^fcrOvS^ CORNELL UNIVERSITY. THE Bosnian p. Winva^v Cibr^rg THE GIFT OF ROSWELL P. FLOWER FOR THE USE OF THE N. Y. STATE VETERINARY COLLEGE. 1897 Cornell University Library RB 25.Z66t 1897 V.I A text-book of special pathological anat 3 1924 000 294 920 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/cu31924000294920 SPECIAL PATHOLOGICAL ANATOMY •y^)^- A TEXT-BOOK SPECIAL PATHOLOGICAL ANATOMY BY ERNST ZIEGLER PROFESSOR OF PATHOLOGY IN THE UNIVERSITY OF FREIBURG TRANSLATED AND EDITED FROM THE EIGHTH GERMAN EDITION BY DONALD MAC ALISTER M.A. M.D. LINACRE LECTURER OP PHYSIO AND TUTOR OF ST JOHN'S COLLEGE, CAMBRIDGE AND HENRY W. CATTELL M.A. M.D. DEMONSTRATOR OF MORBID ANATOMY IN THE UNIVERSITY OF PENNSYLVANIA SECTIONS I — VIII Wefa gork THE MACMILLAN COMPANY LONDON: MACMILLAN & CO. Ltd. All rights reserved Copyright, 1896,, By the MACMILLAN COMPANY. Set 1897. up and electrotyped September, i8g6. Reprinted August, zU / S\bfQ^ ,.1. ' A/ 7 NortoooD ^rfBS J. S. CuBhing & ©0. — Berwick i Smith Norwood Mass. U.S.A. PREFACE Since the publication in 1884 of the first English edition of 2iegler's Special Pathological Anatomy, great advances have been made in our knowledge of its subject-matter. These have been duly embodied in the five successive German editions that have appeared in the meantime. The work has accordingly been so •altered and enlarged that in preparing a third English edition we Jiave had entirely to rewrite the text, and to recast the biblio- graphical and other supplementary portions. The number of pathological papers and monographs to which reference might fitly be made is now so great that only the more recent and important can be dealt with. But the student of historical tastes will find ample references to the earlier literature in the previous English editions ; and by omitting them in this much valuable .space has been gained. The second volume, containing the sections on the alimentary tract with the liver and pancreas, the respiratory and genito- urinary systems, the eye, and the ear, is already in the press and will shortly be published. We hope to follow it with a new version of the part on Q-eneral Pathological Anatomy, -prepared with the author's sanction and assistance from the latest German •edition. We desire here to record our thanks to Dr W. G. Spiller, of Philadelphia, for his help in preparing the translation of Sections VI and VII. DONALD MAC ALISTER HENRY W. CATTELL July, 1896. CONTENTS Section I BLOOD AND LYMPH CHAPTER I. The Blood II. The Lymph Section II THE VASCULAR MECHANISM III. MALFORMATIOlSrS OF THE HeART AND GrEAT VeSSELS IV. Morbid Alterations of the Heart as a Whole V. Morbid Changes in the Endocardium VI. Morbid Changes in the Myocardium .... VII. Infective Granulomata, Tumours, and Parasites the Heart . . .... VIII. Morbid Changes in the Pericardium IX. Morbid Changes in the Arteries X. Morbid Changes in the Veins ..... XI. Morbid Changes in the Lymph-Vessels Section III THE SPLEEN AND THE LYMPH-GLANDS XII. Morbid Changes in the Spleen . ... XIII. Morbid Changes in the Lymph-Glands Section IV THE OSSEOUS SYSTEM XIV. The Bone-Marrow .... XV. Atrophic Affections of Bone XVI. Regeneration and Hypertrophy. vii CONTENTS Section I BLOOD AND LYMPH OlIAPTEK I. The Blood II. The Lymph Section II THE VASCULAR MECHANISM III. Malformations of the Heart and Great Vessels . IV. Morbid Alterations of the Heart as a Whole V. Morbid Changes in the Endocardium .... VI. Morbid Changes in the Myocardium . ... VII. Infectivf, Granulomata, Tumours, and Parasites of THE Heart . . VIII. Morbid Changes in the Pericardium IX. Morbid Changes in the Arteries ..... X. Morbid Changes in the Veins XI. Morbid Changes in the Lymph-Vessels Section III THE SPLEEN AND THE LYMPH-GLANDS XII. Morbid Changes in the Spleen . .... Xni. Morbid Changes in the Lymph-Glands Section IV THE OSSEOUS SYSTEM XIV. The Bone-Marrow . . . . XV. Atrophic Affections of Bone XVI. Regeneration and Hypertrophy. vii Vlll CONTENTS CHAPTER PAGE XVII. Inflammations of Bone ....... 170 XVIII. Infective Granulomata of Bone ... . 183 XIX. Disorders of Osseous Development and Growth 196 XX. Tumours, Cysts, and Animal Parasites of Bone . 231 XXI. Degenerations of the Joints and Synarthroses . 245 XXII. Regeneration and Hypertrophy in Joints . . 250 XXni. Acute and Chronic Inflammations of Joints . 260 XXIV. Tuberculosis and Syphilis of Joints . . 282 XXV. Loose Bodies in the Joints 287 Section V THE MUSCLES AND TENDONS XXVI. The Muscles .... XXVII. The Tendons, Sheaths, and Bursae 291 314 Section VI THE CENTRAL NERVOUS SYSTEM XXVIII. The Spinal Cord and its Malformations . XXIX. Degeneration and Inflammation of the Spinal Cord XXX. The Forms of Myelitis ... ... XXXI. Hydromyelia and Syringomyelia XXXII. Multiple Sclerosis .... XXXIII. Neuronic or Systemic Affections XXXrV. Infective Granulomata and Tumours op the Cord XXXV. The Membranes of the Cord XXXVI. Structure and Functions of the Braix XXXVII. Malformations of the Braix XXXVIII. Disorders of the Cerebral Circulation . XXXIX. Atrophy of the Brain . . . XL. Local Degenerations and Inflammations op the Brain ..... XLI. Infective Granulomata op the Braix XLII. Sclerosis of the Brain .... XLIII. Tumours and Animal Parasites of the Brain XLIV. The Pia Mater and Arachnoid XLV. The Dura Mater, Pineal Gland, and Pituitary Body 323 830 344 849 353 357 370 878 381 388 404 407 412 432 434 436 442 460 CONTENTS OHAl'TEB XL VI. XL VII. XL VIII. XLIX. Section VII THE PERIPHERAL NERVOUS SYSTEM Structure of Peripheral Nerves Degeneration and Inflammation op Nerves Regeneration op Nerves .... Tumours of Nerves Section VIII THE SKIN L. Introductory . . LI. Disorders op Circulation .... LII. Pigmentary Disorders LIII. Atrophy of the Skin LIV. Inflammatory and Parasitic Disorders LV. Inflammatory Hypertrophies and Tumours LVI. Non-Inflammatory Hypertrophies and Tumours LVII. The Sebaceous Glands, Hair, ,\nd Nails . INDEX i-xxxii at end of INDEX OF FIGURES a^'lG. 1. Section through a degenerating patch from the brain '2. Malformation of the heart 3. Heart of a human embryo 4-3 millimetres long 4. Heart of a human em.bryo at the fifth week .... 5. Posterior half of the heart of a human embryo at the fifth week 6. Diagrammatic scheme of the aortic arches of the em.bryo of an am- niotic vertebrate 7. Diagrammatic scheme of the transformations of the aortic arches in a mammal S. Hypertrophy of the left ventricle . . .... 9. Section of fatty endocardium 10. Mucoid degeneration of the connective tissue of the aortic valve 11. Proliferous growth of the endocardium with a thrombus . 12. Mycotic endocarditis of an aortic valve 13. Mycotic endocarditis (pustulosa) of the tricuspid valve 14r. Warty endocarditis (verrucosa) of the aortic valve .... 15. Villous endocarditis (polyposa) 16. Ulcerative endocarditis of the aorta, showing ulcers, valvular per- forations, and valvular thrombi 17. Mycotic endocarditis (villosa), with valvular thrombi, and acute valvular aneurysm 18. Section through an endocarditic vegetation 19. Posterior segment of the mitral valve, with thickened and calcified thrombi, and stenosis of the auriculo-ventricular opening 20. Thickened and distorted aortic valves 21. Aortic insufficiency and mitral stenosis 22. Brown atrophy of the cardiac muscle .... 23. Fatty degeneration of the cardiac muscle . 24. Kupture of the heart in arterio-sclerotic myomalacia . 2.5. Myomalacia cordis .... 26. Fibroid induration of the heart 27. Thrombosis withm the heart .... 28. Partial cardiac aneurysm 29. Mycotic myocarditis 30. Cor villosum 31. Adhesive pericarditis xi XU INDEX OP FIGURES FIO. 32. Granulation-tissue formed within a fibrinous pericarditic deposit of some weeks' duration 61 33. Fatty degeneration of the cells of the intima of the aorta, viewed from the flat surface 65 34. Fatty degeneration of a cerebral capillary 65 35. Hyaline degeneration of the blood-vessels of an atrophic lymph-gland 66 36. Commencing calcification of the middle coat of the aorta . 