 83). 
 
THE MALAEIAL FEYEES. 
 
 The characteristic lesions of malarial poisoning, are certain changes in 
 the blood, the spleen, and the liver. 
 
 In the more intense and acute form of malarial poisoning, the blood 
 contains numerous particles of black or brown pigment, which are either 
 free, or embedded in cells resembling the white blood-cells and the endo- 
 thelium of the blood-vessels. After death, this pigment is found in the 
 blood-vessels throughout the body, but is most abundant in the blood- 
 vessels of the liver and spleen. These organs are then usually of large 
 size, and of a peculiar brown or black coloi'. 
 
 In some of these severe cases, there are also extravasations of blood 
 from the mucous membranes, and in their substance. There may also be 
 general jaundice. 
 
 In the milder and more protracted cases of malarial poisoning, the 
 composition of the blood is altered, and the patients may become pro- 
 foundly auEemic. The spleen becomes the seat of a simple hypertrophy, 
 and may be enormously enlarged. 
 
 The liver may exhibit the changes due to chronic interstitial hepatitis. 
 
 Klebs andTommasi-Crudelli' have described, as occurring in the soil, 
 and in the air at certain times, in the vicinity of Rome, elongated oval 
 spores which are mobile and which, in artificial cultures or on injection 
 into the bodies of animals, develop into long thread-like bacilli. Animals 
 inoculated with these organisms are said to exhibit the clinical and post- 
 mortem characteristics of malarial fever, and their blood to contain the 
 organisms. Similar bacilli have been found in various parts of the body 
 of persons dead of malarial fever, and in the blood of malarial patients in 
 the cold stage, by Marchiafava and Ouboni,^ Ziehl,' Marchand,* McMunn," 
 Dreschfeldt," and others. The experiments of Ceri with cultures and 
 
 ' Archiv f. exp. Path., Bd. xi., p. 122. 
 «Ibid., Bd. xiii., p. 
 
 ^Deutscli. Med. Wocbensoh., Nov. 25tli, 1882. 
 * Virch. Archiv, Bd. 88, p. 104, 1882. 
 'Brit. Med. Jour., 1881, Vol. II., p. 935. 
 'Ibid., 1884, Tol. L, p. 462. 
 
THE MALAEIAL FEVEES. 627 
 
 inoculations were in general confirmatory of those of the earlier obser- 
 Ters. 
 
 The experimental work thus far done in this direction, however, 
 seems altogether too unsystematic, and the justifiable conclusions too in- 
 definite, to permit us as yet to number the malarial among the bacterial 
 diseases, however probable on clinical and other grounds such a conjec- 
 ture may be. 
 
DISEASES OHAEAOTEEIZED BY ALTEEA- 
 TIO]SrS Ilf THE COMPOSITIOI^ OF 
 THE BLOOD. 
 
 There is a group of diseases in which the essential lesion seems to be 
 an alteration in the composition of the blood, although in some members 
 of the group other lesions are also present. This group embraces Chlo- 
 rosis, Pernicious Ansemia, Addison's Disease, Leukaemia and Pseudo- 
 leuksemia. 
 
 CHLOROSIS. 
 
 In many cases of chlorosis the only lesion is the change in the com- 
 position of the blood. 
 
 The Tolume of the blood may be diminished, the red blood-globules 
 contain less haemoglobin, the number of red blood-cells is diminished, 
 there are present red blood-cells some of which are larger and some 
 smaller than the normal cells. 
 
 In a few cases there is also present a congenital smallness of the 
 aorta. 
 
 PERNICIOUS ANEMIA. 
 
 In this disease the same changes in the blood exist as in chlorosis, and 
 there may also be a moderate increase in the number of the white blood- 
 cells. 
 
 There is often fatty degeneration of the walls of the heart, and of the 
 arteries. 
 
 There may be thrombosis of the pulmonary artery. 
 
 The same changes in the marrow of the bones are found as in leu- 
 kaemia. 
 
 There may be ecchymoses in different parts of the body. 
 
 ADDISON'S DISEASE. 
 
 This name is applied to a disease characterized by a peculiar pig- 
 mentation of the skin, certain changes in the supra-renal capsules, and 
 a diminution in the number of red blood-cells. The patients become 
 
ALTEEATIONS IN THE COMPOSITION OF THE BLOOD. 529 
 
 Tery anemic, but are not emaciated. They suffer from cerebral symp- 
 toms, great prostration, syncope, and derangements of the functions of 
 the stomach and intestines. 
 
 The pigmentation of the skin is the symptom which has especially 
 attracted attention. The change in color usually begins and becomes 
 most marked in those parts of the skin which are not covered by the 
 clothing, or are naturally darker colored. The rest of the skin after- 
 wards changes color, but not I'ltviformly, white patches being left. The 
 color is at first a light yellow or brown; this becomes darker until it is 
 of a dark greenish, grayish, or blackish brown. The mucous membrane 
 of the tongue, lips, and gums may be pigmented in the same way. 
 
 Under the name of Addison's Disease different observers have de- 
 scribed cases in which the symptoms and bronzed skin existed without 
 disease of the supra-renal capsules; cases in which the bronzed skin was 
 the only lesion, and cases in which the supra-renal capsules were diseased 
 without symptoms or bronzed skin. 
 
 We hardly know as yet what are really the characteristic lesions of the 
 disease. 
 
 ITie Skin. — The discoloration of the skin is due to deposit of yellow- 
 ish-brown pigment in the deeper layers of the epidermis, especially in 
 the layer covering the papillse and less constantly in the connective tis- 
 sue of the cutis. 
 
 The Brain. — Pigmentation of the gray matter, acute meningitis, 
 chronic meningitis and distention of the ventricles with serum have been 
 observed. 
 
 The Heart— The muscular fibres may be the seat of fatty degenera- 
 tion. 
 
 The Sympathetic Nerves may show a variety of changes apparently 
 due to chronic inflammation, especially the nerves which are in contact 
 with the supra-renal capsules. 
 
 The Supra-renal Capsules.— The most common lesion of these bodies 
 is a tubercular inflammation resembling that which occurs in the lymph- 
 atic glands. 
 
 The supra-renal capsules are large, hard, and nodular; less frequently 
 of normal size or atrophied. On section, they are found to contain 
 cheesy masses, surrounded by zones of gray, semi-translucent tissue. 
 Later the cheesy masses may become calcified, or they may soften 
 
 and break down. 
 
 The grayish zones are composed of tubercle tissue, granulation tissue, 
 
 and- connective tissue. 
 
 Other cases have been described in which the supra-renal capsules 
 were the seat of carcinoma, or of fatty or waxy degeneration. 
 
 The Blood exhibits the same changes as exist in pernicious anjemia. 
 34 
 
530 ALTEEAnONS IN THE COMPOSITION OF THE BLOOD. 
 
 LEUKEMIA (LEUCOCYTH^MIA). 
 
 This disease is characterized by a persistent and progressive increase 
 in the number of white blood-cells in the blood, accompanied by altera- 
 tions of varying amount in the spleen, lymph glands, and bone marrow. 
 Sometimes one, sometimes another of these organs are especially involved. 
 Not infrequently other internal organs, lungs, liver, kidneys, etc., are 
 more or less densely infiltrated with leucocytes, either diffusely or in 
 nodular form. The lymphatic tissue of the gastro-intestinal canal maybe 
 in a condition of hyperplasia. 
 
 Ecchymoses in the serous and mucous membranes, or severe hembr- 
 hages on slight provocation, and fatty degeneration of the heart and kid- 
 neys frequently complicate leuksemia. Aside from various other foreign 
 chemical substances which may exist in t,he blood in leukaemia, there 
 are very frequently found in the blood, marrow, spleen, liver, etc., 
 after death, elongated octahedral crystals, called Gharcofs crystals, 
 which are believed to be formed by a combination of phosphoric acid with 
 some organic base. ' 
 
 For a detailed description of the lesions of the different parts of the 
 body in leuksemia, see chapters on Blood, Spleen, Lymph Glands, Bones, 
 etc. It does not fall within the scope of this work to consider the various 
 theories as to the probable causes of this disease, which is very obscure 
 and but little understood." 
 
 PSEUDO-LEUKEMIA (HODOKIN'S DISEASE). 
 
 In pseudo-leuhmnia, which is very closely related to leukaemia, the 
 anatomical changes in the organs are apparently identical with those of 
 leukaemia, but there is no increase in the number of leucocytes in the 
 blood. Of the internal organs the lymph glands are most apt to be 
 specially affected in pseudo-leuksemia. 
 
 ' For literature of Charcot's crystals, consult Zenker, Arch, ftir Klin. Medicin, 
 Bd. 18, p. 125, 1876. 
 
 ''For literature of leukaemia and pseudo-leukEemia consult Birch-Hirschfeldt: 
 "Lehrbuch der path. Anatomic," 2d Ed. , Bd. II., p. 146. For general consideratiou 
 of the relation of certain diseases of the blood to the blood-forming 0)-gans — 
 spleen, lymph glands, etc., see Cohnheim's " Vorlesungen iiber allgemeine Patholo- 
 gie," Vol. I. 
 
SCORBUTUS, PURPUEA, H^MATOPPIILIA. 
 
 SCORBUTUS (SCURVY). 
 
 This disease appears to result from imperfect nutrition under condi- 
 tions which cannot be considered here, and whose immediate cause we 
 do not understand. The lesions are variable, the most prominent being 
 extravasation of blood in the skin, subcutaneous tissue, and muscles ; 
 swelling and ulceration of the gums. Small and sometimes extensive 
 hemorrhages are apt to occur in the mucous membranes and on serous 
 surfaces. Small ulcers may form in the mucous membranes. Patty 
 degeneration of the heart, liver, and kidneys is not uncommon. The 
 spleen may be large and soft. ISTo constant characteristic changes have 
 been discovered, either in the blood-vessels or the blood, which would 
 satisfactorily account for the extravasations and other lesions. 
 
 The bodies are apt to decompose early. The skin may be mottled 
 with small and large jiurple, blue, brown, or blackish spots produced 
 by degenerative changes in the extravasated blood in the cutis. Some- 
 times ulcers are produced by the perforation of effused blood on to the 
 surface. 
 
 The joints may be inflamed, may contain serum or blood. Barely, 
 the hemorrhages are followed by destruction of the cartilages and ends 
 of the bones. 
 
 Very rarely, there is hemorrhage between the periosteum and bone, 
 and in the bone itself, producing softening and destruction of the bone, 
 and separation of the epiphyses. The sternal ends of the ribs are the 
 most frequent seat of this change. 
 
 PURPURA HEMORRHAGICA (MORBUS MACULOSUS). 
 
 This disease is characterized by the occurrence of ecchymoses in the 
 skin, mucous and serous membranes. Hemorrhages, particularly from 
 the raucous membranes, may be very severe, and even fatal. The cause 
 of the disease is unknown. 
 
532 SCOEBTJTUS, PUEPUEA, H^MATOPHILIA. 
 
 H^MATOPHILIA (HEMORRHAGIC DIATHESIS). 
 
 This disease consists in a liability to hasmorrhage on the slightest 
 provocation, and is dependent upon some constitutional peculiarity which 
 is unknown to us. It is frequently hereditary. An unusual thinness 
 of the intima of the arteries has been noticed in some cases, and other 
 changes have been described, 'but there are no constant lesions associated 
 with the hemorrhages, as yet discovered, which would satisfactorily 
 explain their occurrence. The hemorrhages may be traumatic in origin, 
 or they may occur spontaneously from the mucous membranes. 
 
GOUT. 
 
 The characteristic lesion of gout is the deposit of urate of soda in the 
 articular cartilages, the ligaments of the joints, the ears, and the eye-lids. 
 
 The most frequent situation is the metatarso-phalangeal joint of the 
 great toe. The cartilage may be infiltrated or incrusted with the 
 deposit. 
 
 A very important feature of gout is that patients with the gouty dia- 
 thesis are especially liable to derangements of digestion, and to certain 
 chronic inflammations such as: chronic inflammation of the arteries, 
 chronic bronchitis, and chronic nephritis. 
 
DIABETES. 
 
 It would be expected that so common and well marked a disease as 
 saccharine diabetes should be characterized by definite lesions, but this 
 is not the case. The changes which we find after death are accidental, 
 or the results of the disease. No characteristic lesions have yet been dis- 
 covered. 
 
 Tlie Brain may appear to be entirely normal ; it may be congested ; 
 there may be an increase of serum; the convolutions may be shrunken; 
 there may be meningitis; there may be dilatation of the blood-vessels; 
 small extravasations of blood around the vessels; enlargement of the 
 perivascular spaces, and alterations in the perivascular sheaths, and 
 nervous matter bounding the cavities; there may be tumors at the base 
 of the brain. 
 
 The Spinal Cord may present dilatation of the blood-vessels; dilata- 
 tion of the central canal; changes in the gray matter of the anterior 
 cornua. 
 
 The Lungs. — There may be pleurisy, bronchitis, broncho-pneumonia, 
 lobar pneumonia, gangrene of the lung, chronic pulmonary phthisis. 
 
 The Heart is often small, there may be chronic endocarditis. 
 
 The Stomach and Intestines. — The stomach may be dilated, its walls 
 may be thickened, there may be hemorrhagic erosions of the mucous 
 membrane. In the intestines there may be tubercular ulcers, or ente- 
 ritis. 
 
 The Liver and the Spleen show no marked changes. 
 
 T7ie Pancreas may be atrophied; it may contain abscesses. 
 
 The Kidneys may oe enlarged, they may be the seat of parenchyma- 
 tous or difEuse nephritis, there may be glycogenic degeneration of the 
 epithelium of Henle's loops. 
 
 Tlie Blood. — In a few cases fat has been found in the blood and fat 
 emboli in the vessels of the lungs. 
 
 A considerable number of autopsies are I'ecorded in the "Transactions 
 of the Pathological Society of London," vol. xxxiv., p. 328, and in Fre- 
 rich's monograph on Diabetes. 
 
SUlSrSTEOKE. 
 
 During the hot summer months, cases of sunstroke are of frequent 
 occnrrence in New York. The persons afEected are, for the most part, 
 adult male laborers, usually of intemperate habits. 
 
 It is necessary to separate from the cases of sunstroke proper, when 
 the patient is attacked while exposed to the heat of the sun, the cases 
 of exhaustion from heat and fatigue, which may occur as well in the 
 house. 
 
 The patients who are seriously affected by sunstroke exhibit, during 
 life, an intense heat of the skin, convulsions, and coma. Death in many 
 cases soon ensues. In other cases, the symptoms are more protracted. 
 
 After death, decomposition sets in very early, owing to the state of 
 the weather. In autopsies which I have made within two hours after 
 death, the increased heat of the skin was still maintained. 
 
 The Brain and its membranes were in some cases congested; in others 
 not. Sometimes there was an increased amount of serum beneath the 
 pia mater; sometimes there were small and thin extravasations of blood 
 beneath the pia mater, and between the pia and dura mater. 
 
 In the other viscera there were no lesions except those due to the 
 condition of coma existing before death. The lungs and kidneys were 
 frequently congested. 
 
 In the cases in which cerebral symptoms are protracted for a number 
 of days, the lesions of meningitis have been found after death. 
 
 Attention has been called by Dr. H. 0. Wood, Jr., to the rigid con- 
 dition of the wall of the heart after death, but this rigidity is certainly 
 not present in all cases. 
 
DEATH FEOM BURNII^G. 
 
 Death may be caused by the inspiratioa of smoke and flame ; by 
 drinking of hot fluids ; by the direct contact of flame or hot substances 
 with the external surface of body. It may be due to the direct effect of 
 the agents ; to secondary affections of the viscera, or to the exhaustion 
 produced by long-continued inflammation and suppuration. 
 
 The entire body may be burnt to a coal, or completely roasted, or 
 only a larger or smaller area of the skin be burned. 
 
 We find the burned skin divested of epidermis, and presenting a pe- 
 culiar red, hard, parchment-like appearance. If the patient has lived 
 some time, this is replaced by a suppurating surface. Or there are small, 
 bladder-like elevations of the epidermis. The base of these blisters is 
 red, and they are surrounded by a red zone, or suppuration may have 
 commenced. 
 
 These appearances cannot be produced by heat applied to the skin 
 after death. 
 
 The Brain maybe congested, cedematous, or softened. More fre- 
 quently it is normal. 
 
 The Larynx and Trachea may be congested, and the seat of croupous 
 inflammation. There may be oedema of the glottis. 
 
 The Lungs may be congested and cedematous, or hepatized, or the 
 seat of pyemic infarctions. There may be pleurisy. 
 
 Inflammation of the peritoiieum is not very infrequent. There may 
 be swelling of the solitary and agminated glands of the small intestine. 
 
 The duodenum may be the seat of perforating ulcers and the mucous 
 membrane of entire gastro-intestinal canal may be congested. The Liver, 
 Spleen, and Kidneys may be the seat of parenchymatous degeneration, or 
 of pyaemic infarctions. 
 
DEATH FROM LIGHTNING. 
 
 Persons who are struck by lightning may die instantly ; or may con- 
 tinue for several hours comatose, or delirious, and then either die or 
 recover ; or they may die after some time from the effects of the burns 
 and injuries received. 
 
 The post-mortem appearances are very variable. Sometimes there 
 are no marks of external violence or internal lesions. Sometimes the 
 clothes are burnt and torn, while the skin beneath them is unchanged. 
 Usually there are marks of contusion and laceration, or ecchymoses, or 
 lacerated, punctured wounds, or fractures of the bones, or superficial or 
 deep burns. The track of the electric fluid may sometimes be marked 
 by dark-red arborescent streaks on the skin. Fractures are rare. 
 
 The internal viscera may be lacerated and disorganized from light- 
 nins:. 
 
DEATH FEOM SUFFOOATION.-ASPHYXI2V. 
 
 By suffocation we understand that condition in which air is prevented 
 from penetrating into tlie lungs, without direct pressure on the larynx or 
 trachea. The interruption of the function of resfjiration which is. thus 
 brought about induces the condition known as asphyxia. Many deaths 
 from drowning and strangulation take place in this way. 
 
 The methods in which tlie supply of air may be cut off from the lungs 
 are very various. The mouth and nose may be closed by the hand, by 
 plasters and cloths, by wrapping up the head in cloths, by covering the 
 face with earth, hay, grain, etc. Foreign bodies may be introduced into 
 the mouth, pharynx, and larynx. Blood may pass into the trachea from 
 an aneurism, or from a wound. The glottis may be closed by inflamma- 
 tory swelling. Matters which are vomited may lodge in the larynx. 
 
 On the other hand, injury or disease of the medulla oblongata or par- 
 alysis, or spasm of the muscles of respiration from drugs, tumors press- 
 ing upon tlie air-passages, or diseases of the lungs themselves, may induce 
 asphyxia. 
 
 External Lisped ion. 
 
 The body should be examined for marks of violence, the cavities of 
 the mouth and nose for foreign substances. 
 
 The face may be livid and swollen, or present a natural appearance. 
 The conjunctiva may be congested and ecchymotic. There may be small 
 ecchymoses on the face, neck, and chest. The mouth often contains 
 frothy blood and mucus. The tongue may be protruded. 
 
 Intei'iial Examination. 
 
 The Brain and its membranes maybe congested, or anaemic and oede- 
 matous, or unchanged. 
 
 The Blood throughout the body is unusually dark-colored and fluid. 
 
 The Larynx may contain foreign bodies which have produced the suf- 
 focation. The mucous membrane of the larynx, trachea, and bronchi is 
 congested, and some times ecchymotic. These passages contain frothy 
 blood and mucus. 
 
DEATH FROM STRANGULATIOlSr. 539 
 
 The Lungs are usually congested and cBdematous, but sometimes do 
 not differ from their ordinary appearance. There may be small patches 
 of emphysema near the surface of the lungs. Sometimes, especially in 
 infants, small ecchymoses are found in the costal and pulmonary pleura. 
 
 The Heart usually presents its right cavities full of blood, its left cavi- 
 ties empty; but to this there are frequent exceptions." 
 
 The Abdominal Viscera are usually congested. 
 
 DEATH FROM STRANGULATION— HANGING. 
 
 Strangulation is effected by the weight of the body in hanging, by 
 pressure on the neck with the hands or by some other object, or by con- 
 striction of the neck with a cord or ligature of some kind. Death is 
 usually produced by asphyxia or by asphyxia combined with the effect of 
 the cutting off of the blood supply to the brain by pressure on the large 
 vessels of the neck. In some cases of hanging, death ensues as a result 
 of fracture or dislocation of the cervical vertebrae. 
 
 External Inspection. — The face may be livid and swollen, the eyes 
 prominent, the lips swollen, and the tongue protruded. These appear- 
 ances are, however, often absent. Erection of the penis, ejaculation of 
 semen, and evacuation of fsBces and urine are frequently observed. 
 
 In most cases marks are left«pon the neck by the objects which have 
 directly produced the strangulation. 
 
 In cases of hanging, the marlc about the neck varies considerably in 
 position, direction, and general characters, depending upon the kind of 
 ligature employed, the time of suspension, period after death at which the 
 observation is made, etc. The most common marlc left by a cord about 
 the neck is a dry, dense,- brownish furrow, whose breadth corresponds 
 but in a very general way with the diameter of the cord. In some cases, 
 according to Tidy and others, there may be no mark at all if the hang- 
 ing is quickly accomplished with a soft ligature and tlie body cut down 
 immediately after death. There may be abrasions and ecchymoses of the 
 skin at the seat of ligature. 
 
 In cases of strangulation by the fingers, the marks on the neck may 
 correspond in a general way to the shape of the fingers. 
 
 The application of the same forces immediately after death may pro- 
 duce the same marks as when death is induced by them. 
 
 Internal Examination. — The Brain and its membranes may be con- 
 gested, or there may be extravasation of blood, or there may be- no abnor- 
 mal appearances. The NecJc. — In some cases there is effusion of blood 
 beneath the ligature, rupture of the cervical muscles, fracture of the 
 OS hyoides and cartilages of the larynx, fracture and dislocation of the 
 cervical vertebrse, rupture of the internal vertebral ligaments, and of the 
 inner and middle coats of the carotid arteries. Similar changes may be 
 
640 DEATH FEOM DEOWNING. 
 
 produced in the dead body by the use of great violence. In death from 
 asphyxia, the lesions are similar to those described above. In some 
 cases, for example, where death has occurred from fright or shock, the 
 results of post-mortem examination are entirely negative. 
 
 DEATH FEOM DROWNING. 
 
 In examining the bodies of persons who have been drowned, it is 
 necessary to bear in mind a number of questions which may arise: 
 Whether the person came into the water alive or dead ? How long a 
 time has elapsed since death ? Whether the person committed suicide, 
 or was drowned by accident, or was murdered ? These questions are to 
 be solved sometimes certainly, sometimes with probability, sometimes not 
 at all by the post-mortem examination. Persons dying in the water, to 
 which condition the.term drowning is commonly applied, may die from 
 asphyxia, from exhaustion, from fright or syncope, from diseases of the 
 heart, apoplexy, injuries, etc. While in the majority of cases asphyxia is 
 a predominant or important factor in death by drowning; the condi- 
 tions under which death occurs are so apt to be complex that in the 
 minority of cases only are the lesions of pure asphyxia found after death, 
 while in most cases the bodies present the more or less well-marked 
 lesions of asphyxia, together with those indicative of complicating con- 
 ditions. There are no post-mortem conditions which alone are abso- 
 lutely characteristic of drowning, and it is only by considering all the 
 facts elicited by the autopsy together, that any just conclusion can be 
 arrived at. It should always be borne in mind, moreover, that even the 
 most characteristic of the evidences of drowning are apt to be modified 
 or to disappear as decomposition goes on. 
 
 External Inspection. — Post-mortem rigidity usually sets in early, 
 sometimes immediately after death. Decomposition goes on, especially 
 in summer, with unusual rapidity in bodies which have been removed 
 from the water. Frequently, but by no means constantly, the peculiar 
 roughening of the skin, known as goose skin (cutis anserina) is found, 
 but this may occur after death from other causes. A light, lathery 
 froth, either white or blood-stained, is frequently seen about the month 
 and nostrils within twelve to twenty-four hours after removal of the body 
 from the water, but it may be absent, and may be seen after death from 
 other causes. After the body has lain for several hours in the water 
 (twelve to. twenty-four), the thick skin of the palms of the hands and 
 soles of the feet may become macerated, and thrown into coarse wrin- 
 kles, just as it may after prolonged soaking during life, or in a dead 
 body thrown into the water. The penis and nipples may be retracted 
 and the scrotum shrunken, but this is not constant nor characteristic. 
 
 If the person has struggled in the water and clutched at objects 
 
DEATH FEOM DROWNING. 54]_ 
 
 within his reach, there may be evidences of this in excoriations of the 
 fingers or in the presence of sand, weeds, etc. , under the nails or grasped 
 in the hands. 
 
 External marks of injury, bruises, etc., should be sought for, since 
 persons in diving or on being thrown into the water with homicidal 
 intent may have died from the violence, and not, strictly speaking, from 
 drowning. It should also be borne in mind in such complex cases that 
 injuries, not in themselves fatal, may, when the body is in the water, 
 prove so, on account of the inability of the person to rescue himself or 
 gain time for recovery from the injury, and that then the struggle for 
 breath may be but slight, and the more prominent signs of drowning 
 but little marked. 
 
 INTERNAL EXAMINATION. 
 
 The 5raire.— Congestion of the brain and its membranes is found 
 only in a small proportion of cases. 
 
 The Blood, when death occurs from asphyxia, is usually fluid through- 
 out the body and of a dark color, as in asphyxia from other causes. 
 
 Tlie Air-Passages. — In persons who die from asphyxia, the mucous 
 membrane of the larynx, trachea, and bronchi is usually congested, and 
 the air-passages contain a variable quantity of bloody or mucous froth. 
 In persons dying in the water from other causes than asphyxia, these 
 appearances are absent. Foreign substance from the water, such as sand, 
 weeds, etc., or matters regurgitated from the stomach, may find their way 
 into the air-passages during the act of di'owning, or as a post-mortem 
 occurrence. Thus in bodies washed about on the bottom, sand or mud 
 may get into the air-passages for a certain distance, from the mechanical 
 action of the water. 
 
 The Lungs in typical cases are distended, so that they fill the thorax 
 and cover the heart, l.'he increased size is due partly to congestion, 
 partly to the presence of the fluid in which the person was drowned, 
 which is often inspired during the act of drowning; and partly to the 
 distention of the air- vesicles with air. While in cases of drowning in 
 which there is a struggle, and water is breathed in, the lungs contain 
 more or less fluid, this may, as a result of decomposition, find its way in 
 greater or less quantity into the pleural cavities by transudation, leaving 
 the lungs comparatively empty. It should be remembered, however, 
 that a considerable quantity of reddish fluid may collect in the pleural 
 cavities under other conditions than drowning, as a post-mortem change, 
 by transudation from the blood-vessels, and other adjacent tissues. 
 
 The Heart.— It^ those who die from asphyxia, the right cavities are 
 usually filled with fluid blood, while the left cavities are empty. But 
 where death is due to complex causes, this may not be the case. 
 
 The StomacJi.—The fluid in which the person was drowned, some- 
 
642 DEATH I'EOM DROWNING. 
 
 times mixed with sand, weeds, etc., may be swallowed during the act of 
 drowning. Sand may wash for a short distance into the oeosphagus after 
 death in bodies washing about the bottom. 
 
 The Abdominal Viscera may be congested in joersons who die from 
 asphyxia. 
 
 In persons dying from syncope, shock, etc., we may find no lesions. 
 When the death is partly due to asphyxia, and partly to other causes, the 
 conditions will vary in -vario'us ways, which need not be described in de- 
 tail here. 
 
 In important cases of doubtful drowning, it is desirable to carefully 
 collect and save some of the fluid from the lungs and stomach for micro- 
 chemical examination, since the identification of tbese fluids with those 
 in which the .person was pi'esuniably drowned, will often give certainty 
 to an otherwise doubtful case. 
 
 For the detailed consideration of the anatomical diagnosis of drown- 
 ing, the changes which bodies dead from drowning undergo from decom- 
 position, and the factors bearing on the question of suicide, homicide, 
 etc., we refer to works on Medical Jurisprudence.' 
 
 'Tidy: " Legal Medicine," Vol. II., 342-373. Guy and Ferrier: "Forensic 
 Medicine," 374-385. 
 
DEATH FEOM POISOITING. 
 
 In cases of suspected poisoning which may possibly have a medico- 
 legal bearing, the examination should be made with extreme care and 
 thoroughness. The inspection of the body, and the examination of all 
 the viscera should be thorough and detailed. Every appearance should 
 he noted at the time, and nothing left to the memory. It is well to have 
 xin assistant record the observations as they are made. The disposition 
 of the parts and organs in jars should also be noted at the same time. 
 
 It is important to remember that many poisons destroy life without 
 producing appreciable lesions, and also that many cases of sudden death 
 occur, not due to poisons, and without any discoverable cause. 
 
 In bodies which are exhumed for examination, the tissues may be 
 so changed by decomposition that it is impossible to say whether lesions 
 have or have not existed. In such cases, the careful and separate pre- 
 servation of the viscera, and other parts for chemical examination is often 
 all that can be done. For directions for preserving tissues and organs 
 for the chemist in medico-legal cases, see Part I. (p. 32). 
 
 SULPHURIC ACID. 
 
 The effects of this poison vary with the amount taken and with its 
 strength. Death usually takes place in from two to twenty-four hours 
 after the taking of the concentrated acid. A case of death within an 
 hour is recorded. When the poison is less concentrated, or its effects less 
 intense, the patient may survive for mouths. 
 
 The skin of the face about the mouth may be blackened and charred 
 by the acid. The mouth and pharynx are of a grayish or blackish color, 
 or are covered with a whitish layer, while the deeper tissues are reddened. 
 Sometimes these regions escape the action of the poison. 
 
 The larynx, trachea, and lungs are sometimes acted on, softened and 
 blackened by the accidental passage of the acid into them. This may 
 €ven take place when the acid does not pass into the cesophagus. 
 
 The cesophagus seldom escapes. It is grayish or blackish colored, 
 softened, and the mucous membrane comes off in shreds. If life is pro- 
 
544 DEATH FROM POISONING. 
 
 longed, cicatrices and strictures are formed. The stomach may contain 
 a blackisli pulpy fluid due to the action of the acid on mucus, blood, etc. 
 It is coated on its internal surface with a black, sticky layer beneath 
 which the mucous membrane is reddened. The mucous membrane may 
 be blackened in patches or stripes. The organ may be contracted and 
 the mucous membrane corrugated. Sometimes perforation takes place, 
 and the acid blackens and softens the adjoining viscera. In protracted 
 cases, cicatrices are formed, and the organ is contracted. If the poison 
 is dilute, there may be only the lesions of chronic gastritis. 
 
 The Uood is sometimes thickened, syrupy, acid, and may form thrombi 
 in the vessels. 
 
 The body may be partially preserved from decomposition, owing to 
 the action of the acid upon the tissues. 
 
 Fatty degeneration of the renal epithelium is mentioned by some 
 authors. 
 
 The solution of indigo in sulphuric acid, commonly known as sul- 
 phate of indigo, produces the same lesions as sulphuric acid, and also 
 stains the tissues with which it comes in contact of a dark-blue color. It 
 is stated that an indigo-blue tint is often found in the mucous mem- 
 branes after poisoning by pure sulphuric acid.' 
 
 NITRIC ACID. 
 
 Death may occur very soon after the taking of the poison, but does not 
 usually occur for several hours, and may not take place for several days 
 or weeks. 
 
 The surface of the mucous membrane of the mouth, pharynx, and 
 msopliagus is covered with yellow eschars wherever the acid has touched 
 it. Beneath and around the eschars the tissues are congested and red. 
 The poison may be introduced into the cesophagus without acting on the 
 mouth. The stomach contains a viscous, sanguinolent, yellow or green- 
 ish fluid. The mucous membrane is congested, red, swollen and 
 softened, ecchymotie. It is rarely perforated. The duodenum may be 
 inflamed, and the inflammation extend to its peritoneal coat. The rest 
 of tlie intestines usually escapes the action of the acid. 
 
 The lary7ix is very frequently acted on by the acid. There are yel- 
 low eschars, congestion and swelling of mucous membrane, sometimes 
 oedema of the glottis. The trachea may be inflamed and the lungs con- 
 gested. 
 
 If the patient survives the first effects of the poison, the lesions of 
 chronic inflammation, cicatrization, and contraction, may be found at a 
 later period. 
 
 > Woodman and Tidy: "Forensic Medicine and Toxicology," Ed. 1877, p. 337. 
 
DEATH FEOM POISONING. 545 
 
 The acid nitrate of mercury, if taken in a concentrated form into the 
 stomach, may produce the same lesions as nitric acid. 
 
 HYDROCHLORIC ACID. 
 In fatal cases, death occurs on the average in about twenty-four 
 hours. The lesions are in general similar to those produced by sulphuric 
 and nitric acids, except that the eschars are usually of a whitish color 
 at first, becoming, after a time, discolored and disintegrated. It is also 
 more common to tind false membranes on the inflamed surfaces. 
 
 OXALIC ACID. 
 
 In fatal cases, death may occur within ten minutes (in one case in 
 three minutes) or may be delayed for two or three weeks. The period 
 of death does not depend, as do in general the symptoms, upon the amount 
 and concentration of the poison. 
 
 The mucous membrane of the mouth, jyA«r«/>ia;, and cesopJiagus is 
 usually white and shrivelled, and easily pealed off, and may be covered 
 with brownish vomit from the stomach. The oesophagus maybe much 
 contracted. The stomach is usually contracted and contains a dark- 
 brown, acid, mucous fluid. The mucous membrane of the stomach may 
 be pale, soft, and easily detached, sometimes looking as if it had been 
 boiled in water. Sometimes it is red and congested; sometimes blackened 
 and gangrenous; sometimes peeled off in patches. Perforation is of 
 rare occurrence. If life be prolonged, the whitened condition of the 
 mucous membrane is succeeded by congestion and inflammation. The 
 small intestines may be inflamed. Inflammation of the pleura and per ito- 
 neiom, and congestion of fholiongs, are of occasional occurrence. In some 
 cases of death from oxalic acid there are no well-marked lesions. 
 
 Potassium oxalate produces the same lesions as oxalic acid. 
 
 TARTARIC ACID. 
 
 This acid is seldom used as a poison, but in large doses may prove 
 fatal. The lesions in the cases observed were redness and inflammation of 
 the mucous membrane of the gastro-intestinal canal. 
 
 POTASH, SODA, AND THEIR CARBONATES. 
 These substances are not commonly used as poisons with suicidal or 
 homicidal intent, but may be taken by mistake. They may cause death 
 in a few hours, or life may be prolonged for several weeks. 
 
 The mucous membrane of the mouth, pharynx, (esophagus, and stomach 
 
 is softened, swollen, congested, and inflamed, or may be peeled off. 
 