37. Atheromatous cerebral artery 38. Section of the aorta in acute proliferous aortitis 39. Embolic suppurative arteritis 66 68 70 73 40. Occlusion of a pulmonary vessel by connective tissue after embolism 74 41. Remains of emboli in a branch of the pulmonary artery ... 75 42. Section of a thrombus in process of organisation . . . .76- 43. Diagrammatic section of a ligated vessel 77 44. Syphilitic arteritis 79 45. Tuberculous arteritis 80 46. Periarteritis nodosa . . .80 47. Periarteritis nodosa . 81 48. Aneurysms of the aorta . . 82 49. Aneurysms of the hypogastric artery 83 50. Rupture of the intima and media of the aorta, with the formation of a dissecting aneurysm 85 51. Aneurysmal dilatation and partial rupture of the ascending aorta . 86 52. Obliteration of the right femoral vein . ... 92 53. Varices of leg 93 54. Section of the dark-red spleen-pulp 103 55. Amyloid degeneration in and about the splenic follicles . . . 106 56 . Lymphoid follicle of the spleen with central necrosis . . . 109 57. Portion of tissue and isolated cells from a splenic follicle undergoing partial necrosis ... Ill 58. Hypertrophy of the follicles of the spleen . . . 113. 59. Chronic tuberculosis of the spleen . ... 115 60. Amyloid swelling of the adenoid reticulum . . . US 61. Deposit of pigment-carrying cells in a lymph-gland after resorption of an extravasation of blood . 119 62. Section of a slate-coloured lymph-gland of the lung . . . 120 63. Inflammatory oedema of a lymph-gland, with catarrhal desquam- ation of the endothelium of the lymph-channels .... 121 64. Fibrinous lymphadenitis 122 05. Fibrinous mesh-work in the lymphadenoid follicles of the tonsil in croupous pharyngitis from diphtheria . . . . 123 66. Fibrous hyperplasia of a lymph-gland . . . . 124 67. Recent tuberculosis of a lymph-gland 126 08. Large-celled hyperplasia of a tuberculous lymph-gland . . . 127 69. Alveolar sarcoma of a lymph-gland 132 70. Carcinoma developing in an enlarged axillary lymph-gland . 132 71. Resorption of bone 141 INDEX OF FIGURES xiii PIG. 72. Eccentric atrophy of the lower ends of the tibia and fibula, with osteoporosis 142 73. Senile atrophy of the calvarium 143 74. Hypoplasia of the pubis, ischium, and ilium of the left side . . 144 75. Extreme atrophy of the cranial bones produced by the pressure of the developing brain 145 76. Deformity of the superior and inferior maxillae and their alveolar processes produced by cicatrisation after a burn . . . 146 77. Atrophy of the last thoracic and upper lumbar vertebrae, from the pressure of an aortic aneurysm . 147 78. Section of a vertebra affected with osteomalacia .... 150 79. Osteomalacia of the pelvis . 151 80. Osteomalacia of the tibia 152 81. The formation of new bone on the surface of old bone by means of a layer of osteoblasts 155 82. Myelogenous formation of bone from aggregations of osteoblasts . 156 83. Formation of osteoid trabeculae from proliferous periosteum . 157 84. Periosteal formation of cartilage . 157 85. Formation of bone from cartilage in a callus fourteen days old . 158 86. Formation of bone from connective tissue ..... 158 87. Proliferous periosteum four days after fracture of the bone . 161 88. Longitudinal section through a fracture of the fibula fourteen days old . . . ... ... .162 89. Reunited fracture of the tibia and fibula, with synostosis of the bones 164 90. Fracture of the spine nine months old, with great displacement of the vertebrae 165 91. Fracture of the fibula, repaired by syndesmosis . . . 166 92. Pseudo-arthrosis after fracture of the neck of the femur . . 167 93. Resorption and apposition of bone . . . . 168 94. Apparent dilatation of the radius ... . . 169 95. Necrosis of the lower third of the diaphysis of the femur . . 172 96. jSTecrosis of the left tibia with periosteal bone-formation, following acute osteomyelitis . ... 172 97. Phosphorus-necrosis of the lower jaw . . 176 98. Periosteal hyperostosis of the tibia . . . 177 99. Skeleton of a hand with hyperostosis of the bones . . . 178 100. Ostitis deformans of the head and neck of the femur . . 179 101. Spondylitis deformans ...... . 180 102. Fungous granulations with tubercles from the spongy tissue of the calcaneum ... 183 103. Central tuberculosis of bone in an advanced stage . . . 185 104. Periosteal deposition of bone in chronic myelogenous tuberculosis . 186 105. Osteosclerosis of the femur resulting from chronic tuberculosis 187 106. Tuberculosis of the spinal column 188 107. Formation of osteophytes upon the atrophied cortical layer of the femur in chronic tuberculous arthritis ...... 189 XIV INDEX OF FIGURES FIG. 108. Angular flexure of the vertebral column from the destruction of the first lumbar vertebra 190 109. Angular flexure of the spine with bony ankylosis of the bodies of the vii-xii thoracic vertebrae after partial destruction by tuber- culous disease ......••■• 191 193 193 194 197 199 200 110. Gummatous syphUitic caries of the parietal bone . 111. Syphilitic caries and necrosis of the calvarium 112. Syphilitic hyperostoses of the left femur . 113. Normal endochondral ossification .... 114. Partial agenesis of the bones of the cranial vault in anencephalia 115. New-born micromelic infant, with cretinoid expression of face 116. Skeleton of a female cretinoid dwarf 201 117. Skeleton of a female dwarf . ... 201 118. Head of a microcephalic child (Helen Becker) . . 202 119. Endochondral ossification in a new-bom child with abnormally short limbs ........... 203 120. Bones of the middle finger of the right hand of the cretinoid dwarf of Fig. 116 .204 121. Micromelic pseudo-rachitis (foetal rickets) of the upper limb . . 204 122. Agenesis of the wings of the sacrum with sacro-iliac synostosis . 205 123. Leontiasis ossea .... . . . 208 124. Syphilitic osteochondritis . . .... 212 125. Rickets ... . . .... 214 126. Rickets 216 127. Formation of a medullary space within an epiphysial cartilage in rickets . 217 128. Adult femur with rachitic curvature of the diaphysis . . . 219 129. Adult femur with rachitic flexure of the lower epiphysis . . 219 130. Flat rickety pelvis . .... 220 131. Rickety (pseudo-osteomalacic) pelvis with the promontory of the sacrum sunk forward ....... . 221 132. Congenital hydrocephalus in a child about one year old . 224 133. Scoliosis and kyphosis of the spine .... . 226 134. Spondylolisthesis 228 135. Osseous resorption and apposition in the neighbourhood of a meta- static carcinomatous deposit in the diaphysis of the humerus 231 136. Myelogenous osteosarcoma of the tibia ...... 232 137v Osteosarcoma of the cranium . . . . . . 233 138. Section through an osteoid-chondroma of the humerus . 234 139. Ossifying large-celled sarcoma of the tibia 235 140. Multiple ivory exostoses of the cranium 236 141. Cartilaginous exostosis of the upper diaphysial end of the tibia . 237 142. Ivory osteoma of the parietal bone ....... 238 143. Multiple myelomata of the cranial vault 241 144. Deposit of needle-like crystals of sodium urate in an articular carti- lage . ... 246 145. Senile softening of cartilage . 247 INDEX OP FIGURES XV TIG. 146. Metaplasia of cartilage into mucoid tissue in fungous arthritis 147. Preliminary stage of fibrous intercartilaginous ankylosis 148. Fibrous intercartilaginous ankylosis .... 149. Complete bony ankylosis of the head of the femur with the ace- tabulum ....... 150. Nearthrosis of the hip ...... 151. Bony ankylosis of the lower jaw ..... 152. Chronic dry ulcerative arthritis 153. Chronic arthritis deformans .... 154. Arthritis and ostitis deformans with arborescent lipoma of the hip- joint .......... 155. Chronic polyarthritis deformans ..... 156. Arthritis deformans of the head of the femur . 157. Arthritis deformans of the head of the femur . 158. Spondylitis deformans 159. Chronic ankylosing arthritis .... 160. Hand with gouty nodes about the joints . 161. Tuberculous (fungous) arthritis ... 162. Tuberculous arthritis . . ... 