 It may be blackened from local changes in the blood. The mucous 
 
 membrane of the larynx and trachea may also be swollen and infl.amed. 
 
 35 
 
546 DEATH FROM POISONING. 
 
 If life is prolonged for some time, cicatrices and strictures of the 
 msopliagus and stomach are apt to be produced as a result of the repara- 
 tive inflammation. 
 
 AMMONIA. 
 The vapor of strong ammonia may cause death from inflammation of 
 the larynx and air passages. The strong solution of ammonia produces 
 lesions similar to those of potash and soda. The larynx, trachea, and 
 h'onchi are frequently inflamed and may be covered with false membranes. 
 Fatal inflammation of the rectum and colon has been produced by an 
 enema of strong solution of ammonia. 
 
 POTASSIUM NITRATE. 
 
 Accidental poisoning sometimes occurs from large doses of this salt. 
 In the observed cases, there was intense congestion and inflammation of 
 the stomach and intestines, and in one case a small perforation of the 
 stomach. 
 
 For the effects of several infrequently employed salts of the alkalies 
 and alkaline earths, which for the most part produce simple inflamma- 
 tion of the gastro-intestinal canal, we refer to special works on Toxi- 
 cology. 
 
 PHOSPHORUS. 
 
 Poisoning by phosphorus is much more common in France and Ger- 
 many than in this country. Some of the forms of rat poison of which 
 this is a frequent ingredient and the ends of matches are common media 
 for its administration. It is more often used with suicidal than homici- 
 dal intent. 
 
 The post-mortem appearances vary according to the length of time 
 which elapses before death, which may be from a few hours to several 
 months. 
 
 If death takes place in a few hours, the only lesions may be 
 those produced by the direct local action of the poison. The mouth, 
 pharynx, and oesophagus usually escape. The stomach may be only 
 slightly reddened, or there may be patches of inflammation and erosion. 
 The contents of the stomach are often mixed with blood, and may have 
 the peculiar smell of phosphorus. There may be little bits of wood 
 present when the poison has been taken from the heads of lucifer 
 matches. It is said that the mucous membrane of the stomach may emit 
 a phosphorescent light in the dark. 
 
 If death does not ensue until after several days, the lesions are 
 more marked. The body is usually jaundiced. There may be ecchy- 
 mosis beneath the pericardium, pleura, and peritoneum, in the lungs, the 
 kidneys, the bladder, the uterus, the muscles, and the subcutaneous con- 
 nective tissue, and bloody fluid in the visceral cavities. 
 
DEATH FROM POISONtNG. 54-7 
 
 ,^..^^l ^Tv ^^^^/f "'^^^^^ '«««^^«^. the walls of the Uood-vessels, and 
 
 S faSvl : '"'' at"""'" '' ^'^ ^^^"^^^ ™^y '^^ - th« -•edition 
 
 of fatty degeneration. The blood is usually dark and fluid 
 
 The Stomach sometimes presents lio very striking changes. There 
 may be small circumscribed spots of inflammation, erosion, or gangrene, 
 and occasionally perforation. The most constant change is a granular 
 degeneration of the cells which fill the gastric follicles. In consequence 
 01 tnis, the mucous membrane appears thickened, opaque; of white 
 gray, or yellow color. ' 
 
 The Small Intestine appears normal or is congested. 
 
 The Liver is found in different degrees of parenchymatous and fatty 
 degeneration, and is often stained yellow from the jaundice. It is usually 
 increased m size, and of a grayish, grayish-yellow, or light-yellow color, 
 unless stained by the bile. Less frequently the centres of the acini 
 are congested, or the entire liver is congested, or there are small hemor- 
 rhages m the liver-tissue. The liver may be soft, flabby, and smaller 
 than normal. In the interstitial tissue of the liver and along the branches 
 of the portal vein there may be marked infiltration with small spheroidal 
 cells. 
 
 The Kidneys often present parenchymatous and fatty degeneration of 
 the epithelium. The mesenteric glands may be soft and swollen. 
 
 ARSENIC. 
 
 This poison is very frequently employed with suicidal intent. Death 
 may occur in a longer or shorter time from the direct irritative effects of 
 the poison upon the gastro-intestinal canal, with the symptoms which 
 usually accompany the ingestion of irritant poisons; or it may occur with 
 symptoms of collapse, or coma, or shock; or the symptoms may resem- 
 ble those of cholera. The average time of death in acute fatal cases is 
 about twenty hours, but death has occurred in twenty minutes, and has 
 been prolonged for two or three weeks. 
 
 The mouth, pharynx, and oesophagus may be inflamed, but are more 
 frequently unaltered. The stomach may be empty or contain mucus 
 mixed with blood. The arsenic, in substance, may be found adherent to 
 the mucous membrane or mixed with the contents of the organ. It has, 
 in rare cases, been found encysted in the stomach, in considerable quanti- 
 tity. When invisible to the naked eye, a microscopical examination of the 
 stomach contents will not infrequently reveal characteristic crystals of 
 arsenious acid or some of its compounds. The stomach may be contracted 
 and its mucous membrane corrugated. The entire inner surface may be 
 red and inflamed, or there may be patches or streaks of inflammation or 
 deep congestion. The inflamed and congested patches may bo thickened 
 and covered with false membrane mixed with larger and smaller particles 
 
548 DEATH FEOM POISONING-. 
 
 or masses of the poison. Ulceration, perforation, and gangrene are rare. 
 Blood may be extravasatcd into the mucosa and submucosa, and with the 
 congestion, give the mucous membrane a very dark-red or brown appear- 
 ance. Frequently the mucous membrane is studded with small petechia. 
 Sometimes the arsenic is converted in the stomach into the yellow sul- 
 phide. There may be acute gastritis even when the poison is ab- 
 sorbed by the skin or otherwise, and not introduced into the stomach. 
 Taylor mentions a case in which the coats of the stomach were thick- 
 ened and gelatinous, but not congested. The epithelium of the gastric 
 glands may undergo granular and fatty degeneration. 
 
 The entire length of the intestine may be congested and inflamed, 
 but the action of the poison does not usually extend beyond the duode- 
 num. In some cases, the solitary follicles. Peyer's patches, and mes- 
 enteric glands are swollen. Inflammation of the bladder mid peritoneum , 
 and congestion and oedema of the brain have been observed, but are 
 neither frequent nor in any way characteristic. 
 
 Fatty degeneration of the muscles, liver, kidneys, blood-vessels, and 
 vesicular epithelium of the lungs may be produced in arsenical j^oison- 
 
 ing. 
 
 Alterations in the spinal cord indicative of acute myelitis have been 
 described by Popon as occurring in dogs poisoned with arsenious acid.' 
 
 The walls of the stomach and intestines, and other parts of the body 
 may be preserved from decomposition for a long time after death by ar- 
 senical poisoning. 
 
 It should always be borne in mind, in examining cases of suspected 
 arsenic poisoning, that death may be produced by arsenic and its com- 
 pounds without any appreciable lesions. While, in general, it may be 
 said that, in the cases in which no lesions are discovered, death has been 
 rapid, the death may be delayed in such cases until long after a period 
 at which, in other cases, marked inflammatory changes have occurred. 
 
 Compounds of arsenic, such as the chloride, and sulphide, and the 
 arsenite (Scheele's green; Paris green) are sometimes used for suicidal 
 purposes, and produce lesions similar to those of arsenious acid. Paris 
 green is a favorite article in New York, particularly among Germans, 
 for suicidal purposes. It is usually taken in considerable quantities, and 
 and is often found in the stomach after death.'' 
 
 'Popon: " Ueber die Veranderungen im Eilckenmarke nach Vergif tung mit 
 Arsen," etc. Virch. Arch., Bd. 93, p. 351. 
 
 ' It is advisable, in cases of suspected arsenic poisoning, particularly if tlie 
 body have lain for some time, as in exhumations, to preserve, not only all of the 
 internal organs entire for the chemist, but also portions of the muscles (back, 
 thigh, arm, and abdomen), and also one of the long bones, preferably the femur,, 
 since arsenious acid and its compounds are quite diffusible, and may be present 
 in proportionately larger quantity in other parts than in the gastro-intestinal canal. 
 
DEATH FEOM POISONING. 549 
 
 CORROSIVE SUBLIMATE. 
 
 The mucous membrane of the motUh and throat may be swollen, in- 
 flamed, or have a grayish-white appearance. The m&opliagus may be 
 swollen and white, or congested, or unaltered. The mucous membrane 
 of the stomach is usually congested or inflamed, or there may be patches 
 of softening, ulceration, or gangrene. Perforation is of rare occurrence. 
 Small ecohymoses in the mucosa are not uncommon. Sometimes there 
 is little or no change in the stomach. Sometimes the mucous membrane 
 -of the stomach is slate-colored from the deposition of metallic mercury 
 from the decomposed salt. The intestines may appear normal, or there 
 may be patches of congestion and eccliymosis. 
 
 The larynx and trachea may be congested. The kidneys may show 
 parenchymatous and fatty degeneration of the epithelium. 
 
 LEAD. 
 
 The different preparations of lead may prove fatal, either from the 
 immediate effect of large doses or from the gradual effects of repeated 
 small doses. Although there may be marked symptoms during life, the 
 post-mortem lesions are few and variable. 
 
 Large doses may produce acute gastritis, and sometimes a whitening 
 of the mucous membrane. The intestines are generally contracted, and 
 there may be fatty degeneration of the renal epithelium; very frequently 
 there are no appreciable lesions. 
 
 In chronic lead-poisoning the intestines may be contracted, the vol- 
 untary muscles flabby and light-colored, or partially replaced by connec- 
 tive tissue, and there may be chronic meningitis. 
 
 COPPER. 
 
 Acute poisoning by salts of copper is not very common, but it is of 
 occasional accidental occurrence, and the salts are infrequently used with 
 suicidal intent. The sulphate and acetate are the most important salts 
 in this respect. Soluble salts of copper may be formed m the use ot 
 copper cooking utensils, and accidents most frequently occur in this 
 
 "^^ The post-mortem appearances are somewhat variable. The pharynx 
 and oesophagus may be somewhat inflamed or unchanged The niucous 
 ■membrane of the stomach and intestines may be inflamed, ulcerated, oi 
 gangrenous, and perforat^cn^^n^F^^^onit^^ 
 
 ^n;T~;bj;"ti;;a^;;^;v;^hole of the mtemal organs, and to weigh the muscle 
 Id boTes i: ll as the whole body at the autopsy, in o^d- ^ha^e^^^^^^^^^^^^^ 
 of the chemist, in case arsenic be found, may rest upon a definite basis and be 
 Z Mtle as possible dependent upon estimates whose value may be questioned by 
 lawyers, should the case come into the courts. 
 
650 DEATH FEOM POISONING. 
 
 membrane may have a diffuse greenish color, or particles of the salt may 
 be found adhering to it. 
 
 TARTAR EMETIC. 
 
 • This preparation of antimony may prove fatal when administered in 
 a single large dose or in repeated small doses. The post-mortem lesions 
 are not constant. In oases of chronic poisoning there are usually no 
 appreciable lesions. 
 
 In cases of acute poisoning, there may be evidence of acute inflamma- 
 tion of the msophagus, stomach, intestines, and peritoneum. Sometimes 
 the stomach-exhibits no lesions, while the intestine is involved. The 
 larynx and lungs may be deeply congested. 
 
 VEGETABLE IRRITANTS. 
 
 Aloes, colocyntli, gamboge, jalap, scammony, savin, croton oil, colclii- 
 cum, verafria, hellebore, elaterium, and turpentine. 
 
 All these drugs may produce poisonous effects. The post-mortem 
 lesions are congestion, inflammation, and sometimes ulceration of the 
 gasbro-intestinal mucous membrane; but these lesions are sometimes 
 present and sometimes absent. 
 
 CANTHARIDES. 
 
 This substance may be given in powder or tincture. The entire 
 length, or only a portion of the alimentary canal may be congested or 
 inflamed. There may be patches of gangrene of the mucous membrane 
 of the stomach. When the poison was taken in substance, a microscopi- 
 cal examination of the contents of the alimentary canal or of the mucous 
 membrane may reveal the glistening green and gold particles of the fly. 
 
 The kidneys, ureters, and bladder may be congested and. inflamed. 
 There is sometimes congestion of the brain and its membranes. 
 
 OPIUM. 
 
 The post-mortem appearances in persons who have died from opium 
 poisoning are inconstant and not characteristic. Congestion of the 
 brain aiid its membranes, with serous effusion in the membranes and ven- 
 tricles, and congescion of the lungs, are changes occasionally seen, but 
 they are frequently entirely absent, and when present are not character- 
 istic of death from this poison. 
 
 POISONOUS FUNGI. 
 
 The action of these substances varies greatly, and the post-mortem 
 appearances are inconstant and not characteristic. In general, when 
 any lesions are present, they are these of gastro-intestinal irritation or 
 of venous congestion, or both. 
 
DEATH TEOM POISONING. 351 
 
 Microscopical examination may reveal characteristic fragments of 
 fungi in the contents of the alimentary canal. 
 
 HYDROCYANIC ACID. * 
 
 This poison in fatal doses may destroy life in a very short time. The 
 post-mortem appearances are inconstant and not characteristic. The 
 skin may be livid and the muscles contracted. The stomach may be con- 
 gested or normal. The most frequent internal appearances are those 
 of general venous congestion. Under favorable conditions the odor 
 of prussic acid may be detected in the stomach or blood or brain or^other 
 parts of the body. It may be absent in the stomach and present in other 
 parts of the body. If the patient have lived for some time, the odor 
 may be absent altogether. 
 
 Cyanide of potassium may produce the same lesions as prussic acid, 
 and there is the same inconstancy in their occurrence. 
 
 Nitroienzole. — This substance produces general venous congestion, 
 and the odor of the oil of bitter almonds may be more or less well marked 
 in the body after death. 
 
 CARBOLIC ACID. 
 
 "When this poison is taken into the stomach, the mucous membrane 
 of the mouth, msophagus, and stomach may be white, corrugated, and par- 
 tially detached in patches, and the edges of the affected parts may be 
 hypersemic, or there may be patches of extravasation. Brownish 
 Shrunken patches may be present about the mouth. The 'brain and 
 meninges may be congested. There may be congestion and oedema of 
 the lungs, and congestion of the liver and spleen. The blood is usually 
 dark and fluid. The urine is usually of a dark or greenish color. The 
 odor of the poison may be evident in the body and in tlie urine. 
 
 ALCOHOL. 
 
 The difEerent preparations of alcohol, when taken in concentrated 
 form or in large quantities, sometimes produce sudden coma and death 
 in from half an hour to several hours. In acute poisoning, if death 
 have followed soon after the ingestion of the poison, the body may resist 
 decomposition for an unusual length of time. The stomach and tissues 
 may even have a more or less well-marked alcoholic odor. The stomach 
 and even the cesophagus and duodenum may be of a deep-red color. There 
 may be punctiform ecchymoses in the gastric mucous membrane. In 
 many cases, the stomach is apparently quite normal. There is apt to be 
 venous congestion in some of the internal organs, but this is not con- 
 stant. There is frequently congestion and sometimes extravasation of 
 blood in the irai7i and its membranes and oedema of the membranes or 
 
652 DEATH FEOM POISONING. 
 
 of the brain substance, or both. There may be a serous effusion in the 
 ventricles of the brain. Tlie bladder is frequently distended with urine, 
 as in other cases in which death is preceded by a period of uncon- 
 sciousness. ' 
 
 Chronic alcoholic poisoning is of a different nature. The subjects 
 of it may die from some other disease, or they die after a debauch with- 
 out anything else to account for their death. In the latter case, there 
 may be delirhun tremens, or the patient dies exhausted and comatose. 
 Chronic alcoholism is not infrequently mistaken clinically for meningi- 
 tis. The post-mortem lesions are sometimes marked, sometimes ab- 
 sent. There may be chronic pacchymeningitis resulting in thickening of 
 the diora mater and its close adherence to the skull. The pia mater may 
 be thickened and oedematous. The train may be normal or oedematous 
 or atrophied. The lungs are frequently congested. The heart may be 
 thickly covered with fat, and its walls may be flabby and fatty. The 
 stomach frequently presents the lesions of chronic gastritis. The liver 
 may be cirrhotic, with or without fatty infiltration. The kidneys may 
 present the lesions of parenchymatous or fatty degeneration or of chronic 
 diffuse nephritis. 
 
 It should always be remembered, however, that all or a part of the 
 above lesions may be absent in the bodies of drunkards and, further- 
 more, that the same lesions may be due to other causes. 
 
 CHLOROFORM. 
 
 Chloroform may cause death when it is taken in fluid form into the 
 stomach, or when inhaled. Death from swallowing liquid chloroform is 
 rare, and its immediate cause is usually uncertain. The post-mortem 
 changes are variable; sometimes there are no lesions. In some cases 
 there is simple reddening of the gastric mucous membrane, occasionally 
 there is acute gastritis, or ulceration of the mucous membrane. The 
 odor of chloroform may, or may not, be evident. Discoloration and 
 softening of the mucous membrane of the pharynx, oesophagus, and 
 duodenum have been observed. There may be general venous conges- 
 tion; the heart may be flabby. Bubbles of gas have been frequently 
 seen in the blood, but this is not characteristic. Death from inhalation 
 of chloroform is a not infrequent accident in surgical practice. After 
 death from inhalation, the results of the examination are usually quite 
 negative. 
 
 ETHER. 
 
 The inhalation of ether occasionally causes death. The post-mortem 
 examination is negative. The ingestion of fluid ether may induce inflam- 
 mation of the stomach. The odor of ether may be perceptible if the 
 autopsy is made soon after death. 
 