163. Tuberculous caries about the acetabulum of the left hip-joint 164. Section through an atrophic muscular bundle from a case of pro- gressive spinal amyotrophy . 165. Progressive muscular atrophy . ... 166. Dropsical muscle-fibres ... ... 167. Transverse section through a muscle-bundle containing dropsical fibres 168. Waxy degeneration or coagulative necrosis in typhoid fever . 169. Spinal amyotrophy with lipomatosis ..... 170. Lipomatosis with atrophy of the calf-muscles ..... 171. Muscle-fibres in process of regenerative proliferation, taken from wounds of different ages .... ... 172. Ossification in a ' drill ' bone . . 173. ' Hour-glass ' hygroma of the sheath of the digital flexor tendons . 174. Section through a dilated prepatellar bursa with free and fixed rice-like bodies . 175. Sessile rice-like bodies from a prepatellar bursa 176. Wall of the thickened bursa of the olecranon with nodular fibrous growths . ........ 177. Scheme of the position and connexions of the ganglion-cells and posterior roots of the spinal cord .... 178. Diagrammatic cross-section of the spinal cord showing the tracts of the white matter ..... .... 179. Diagram of' the nuclei of the cerebral nerves in the floor of the fourth ventricle ........ 180. Atrophy of the left anterior horn from intra^uterine amputation of the left fore-arm 181. Contraction of the vertebral canal by crushing and protrusion of the sixth thoracic vertebra . PAGK 249 253 254 257 258 265 267 268 269 270 271 274 276 279 283 284 285 296 297 298 298 298 301 302 304 311 315 318 318 319 324 325 326 330 331 XVI INDEX or FIGUKES FIG. 1 a(;k 182. Compression of the lumbar cord by cavernous tissue with dilated veins formed on the dorsal surface of the pia mater . . 332 183. Transverse section through the apex of the left anterior horn of a normal spinal cord at the level of the fourth cervical nerves . 335 184. Transverse section through the apex of an atrophic anterior horn at the level of the fourth cervical nerves . . . 335 185. Degeneration of the cord from compression . . . 336 186. Myelitis from compression ...... . 337 187. Sclerotic tissue from the posterior column (disseminated sclerosis) 338 188. Grey gelatinous degeneration of the anterior horn of the cord . 339 189. Ascending degeneration of the cord above a compressed portion . 342 190. Ascending degeneration of the cord 342 191. Sclerosis and contraction of the entire grey matter of the cord . 346 192. Transverse sclerosis of the cord 347 193. Hydromyelia with sclerosis of the surrounding tissue . . 349 194. Syringomyelia in the region of the posterior columns of the cervdcal cord 350 195. Gliosis and syringomyelia in the lumbar region of the cord . 350 196. Cervical region (multiple sclerosis) .... 353 197. Thoracic region (multiple sclerosis) .... 353 198. Lumbar region (multiple sclerosis) .... 353 199. Multiple (secondary) sclerosis ... . 354 200. Multiple (primary) sclerosis . . . . 354 201. Disseminated sclerosis of the brain . . .... 355 202. Tabes dorsalis in an advanced stage . . . . 359 203. Transverse section of the posterior white columns in tabes dorsalis 359 204. Sclerosis and cicatricial contraction of the left anterior horn of the fourth cervical nerve after acute anterior poliomyelitis . . 363 205. Gelatinous degeneration of both anterior horns of the lun>bar region, with total loss of the ganglion-cells and nerve-fibres, after acute anterior poliomyelitis . . . . .363 206. Amyotrophic lateral sclerosis .... . . .366 207. Degeneration and sclerosis of the column of Burdach , of the column of Goll, and of the crossed pyramidal tracts . . . 368 208. Combination of sclerosis of the posterior columns with marginal sclerosis ...... . . 368 209. Tuberculous spinal meningitis . . . 374 210. Syphilitic induration and adhesions in the lumbar cord . 375 211. Venous angioma of the pia mater .... . 377 212. Fibroma and papillomatous angio-sarconia of the cauda equina with central glioma of the lumbar cord .... 378 213. Papillomatous angio-sarcoma with hyaline degeneration . . . 378 214. External surface of the left cerebral hemisphere .... 382 215. Median surface of the cerebrum 383 216. Frontal section of the cerebrum 384 217. Diagrammatic scheme of the course of the nerve-fibres within the brain {after Ramon y Cajal) 3S5 INDEX OP FIGURES Xvii f'G- PAdK 218. Basal aspect of the cerebral axis 219. Head of the mici-ocephalic child Helen Becker 220. Brain of the microcephalic child Helen Becker 221. Brain weighing 600 grammes . 222. Hypoplasia and microgyria 223. Frontal section through the brain of Fig. 222 224. Frontal section through the brain of a .deaf-mute with bilateral hypoplasia and partial agenesis of the temporal lobes and the cortex of the insula .... . 393 225. Agenesis of isolated portions of the cerebral convolutions . . 394 226. Porencephalic left hemisphere of a child of ten weeks . . . 395 227. Porencephalic right hemisphere of a child of ten weeks . . . 395 228. Congenital ventricular and meningeal hydrocephalus . . . 397 229. Frontal section through the brain of a hydrocephalic idiot . . 399 230. Hypoplasia of the cortex of the cerebellum 401 231. Atrophy of the cerebral cortex in progressive paralytic dementia . 408 232. Degenerate and disintegrating nerve-cells and nerve-fibres . . 412 233. Fatty degeneration of the ganglion-cells and the blood-vessels ., 413 234. Calcified ganglion-cells and nerve-fibres 413 235. Teased preparation from a degenerating patch in the brain, with hypertrophic neuroglia 414 236. Section from the border of a patch of softening in the brain (en- cephalomalacia) .... 415 237. Ischaeriiic softening of the cerebral cortex 418 238. Ischaemic softening of the brain 420 239. Apoplectic cicatrix from the centre of a cerebral hemisphere . . 423 240. Frontal section through the infundibulum of a brain with a bullet- wound ............ 425 241. Experimental encephalitis produced by a puncture through the cerebral cortex of a rabbit . 426 242. Transverse section of a bullet-wound in the brain .... 427 243. Section from a nodose ganglionic neuroglioma of the central lobe of the cerebrum 437 244. Telangiectatic glioma 437 245. Glioma of the pons and medulla oblongata 438 246. Section from a cerebral glioma, with stellate cells .... 439 247. Chronic meningo-encephalitis with atrophy of the cerebral cortex . 447 248. Chronic disseminated tuberculous meningo-encephalitis . . ■ 448 249. Large solitary tubercle of the cerebellar pia mater .... 450 250. Gummatous syphilitic meningo-encephalitis 452 251. Alveolar endothelioma of the pia mater 455 252. Papillomatous carcinoma of the choroid plexus . . . .456 253. Papillomatous carcinoma with gelatinous degeneration of the stroma from the choroid plexus 457 254. Endothelioma of the dura mater .462 255. Section from a psammoma of the dura mater . . . 463 256. Degeneration of the sciatic nerve 471 XVIU INDEX OF PIGUKES FIG. 257. Advanced degeneration of the motor nerves in a case of atrophy of the anterior horns of the spinal cord 471 258. Transverse section from an atrophic sciatic nerve (multij)le scle- rosis) 472 259. Chronic neuritis with partial atrophy of the nerve-fibres . . 474 260. Old and newly-formed nerve-fibres 478 261. Section of a fasciculus of the median nerve just above the point of severance by a stab four months previously .... 479 262. Amputational neuroma of the sciatic nerve in longitudinal section (amputation nine years previously) 479 263. Multiple neurofibromata 481 264. Multiple fibromata in one of the nerves of the sciatic plexus . . 482 265. Plexiform neuroma of the sacral region 483 266. Lobulated plexiform neuroma of the temporal region and neuro- fibroma of the vagus {after Bruns) 484 267. Acne rosacea 491 268. Endemic vitiligo 497 269. Atrophy and cystic degeneration of the hair-follicles and sebaceous glands of the scalp 500 270. Section through a syphilitic mucous patch (condyloma latum ani) . 504 271. Section through the margin of a blister due to a burn . . . 505 272. Blister from a burn in process of healing 507 273. Miliaria crystallina . 512 274. Acute pemphigus ... . . ... 514 275. Section of a variolous vesicle becoming pustular . . . 518 276. Colony of Streptococcus erysipelatis . . . . 522 277. Section of the skin in erysipelas buUosum 523 278. Phlegmon of the subcutaneous tissue, with an oedematous bulla . 524 279. Malignant pustule ... . . ... 526 280. Hypertrophic lupus of the face . 533 281. Patch of lupus vulgaris 534 282. Initial sclerosis of syphilis ... 535 283. Pustular syphilide (infantile syphilitic pemphigus) .... 537 284. Leontiasis leprosa ... 589 285. Ulcerous leprosy (lepra mutilans) of the leg and foot . . 540 286. Leprous node of the skin 541 287. Cup or scutulum of favus . . 543 288. Hair affected with favus . . 544 289. Section of the skin in scabies 546 290. Longitudinal section of a node of moUuscum contagiosum . . 547 291. Section of a corn . 543 292. Cutaneous horn removed from the back of the hand . . . 549 293. Cutaneous horn from the arm 549 294. Condyloma acuminatum 549 295. Lymphangiectatic elephantiasis of the leg 551 296. Congenital ichthyosis 555 297. Congenital ichthyosis 556 INDEX OF FIGURES xix FIG. 298. Ichthyotic wart . ........ 556 299. Congenital cavernous angioma of the skin .... 557 300. Section of a hypertrophic angioma of the skin and subcutaneous tissue . 558 301. Subcutaneous cavernous lymphangioma .... . 559 302. Section through two papillae from a tuberous hard wart . 560 303. Section through a slightly tuberous soft wart 561 304. Neurofibroma moUuscum 562 305. Multiple neurofibromata of the skin 563 306. Neuromatous elephantiasis or pachydermia of the thigh . . 564 307. Skin with neurofibromata from a case of pachydermia (Fig. 306) . 565 308. Atrophy and cystic degeneration of the hair-follicles and sebaceous glands of the scalp 571 SECTION I BLOOD AND LYMPH CHAPTER I THE BLOOD 1. The blood is a liquid of peculiar composition, abounding in cells or corpuscles, and equivalent in amount to about one- thirteenth of the body-weight. A cubic millimetre of the blood of a man contains on the average 5,200,000, that of a woman about 4,800,000, red corpuscles, with from 5,000 to 10,000 white corpuscles. Thus for every white corpuscle there are from 500 to 1,000 red corpuscles. In 100 cubic centimetres of blood there are in men 14.5 grammes of haemoglobin, and in women, 13.2 grammes (Hufnee). The amount of blood even in health is subject to considerable variation ; it maj^ under certain pathological conditions, differ notably from the average proportion given above. When the amount of blood in the body is simply increased, without change in its composition, the condition is described as plethora vera ; when the increase is due to an augmentation of the water and the salts, we speak of the condition as plethora serosa. Diminution of the total amount of blood in circulation is called anaemia or oligaemia; concentration of the blood, through loss of water and salts, the blood-albumen remaining normal in amount, is termed anhydraemia ; relative dilution of the blood, from diminution of the albumen it contains, is desig- nated hydraeiuia or hypalbuminosis. Plethora vera may occur when, before the removal by surgical operation of parts of the body, the blood has been pressed back from them into the general circulation to prevent haemorrhage, as in amputation by Esmaech's bloodless method (^plethora apo- coptica) ; or when blood has been injected directly into the vascular system. The complete emptying of the placenta in par- turition may force an excessive amount of blood into the body of the new-born infant, and so give rise to temporary plethora. Plethora caused by such an increase of the blood in circula- tion is a transient condition, the organism promptly excreting the excess of water and then destroying the surplus of red corpuscles. True plethora, however, of a more abiding kind, occurs in specially predisposed persons whose luxurious habits of life favour exces- sive blood-formation. This excess, in certain cases, may be so 4 THE BLOOD [CHAP. I considerable as to be recognisable during life, by means of the abnormally large, full, and at times tense pulse, and the unusually powerful action of the heart ; and after death by the increased capacity and fulness of the entire vascular system, as well as by the cardiac hypertrophy thereby induced. Plethora serosa as a transient condition may result from an increased supply of water to the blood. As a chronic condition, it may be due to diminished excretion of water, from disease of the kidneys or the heart. Simple hydraemia results from abnor- mal loss and insufficient re-formation of the blood-albumen : anhydraemia, from increase of the water excreted and defi- ciency of that ingested. After severe haemorrhage more water is taken up by the blood, and the condition of hydraemia follows and persists until the loss of albumen and red blood-corpuscles is again made good. Anaemia may occur from single or repeated haemorrhages, abnormal disintegration of blood, and insufficient formation of red corpuscles. Its characteristic symptom is the diminution of the amount of haemoglobin in the blood. The proportion may fall to six or even three grammes per 100 cubic centimetres of blood. Usually the number of red corpuscles is somewhat reduced, and the result is oligocythaemia. In chlorosis, however, the causes of which are as yet undetermined, the red blood-corpuscles are deficient in haemoglobin, but their number is not diminished. Increased destruction of the red blood-corpuscles is fre- quently referable to special causes acting injuriously on the blood. It occurs after burns of the skin, and from the action of many poisons, such, for example, as sulphuretted hydrogen, ar- seniuretted hydrogen, potassium chlorate, picric acid, toluylene- diamine, and many of the poisonous fungi. Infective diseases accompanied by fever may also exercise a destructive influence on the blood, owing to the action of their specific poisons and to the abnormal increase of the body-heat ; and the like result may follow from the presence of certain parasites in the blood, as in malaria. Excessive cooling of the skin in specially-disposed persons may occasion a destruction of the red blood-corpuscles (periodic or paroxysmal haemoglobinuria). There are also several forms of severe anaemia which are grouped together as pernicious anaemia, among the features of which is increased blood-destruc- tion or haematolysis, but the cause of this is still uncertain. These forms are therefore provisionally termed cryptogenetic anaemias. In some cases the condition is connected with defi- nite physiological conditions, or with organic diseases, such as for example pregnancy or childbirth, ulcerative affections of the bowels, or the presence of intestinal parasites {Bothriocephalus) . In other cases no organic disease is demonstrable, the anaemia appearing as a primary blood-disease. In the two instances last named opinions differ as to the cause of the blood-changes ART. 1] CAUSES OF ANAEMIA 5 whether they are due to an alteration in the blood-plasma, to the presence of specific poisonous substances in the blood causing its destruction, or to some abnormal frailty on the part of the blood- corpuscles. Deficiency in the formation of blood should be admitted as a cause of anaemia only when we can demonstrate the presence of morbid conditions in the bone-marrow, where especially the pro- dviction of red corpuscles takes place, or when defective food- supply or disease in the alimentary tract or in other organs has obviously caused impairment of the general nutrition, the evi- dence of any active blood-destruction being at the same time wanting. Even in such cases, however, it is often impossible to make out the connexion between the organic disease and the anaemia. There is, for example, a form of cachectic