DEATH FROM POISONING. 553 
 
 CHLORAL HYDRATE. 
 There are no characteristic post-mortem appearances after death by 
 chloral Hyperemia of the brain, and the odor of the drug have been 
 noticed. 
 
 STRYCHNIA-NUX VOMICA. 
 
 The post-mortem appearances after poisoning by these drugs are not 
 characteristic, and are inconstant. The body is usually relaxed at the 
 ime of death, but the rigor mortis usually comes on early and remains 
 long. There may be congestion of the brain and spinal cord, and some- 
 times of the lungs and stomach. 
 
 CONIUM, ACONITE, BELLADONNA, LOBELIA INFLATA DIGITALIS 
 
 STRAMONIUM. 
 
 These vegetable poisons are administered in their natural form of 
 leaves, berries, and roots, or in tinctures, infusions, and extracts, or in 
 the form of their active alkaloid principles. 
 
 If the leaves, berries, or seeds are given, they may be detected in the 
 contents of the stomach by microscopic examination. Otherwise the 
 results of autopsies are not characteristic. 
 
 The brain and its membranes, and the lungs, may be congested. The 
 stomach may present patches of congestion, inBammation, and extrava- 
 sation, or its entire mucous coat may be inflamed, or it may appear 
 normal. 
 
 Microscopical examination of the contents of the alimentary canal 
 may reveal characteristic seeds, or fragments of leaves.' 
 
 CARBONIC OXIDE. 
 
 This is one of the gases formed in the burning of charcoal, and 
 forms one of the ingredients of illuminating gas. The most character- 
 istic post-mortem appearance is the cherry-red color of the blood, and of 
 the tissues and viscera which contain blood. The presence of carbonic 
 acid in the gas may obscure the bright-red of the carbonic oxide by the 
 dark color which it induces in the blood. 
 
 CARBONIC ACID. 
 
 The lesions are essentially those of asphyxia, but the brain is said to 
 be more frequently congested than in asphyxia by simple obstruction of 
 respiration. 
 
 For a more detailed consideration of poisons, tlieir effects, modes of detec- 
 tion, etc., consult: Taylor, on Poisons. Maschka's "Handbuch der Gericht- 
 
 ' Consult Guy and Ferrier : "Forensic Medicine," p. 534. 
 
554: DEATH FEOM POISONING. 
 
 lichen Medicin," Bd. II. ' Woodman and Tidy : " Forensic Medicine." Wormley's 
 " Micro-chemistry of Poisons," contains a series of good plates of the microscopi- 
 cal appeai-ances of various forms of crystals of poisonous substances. 
 
 Lesser's "Atlas der G-erichtlichen Medicin" contains a series of fine colored 
 plates, showing the appearance of the stomach after the action of various poisons. 
 The small work of Guy and Ferrier, on Forensic Medicine, contains in very com- 
 pact and reliable form, much information on the general subjects treated in the 
 foregoing section. 
 
INDEX. 
 
 Abbe's condenser, use of, in examin- 
 ing bacteria, 91 
 Abdominal cavity, examination of, in 
 adults, 15, 23 
 cavity, examination of, in 
 
 children, 37 
 cavity, methods of opening, 
 
 15 
 cavity, serum in, as a result 
 of post-mortem changes, 
 15 
 pregnancy, 438 
 Abscesses, formation of, in inflamma- 
 tion, 99 
 of brain, isl 
 pysemic, 514 
 Accessory spleens, 25 
 Achorion Schonleinii, 76 
 Acid, carbolic, poisoning, lesions of, 551 
 carbonic, poisoning, lesions of, 
 
 553 
 chromic, use of, in decalcifying 
 
 tissues, 40 
 hydrochloric, poisoning, lesions 
 
 of, 545 
 hydrocyanic, poisoning, lesions 
 
 of, 551 
 nitric, poisoning, lesions of, 544 
 nitric, use of, in decalcifying tis- 
 sues, 40 
 osmic, use of, in preserving tis- 
 sues, 42 
 oxalic, poisoning, lesions of, 545 
 picric, use of, in decalcifying, 40 
 picric, use of, in preserving sedi- 
 ments, exudations, casts, etc., 
 42 
 sulphuric, poisoning, lesions of, 
 
 543 
 tartaric, poisoning, lesions of, 545 
 Aconite poisoning, lesions of, 558 
 Actinomycosis, 77 
 Acute yellow atrophy of liver, 342 
 
 yellovsr atrophy of liver, micro- 
 cocci in, 80 
 Addison's disease, lesions of, 528 
 Adenoma, general consideration of, 140 
 characters and varieties of, 
 142 
 
 Adeno-sarcoma, 131 
 Agar-agar, use of, in cultivating bac- 
 teria, 94 
 Ague-cake, 364 
 
 Air, presence of, in blood air emboli, 57 
 Alcohol poisoning, lesions of, 551 
 
 use of, in preserving tissues, 41 
 Alimentary canal, 293 
 Aloes poisoning, lesions of, 550 
 Alveolar carcinoma, 152 
 
 sarcoma, 130 
 Ammonia poisoning, lesions of, 546 
 Amoeba, occurrence of, in dysentery, 66 
 Amyelia, 199 
 Amyloid degeneration, 61 
 
 degeneration, methods of 
 staining tissues in, 63 
 - degeneration, conditions of, 62 
 degeneration, parts most fre- 
 quently affected by, 62 
 Anaemia, changes of blood in, 55 
 
 changes of marrow cells in, 
 
 456 
 effects of, on tissues and or- 
 gans, 56 
 general effects of, 49 
 nature and effects of, 49 
 pernicious, 528 
 Aneurism, cirsoid, 275 
 
 dissecting, 276 
 
 false, 279 
 
 fusiform, 276 
 
 of the aorta, 276 
 
 of the blood-vessels, 275 
 
 of the coronary arteries, 277 
 
 of the heart, 269 
 
 of the heart-valves, 268 
 
 of the pulmonary arteries, 
 
 277 
 sacculated, 276 
 spurious, 279 
 Aneurismal varix, 279 
 Angioma cavernosum, 140 
 
 telangiectoides, 139 
 Angiomata, general characters of, 138 
 Angio-sarcoma, 129 
 Anhydrsemia, 55 
 
 Anilin colors, uses of, in staining bac- 
 teria, 89, 90 
 
556 
 
 INDEX. 
 
 Animal parasites, 66 
 Ante-mortem heart-clots, 19, 269 
 Anthracosis, 65 
 Anthrax bacillus, 82, 524 
 
 bacillus in blood, 58 
 lesions of, 524 
 
 lesions and bacteria of, 83, 524 
 Anus, atresia of, 313 
 Aorta, examination of arch of, before 
 removal from body, 18 
 aneurism of, 276 
 aneurism, dissecting, of, 279 
 atheroma of, 274 
 malformations of, 256 
 stenosis of, 277 
 Apoplectic clots, methods of examin- 
 ing, 12 
 Arnold, J., researches of, on lymphatic 
 
 tissues in organs, 291 
 Arteries, aneurism of, 275 
 dilatation of, 275 
 effect of contraction of, when 
 in obliterating endarteritis, 
 275 
 inflammation of (see arteritis), 
 
 271 
 rupture of, 278 
 tumors of, 280 
 wounds of, 278 
 Arteritis, acute, 271 
 
 chronic, 272 
 syphilitic, 185, 374 
 Arsenic poisoning, lesions of, 547 
 
 poisoning, pi-ecautions to be 
 taken in examining for, 548 
 Arthritis, acute, 470 
 chronic, 471 
 chronic rheumatic, 471 
 deformans, 471 
 purulent, 470 
 sero-fibrinous, 470 
 serous, 470 
 tubercular, 472 
 uritica, 472 
 Ascaris lumbricoides, 71 
 maritima, 73 
 mystax, 73 
 Asending gray degeneration of spinal 
 
 cord, 193 
 Aspergillus, 77 
 Asphyxia, lesions of, 538 
 Atelectasis of lungs, 333 
 Atheroma, 278 
 
 of aorta, 274 
 of blood-vessels, 273 
 Atheromatous cysts of blood-vessels, 
 274 
 ulcers of blood-vessels, 
 274 
 Auricles of heart, method of examin- 
 ing, 20 
 Autopsies in cases of suspected poison- 
 ing, 32, 543 
 
 Bacilli, pathogenous, 82 
 
 Bacilli, zymogenous, 83 
 Bacillus anthracis, characters and re- 
 lations to anthrax, 82, 524 
 butyricus, 82 
 genus, characters of, 82 
 Kochii (see B. tuberculosis), 83, 
 
 507 
 lepras, 83, 520 
 malariae, 83, 526 
 subtilis, 82 
 syncyanum, 83 
 tuberculosis, characters of, 83, 
 
 507 
 tuberculosis, cultivation of, 
 
 511 
 tuberculosis, presence of, in 
 tubercle tissue, 103, 504, 508 
 tuberculosis, metlaods of stain- 
 ing, 509 
 tuberculosis, references to lit- 
 erature of, 511 
 of cholera, 83, 502 
 of glanders, 83, 515 
 of malignant (vdema of mice, 
 
 pigs, and rabbits, 83 
 of septicsemia of mice, 83 
 of typhoid fever, 83, 491 
 Bacteria action of disinfectants on, 78 
 artificial cultivation of, 91 
 artificial cultivation of, care 
 
 and skill required in, 95 
 artificial cultivation on Agar- 
 agar, 94 
 artificial cultivation on gela- 
 tinized blood-serum, 94 
 artificial cultivation on gelati- 
 nized bouillon, 93 
 artificial cultivation on Ja- 
 panese isinglass, 94 
 artificial cultivation on pota- 
 toes, 92 
 classification of, 79 
 double staining of, 90, 510 
 effects of temperature on, 78 
 filamentous, see bacilli, 82 
 Gram's method of staining, 90 
 in chicken cholera, 82 
 in emboli, 53 
 in false membrane of croupous 
 
 infiammation, 109 
 in kidneys, method of preser- 
 vation of tissue for study 
 of, 34 
 in putrefaction, 78 
 in pyelo-nepLritis, 83 
 in septicaemia of rabbits, 82 
 in syphilitic inflammation, 105 
 in thrombi, 53 
 
 local effects of, in tissues, 85 
 methods of studying, 85 
 morphology and physiology of, 
 
 77 
 of pneumonia, 82, 228 
 of relapsing fever, 85, 494 
 of syphilis, 105 
 
INDEX. 
 
 557 
 
 Bacteria, references to literature of, 95 
 relations to disease, 85 
 speedy appearance of, in dead 
 
 body, 85 
 spiral-celled, 84 
 spiro, 84 
 
 spores of, method of destroy- 
 ing, 93 
 spores of, vulnerability of, 78 
 Bacterium, seruginosum, 81 
 
 characters of the genus, 81 
 chromogenous species of, 81 
 lineola, 81 
 
 pathogenous species of, 81 
 synxanthum, 81 
 termo, 81 
 
 zymogenous species of, 81 
 Balanitis, 435 
 
 Belladonna pnisoning, lesions of, 553 
 Bile-ducts, lesions of, to be looked for 
 at autopsies, 27 
 method of detecting patu- 
 
 ■lousness of, 27 
 method of opening and ex- 
 aming, 27 
 Biliary calculi, 357 
 
 passages, lesions of, 356 
 Bilirubin, crystals of, in blood, 57 
 Bismark brown for staining fresh tis- 
 sues, 40 
 Bladder, gall, lesions of, 357 
 
 urinary, absence of, 395 
 urinary, calculi in, 400 
 urinary, changes in size of, 
 
 396 
 urinary, cysts of, 399 
 urinary, dilatation of, 396 
 urinary, diverticula of, acquir- 
 ed, 396 
 urinary, diverticula of, con- 
 genital, 395 
 urinary, extroversion of, 395 
 urinary, foreign bodies in, 400 
 urinary, hemorrhage of, 397 
 urinary, herniae of, 396 
 urinary, hypersemia of, 397 
 urinary, hypertrophy of, 396 
 urinary, inflammation of, see 
 
 cystitis, 397 
 urinary, malformations of, 395 
 urinary, methods of preserv- 
 ing, 29 
 urinary, of young children, 
 contents and intra-uterine 
 lesions of, 39 
 urinary, parasites of, 400 
 urinary, perforation of, 397 
 urinary, removal and exami- 
 nation of, 29 
 urinary, rupture of, 396 
 urinary, tumors of, 399 
 Blood, air in, 57 
 
 alterations of, reference to lite- 
 rature, 58 
 anhydrsemia, 55 
 
 Blood, bilirubin, crystals in, 57 
 
 cells containing red blood-cells, 
 
 465 
 changes in composition of, 55 
 changes in circulation of, 49 
 changes of, in Addison's disease, 
 
 528 
 changes of, in ancemia, 55 
 changes of, in chlorosis, 528 
 changes of, in Hodgkin's disease, 
 
 530 
 changes of, in leucocythaemia, 
 
 56, 530 
 changes of, in leucocytosis, 56 
 changes of, in leukaemia, 56, 530 
 changes of, in pernicious anae- 
 mia, 528 
 coagulability of, changes in, 55 
 counting, apparatus for, 58 
 difference in distribution of, in 
 
 life and after death, 9 
 endothelial cells in, 57 
 extravasated, changes in, 50 
 fat in, 57 
 
 foreign bodies in, 57 
 hydraemia of, 55 
 in melaneenia, 56 
 parasites in, 58 
 pigment in, from inhaled dust, 
 
 57 
 pus-cells, in, 57 
 Blood-serum, gelatinized, preparation 
 
 of for cultivation of bacteria, 94 
 Blood-vessels, amyloid degeneration of, 
 271 
 atheroma of, 273 
 atrophy of, 270 
 calcification of, 271 
 development of, in in- 
 flammation, 101 
 fatty degeneration of, 270 
 fatty ulcers of, 271 
 hypertrophy of, 270 
 inflammations of ,271, 282 
 method of preserving, 14 
 Blue milk, bacillus which produces color 
 
 of, 82 
 Bone, 450 
 
 abscess, 456 
 
 atrophy of, 466 
 
 caries of, 461 
 
 cysts of, 469 
 
 decalcification of, method of, 40 
 
 dislocations of, 451 
 
 disturbances of circulation in, 
 
 450 
 fractures of, 451 
 hemorrhage, 450 
 hyperaemia of, 450 
 inflammation of, see osteitis, 453 
 inflammation of marrow of, see 
 
 osteomyelitis, 459 
 mari-ow, alterations in leukaemia 
 
 and pseudo-leukaemia, 464 
 necrosis of, 460 
 
558 
 
 INDEX. 
 
 Bone, of young children, examination 
 of, 39 
 osteomalacia, 464 
 parasites of, 469 
 rachitis, 462 
 
 syphilis, congenital, of, 457 
 tumors of, 466 
 wounds of, 451 
 Bothriocephalus cordatus, 71 
 cristatus, 71 
 latus, 71 
 Brain, abscess of, 181 
 ansemia of, 178 
 cysts in, 184 
 emboli of, 175 
 hemorrhage in, 178 
 laernia of, 189 
 hypersemia of, 177 
 hypertrophy and atrophy of, 186 
 inilanimation of, see encephali- 
 tis, 181 
 inilammation, syphilitic of, 185 
 inflammation, tubercular of, 185 
 inflammatory softening of, 181 
 lesions of, in the chronic insane, 
 
 186 
 location of lesion in, 11 
 malformations of, 188 
 membranes of, 158 
 method of examination and dis- 
 section of, 11, 12 
 method of preserving, 13 
 method of removal from skull, 
 
 11 
 oedema of, 178 
 parasites of, 188 
 pigmentation of, 187 
 pus-cells in tissue of, 182 
 red softening of, 176 
 sclerosis of, 182 
 softened areas in, method of 
 
 studying, 14 
 summary of surface lesions to be 
 
 looked for at autopsies, 11 
 thrombosis of, 175 
 tumors of, 187 
 ventricles of, lesions of, 171 
 weight of, 11 
 white and yellow softening of, 
 
 176 
 wounds of, 183 
 Brain-sand, composition of, 174 
 
 in choroid plexus, 174 
 in pacchymeningitis, 160 
 Bright's disease, see nephritis, 380 
 Bronclii, abnormal contents of, 31 
 
 appearances to be noted in au- 
 topsies, 21 
 inflammation of, see bronchi- 
 tis, 217 
 method of opening, 21 
 method of preserving, 31 
 tumors of, 319 
 Bionchiectasia, 218, 341 
 Bronchitis, acute catarrhal, 317 
 
 Bronchitis, acute croupous, 318 
 acute general, 217 
 capillary, 217, 233 
 chronic catarrhal, 218 
 chronic croupous, 218 
 in acute phthisis, 244 
 in chronic phthisis, 249 
 
 Broncho-pneumonia, 333 
 
 Bronze-liver, 341 
 
 skin in Addison's disease, 529 
 
 Brood-capsules of ecchinococcus cysts, 
 69 
 
 Brown induration of lung, 231 
 
 Brownian movement in micrococci, 79 
 
 Burning, lesions in death from, 536 
 
 Cachexia, development of, in malignant 
 
 tumors, 115 
 Cadaveric hypostasis, 4 
 
 lividity, 4 
 Calcareous degeneration, 64 
 Calcification, 64 
 
 Calcium carbonate in vesical calculi, 
 400 
 oxalate, in vesical calculi, 401 
 Calculi, biliary, 357 
 vesical, 400 
 Calvarium, changes of, to be noticed at 
 autopsies, 10 
 depressions of, by Pacchio- 
 nian bodies, 10 
 method of removing, 9 
 Cancer, see carcinoma, 144 
 Cantharides poisoning, lesions of, 550 
 Capillaries, blood, lesions of, 283 
 Capillary hemorrhage in brain, 174 
 Capsule, brood, of echinococcus, 69 
 
 supra-renal, changes in, by de- 
 composition, 25 
 supra-renal, general appear- 
 ance of, 24 
 supra-renal, lesions of, 35, 377 
 supra-renal, method of pre- 
 servation, 25 
 supra-renal, of children, 38 
 Caput succedaneum, 35 
 Carbolic acid poisoning, lesions of, 551 
 acid to be avoided in preserv- 
 ing microscopical specimens, 
 46 
 Carbonates of soda and potash poison- 
 ing, lesions of, 545 
 Carbonic acid poisoning, lesions of, 553 
 oxide poisoning, lesions of, 553 
 Carcinoma, alveolar, 152 
 colloid, 151 
 cylindrical-celled, 15 
 enoephaloid or medullary, 
 
 151 
 fibrous (scirrhous), 151 
 flat-celled or epithelioma, 
 
 147 
 forms of, 146 
 
 general considerations on, 
 1,40 
 
INDEX. 
 