anaemia which is met with in certain pathological conditions of the lymphadenoid tissues (Arts. 30 and 35), of the spleen, of the lymph-glands, and of the intestine, though the formation of blood in the bone-marrow is not perceptibly impaired. Increased destruction of red blood-corpuscles is often capa- ble of demonstration by the microscope, the blood containing morbidly-altered red corpuscles and the products of their dis- integration. The altered and dying red blood-corpuscles often exhibit the most varied and diverse forms : thus we have globular, spindle- shaped, crescent-, club-, bobbin- and nail-shaped varieties ; others again are drawn out into threads, constricted in the middle, or wholly irregular. This condition is known as poikilocythaemia. Occasionally very small or very large red blood-corpuscles are met with, and these are termed respectively micrbcytes and macrocjrtes. Portions of the stroma of the red corpuscles may also display partial discoloration, while other portions are strongly coloured, and in some cases the several constituents of the cor- puscle appear to be separated {plasmoschisis'). Besides these corpuscular forms, which are undoubtedly due to disintegration, we find in grave anaemia others which we must regard as immature or morbidly altered embryonic forms of the red corpuscle. Of this nature are the nucleated red corpuscles, which are normally to be found only in the bone-marrow. The normal embryonic forms, which are nucleated cells of ordinary size, have been termed normoblasts, the morbid embryonic forms, which are abnormally large, megalohlasts. The diameter of the latter may be twice or even four times that of the normal cor- puscle. According to Ehklich and Mullbb, megalohlasts are chiefly met with in severe pernicious anaemia, and exemplify a morbid mode of blood-formation, which in normal conditions occurs onlj- during the period of embryonic development. It is to be noted, however, that in pernicious anaemia not only is the rate of blood-destruction augmented, but the rate of formation of 6 THE BLOOD [CHAP. I blood in the bone-marrow, which in this affection contains numer- ous embryonic forms of the red blood-cells, is simultaneously increased (Cohnheim, Rindfleisch, Neumann, Muller). It is not possible, however, to decide whether the multiplication of the normoblasts and the appearance of megaloblasts in the bone- marrow is caused by a primary disorder of that tissue, or is the consequence of an antecedent disease of the blood. In the latter case the phenomenon would indicate an increased growth of the haematoblasts of the bone-marrow with a view to the restoration of the blood. According to Stinzing and Gumprecht, the average proportion of the dry residue in normal blood is in man 21-6 per cent., and in woman 19'8 per cent. In severe anaemia this proportion may sink to 8-5 per cent., so that a condition o.f hydraemia is present. Oligaemia may however exist, though the composition of the blood remains normal. In leukaemia (Art. 2), on the contrary, the pro- portion of dry residue is relatively high, though the amount of haemoglobin is diminished. The proportion of haemoglobin in the blood varies considerably at different ages. It is highest at birth ; in the first years of life it falls to one-half, rising again between the fifth and forty-fifth year to about two-thirds of its original amount ; thereafter it again declines. During gestation the proportion of haemoglobin is diminished. The researches of Bollinger and Heissler furnish the following data concerning the variations of the quantity of blood in the lower animals : in pigs, from 2-2.5 to 8-70; in horned cattle, from 6-03 to 10 ; in dogs, from 4-4 to 12-4 ; in horses, from 5-9 to 13-5 ; in sheep, from 6-56 to 10-43 per cent., of the body-weight. Fat pigs are remarkably poor in blood. The amount of fat in the blood, which normally is very small and during digestion reaches about 1-2 per cent., may under pathological conditions reach a much higher percentage, the blood becoming milky and turbid from the small oil-globules (lipaemia) it contains. The amount ol fibrin-ferment contained in the blood is, in diseased condi- tions, subject to considerable variation ; so that on post-mortem examination we can distinguish certain cases in which there is an abundant formation of fibrin, or liyperinosis ; and in other cases a deficiency of fibrin-formation, or hypinosis. The former condition is found especially in inflammatory diseases, such as croupous pneumonia and erysipelas ; the latter, in death by suffocation, and in poisonmg by sewer-gas, by alcohol, and by hydrocyanic acid. We can remove the anaemia resulting from haemorrhage by the transfusion of blood, that is, by supplying to the affected person blood capable of perform- ing its functions. Transfusion into the human subject of the blood of lower animals serves no purpose, but rather causes further injury, inasmuch as the human red corpuscles break down in the blood-serum of animals. The same thing happens when the blood of one species of animal is injected into the vascular system of an animal of another species. References on Plethora, Anaemia, Hydraemia. Lipaemia, and Transfusion. Bierfreuxd: Haemoglobin in surgical diseases Langenbeck's Arch, xli 1891 Biermer: Pernicious anaemia Corresp. f. Schweiz. Aerzte ii 1872 BiRCH-HiRSciiFELD : Epidemic haemoglobinuria in infants D meet Woch 1879 AUT. 1] PLETHORA, ANAEMIA, ETC. 7 BiRCH-HiRSCHFELD and Ehrlich: Grave anaemias Verh. Congr.f. inn. Med. XI Wiesbaden 1892 BizzozERO and Sanguirico : Transfusion A. ital. de biol. vii 1886 Blechmann : Pathology of the bone-marrow A . d. Heilk. xix 1878 Bollinger: Haemoglobinuria in horses Z.f. Thiermed. in; Plethora vera Munch, med. Woch. 1886 "CoHNHEiM : Allqem. Path, i 1882 ; The bone-marrow in pernicious anaemia V. A. 68 1876 Darbmberg: Destructive action of blood-serum A. de med. exp. in 1891 Ehklich : Colorimetry of the blood Gesamm. Mittheil. i Berlin 1891 EiCHHORST : Die progressive perniciose Andmie Leipzig 1878 ; Art. Chlorosis Eulefiburg's Realencyklop. 1894 (with references) ■d'EspiNE and Picot : Pernicious anaemia in infants Rev. de med. x 1890 <3rABBi : Normal haematolysis Ziegler's Beitrdge xiv 1893 •Graeber : Zur Tclinischen Diagnostik der Blutkrankheiten Leipzig 1888 Gram : The size of the red corpuscles in health and disease Fortschr. d. Med. II 1884 Grossglick : Hydraemic plethora A. de physiol. n 1890 ■GuMPRECHT : Lipaemia D. med. Woch. 1894 (with references) Halla : Haemoglobin and corpuscles in acute fevers Prag. Z. f. 'tieilk. iv 1883 Haybm : Du sang et de ses alterations organiques Paris 1889 Heisslek : The theory of plethora Munch, pathol. Arbeiten Stuttgart 1886 Hoppk-Sbyler : Physiol. Chemie Berlin 1877-81 vosr HossLiN : Excretion of haematin and albumen in chlorosis Munch, med. Woch. 1890 Hunter : Pernicious anaemia Lancet 1888, 1890, Practitioner 1888-89 ; Transfusion Journ. of Anat. xxi and B. M. J. 1887 Immermann : D. A. f. klin. Med. xiii, Ziemssen's Cyclop, xvi New York 1877 Krugbr : Foetal blood at birth V. A. 106 1886 Laache: Die Anamie Christiania 1883, D. med. Woch. no. 43 1884 Labadie-Lagrave : Traite d. malad. du sang Paris 1893 Lbichtenstern : Hamoglobingehalt d. Blutes Leipzig 1878 Lichtheim : Periodic haemoglobinuria Volkmann's klin. Vortrage 134 1878, Corresp. f. Schweiz. Aerzte 1883 VON Limbeck : Klin. Pathol, d. Blutes Jena 1892 (with references) LxjKJANOw: Allgem. Path. d. Blutes u. d. Lymphe Leipzig 1892 (with refer- ences) Mackenzie : Anaemia B. M. J. 1891 Maissurianz : Exper. Studien ilb. d. Verdnd. d. Blutkbrper im Fieber Dorpat 1882 Maurbl : Z/anemie'par insuffisance de I'he'matose Paris 1891 MiJLLBR, Fr. : Pernicious anaemias Charite-Ann. xiv 1889 ; Examination of blood Cent. f. allgem. Path, in 1892 (with references) ; Atypical blood- formation in pernicious anaemia D. A. f. klin. Med. n 1893 (with refer- ences) MiJLLER : Progressive pernicious anaemia