 559 
 
 Carcinoma, gland-celled, 150 
 melano, 153 
 
 modes of extension, 145, 146 
 moUe, 151 
 myxomatodes, 152 
 simplex, 150 
 
 structure and origin of, 144 
 telangiectoides, 151 
 variability in shape of cells 
 of, 145 
 Caries of bone, 461 
 Cartilaginous tumors, see chondroma, 
 
 133 
 Casts, preservation of, 43 
 Cavities in lungs in chronic miliary 
 tuberculosis, 243 ' 
 in phthisis, 249 
 of heart, contents of, 19 
 Catarrhal inflammation, acute, of mu- 
 cous membranes, 106 
 inflammation, chronic, of 
 mucous membranes, 107 
 Celloidin, preservation of specimens 
 embedded in, 44 
 use of, in embedding, 43 
 Cellular inflammation, 97 
 Cephalhaematoma in the new-born, 36 
 Cephalocele, 189 
 Cercomonas intestinalis, 66 
 Cerebellum, method of dissection of, 12 
 Cerebral arteries, examination of, at 
 autopsies, 11 
 ganglia, location of lesions in, 
 
 13 
 ganglia, methods of dissection 
 of, 12 
 Cerebro-spinal meningitis, 496 
 
 meningitis, micrococci 
 in, 80, 497 
 Cestode worms, 67 
 Charbon, lesions and bacilli of, 524 
 Charcot's crystals in leuksemia, 530 
 Cheesy degeneration, 60 
 
 degeneration in acute phthisis, 
 
 245 
 degeneration in chronic phthi- 
 sis, 247 
 degeneration of lymph-glands 
 in scrofula, 288 
 Children, changes in appearance of, 
 immediately after birth, 35 
 chronic internal hydrocepha- 
 lus in, method of removing 
 brain, 36 
 examination of thorax and 
 
 abdomen, 37 
 new-bom, cephalhsematoma 
 
 in, o6 
 new-born, examination of 
 
 head, 36 
 new-born, post-mortem ex- 
 amination of, in general, 
 32 to 39 
 Chloral hydrate poisoning, lesions of, 
 553 
 
 Chloral hydrate, use of solution of, for 
 
 preserving cysts, etc., 45 
 Chloroform poisoning, lesions of, 553 
 Chloroma, 131 
 Chlorosis, 528 
 Cholera, bacteria of, 83, 502 
 
 lesions of, 501 
 Cholestearin crystals in softening of 
 brain, 176 
 developed from fat in 
 fatty degeneration, 61 
 Chondroma, characters, varieties, and 
 
 situations, 133 
 Choroid plexus, brain-sand in, 174 
 
 corpora amylacea in, 
 
 174 
 cysts of, 12, 174 
 tubercles in, 168 
 Chromic acid mixture, composition and 
 use of, in hardening tissue, 41 
 acid, use of, in decalcifying 
 bone, 40 
 Chromogenous micrococci, 79 
 Cicatricial tissue, formation of, in in- 
 flammation, 101 
 Circulation of blood, morbid changes 
 in, 49 
 of blood, inflammation, 98 
 Cirrhosis of liver, 344 
 Cirsoid aneurism, 375 
 Clitoris, malformations of, 405 
 Cloacte in connection with intestines, 
 
 312 
 Clots, apoplectic in brain, 13, 179 
 
 heart, characters and significance 
 of, 19, 369 
 Coagulation necrosis in acute phthisis, 
 344 
 necrosis in croupous in- 
 flammation, 60, 109 
 necrosis in infarctions, 59 
 necrosis, nature, condi- 
 tions, and effects of, 59 
 Coenum, inflammation of, 318 
 Cohnheim's hypothesis of embryonal 
 
 origin of tumors, 116 
 Cohn's classification of bacteria, 79 
 Colchicum poisoning, lesions of, 550 
 Colitis, catarrhal, acute, 317 
 
 catarrhal, chronic, 317 
 croupous, 318 
 ulcerative, 318 
 Colloid carcinoma, 151 
 
 degeneration, 63 
 Colon, lesions of solitary foUioles of, 
 318 
 transverse, position of, 16 
 Colocynth poisoning, lesions of, 550 
 Comedones, 119 
 Comma bacillus, 503 
 Compound granular corpuscle, nature 
 of, 176 
 ovarian cysts, 436 
 Condenser, Abbe's, in examination of 
 bacteria, 91 
 
660 
 
 INDEX. 
 
 Condyloma of vulva, 407 
 Conium poisoning, lesions of, 553 
 Connective tissue, inflammations of, 96 
 tissue, new formation of, in 
 inflammation, 100, 102 
 Contusions, ante-mortem, 7 
 post-mortem, 7 
 Convolutions of brain, significance of 
 
 flattening of, 10 
 Cooling of body after death, 5. 6 
 Copper poisoning, lesions of, 549 
 Cord, spinal, lesions of, 14, 190 
 
 spinal, method of removal, 14 
 spinal, post-mortem changes in, 14 
 Coronary arteries, effects of closure on 
 
 heart, 275 
 Corpora amylacea, 62 
 
 amylacea in choroid plexus, 174 
 amylacea in softening of brain, 
 
 176 
 cavernosa penis, inflammation 
 of, 436 
 Corrosive sublimate poisoning, lesions 
 of, 549 
 sublimate, use of, in steriliz- 
 ing vessels, etc., 93 
 Craniotabes, 463 
 
 Cranium, base of, examination of, 13 
 Creases of neck, liable to be mistaken 
 
 for marks of hanging, etc., 8 
 Croton oil poisoning, lesions of, 550 
 Croupous inflammation, coagulation 
 necrosis in, 60 
 inflammation of mucous 
 membranes, 108 
 Cryptorchismus, 437 
 Cuticula of echinococcus cysts, 69 
 Cyanide of potassium poisoning, lesions 
 
 of, 551 
 Cylindroma, 130 
 Cystic kidney, 391 
 Cysticercus cellulosse, 68 
 
 tEenia mediocanellata, 68 
 Cystin calculi, 401 
 Cystitis, catarrhal acute, 397 
 
 catarrhal chronic, 398 
 croupous, 398 
 gangrenous, 398 
 tubercular, 398 
 Cystocele, 408 
 
 vaginal, 396 
 Cysto-sarcoma, 131 
 Cysts, classification of, 119 
 congenital, 119 
 dermoid, 118 
 exudation, 119 
 formed around foreign bodies, 
 
 119 
 formed by softening of tissue, 
 
 119 
 formed in spaces in new growths, 
 
 119 
 in brain, 184 
 
 method of preserving for mu- 
 seum specimens, 45 
 
 Cysts, of ecchinococcus, 69 
 retention, 119 
 
 Death, causes of, in general, 3 
 
 sudden, frequent obscurity of 
 causes of, 3 
 Decalcification of bone, methods of, 40 
 Degeneration, amyloid, 61 
 
 amyloid, method of stain- 
 ing tissues in, 62 
 amyloid, parts most fre- 
 quently seat of, 62 
 calcareous, 64 
 colloid, 63 
 cheesy, 60, 345, 247 
 fatty, 60, 61 
 hyalin, 63 
 mucoid, 63 
 
 of tissues in general, 59 
 parenchymatous, 60 
 waxy, see amyloid, 61 
 Degenerations, secondary, in braiiL 
 
 lesions, 180 
 Dermoid cysts, 118 
 Descending gray degeneration of spinal 
 
 cord, 193 
 Desmo-bacteria, 82 
 Diabetes, lesions of, 534 
 Diapedesis, hemorrhage by, 50 
 
 in infiammation, 99 
 Diaphragm, position and height of, 17 
 Diffuse inflammation of the viscera 111 
 Digitalis poisoning, lesions of, 553 
 Diphtheria, 498 
 
 micrococci in, 80, 499 
 Diphtheritic inflammation of mucous 
 
 membranes, 108 
 Diplococcus, 79 
 Discolorations of body after death, 4 
 
 of internal organs in pu- 
 trefaction, 15 
 Disinfectants, action of, on bacteria, 
 
 79 
 Displacement of organs by putrefactive 
 
 gases, 5 
 Dissecting aneurism, 376 
 Distoma hematobiura, 58, 67 
 hepaticum, 67 
 lanceoleatum, 67 
 sinense, 67 
 Dochmius duodenalis, 72 
 Dropsy, nature of, 51 
 Drowning, examination of body in 
 cases of, 540 
 lesions of, 541 
 Drysdale's corpuscles, 428 
 Duodenum, method of opening and pre- 
 serving, 37 
 ulcers of, 316 
 Dura mater, hemorrhages of, 157 
 
 mater, inflammation of, see pac- 
 
 chymeningitis, 158 
 mater, lesions to be looked for at 
 
 autopsies, 10 
 mater, method of preserving, 13 
 
INDEX. 
 
 561 
 
 Dura mater, method of removing from 
 body, 10 
 mater, perforation of, by Pacchi- 
 onian bodies, 10 
 mater, structure of, 157 
 mater, thrombosis of sinuses of, 
 
 157 
 mater, tumors of, 161 
 mater, spinalis, hemorrhage, and 
 
 other lesions of, 190 
 mater, spinalis, preservation of, 
 15 
 Dyscrasia of tumors, 115 
 Dysentery, 318 
 
 Echinococcus, 68 
 
 cysts, preservation of, 
 
 for museums, 45 
 exogena, 70 
 in blood, 58 
 multilooularis, 70, 355 
 scolecipariens, 70 
 Ecchondroses, 134 
 Ecchymoses of skin, post-mortem, 7 
 
 nature of, 50 
 Ecchymosis, ante-mortem and post- 
 mortem, 4 
 Ehriich's method of staining tubercle 
 
 bacillus, 509 
 Elaterium poisoning, lesions of, 550 
 Elephantiasis, dilatation of lymph-ves- 
 sels in, 285 
 of vulva, 407 
 Embedding in celloidin, 43 
 methods of, 42 
 Emboli, fat, 57 
 
 infectious, effects of, 53 
 Embolic infarctions, most frequent seat 
 
 of, 54 
 Embolism, effects and occurrence of, 
 53, 53 
 fat, 57 
 in brain, 175 
 of cerebral arteries, most 
 
 common seat of, 177 
 nature of, 53 
 Embryonal origin of tumors, Cohn- 
 
 heim's hypothesis of, 116 
 Emigration of vs^hite blood-cells, 98 
 Emphysema of lungs, 323 
 Empyema, 313 
 Encephalitis, 181 
 
 chronic interstitial, 183 
 in new-born, 183 
 Encephalocele, 189 
 Encephaloid cancer, 151 
 Endarteritis, acute, 271 
 
 chronic, 272 
 obliterans, 372 
 syphilitic, 374 
 Endartery (see terminal artery), 53 
 Endocarditis, acute, 364 
 
 chronic, 366 
 malignant, 265 
 tubercular, 267 
 36 
 
 Endocarditis, ulcerative, 80, 365, 266 
 Endocardium, structure of, 264 
 
 discolorations of, 30 
 Endometritis, acute catarrhal, 415 
 
 chronic catarrhal, 416 
 croupous, 416 
 puerperal, 417 
 syphibtio, 416 
 tubercular, 416 
 Endophlebitis, 383 
 Endothelioma, general characters and 
 
 situation of, 132, 133 
 Enteritis, catarrhal acute, 315 
 catarrhal chronic, 315 
 croupous, 315 
 suppurative, 316 
 Eosin, use of, m staining tissues, 44 
 Epididymitis, acute, 440 
 Ependyma, cysts of, 174 
 
 examination of, at autopsy, 
 
 13 
 inflammations of, see 
 
 ependymitis 172 
 method of preserving, 13 
 tumors of, 174 
 Ependymitis, acute and chronic, 173 
 
 tubercular, 169 
 Epispadia, 434 
 Epithelial pearls in epithelioma, 148 
 
 tumors, 140 
 Epitheliomata, characters of, 147 
 
 most frequent situation 
 of, 150 
 Erysipelas, characters of, 533 
 
 micrococci of, 80, 523 
 Ether poisoning, lesions of, 553 
 Exostoses, 135 
 
 Extra-uterine pregnancy, '433 
 Extravasation of blood in contusions, 
 
 7 
 Exudations, inflammatory nature and 
 origin of, 51. 99 
 method of preserving, 42 
 Eye, method of hardening and removal 
 of, 13, 14 
 
 Fallopian tubes, changes in size and 
 
 position of, 430 
 tubes, coairaon lesions of, 
 
 to be looked for, 31 
 tubes, cysts of, 431, 
 tubes, dilatation of, 430 
 tubes, hemorrhage of, 430 
 tubes, inflammation of, see 
 
 salpingitis, 431 
 tubes, malformations of, 430 
 tubes, position, shape, and 
 
 dimensions of, 31 
 tubes, tumors of, 431 
 
 False membrane in croupous inflamma- 
 tion, 109 
 neuromata, 138 
 Farcy, characters and bacilli of, 515 
 Fat-emboUsm, 57 
 
562 
 
 INDEX. 
 
 Fat in tissues, method of demonstrat- 
 ing, 61 
 necrosis, in pancreas, 370 
 Fatty degeneration, 60, 61 
 
 infiltration, 60 
 Female generative organs, removal of, 
 29 
 generative organs, lesions of, 
 29, 405 
 Fever, inflammatory, see pyaemia, 512 
 malarial, lesions and bacteria of, 
 
 526 
 relapsing, 494 
 
 relapsing, spivilliim of, 85, 494 
 splenic, lesions and bacteria of, 
 
 83, 534 
 suppurative, see pyaemia, 512 
 surgical, see pyaemia, 513 
 traumatic, see pyaemi;!, 512 
 typhoid, see typhoid fever, 485, 
 typhus, 493 
 Fibrin, formation of, in inflammation, 
 
 99 
 Fihro-carcinoma (scirrhous), 151 
 Fibroma, durum and moUe, 131 
 
 forms and characters of, 121 
 intracanalicular, 123 
 usual situations of, 132 
 Fibro-myoma, 186 
 Filamentous bacteria, 83 
 Filaria medinensis, 74 
 
 sanguinis hominis, 58, 75 
 Flukes, 67 
 
 Foetal tissues, preservation of, 39 
 Foetus, deteriuination of age of, 32, 34 
 Fourth ventricle of brain, method of 
 
 opening, 12 
 Fractures, ante-mortem and post-mor- 
 tem, 8 
 intra-uterine, 35 
 Fraenkel's method of double staining 
 of tubercular sputum and sections, 
 510 
 Fi'eezing microtome, 40 
 Ifresh tissues, method of studying, 40 
 Fuchsia, use of, iu staining bacteria. 89 
 acid for staining nerve-tissue, 
 203 
 Fungi, parasitic, 76 
 
 poisoning by, lesions in, 550 
 reference to literature of, 77 
 
 Gall-bladder, dilatation of, 357 
 
 bladder, lesions of, :^56 
 
 bladder, opening of, at autopsy, 28 
 
 bladder, tumors of, 359 
 
 ducts, constriction aud occlusion 
 of, 357 
 
 ducts, dilatation of, 357 
 
 ducts, inflammations of, 356 
 
 ducts, method of examining, 27 
 
 ducts, tumors of, 359 
 
 stones, b57 
 Gastritis, catarrhal, acute and chronic, 
 304 
 
 Gastritis, croupous. 305 
 
 suppurative, 305 
 toxic, 306 
 
 Gamboge poisoning, lesions of, 550 
 Ganglia, cerebral, localization of le- 
 sions in, 13 
 cerebral, method of dissec- 
 tion, 12 
 Gangrene of lungs, 224 
 Gas in intestines in young children, 39 
 
 in pericardium, 255 
 Gelatin bouillon for bacteria cultures. 
 
 93 
 Generative organs, female, lesions of, 
 39, 405 
 organs, female, preserva- 
 tion and removal of, 29, 
 30,31 
 organs, male, lesions of , 29, 
 
 434 
 orgaos, male, removal of, 
 
 29 
 organs of young children, 
 position and characters 
 of, 39 
 Genito-urinary organs, removal and 
 
 preservation of, 39 
 Gentian-violet for staining bacteria 89 
 Giant cells in tubercle tissue, 103, 506 
 celled or myeloid sarcoma, 128 
 Glauders, lesions and bacteria of, 83, 
 
 515, 516 
 Glioma, general characters of, 135 
 
 varieties and situations of, 136 
 Gloraerulo-nephritis, see Bright's dis- 
 ease, 383 
 Glossitis, 296 
 
 parenchymatous, 297 
 syphilitic, 297 
 tubercular, 297 
 Gluge's corpuscles, nature of, 176 
 Goitre, 375 
 Gonocoi-cus, 80, 403 
 Gonorrhoea, 403 
 Gout, lesions of, 533 
 Grain's method of staining bacteria, 
 
 90 
 Granulation tissue, characters and for- 
 mation of, 100 
 Granuloma, infective, 120 
 Gravel, see calculi, 400 
 Gray degeneration, secondary, of spinal 
 
 cord, 193 
 Guinea worm, 74 
 Gummata, 105 
 
 Hanging, lesions in death from, 539 
 
 marks of, liable to be con- 
 founded with natural 
 creases of neck, 8 
 Hardening and preservation of tissues, 
 
 41 
 Head, method of examination of, 9 
 Heart, amyloid degeneration of, 263 
 
INDEX. 
 
 663 
 
 Heart and great vessels, malforma- 
 tions of, 256 
 
 aneurism of, 269 
 
 animal parasites of, 370 
 
 atrophy of, 259 
 
 cal<-iflcation of, 264 
 
 changes in, from thrombosis and 
 embolism of coronary arterv 
 264 ■> Jj 
 
 changes in position of, 258 
 clots, 19, 269 
 
 •concentric hypertrophy of, 260 
 contents of cavities of, 19 
 dilatation of, 261 
 displacements of, 258 
 fatty degeneration of, 263 
 fatty infiltration of, 363 
 hypertrophy of, 360 
 inflamm;ttion of, see myocardi- 
 tis, 367 
 in young children, 37 
 lipomatosis of, 363 
 method of opening, 19 
 method of preserving, 20 
 method of removal from body, 
 18 ^' 
 
 mucous degeneration of, 263 
 parenchymatous degeneration 
 
 of, 363 
 position of, in body, 17, 18 
 rupture of, 259 
 softening of, from thrombosis 
 
 and embolism, 364 
 thickness of walls of, 20 
 thrombosis of, 269 
 tumors of, 276 
 uncovered area of, 17 
 valves, aneurism of, 268 
 valves, degeneration of, 367 
 valves, fenestration of, 368 
 valves, general examination of, 
 
 19 
 valves, hemorrhage in, 369 
 valves, inflammation of, see en- 
 docarditis, ^64 
 valves, method of preserving, 20 
 valves, method of testing sufiS- 
 
 ciency of, 18 
 valves, position of, 18 
 valvular openings of, size of, 19 
 ventricles, estimation of size of, 
 
 20 
 vfalls of, effect of decomposi- 
 tion on, 20 
 waxy degeneration of, 363 
 weight of. 30 
 wounds I if, 258 
 Hematocele, ante-uterine, 415 
 
 of tunica vaginalis testis, 
 
 439 
 peri-uterine, 415 
 retro-uterine, 415 
 Hematoidin from changes in extra- 
 
 vasated blood, 50 
 Hematoma, nature of, 60 
 
 Hematometra, 412 
 Hematophilia, 532 
 Hematoxylin, formula for, 44 
 Hemorrhage by diapedesis, 50 
 by rhexis, 49 
 causes of, 50 
 changes in extravasated 
 
 blood in, 50 
 from umbilical cord in 
 
 young children. 35 
 intermeningeal, 163 
 modes of, 49 
 of brain, 174 
 of dura mater, 157 
 of pia mater, 163 
 Hemorrhagic diathesis, 582 
 
 infarctions, changes in, 
 
 53 
 infarctions, mode of for- 
 mation, 53 
 infarctions, nature of, 50 
 Hellebore poisonmg, lesions of, 550 
 Hepatitis, acute, 343 
 
 chronic, interstitial, 844 
 peri, 350 
 purulent, 343 
 syphilitic, 348 
 tuljercular, 349 
 Hepatization in phthisis, 244, 246 
 
 in pneumonia, 225, 233 
 Hermaphroditism, 434 
 Hernia, iutestino-vagiaalis, 408 
 recto-vaginalis, 408 
 vesico-vaginalis, 408 
 Heterologous tumors, 112 
 Histoid or connective-tissue tumors, 
 
 117 
 Hodgkin's disease, 292, 365 
 Homogeneous immersion lenses for 
 
 studying bacteria, 91 
 Homologous tumors. 112 
 Hooklets of taenia echinonoccus, 70 
 Ho'se-'hoe kidney, 379 
 Howship's lacunae in bone, 455 
 Hyalin degeneration, 62 
 Hydatids, see ecchinococcus, 69 
 Hydatid ruoles, 134 
 Hydraemia, 55 
 Hydreacephalocele, 189 
 Hydrocele, 438 
 
 Hydrocephalus, acute tubercular, 170 
 chronic, internal in 
 children, method of 
 removing brain in, 
 86 
 congenital, 173 
 externus, 189 
 forms of, 173 
 internus, 188 
 primary, in adults, 174 
 secondary, 173 
 Hydrochloric acid poisoning, lasionsof, 
 
 545 
 H.vdrocyanic acid poisoning, lesions of, 
 551 
 
564 
 
 INDEX. 
 
 Hydromeningocele, 189 
 Hydrometra, 413 
 Hydiomyelocele, 199 
 Hydronephrosis, 390 
 Hydropericardium, 254 
 Hydrophobia, 517 
 
 Hydrorrachis, interna and externa, 199 
 Hydrostatic test of aeration of lungs, 
 
 38 
 Hydrothorax, 208 
 Hydrosalpinx, 430 
 Hymen, lesions of, 405 
 Hypersemia, effects of,in general, 49 
 Hypertrophy of heart, 260 
 Hypospadia, 484 
 Hypostasis, cadaveric, 4 
 Hypostatic pneumonia, 330 
 
 lohorrhEemia. see pysemia, 512 
 Incarceration of intestines, 318 
 Indigo-sulphate poisoning, lesions of, 
 
 544 
 Infarction, embolic, most frequent seat 
 of, 54 
 hemorrhagic, changes in, 58 
 hemorrhagic, mode of for- 
 mation of, 53 
 hemorrhagic, nature of, 50 
 white, 53 
 Infectious diseases, relations of bacte- 
 ria to, 85 
 Infective granuloma, 12 
 Infiltration, fatty, 60 
 Inflammation, catarrhal, of mucous 
 membranes, 107 
 cellular, 97 
 
 chronic, vpith forma- 
 tion of connective 
 tissue, 103 
 classification of, 96 
 croupous, coagulation 
 
 necrosis in, 60 
 croupous, of mucous 
 
 membranes, 108 
 diffuse, of viscera. 111 
 formation of abscesses 
 
 in, 99 
 formation of blood- 
 vessels, 101 
 formation of cicatricial 
 
 tissue in, 101 
 formation of exuda- 
 tions in, 99 
 formation of granula- 
 tion-tissue in, 100 
 forms of, in connec- 
 tive tissue, 96 
 forms of, in mucous 
 
 membranes, 106 
 forms of, in viscera, 
 
 110 
 interstitial, of viscera, 
 
 110 
 parenchymatous, of 
 viscera, 110 
 
 Inflammation, purulent, of mucous 
 membranes, 107 
 syphditic, 103, 109 
 tubercular, 102, 109 
 tubercular, with sim- 
 ple inflammation,. 
 108 
 with production of se- 
 rum, fibrin, and pus, 
 98 
 with production of 
 serum, fibrin, and 
 pus, and new con- 
 nective tissue, 100 
 Inflammatory' softening of brain, 181 
 Infusoria in intestinal contents, 67 
 Injection, interstitial, mode of, in har- 
 dening tissues, 42 
 Internal examination, mode of, in au- 
 topsies, 8 
 Interstitial inflammation of viscera,. 
 110 
 injection, 43 
 pneumonia, 235 
 pregnancy, 433 
 Intestines, cadaveric lividities in, 36 
 concretions in, 330 
 diverticula of, 313 
 incarceration of, 313 
 intussusception of, 314 
 large, inflammation of, see 
 
 colitis, 317 
 lesions of, caused by embo- 
 li, 317 
 malformations of, 313 
 method of opening, 26 
 method of preservation, 36 
 method of procedure with, 
 in suspected poisoning,. 
 36 
 method of removal, 23, 35 
 method of testing for amy- 
 loid degeneration, 36 
 of young children, gas in, 
 
 39 
 more common lesions of, 
 
 38 
 parasites of, 331 
 postmortem changes in, 
 
 36 
 resume of more common 
 
 lesions, 36 
 rupture of, 315 
 small, inflammation of, see 
 
 enteritis, 315 
 small, position of, and con- 
 dition at autopsies, 16 
 small, ulcers of, 317 
 solitary and agminated 
 
 glands of, 316 
 strangulation of, 813 
 transposition of, 315 
 tumors of, 319 
 ulcers of, 316, 318 
 ulcers, syphilitic, of, 819 
 
INDEX. 
 
 Intestines, ulcers, tubercular, of, 315 
 ulcers, typhoid, of, 486 
 ■wounds of, 315 
 -Intracanalicular fibroma, 133 447 
 Intussusception of intestines '314 
 J-odine, use of, in staining bacteria by 
 Gram's method, 90 
 use of, in testing for amyloid 
 degeneration, 34 
 
 ■Jalap poisoning, lesions of, 550 
 Janeway's case of thrombosis of portal 
 
 vein from fish bone, 337 
 Japanese isinglass, use of, in cultivat- ■ 
 
 ing bacteria, 94 
 Joints, diseases of, 470 
 
 foreign bodies in, 473 
 inflammations of, see arthritis 
 470 ' 
 
 tumors of, 473 
 
 Kidneys, atrophied, 384 
 
 Bright's disease of, classifica- 
 tion of, 380 
 calculi of, 393 
 changes in position of, 379 
 congestion of, 380 
 cysts of, 391 
 embolism of, 390 
 examination and removal of, 
 
 at autopsies, 23 
 fatty infiltration of, 388 
 hydronephrosis, 390 
 inflammation around, 393 
 inflammation of, see nephri- 
 tis, 380 
 injection of vessels of, for 
 
 preservation, 24 
 large white, 382, 384 
 macroscopical appearance of, 
 
 23 
 malformations of, 379 
 methods of preservation of, 34 
 methods of removal from 
 
 body, 23 
 parasites of, 394 
 of young children, resume of 
 
 lesions of, 38 
 pareachymatous degeneration 
 
 of, :;4 
 pelvis of, calculi in, 392 
 pelvis of, examination of, 34 
 post-mortem changes in, 33 
 preservation of, for study of 
 
 bacteria, 34 
 size and weight of, 33 
 study of fresh tissue of, 34 
 thrombosis of, 390 
 tumors of, 393 
 waxy, 34, 385 
 
 Koch's method of solid culture for bac- 
 teria, 91 
 
 Klihne's theory of cause of rigor mortis, 
 6 
 
 565 
 
 Lardaceous degeneration, see waxy de- 
 generation, 61 
 Large white kidney, 382, 384 
 Laryngitis, catarrhal, acute, 205 
 
 catarrhal, chronic, 206 
 croupous, 306 
 syphilitic, 306 
 tubercular, 307 
 Larynx and trachea, tumors of, 305 
 
 inflammation of, see laryngi- 
 tis, 205 
 in young children, examina- 
 tion of, 38 
 malformations of, 205 
 method of preservation of, 33 
 method of removal of, 33 
 perichondritis of , 306 
 Lateral ventricles of brain, examina- 
 tion of, 13 
 Lead poisoning, lesions of, 549 
 Leiomyoma, 136 
 Lepra ansesthetica, 301 
 bacilli of, 83, 530 
 lesions of, 520 
 Leprosy, see lepra, 520 
 Leptomeningitis, 163 
 Leptothrix buccalis, 84 
 Lesions, extent of necessary, to cause 
 
 death, 3 
 Leucooyth^mia, lesions of, in general, 
 530 
 lesions of, in blood, 
 
 56 
 lesions of, in bones, 
 
 464 
 lesions of, in lymph- 
 glands, 391 
 lesions of, in spleen, 
 365 
 Leucocytosis, nature and occurrence 
 
 of, 56 
 Leuksemia, see leuoocythsemia, 530 
 
 nucleated red blood-cells in, 
 365 
 , pseudo, 293 
 
 Lightning, lesions in death from, 537 
 Lipssmia, 57 
 Lipoma, characters and situations of, 
 
 133 
 Liver, abscess of, 343, 344 
 
 acute yellow atrophy of, 343 
 acute yellow atrophy of, micro- 
 cocci in, 80 
 amyloid degeneration of, 340 
 anaemia of, 334 
 atrophy of, 338 
 bronze, 341 
 changes in position, size, and 
 
 shape of, 16, 333 
 cirrhosis of, 344 
 congestion of, 334 
 cysts of, 353 
 
 fatty degeneration of, 339 
 fatty infiltration of, 338 
 gummata of, 349 
 
566 
 
 mcEx. 
 
 Liver, hemorrhage of, 336 
 
 hepatic artery, lesions of, 336 
 hepatic veins, lesions of, 338 
 "hob-nail," 344 
 hypersemia of, 334 
 inflammations of, see hepatitis, 
 
 343 
 lymphatic tissue, hyperplasia of, 
 
 351 
 malformations of, 333 
 metastatic abscesses of, 344 
 method of examination of, 27, 
 
 28 
 method of preservation of, 28 
 method of removal of, from 
 
 body, 27 
 miliary lymphoma in, 351 
 " nutmeg," 335 
 of young children, appearances 
 
 of 39 
 parasites of, 353 
 paiencliymatous degeneration 
 
 of, 338 
 pigmentation of, 341 
 portal vein of, lesions of, 336 
 position of, in body, 16 
 post-mortem discoloration of, 
 
 28 
 resume of lesions to be looked 
 
 for at autopsies, 28 
 rupture of, 336 
 size and weight of, 28 
 tumors of, 351 
 waxy degener«tion of, 340 
 ■wounds of, 336 
 Lividity, cadaveric, 4 
 
 post-mortem in internal or- 
 gans, 15 
 Lobar pneumonia, acute, 225 
 Lobelia inflata poisoning, lesions of, 553 
 Locomotor ataxia, 196 
 Longitudinal sinus of dura mater, ex- 
 amination of, 10 
 Lungs, acute miliary tuberculosis of, 
 237 
 atelectasis of, 223 
 brown induration of, 231 
 congestion of, 221 
 emphysema of, 222 
 gangrene of, 224 
 general examination of, at au- 
 topsies, 20 
 hemorrhage of, 221 
 hydrostatic test for presence of 
 
 Hirin, 38 
 inflammation of, 224 
 injuries of, 220 
 malformations of, 220 
 method of examining at autop- 
 sies, 21 
 method of preservation of, 21 
 method of removal of, 20 
 non-aerated, in new-born chil- 
 dren, 38 
 oedema of, S21 
 
 Lungs of still-born children, 37 
 of children born alive, 38 
 parasites in, 251 
 pneumonia, acute lobar of, 225 
 pneumonia broncho, 230, 232 
 pneumonia, compli'cating, 230 
 pneumonia, interstitial, 235 
 pneumonia of heart disease, 231 
 pneumonia, secondary, 230 
 pneumonia, syphilitic, 336 
 stnrcture of, 207 
 tumors of, 250 
 Lupus, micrococci in, 80 
 
 relations of bacteria to, 519 
 structure of nodules of, 518 
 Lymphangiectasis, 285 
 Lymphangioma, 140, 285 
 Lymphangitis, 284 
 
 Lymphatic follicles of intestines, lesions 
 of, 316 
 tissue in various organs, 281 
 Lymhoma, 120, 291, 292, 351 
 Lympho-sarcoma, 127 
 Lymph-glands, amyloid degeration of. 
 291 
 glands, atrophy of, 290 
 glands, enlargements of, 291 
 glands, hyalin degeneration of, 
 
 291 
 glands, hyperplasia of, 291 
 glands, inflammation of, acute,. 
 
 286 
 glands, inflammation of, chron- 
 ic, 287 
 glands, inflammation of, witlx 
 
 cheesy degeneration, 288 
 glands, inflammation of, 
 
 scrofulous, 2S8 
 glands, inflammation of, syphi- 
 litic, 290 
 glands, inflammation of, tuber- 
 cular, 289 
 glands, parasites of, 292 
 glands, pigmentation of, 287 
 glands, structure and relations 
 
 of, to disease, 285 
 glands, tumors of, 292 
 vessels, dilatation of, 285 
 vessels, inflammations of, 284 
 vessels, lesions of, 283 
 vessels, tumors of, 285 
 
 Macroglossia, 285, 296 
 
 Malarial fever, bacteria in, 83, 526 
 
 fever, lesions of, 526 
 Malignant pustule, 8a, 524 
 Mamma, female, cysts of, 446 
 
 female, hemorrhage of, 445 
 female, inflammation of, see- 
 mastitis, 445 
 female, malformations of, 
 
 444 
 female, nipple of, eczema and 
 
 ulcers, 446 
 female, tumois of, 446 
 
INDEX. 
 