Inaug. Diss. Zurich 1877 Neumann : Bone-marrow in pernicious anaemia Berl. klin. Woch. 1877 VON Noorden: Grave anaemias Charite-Ann. xvi 1891 ; Path, des Stoffwechsels Berlin 1893 OsLER : Pernicious anaemia Cent. f. med. Wiss. 1877 Quincke: V. A. 54: 1871; Volkmann's klin. Vortrage 100 1876 ; D. A. f. klin. Med. XXV, xxvii 1880 QuiNQUAUD : Blood-lesions in various diseases A . gen. de med. 1879 von Keoklinghausen : Allgem. Path. d. Kreislaufs u. d. Erndhrung Stuttgart 1883 Rbinert : Die Zdhlung d. Blutkorperchen Leipzig 1891 (with references) RiEDBR : Atlas d. klin. Mikroskopie d. Blutes Leipzig 1893 Kindfleisch : Defective blood-formation in pernicious anaemia V. A. 121 1893 8 THE BLOOD [CHAP. I Sadler : Estimation of corpuscles and haemoglobin Fortschr. d. Med. (supple- ment) 1892 ScHAUMANN I Bothryocephalen-Anamie Berlin 1894 ScHiFF, H. : The red corpuscles in infants Prager Z. f. Heilk. xi 1890 Stierlin: Estimation of corpuscles and haemoglobin in infants D. A. f. klin. Med. XLV 1889 Stihzing and Gumprecht : Proportion of water and dried residue in the blood in health and disease D. A. f. klin. Med. liii 1894 (with references) TuMAS : Variations in the blood in certain infective diseases D. A. f. klin. Med. XLi 1887 Vanlair and Masius : De la microcylhe'mie Brussels 1877 "Vikrordt: Daten und Tabellen f. Mediciner Jena 1893 VoGEL : Virchow's Handb. d. spec. Path. Erlangen 1854 Waldstein : Progressive anaemia with subsequent leukaemia V. A. 91 1883 Weintraud: Changes in the red corpuscles V. A. 131 1893 Worm-Muller : Transfusion u. Plethora Christiania 1875 2. The proportion of white corpuscles in the blood (which usually ambunts on the average to one white cell to five hundred red) is subject, even under physiological conditions, to great vari- ation, being markedly increased during digestion and during gestation. Under pathological conditions this increase may reach still higher degrees, and may be associated Avith a diminution of the red blood-cells. If the condition of increase is transient it is spoken of as leueooytosis ; if lasting, as leukaemia. Pathological leucocjrtosis may occur, though not invariably, after haemorrhages, in cachectic conditions accompanying malig- nant disease (Reinbach), and just before death. It is met with in a large class of diseases that are accompanied by inflammatory exudations (inflammatory leucocytosis), such as croupous pneu- monia, inflammations of the serous membranes, pyaemia, ery- sipelas, scarlet fever, diphtheria, and quinsy. It is absent, on the other hand, in measles and influenza. In typhoid fever the proportion of leucocytes may even diminish. Experimentally, leucocytosis may be induced in animals by the injection of pus- micrococci, sterilised cultures of certain bacteria, bacterial proteins or albumoses, vegetable proteins, hemialbumose, and nucleinic acid, as well as by the administration of certain blood-poisons. The leucocytosis is usually preceded by a transient diminution of the leucocytes (hypoleucocytosis), which, according to Goldscheider and Jacob, is caused by the retention of the leucocytes within the capillaries of the viscera, and especially in those of the lungs. Physiological leucocytosis is seldom marked in degree (on the average it amounts to 33 per cent., Rieder), and it leaves unaffected the proportion between the different forms of leu- cocytes. Inflammatory leucocytosis reaches a higher degree of intensity, especially in pneumonia. Thus a proportion of one leu- cocyte to 100, or even to 15 or 20 red corpuscles, may occur, and the increase is generally confined to the multinuclear leucocytes. The causation of pathological leucocytosis is not certainly es- tablished. It is supposed by most authorities that an increased ART. 2] LEUKAEMIA 9 supply of leucocytes is carried to the blood from tlie parts in which leucocytes are normally produced; but perhaps there is also an increased production of these cells. The latter hypothesis would seem to correspond best with the observed facts. The change in the blood known as leukaemia (Virchow) is characterised by a more or less considerable increase of white blood-cells, accompanied in general by a corresponding reduction in the number of red corpuscles. The proportion between the two may be so altered that their numbers become equal, or in extreme cases the white may slightly outnumber the red. Of the white corpuscles, the uninuclear cells in particular are increased above the normal proportion, while among the red blood-cells nucleated forms are met with. In well-marked leukaemia the blood is strikingly pale, clear, and limpid. The heart and the large blood-vessels often contain after death peculiar clay-coloured clots, rich in white corpuscles, instead of the usual semi-translucent fibrinous deposits ; or the clots are covered with a white, creamy, pus-like film composed of colourless cells. The diagnosis of less-marked cases of leu- kaemia may require the aid of the microscope, by means of which even a slight relative increase in the proportion of white cells may be recognised. The increase of the white blood-cells in leukaemia is primarily referable to an increased supply of cells from those organs which produce leucocytes. Accordingly the spleen, the lymph-glands, and the marrow of the bones, show in different degrees and com- binations signs of hyperplastic proliferation ; sometimes only one or two of the above organs are altered and increased in bulk, or all three may exhibit proliferation. We can thus distinguish lymphatic, splenic (lienal), and myelogenous forms of leukaemia, as well as combinations of these forms. Further proof of this mode of origin is afforded by the fact that the blood contains cell- forms which correspond with the characteristic cells of the organs indicated. Thus in lymphatic leukaemia we find chiefly the small uninuclear cell-forms, which correspond to the cells of lymphaden- oid tissue. On the other hand in myelogenous and mixed leu- kaemias large uninuclear cells appear, which correspond to those found in the bone-marrow (myelocytes) but not in normal blood ; in this case, too, the eosinophile cells in the blood are increased in number. Finally, it is capable of demonstration that in leukaemia the tissu6-elements of the organs which produce leucocytes exhibit abundant examples of karyokinetic cell-division. It is to be noted, however, that an increase of the colourless cells may un- doubtedly take place outside of the above-named organs (Bizzo- ZERO, Spronck, MtJLLER, Strobe), for the leucocytes have been observed to divide by mitosis, not only in the circulating blood but also within certain organs in which they are retained ; in this lO THE BLOOD [CHAP. I way their number is further increased. It is also possible that those cells which reach the blood-current are in part endowed with a longer life than the ordinary leucocytes. The last-named phenomena suggest an explanation of the fact that in very rare cases (Leube, Fleischer) leukaemia may occur unaccompanied by any recognisable changes in the spleen, the marrow of bone, or the lymph-glands. Moreover, there is nothing to prevent us assuming that from organs not perceptibly hypertrophied an ab- normal number of colourless cells may be supplied to the blood. The diminution of the number of red corpuscles which takes place in the majority of cases of leukaemia is referable to the fact that the process of their formation is disordered. The nucleated red corpuscles, which are specially apt to appear in the blood in myelogenous and mixed leukaemias, are to be regarded as immature cells that have escaped from the marrow of bone. The richness of the blood in colourless cells generally leads to secondary changes in the different organs. These are indicated chiefly by an accumulation of leucocytes in the capillaries, and later on by the migration of some of them into the tissues. Such leukaemic infiltrations occur mainly in the liver, but are