 567 
 
 Mamma, male, lesions of, 449 
 Marrow of bone, anaemia , 405 
 
 of bone, alterations in leukae- 
 mia, 464 
 of bone, inflammation of, see 
 osteomyelitis, 459 
 Mastitis, acute, 445 
 
 chronic, 445 
 "Measle," 67 
 Measles, micrococci in, 80 
 Meconium in intestines of young; chil- 
 dren, 39 
 Mediastinum, description of, 251 
 
 inflammation of, 351 
 tumors of, 353 
 Medulla oblongata, examination of, 12 
 Medullary cancer, 151 
 Melaneemia, blood in, 56 
 
 deposit of pigment in or- 
 gans in, 56 
 Melano-carcinoma, 153 
 
 sarcoma. 127 
 Me.mbranes of brain, lesions of, 157 
 Meningitis, 113 
 
 acute cellular, 164 
 acute simple, 165 
 chronic, l67 
 epidemic cerebro- spinal, 
 
 80, 496 
 syphilitic, 171 
 tubercular, 167 
 Metastasis of tumors, 114 
 Methyl-violet for staining amyloid and 
 
 bacteria, 63, 509 
 Methylen-blue for staining bacteria, 
 
 89, 510 
 Metritis, acute. 416 
 chronic. 417 
 puerperal, 417 
 Micro-bacteiia, 81 
 
 organisms, 77 
 Microcephalia, 189 
 Micrococci, chromogenous, 79 
 pathogenous, 80 
 zymogenous, 80 
 Micrococcus, characters of, 79 
 luteus. 80 
 prodigiosus, 80 
 urese. 80 
 Microcytes in blood, 56 
 Microsporon furfur, 77 
 Microtome, freezing, of Thoma, 40 
 
 sliding of. Thoma. 44 
 Miliary tubercles, characters of, 103, 237, 
 
 241,-506 
 Moles, hydatid, 184 
 
 pigmented, 128 
 Morbus maculosus, lesions of, 531 
 Moulds, 76 
 Mouth, gangrene of, 295 
 
 hypertrophy of, 394 
 inflammations of, see stoma- 
 titis, 294 
 malformations of, 393 
 tumors of, 295 
 
 Mucoid degeneration, 63 
 Mucous membranes, inflammation of, 
 catarrhal, 106 
 membranes inflammation of, 
 
 ci-oupous, 108 
 membranes, inflammation of, 
 
 diptheritic, 108 
 membranes, inflammation of, 
 
 purulent, 107 
 membranes, inflammation of, 
 
 syphilitic, 109 
 membranes, inflammation of, 
 
 tubercular, 109 
 membranes, polypi of, 123 
 membranes, structure of, 106 
 patch on mucous membranes, 
 110 
 Miiller's fluid, formula for and use of, 
 
 41, 4-2 
 Multilocular cysts of ovary, 426 
 Mumps, 373 
 
 Muscle, heart, method of preserving, 80 
 voluntary striated, 475 
 voluntary striated, atrophy, 
 
 simple of, 478 
 voluntarj' striated, atrophy, 
 
 progressive of, 478 
 voluntary striated, degenera- 
 tions of, 478 
 voluntary striated, degenera- 
 tion, fatty, of, 480 
 voluntary striated, degenera- 
 tions, hyalin, of, 480 
 voluntary striated, degenera- 
 tions, waxy, of, 480 
 voluntary striated, enboli of, 
 
 475 
 voluntary striated, hemorrhage 
 
 of, 475 
 voluntary striated, fatty infil- 
 trations of, 479 
 voluntary striated, hypertro- 
 phy of, 481 
 voluntary striated, hypertro- 
 phy, pseudo-, of, 479 
 voluntary striated, inflamma- 
 tion of, see myositis, 475 
 voluntary striated, lipomato- 
 sis of, 479 
 voluntary striated, parasites 
 
 of, 483 
 voluntary striated, rupture of, 
 
 475 
 voluntary striated, tumors of, 
 
 481 
 voluntary striated, wounds of, 
 475 
 Museums, preservation of specimens 
 
 for, 44 
 Mycosis intestinalis, 321 
 Myelitis, acute, 194 
 ohronii^, 196 
 disseminated, 195 
 of anterior cormia, polio-mye- 
 litis anterior, 195 
 
568 
 
 INDEX. 
 
 Myeloid or gianf-celled sarcoma, 128 
 Myocarditis, acute purulent, 367 
 
 chronic interstitial, 268 
 interstitial, 267 
 syphilitic, 268 
 Myoma, 136 
 
 laevicellulare, 136 
 striocellulare, 187 
 Myomalacia of heart, 364 
 Myosin, coagulation of, in rigor mor- 
 tis, 6 
 Myositis, acute parenchymatous, 476 
 chronic interstitial, 476 
 ossificans. 477 
 suppurative, 475 
 syphilitic, 478 
 tubercular, 478 
 Myxomata, 122, 123, 124 
 Myxo-sarooma, 131 
 
 Nabothi ovula on cervix uteri, 81 
 Nsevi, vascular, 139 
 Necrosis, coagulation, in acute and 
 chronic phthisis, 244, 247 
 coagulation, in croupous in- 
 flammation, 60, 109 
 coagulation, in infarctions, 59 
 coagulation, nature and con- 
 ditions of occurrence of, 
 59 
 simple, nature and varieties 
 
 of, 59 
 of bone, 460 
 
 of tissue as result of inflam- 
 mation, 99 
 phosphorus, of bone, 461 
 pj-esence of bacteria in, 59 
 Nematode worms, 71 
 Nephritis, diffuse acute, 383 
 
 diffuse chronic, 3S3 
 interstitial acute, 386 
 interstitial chronic, 387 
 parenchymatous acute, 381 
 parenchymatous chronic, 382 
 peri-, 393 
 pyelo-, acute, 388 
 pyelo-, chronic, 389 
 suppurative, 388 
 tubercular, 389 
 Nephro-phthisis, 389 
 Nerve, optic, preservation of, 14 
 Nerves, changes in, after division, 200 
 inflammation of, see neuritis, 
 
 201 
 peripheral, lesions of, 200 
 tumors of, 201 
 Nerve-tissue, methods of preservation 
 and study of, 203 
 staining, Weigert's method 
 of, 203 
 Nervous system, 157 
 Neuritis, acute and chronic, 201 
 leprous, 201 
 syphilitic, 201 
 tubercular, 201 
 
 Neuroma, characters and varieties of. 
 
 138 
 New-born children, changes in appear- 
 ance, soon after death, 35 
 children, post-mortem ex- 
 amination of. 33 to 39 
 Nitrate of mercury, poisoning by, 545 
 of potassium poisoning, lesions 
 of, 546 
 Nitric acid poisoning, lesions of, 544 
 
 acid, use of, in decalcifying 
 bone, 40 
 Nitro-benzole poisoning, lesions of, 551 
 Noma of vulva, 4(l6 
 Nutmeg liver, 335 
 Nux vomica poisoning, lesions of, 553 
 
 Obliterating endarteritis, 272 
 
 thrombi, 51 
 (Edema glottidis, 206 
 
 glottidis post mortem, 22 
 nature of, 51 
 Oesophagitis catarrhal, 298 
 croupous, 298 
 Oesophagus, cysts of, 300 
 
 dilatation of, 299 
 malformations of, 298 
 method of preservation of, 
 
 22 
 method of removal of, 22 
 perforation and rupture, 
 
 299 
 softening post mortem, 
 
 303 
 stenosis of, 300 
 tumors of, 300 
 ulceration of, 299 
 veins of, dilatation of, 300 
 Oidium albicans. 77 
 Omentum, position of, 16 
 Oophoritis, 424 
 
 syphilitic, 425 
 tubercular, 425 
 Opium poisoning, lesions of, 550 
 Optive nerve, method of hardening, 14 
 Orchitis, acute, 439 
 
 chronic, 440 
 syphilitic, 441 
 tubercular, 440 
 Organs, method of preservation, 41 
 
 of young children, preserva- 
 tion of, 39 
 Osmic acid, use of, in preserving tissue, 
 
 42 
 Osteitis, 453 
 
 condensing, 455 
 rarefying, 454 
 suppurative, 456 
 syphilitic, 457 
 tubercular, 457 
 Osteoblasts, 452 
 Osteoclasts. 454 
 Osteoma, characters and situation of, 
 
 135 
 Osteomalacia, 464 
 
nSTDEX. 
 
 669 
 
 Osteomyelitis, 459 
 
 idiopathic, 459 
 malignant, 459 
 traumatic, 460 
 Osteophytes, 135, 452 
 Osteo-sarcoma, 189 
 Osteo-sclerosis, 455 
 Ovarian pregnancy, 433 
 Ovaries, appearance, size, weight of, 
 31 
 changes in size and position 
 
 of, 424 
 cysts of. 426, 429 
 hemorrhage and hypeisemia 
 
 of, 424 
 inflammation of, see oophori- 
 tis, 424 
 malformations of, 423 
 method of preservation of, 81 
 removal of, 29 
 tumors of, 425 
 Ovula Nabothi in cervix uteri, 31, 119 
 Oxalic acid poisoning, lesions of, 545 
 Oxide, carbonic, poisoning, lesions of, 
 
 553 
 Oxyuris vermioularis, 72 
 
 Pancreas, amyloid degeneration of, 370 
 atrophy of, 370 
 calculi in ducts of, 371 
 cirrhosis of, 369 
 cysts of, 371 
 degeneration of, 370 
 displacements of, 372 
 fat-necrosis of, 370 
 fatty degeneration and infil- 
 tration of. 370 
 hemorrhage of, 369, 370 
 inflammation of, see pancrea- 
 titis, 369 
 malformations of, 372 
 method of examination, 
 weight, size, etc., of, 28, 
 29 
 tumors of, 371 
 Pancreatic ducts, lesions of, 371 
 Pancreatitis, chronic interstitial, 369 
 parenchymatous. 369 
 suppurative, 369 
 syphilitic and tubercular, 
 370 
 Pacchionian bodies, 16 '■ 
 Pacohymeningitis, forms of, 158 
 
 syphilitic and tu- 
 bercular, 160 
 Papillomata, sarcomatous, 131 
 Parametritis, 417 
 Paraphimosis. 435 
 Parasites, animal, 66 
 
 animal, methods of preserva- 
 tion and study, 75 
 ■vegetable, 76 
 Parenchymatous degeneration, 60 
 
 inflammations of vis- 
 cera, 110 
 
 Parietal thrombi, 51 
 Paris green poisoning, lesions of, 548 
 Parotid gland, inflammation of, 373 
 gland, parasites of, 374 
 gland, tumors of, 374 
 Parovarium, cysts of, 430 
 Pathogenous bacteria, 80, 81, 82 
 Pathological tissues, preservation of, 40 
 Pearls, epithelial, in epithelioma, 148 
 Pelvis of kidney, examination of, 24 
 Penis, calcification of, 436 
 condyloma of, 436 
 enlargements of, 435 
 hemorrhage of, 435 
 inflammation of, 435 
 injuries of, 435 
 mnlformations of, 434 
 method of removal from body 
 
 29 
 ossification of, 436 
 tumors of, 436 
 ulcers of, 436 
 Periarteritis, 271 
 Peribronchitis in acute phthisis, 244 
 
 in chronic phthisis, 247 
 Pericarditis, 255 
 
 tubercular, 256 
 Pericardium, adhesions of, 256 
 
 calcification of, 264 
 dropsy of, 
 extravasation of blood 
 
 in, 254 
 gas m, 255 
 hemorrhage of, 254 
 inflammation of, 355 
 injuries of, 254 
 methoil of opening, 18 
 perforation of, 254 
 serum in, 18 
 thickenings of, 18 
 tumors of, 256 
 Perihepatitis, 350 
 Perimetritis, 417 
 Perinephritis, 392 
 
 Periosteum, inflammation of, see peri- 
 ostitis, 451 
 Periostitis, acute, simple, 451 
 fibrous. 452 
 
 infective, micrococci of, 80 
 ossifying, 452 
 suppurative, 451 
 syphUitio, 452 
 tubercular, 453 
 Periphlebitis, 383 
 Perisplenitis, 365 
 
 Peritoneum, inflammation of, see peri- 
 tonitis, 322 
 malformations of, 332 
 parasites of, 332 
 structure of, 321 
 tumors of, 329 
 Peritonitis, acute, 333 
 
 acute cellular, 323 
 acute exudative, 324 
 chronic adhesive, 336 
 
570 
 
 nSTDEX. 
 
 Peritonitis, chronic cellular, 325 
 
 chronic exudative, 338 
 chronic, with serum, fibrin, 
 
 and pus, 328 
 chronic, with thickening of 
 
 peritoneum, 329 
 hemorrhagic, 328 
 tubercular, 329 
 Pernicious ansemia, 528 
 Petechiee, 50 
 
 Pharyngitis, catarrhal, 298 
 croupous, 298 
 submucous, 298 
 Pharynx, examination of, in children, 
 38 
 inflammation of, 298 
 lupus of, 299 
 malformations of, 298 
 removal and examination of, 
 
 22 
 tumors of, 301 
 ulcerations of, 299 
 Phimosis, 435 
 Phlebectasia, 280 
 Phlebitis, 282 
 
 syphilitic, 283 
 tubercular, 383 
 Phleboliths, 52, 281 
 Phosphates in vesical calculi, 400 
 Phosphorus poisoning, lesions of, 546 
 Phtliisis, acute. 243 
 
 chronic, 245 
 Pia mater, collection of serum in, 10 
 mater, examination of, 10 
 mater, fatty degeneration of cells 
 
 along vessels of, 166 
 mater, hemorrhage and hypersemia 
 
 of, 163 
 mater, inflammation of, see menin- 
 gitis, 163 
 mater, localized thickenings of, 162 
 mater, method of preserving, 13 
 mater, oedema of, 163 
 mater, opacities of, 10 
 mater. Pacchionian bodies of, 162 
 mater, parasites and pigmentation 
 
 of, 171 
 mater, structure of, 161 
 mater, tumors of, 171 
 mater spinalis, lesions of, 191 
 Picric acid, use of. for decalcifying, 40 
 acid, use of, in preserving sedi- 
 ments, casts, etc., 43 
 Pigment in blood, 56, 57 
 Pigmentation of lymph-g ands, 287 
 
 of tissues, 64 
 Pin -worm, 73 
 Pineal gland, 174 
 Pituitary body, 175 
 Pityriasis versicolor, fungus of, 77 
 Placenta, amyloid degeneration of, 434 
 apoplexy of, 433 
 cysts of, 434 
 
 fatty degeneration of, 434 
 hemorrhage of, 433 
 
 Placenta, inflammation of, see placen- 
 titis, 433 
 Placentitis, 433 
 Pleura, hemorrhage in, 308 
 
 inflammation of, see pleurisy, 
 
 208 
 tumors of, 216 
 Pleural cavities, examination of, 20, 37 
 cavities, method of determin- 
 ing presence of air in, 17 
 cavities, serum in, as a result 
 of decomposition, 20 
 Pleurisy, acute, 209 
 chronic, 215 
 dry, 209 
 
 with effusion, 209 
 with production of serum, 
 
 fibrin, and pus, 213 
 subacute, 209 
 tubercular, 215 
 Plexiform neuroma, 138 
 Pneumonia, broncho-, 232 
 
 diffuse, in acute phthisis, 
 
 343 
 diffuse, in chronic phthisis, 
 
 246 
 interstitial, 235 
 interstitial, in chronic 
 
 phthisis, 246 
 lobar acute, 825 
 lobar, micrococci in, 80, 82, 
 
 228 
 of heart disease, 231 
 secondary and complicat- 
 ing, 230 
 syphilitic, 336 
 Poisoning, lesions of, by alcohol, 551 
 lesions of, by aconite, 553 
 lesions of, by aloes, 550 
 lesions of, by arsenic, 547 
 lesions of, by belladonna, 553 
 lesions of, by cantharides, 
 
 550 
 lesions of, by carbolic acid, 
 
 551 
 lesions of, by carbonic acid, 
 
 553 
 lesions of, by carbonic ox- 
 ide, 553 
 lesions of, by chloral hy- 
 drate, 553 
 lesions of, by chloroform, 
 
 553 
 lesions of, by colohicum, 550 
 lesions of, by colocynth, 550 
 lesions of, by conium, 553 
 lesions of, by copper, 549 
 lesions of, by corrosive sub- 
 limate, 549 
 lesions of, by croton oQ, 55C 
 lesions of, by digitalis, 553 
 lesions of, by elaterium, 550 
 lesions of, by ether, 553 
 lesions of, by gamboge, 55 
 lesions of, by hellebore, 550 
 
INDEX. 
 
 571 
 
 Poisoning, lesions of, by hydrochloric 
 
 acid, 545 
 lesions of, by hydrocyanic 
 
 acid, 551 
 lesions of, by indigo-sul- 
 phate, 544 
 lesions of, by jalap, 550 
 lesions of, by lead, 549 
 esions of, by lobelia inflata, 
 
 553 
 lesions of, by nitric acid, 
 
 544 
 lesions of, by nitro-benzole, 
 
 551 
 lesions of, by nux vomica, 
 
 553 
 lesions of, by opium, 550 
 lesions of, by oxalic acid, 
 
 545 
 lesions of, by phosphorus, 
 
 546 • ' ^ ^ 
 
 lesions of, by potash, 545 
 lesions of, by potassium cy- 
 anide, 551 
 lesions of, by potassium ni- 
 trate, 546 
 lesions of, by savin, 550 
 lesions of, by scamnaony, 
 
 550 
 lesions of, by Scheele's 
 
 green, 548 
 lesions of, by soda, 545 
 lesions of, by stramonium, 
 
 553, 
 lesions of, by strychnia, 
 
 553 
 lesions of, by sulphuric acid, 
 
 543 
 lesions of, by tartar emetic, 
 
 550 
 lesions of, by tartaric acid, 
 
 545 
 lesions of, by turpentine, 
 
 550 
 lesions of, by vegetable irri- 
 tants, 550 
 lesions of, by veratria, 550 
 general considerations on 
 autopsies in cases of, 33, 
 543 
 Poliomyelitis anterior, 195 
 Polypi of mucous membranes, fibrous, 
 122 
 of mucous membranes, myxo- 
 matous, 124 
 of mucous membranes, sarco- 
 matous, 131 
 Porencephalie, 184 
 Portal vein, dilatation of, 337 
 vein, embolism of, 336 
 vein, examination of, 27 
 vein, inflammation of, 336 
 vein, rupture of, 337 
 vein, thrombosis of, 336 
 Posterior spinal sclerosis, 196 
 
 Post-mortem changes in internal or- 
 gans, 26 
 cooling of body, 5 
 distribution of blood in 
 
 body, 9 
 elevation of temperature,. 
 