not wholly absent in other organs and tissues. Sometimes they form not only diffuse infiltrations, but also more definite deposits, which, in the form of greyish-white nodular patches, can be recognised without the aid of the microscope ; they are spoken of as leu- kaemic lymphomata. These aggregations originate not simply in a passive accumulation of leucocytes ; the cells probably increase also by subdivision and multiplication in situ. In the blood, in the spleen, and in the bone-marrow of those affected with leukaemia Charcot's crystals are not infrequently found after death. These are recognisable as sharp acicular octahedral crystals. The aetiology of leukaemia is not known. It is improbable that all the diseases which are designated as leukaemia at the pres- ent time have the same genesis and causation. The course of the disease is usually a chronic one, though acute cases are occasion- ally met with. The proportion of multinuclear cells under normal conditions amounts to about 70 per cent., that of eosinophile cells to about 1 or 2 per cent., of the colourless elements of the blood (Zappert). The view that leukaemia is the result of disease of the blood-producing organs is maintained chiefly by ViRCHOw, Neumann, Mosler, Ehrlich, and Muller ; while Biesiadecki, Renaut, Lowit, and others believe it to be a primary disease of the blood itself, in which the colourless elements, perhaps in consequence of some patho- logical alteration of the blood-plasma (Lowit), do not pass through the normal cycle of changes, but retaining their vitality are deposited in the tissues, and so lead to organic disorders. The peculiarities of the cells appearing in the blood, and in particular the occurrence of cells which resemble those of the bone- marrow, and like them present the same neutrophile granulation (Ehrlich), support the theory that lukaemia is primarily a disease of the organs that ART. 2] LBTTCOCYTOSIS AND LEUKAEMIA H produce the red and white blood-corpuscles. This does not exclude the possi- bility that the colourless cells which reach the blood may increase within the vessels in some pathological manner, and maintain their vitality beyond the normal period. It is a noteworthy fact, however, that afiections of the spleen and of the lymph-glands (see Sect. Ill), which are anatomically identical with those occurring in leukaemia, may exist without any accompanying leukaemia (pseudo-leukaemia, splenic and lymphatic anaemia). Thus hypertrophy of the spleen and lymph-glands does not always lead to an increased influx of colour- less cells into the blood. Summaries of the present state of our knowledge of leucocytosis and of leukaemia are given in the memoirs of Ribder and Mullee, cited below. References on Leucocytosis and Leukaemia. Askanazy: Acute leukaemia V. A. 137 1894 BiONDi : White corpuscles in leukaemia A. p. le scienze med. xiii 1889 BizzozEKO : V. A. 97, 99; Cent./, med. Wiss. 1868, 69, 79 Chabcot and Robin : Crystals Comptes rend. Soc. de biol. no. 49 v 1853 Ehrlich : Colorimetry of the blood Gesamm. Mittheil. i Berlin 1891 EiCHHORST : Acute leukaemia V. A. 130 1892 Felsenthal : Haematology A. f. Kinderheilh. xvi 1892 Fleischer and Penzoldt: D. A.f. klin. Med. xxvi Leukaemia 1880 Gabeitschewski : Eosinophile cells in bronchial asthma A. f. exp. Path. 28 1890 Geigel : Red corpuscles in pseudo-leukaemia D. A. f. klin. Med. xxxvii 1885 Goldscheidbr and Jacob : Variations in leucocytosis Z. f. klin. Med. 25 1894 (with references) Hayem ; Du sang Paris 1889 JoAS : Inflammatory leucocytosis Ziegler's Bekrage x 1891 Kanthack : Leucocytosis from bacterial products B. M. J. 1892 Labadie-Lagrave : Maladies du sang Paris 1893 VON Limbeck : Inflammatory leucocytosis Z. f. Heilk. x 1889 ; Leukaemia and leucocytosis Cent. f. allgem. Path, ii (p. 922) ; Klin. Pathol, d. Blutes Jena 1892 LowiT : Wien. Sitzungsher. 88 1883, 92 1885, 95 1887 ; Physiol, fc. Pathol, d. Blutes Jena 1892; Leukaemia Cent.f. allgem. Path, v 1894 Maurel : Recherches exper. sur les leucocytes Paris 1891 MosLEK : Ziemssen's Cyclop, viii New York 1878 MuiE : Leucocythaemia Journ. of Path. 1 1892 MiJLLER, H. Fr. : Leukaemia D. A. f klin. Med. xlviii 1891; Lymphaemia ibid. L 1892 and Ziemssen's Arheiten ill 1893 ; Morphology of leukaemic blood Cent. f. allgem. Path, v 1894 (with references) MtJLLER and Rieder: Eosinophile cells D. A.f. klin. Med. xlviii 1891; Ziemssen's Arbeiten in 1893 Neumann: Cent, f med. Wiss. 1868-69; Arch. f. Heilk. xi; Berl. klin. Woch. 1878; V.A. 116 1889 Reinbach: Leucocytes in malignant disease A.f. klin. Chir. xlvi 1893 RiCHTER and Spieo : Leucocytosis from cinnamic acid A. f. exp. Path. 34 1894 Rieder : Leukocytose Leipzig 1892 (with references) ; Atlas d. Blutes Leip- zig 1893 Robert: Leucocythaemia Jourra. of Path. 1892 Schmidt: Formation of corpuscles in liver and spleen Zieglefs Beitrage xi 1892 ScHULz : Leucocytosis D. A.f. klin. Med. li and Ziemssen's Arbeiten in 1893 TcHiSTOViTCH : Fibrinous pneumonia Annal. de I'Inst. Pasteur v 1891 Troje : Leukaemia and pseudo-leukaemia Fortschr. d. Med. x Vehsemeyer : Leukaemia Miinch. med, Woch. 1893 12 THE BLOOD. [CHAP. I, AKT. 2 ViRCHOw: Cellular pathology (Berlin 1859) London 1860, Gesamm. Abhandl. 1862 VoGEL : Disorders of the composition of the blood Virchow's Handb. d. spec. Path. 1 Erlangen 1854 Waldeyer: Hyperplasia of bone-marrow V. A. 52 1871 Wertheim : Blood-formation in leukaemia Z. f. Heilk. xii 1891 Westphal: Charcot's crystals in lymph D. A.f. klin. Med. xlvii 1891 Zappert : Eosinophile cells in the blood Z. f. klin. Med. 23 1893 Zenker : Charcot's crystals D. A.f. klin. Med. xviii 1876 CHAP. II, ART. 3] THE LYMPH 13 CHAPTER II THE LYMPH 3. The lymph is a liquid transuded from the blood-vessels, together with certain products of tissue-metabolism, and in special parts also (e.g. the lacteals) substances brought to the lymph from t '\ K \ ^. h Fig. 1. Sbction through a degenerating patch from the brain. (Perosmic acid preparation : X 200) a blood-vessel filled with blood b tunica media c adventitia with its lymph-sheath d unaltered neuroglia-cells e fatty neuroglia-cells / binuclear neuroglia-cells g sclerotic tissue h lymphoid cells hi lymphoid cells containing a few oil- globules. Ji2 fat-granule carriers hs pigmen1>granule cells, some contain- ing red corpuscles without. The lymph-glands contribute a number of lymphoid elements in addition to the few cells derived from the blood. 14 THE LYMPH [CHAP. II, AET. 3 Morbid conditions of the blood, as well as diseases of the tissues, accordingly give rise in general to changes in the lymph ; and sub- stances taken up into the tissues from without very frequently reach the lymphatic channels. Many of the changes in question are not physically demonstra- ble, being due to substances that are dissolved in the lymph. As regards the morphological elements of the pathologically altered lymph, the changes in them relate to the number and nature of the cells it contains, and to the addition of products of the disintegration of the tissues, or of foreign matters derived from without. As illustrative of such changes in the normal contents of the lymph, we may refer to Fig. 1, representing the degenera- tive process resulting from a haemorrhage in the brain. Here the circumvascular lymph-vessels (Fig. 1 c) contain, along with the unchanged lymphoid elements, certain cells which are loaded partly with colourless (Aj Ag) detritus of the brain-substance, partly with disintegrated blood-corpuscles (A3). In a lymphatic vessel pro- ceeding from an inflamed tissue the number of cellular elements in the lymph is very markedly increased. Often mixed with the lymph are found cast-off endothelial cells, some subdividing, others degenerate. Not infrequently local coagulation of the lymphatic contents, with the formation of fibrin, is observed. If a new growth has broken into a lymphatic vessel, we may find the tumour-cells in the lymph. Where bacteria have invaded