 6 
 examinations, external 
 
 inspection, 4-8 
 examinations, internal, 
 
 order to follow, 8 
 examinations, method of 
 
 making, 3-39 
 fractures, 8 
 heart-clots, 19, 269 
 lividity, 4 
 putrefaction, 5 
 stiffening of body, 6 
 wounds, 8 
 Potash poisoning, lesions of, 545 
 Potassium cyanide poisoning, lesions 
 of, 551 
 nitrate poisoning, lesions 
 of, 546 
 Potatoes, sterilized, for cultivating bac- 
 teria, 92 
 Pregnancy, extrauterine, 432 
 Preservation and hardening of tissues,. 
 40, 41, 44, 45 
 and hardening of organs 
 in poisoning cases, 31^ 
 548 
 of tumors, 120 
 Prickle-cells in epithelioma, 147 
 Proglottides of tape-worms, 67 
 Prostate, atrophy of, 443 
 
 concretions in, 444 
 hypertrophy of, 443 
 inflammations of, 443 
 parasites of, 444 
 preservation of, 29 
 removal of, 39 
 tumors of, 444 
 Protozoa, 66 
 Psammoma, 131, 161 
 Pseudo-hermaphrodites, 405 
 
 hypertrophy of muscle, 479 
 leukaemia, 530 
 Psorospermice of liver, 66 
 Pulmonary arteries, aneurism of, 377 
 
 arteries, malformations of, 
 256 
 Purpura hemorrhagica, 531 
 Puerperal fever, bacteria in, 80 
 
 metritis and endometritis, 
 417 
 Purulent infection, see pyaemia, 512 
 Pus, blue, bacteria of, 81 
 cells in blood, 57 
 
 formation of, in inflammation, 98, 
 99 
 Putrefaction after death, 5, 15, 85 
 Pyaemia, bacteria of, 80, 513 
 
 lesions of, 512 
 Pyelitis, micrococci in, 80 
 
572 
 
 INDEX. 
 
 Pyelo-nephritis, acute, 388 
 
 chronic, 389 
 
 species of bacteria in, 
 82 
 Pyo-pneumothorax, 313 
 Pyo-salpinx, 431 
 
 Rabies, 517 
 
 Rachitis, 462 
 
 Ranula, 119, 374 
 
 Ray-funguB, 77 
 
 Rectocele vaginalis, 408 
 
 Rectum, inflammation of, 319 
 
 Recto-vaginal flstulse, 409 
 
 Relapsing fever, 494 
 
 fever, bacteria of, 85, 495 
 
 Renal calculi, 393 
 
 Respiratory system, lesions of, 305 
 
 Rhabdonema strongyloides, 75 
 
 Rhabdomyoma, 137 
 
 Rhexis, hemorrhage by, 49 
 
 Rickets, 462 
 
 Rigor mortis, absence of, in foetuses 
 before term, 7 
 mortis, nature and cause of, 6 
 order of occurrence and contin- 
 uance of, 6, 7 
 
 Ring-worm fungus, 76 
 
 Rod bacteria, characters of, 81 
 
 Rosanilin, use of, in staining bacteria, 
 89 
 
 Round-worms, 71 
 
 Saccharomyces albicans, 77 
 Salivary glands, lesions of, 373 
 Salpingitis, 431 
 Sarcina ventriculi, 81 
 Sarcoma, alveolar, 130 
 
 angio-, 129 
 
 cysto-, 131 
 
 general characters of, 13 i 
 
 lympho-, 127 
 
 melano-, 127 
 
 myeloid or giant-celled, 127 
 
 myxomatodes, 131 
 
 osteo-, 129 
 
 round-celled, 126 
 
 spindle-celled, 125 
 Savin poisoning, lesions of, 550 
 Scammony poisoning, lesions of, 550 
 Sjars and tattoo marks, 8 
 Soheele's green poisoning, lesions of, 
 
 548 
 Scirrhous carcinoma, 151 
 Sclerosis of brain, 182 
 
 of spinal cord, 193, 196 
 Soolex of tape-worm, 67 
 Scorbutus, lesions of, 531 
 Scrofula, inflammation of lymph-glands 
 
 in, 288 
 Scrotum, lesions of, 437 
 Scurvy, 581 
 Secondary degenerations in spinal cord, 
 
 192 
 Section-cutting, 44 
 
 Seminal vesicles, 442 
 Septicsemia, see pyeemia, 512 
 Septo-pyEemia, see pyaemia, 513 
 Serum in pleural cavities from post- 
 mortem changes, 20 
 Sinus, longitudinal of dura mater, ex- 
 amination of, 10, 13 
 Skull, base of, examination of, 10 
 
 method of opening, 9 
 Small intestines, examination and le- 
 sions of, 16, 315 
 pox, micrococci in, 81 
 Soda poisoning, lesions of, 545 
 Sodium chloride, use of, in studying 
 
 fresh tissues, 40 
 Softening of brain, 12, 176 
 
 of internal organs, post-mor- 
 tem, 16 
 Solitary tubercles of brain, 185 
 Spermatocele, 439 
 Sphero-bacteria, 79 
 Spina bifida, 199 
 
 Spinal cord, ascending gray degenera- 
 tion of, 193 
 cord, cysts of, 198 
 cord, spcondaxy degenerations 
 
 of, 192 
 cord, descending gray degene- 
 ration of, 193 
 cord, examination of, 14, 16 
 cord, gummata of, 198 
 cord, hemorrhage of, 193 
 cord, inflammation of, 194 
 cord, injuries of, 193 
 cord, lesions of, 190, 192 
 cord, malformations of, 199 
 cord, pia mater of, post-mortem 
 
 changes in, 14, 191 
 cord, preservation of, 14 
 cord, sclerosis of, 196 
 cord, tubercles of, 198 
 cord, tumors of, 198 
 Spirillum rugula, 84 
 serpens, 84 
 Spiro-baoteria, 84 
 Spirochsste denticola, 83 
 
 Obermeieri, 85, 494 
 plicatilis, 85 
 Spleen, abscess of, 363 
 
 alterations of, in leukaemia, 
 
 365 
 amyloid degeneration of, 366 
 atrophy of, 866 
 changes in blood content of, 
 
 361 
 displacements of, 368 
 examination, size, weight, etc., 
 
 of, 25, 38 
 general relations of the vascular 
 
 system, 360 
 infarctions of, 361 
 inflammations of, see splenitis, 
 
 363 
 malformations of, 367 
 parasites of, 367 
 
INDEX. 
 
 573 
 
 Spleen, pigmentation of, 367 
 rupture of, 360 
 sago, 366 
 tumors of, 367 
 waxy degeneration of, 366 
 wounds of, 360 
 Splenic fever, 82, 534 
 Splenitis, acute hyperplastic, 362 
 chronic indurative, 363 
 peri-, 365 
 suppurative, 863 
 syphilitic, 364 
 tubercular, 365 
 Spores of bacteria, destruction of, 93 
 Sputum, examination of, for bacilli of 
 
 tuberculosis, 509 
 Staining, methods of, 44 
 Sterilizer, steam, for bacteria, 92 
 Stomacace, 294 
 
 Stomach, attachments and position of, 
 16, 17 
 calcification of, 312 
 dilatation of, 309 
 erosions, hemorrhagic, of, 308 
 hemorrhage of, 303 
 inflammation of, see gastritis, 
 
 304 
 injuries and rupture of, 303 
 malformations of, 802 
 opening, removal, and preser- 
 vation of, 27 
 post-mortem changes in, 303 
 tumors of, 309 
 ulcers of, 306, 809 
 waxy degeneration of, 812 
 Stomatitis, catarrhal and croupous, 294 
 syphilitic and tubercular, 
 
 296 
 ulcerosa, 294 
 Stomatite ulcero-membraneuse, 294 
 Stramonmm poisoning, lesions of, 553 
 Strangulation, lesions in, 8, 539 
 Strawberry marks, 139 
 Streptococcus, 80 
 Strongylus gigas, 73 
 
 longevaginatus, 73 
 Struma, 375 
 
 Strychnia poisoning, lesion of, 553 
 Subclarian artery, stenosis of, by athe- 
 roma of aorta, 278 
 Sublimate, corrosive, poisoning, lesions 
 
 nf ^49 
 Sublingual gland, inflammation of, 373 
 Submaxillary gland, inflammation of, 
 373 
 tumors of, 374 
 Suffocation, lesions in death by, 538 
 Sulphuric acid poisoning, lesions of, 
 
 543 
 Sunstroke, lesions of, 535 
 Suppuration, micrococci in, 81 
 Supra-renal capsules, lesions ot, 877, 
 378 
 capsules, removal, size, 
 etc., of, 23, 24, 35, 38 
 
 Syphilitic inflammation, 103 
 
 inflammation of mucous 
 
 membrane, 109 
 inflammation, bacteria of, 80, 
 
 105 
 
 Tabes dorsalis, 196 
 Taenia cucumerina, 71 
 echinococcus, 68 
 flavopuntata, 71 
 madagascariensis, 71 
 mediocanellata, 68 
 nana, 71 
 saginata, 68 
 solium, 67 
 Tape-worms, see taenia, 67 
 Tartar emetic poisoning, lesions of, 550 
 Tartaric acid poisoning, lesions of, 545 
 Tattoo marks and scars, 8 
 Temperature, change of, in body after 
 
 death, n 
 Teratoid tumors, teratoma, 118, 353 
 Terminal arteries, 58 
 Testicles, atrophy of, 438 
 cysts of, 443 
 inflammation of, see orchitis, 
 
 439 
 malformations of, 437 
 method of removal and pre- 
 servation of, 39 
 parasites of, 442 
 tumors of, 441 
 Thoma's microtomes, 40, 44 
 Thorax, method of examination, 15, 17 
 Thread-worms, 72 
 Thrombi, bacteria in infectious, 52 
 canalization of, 53 
 compositions, varieties, 
 changes, and effects of, 53 
 obliterating, 51 
 organization of, 53 
 Thrush, 77 
 
 Thymus gland in children, 37 
 Thyroid gland, amyloid degeneration 
 of, 375 
 gland, colloid degeneration of, 
 
 875 
 gland, goitre, 375 
 gland, hyperaemia and inflam- 
 mation of, 375 
 gland of young children, 38 
 gland, parasites of, 876 
 gland, struma of, 375 
 gland, tumors of, 375 
 Tissues, method of preservation of, 39, 
 
 41 
 Tongue, cysts of, 397 
 
 hypertrophy of, 296 
 inflammatLon of, see glossitis, 
 
 296 
 malformations of, 296 
 tumors of, 297 
 Trachea, inflammation of, see trachei- 
 tis, 305 
 malformations of, 205 
 
574 
 
 INDEX. 
 
 Trachea, of children, 38 
 
 preservation of, 33 
 tumors of 207 
 Transudation, nature of, 51 
 Trematode worms, 67 
 Trichina spiralis, 58, 73, 74 
 Trichocpphalus dispar, 73 
 Trichomonas vaginalis, 66 
 Trichophyton tonsurans, 76 
 Tubercle bacilli, 83, 504, 507, 508, 509, 
 511 
 granula, 103 
 tissue, 102, 506 
 Tubercles, miliary, 103, 506 
 
 solitary, of brain. IfiS 
 Tubercular inflammation, 102, 103 
 Tuberculosis, acute miliary of lung, 237 
 bacillus of, 83, 504, 507, 
 
 508. 509, 511 
 characters and causes of, 
 
 504 
 chronic miliary of lungs, 
 
 241 
 general and localized, 
 
 505 
 lesions of, 506 
 Tubes, Fallopian, lesions of, 430 
 
 Fallopian, position, shape and 
 dimensions of, 31 
 Tubal pregnancy, 433 
 Tumors, benign. 114 
 
 cachexia from, 115 
 
 causes of, 116 
 
 characters of, in general, 112 
 
 classification of, 117 
 
 Cdmplex, congenital forms of, 
 
 118 
 complex, nomenclature of, 130 
 Cohuheim's hypothe-iis of ori- 
 gin of, 116 
 degenerations of, 113 
 epithelial, 140 
 heterologous and homologous, 
 
 113 
 malignancy of, 114 
 metasta.ses of, 114 
 methods of preservation of, 
 
 120 
 modes of growth of, 113 
 parts of, best adapted for 
 
 study, 117 
 shapes of, 113 
 special forms of, 121 
 teratoid, 118 
 vessels of, 112 
 Turpentine poisoning, lesions of, 550 
 Typhlitis, 318 
 Typhoid fever, 485 
 
 fever, bacteria of, SO, 83, 491 
 fever, complicating and sec- 
 ondary lesions of, 489 
 fever, hemorrhages and in- 
 farctions in, 488 
 fever, intestinal lesions of, 
 485 
 
 Typhoid fever, mesenteric glands in 
 488 
 fever, peritonitis in, 488 
 fever, spleen, lesions of, in, 
 488 
 Typhus fever, lesions of, 498 
 
 Ulcerative endocarditis, 80, 265 
 Umbilical cord, examination of, 35 
 Urachus, 395 
 
 Urates in vesical calculi, 400 
 Ureter, examination of, 33 
 Urethra, dilatations of . 401 
 examination of, 29 
 inflammations of, see urethri- 
 tis, 403 
 malformations of, 401 
 perforation of, 403 
 preservation of, 39 
 prolapse of mucous mem- 
 brane of, 504 
 rupture and strictures of, 402 
 tumors and ulcers of, 404 
 wounds of, 402 
 Urethritis, 403, 404. 
 Urinary apparatus, lesions of, 379 
 Uric acid in vesical calculi, 400 
 Uterus, amyloid degeneration of, 41 
 anteflexion of, 413 
 anteversion of, 412 
 changes during menstruation, 
 
 30 
 changes in size and position of, 
 
 411, 413 
 cysts of, 423 
 dilatation of, 411 
 elevation of, 413 
 enlarged condition after preg- 
 nancy, 30 
 enlargement of, 411 
 fatty degeneration of, 418 
 hematocele of, 415 
 hemorrhage and hypersemia of, 
 
 414 
 hernise of, 413 
 inflammation, see metritis, 415, 
 
 416, 417 
 inversion of, 413 
 latero-flexion of, 412 
 latero- version of, 413 
 malformations of, 410 
 obliteration of cavity of, 411 
 parasites of, 423 
 perforation of, 414 
 polypi of, 419 
 prolapse of, 413 
 retroflexion and retroversion 
 
 of, 413 
 rupture of, 414 
 size, position, removal, etc., 
 
 of, 29, 30, 31 
 tumors of, 419 
 ulcerations of, 418 
 versions of, 412 
 waxy degeneration of, 418 
 
INDEX. 
 
 575 
 
 Vagina, cysts of, 410 
 
 dilatations of, 408 
 
 fistulas of, 409 
 
 gangrene of, 409 
 
 hernise of, 408 
 
 inflammation of, see vaginitis, 
 
 409 
 malformations of, 407 
 parasites of, 410 
 perforations of, 408 
 prolapse of, 408 
 removal, preservation, etc., of, 
 
 30, 31 
 tumors of, 410 
 wounds of, 408 
 Vaginitis, 409 
 
 Valves of heart, examination, removal, 
 preservation, etc., of, 18, 19, 
 20 
 of heart, lesions of, see endocar- 
 ditis, 264 
 Varicose aneurism, 279 
 Variola, micrococci of, 81 
 Vegetable parasites, 76 
 Vein, portal, examination of, 27 
 portal, lesions of, 336 
 stones, 52 
 Veins, animal parasites in, 283 
 dilatation of, 280 
 inflammation of, see phlebitis, 
 
 282 
 perforations of, 282 
 rupture of, 281 
 tumors of, 283 
 wounds of, 281 
 Ventricles of brain, examination of, 
 12 
 of brain, lesions of, 171, 173, 
 
 174 
 of heart, examination of, 19 
 
 20 
 of heart, lesions of, see en- 
 docarditis, 264 
 Veratria poisoning, lesions of, 550 
 Vermiform appendix, lesions of, 319 
 
 Vernix caseosa, 35 
 Vertebrae, examination of, 14 
 Vesical calculi, 400 
 Vesicovaginal tistulge, 409 
 Vesicute seminales, examination and 
 preservation of, 29 
 seminales, lesions of, 442 
 Violet-methyl, use of in staining amy- 
 loid, 62 
 Viscera, inflammations of, in general, 
 
 110, 111 
 Vulva, changes in size of, 408 
 cysts of, 407 
 
 examination and removal of, 30 
 gangrene of, 406 
 hemorrhage and hypersemia of, 
 
 403 
 inflammation of, 406 
 lupus of, 406 
 malformations of, 405 
 cedema of, 406 
 tumors of, 406 
 
 Warts, sarcomatous, 131 
 Wandering kidnt^ys, 380 
 Water test for aeratiun of lungs, 38 
 
 test for suflicieacy of heart 
 valves, 18 
 Waxy degf»neration, 61 
 Weigert's methods of staining nerve- 
 tissue, 203 
 Whip-worm, 72 
 Wickersheimer's fluid, formula and use 
 
 of, 45 
 Worms, 67 
 
 Wounds, examination of, 8 
 healing of, 100 
 
 Xanthin calculi, 401 
 
 Yeasts, 76 
 Yellow fever, 500 
 
 Zoogloea colonies of bacteria, 78 
 Zymogenous bacteria, 80, 81, 82