the tissues, colonies of microbes may develope in the lymph-channels. SECTION II THE VASCULAR MECHANISM CHAP, ni, ART. 4] MALFORMATIONS 17 CHAPTER III MALFORMATIONS OF THE HEART AND GREAT VESSELS 4. Malformations of the heart are of frequent occurrence, and have great practical importance, inasmuch as they often on the one hand cause non- viability of the foetus, and on the other, where life after birth is possible, induce conditions of more or less imperfect circulation, and a disposition to other and more extensive lesions. Not infrequently also, in circumstances involv- ing great demands upon the activity of the malformed heart, they lead ultimately to a fatal issue. In most cases we have to deal with primary arrest of develop- ment and with disturbances of growth, resulting in an imperfect development of some part of the heart or in abnormality of its position and configuration. Only in rare instances do morbid processes in utero, such as inflammations, inhibit or disturb the normal development of the heart. In the majority of cases the primary failure lies in the absence or defective development of the septa which divide the simple cavity of the embryonic heart into a right and a left ventricle, and into a right and a left auricle, and the truncus arteriosus into the aorta and pulmonary artery. In addition to these defects we meet with malformations of the valves, stenosis and closure of the auriculo-ventricular, the arterial, and the venous orifices ; and lastly malposition and faulty development of the large arterial trunks and their branches, and of the veins entering the auricles. Stenosis of the pulmonary artery (Fig. 2 d dj), a somewhat frequent malformation, may involve the arterial trunk as well as the conus arteriosus and the ostium, the valves being at the same time more or less malformed. Sometimes there is complete clos- ure or atresia of the pulmonary orifice. These malformations occur in association both with closed and complete ventricular septa and with defects (e) in the ventricular or auricular septum, the former combination being however infrequent. Very often these malformations are combined with anomalies in the position of the large arterial trunks, both of these vessels arising from the right ventricle, or the aorta from the right ventricle (a e) and the pulmonary artery from the left ventricle (d d^), a condition which might be termed transposition of the arterial trunks. If 18 MALFORMATIONS OF THE HEART [chap. Ill the diameter of the puhnonary orifice measure less than a, certain amount, the pulmonary circulation can be adequately maintained only when the ductus arteriosus remains patent. Fig. 2. Malformation of the heart. {With transposition of the large blood-vessels, stenosis of the pulmonary orifice, and defect of the anterior part of the ventricular septum : from Rokitansky) a right ventricle opened near its margin i stenosed riglit ostium venosum c aorta arising from tlie right ventricle d orifice of the pulmonary artery rfj lying posteriorly e defeotoltheanteriorventricular septum / anterior portion of the septum extend- ing to the aorta on the left, between the anterior and left segment of the valve g membranous portion of the light side of the pulmonary artery Stenosis and atresia of the aorta occur, like the analogous conditions of the pulmonary artery, both with and without defect of the interventricular septum. These malformations are some- AKT. 4] DEFECTS OF THE SEPTA 19 times accompanied by transposition of the aorta, or may be com- bined with other forms of cardiac malformation. When the aortic orifice is markedly constricted or entirely closed, the ventricular septum being properly developed, the foramen ovale and the ductus arteriosus usually remain open, so that the circulation is carried on chiefly by the action of the right heart, and the blood of both the systemic and the pulmonary circulations is driven through the pulmonary artery. The left ventricle and left auricle are in these cases generally small and imperfectly developed. Stenosis of the aorta between the opening of the ductus arte- riosus and the origin of the left subclavian (^isthmus aortae), a slight form of which is not infrequent, may in exceptional cases be very marked ; and instances are described in which the aorta is entirely closed, or even wholly wanting. The collateral circu- lation is then established by means of anastomoses between the branches of the subclavian and the descending thoracic and abdom- inal aorta. Stenosis and atresia of the venous orifices occur in the right as well as in the left auricle. Misplacement (or transposition) of the large blood-vessels occurs along with other malformations of the orifices, of the ves- sels, and of the septa, as well as in the absence of such malfor- mations. In these cases the vessels sometimes maintain their connexion with their proper ventricles ; at other times an inter- change takes place. Defects of the ventricular septum may involve the entire partition (^cor hiloculare hiatriatum), in which case only one ven- tricle is present. They are more frequently, however, limited to the anterior or posterior region of the septum, or even to a por- tion of one of these. The defect may be combined with a like defect of the auricular septum (^cor hiloctilare), or with malforma- tions of the arterial trunks and orifices, as well as of the venous orifices. Persistence of the truncus arteriosus may be associ- ated with defects of the anterior septum ; the latter however occurs much more frequently in association with stenosis of the pulmonary artery. In partial defects of the septum the aorta is generally displaced to the right. Defects of the auricular septum, more or less extensive, are met with either by themselves, or in conjunction with other malformations. Most frequently the foramen ovale remains open; less often a defect is found beneath the membranous margin of the foramen. Total absence of the septum constitutes the cor hiloculare hiventriculare. Malformations of the valvular segments may occur in the auriculo- ventricular valves, which are sometimes abnormally short, or adherent to each other ; abnormal constriction and occlusion of the orifices are also met with. In the latter condition the circula- 20 MALFORMATIONS OF THE HEART [CHAP. Ill tion can take place only when an opening persists in the auricular septum. The number of the segments of the semilunar or sigmoid valves may be excessive or defective at either of the arterial orifices. Persistence of the ductus arteriosus is brought about chiefly as a result of other defects in development, such as stenosis of the pulmonary artery, of the aorta, or of one of the venous orifices. It also occurs apart from any other form of cardiac malformation. From their complexity, it is not always easy to gain a clear conception of the genesis of these malformations. More exact knowledge of the history of the development of the heart, which we owe to His and Born, has materially aided our understanding of their origin, in regard both to defects of the septa and to malformations of the arterial and venous orifices. The human heart is originally formed out of a straight tube, which later on becomes curved and S-shaped (Hbrtwig). From the anterior extremity of this arise the two primitive aortic arches, while its posterior extremity receives the two vitelline veins (venae omphalo-mesentericae). When the tube (Fig. 3) has reached a certain size and position in the embryo, the several parts become differentiated, the widening venous portiou and the arterial portion being separated by a narrower tube, the auricular canal (ac) ; the cavities are thenceforward recognisable as auricle (a) and ventricle (v). At the same time the auricles develope lateral pouches (aa), which become the appendices auricularum. Fig. 3. Heart of a human embryo 43 millimetres long. (From His) V ventricle ac auricular canal a auricle with appendix auriculae aa ta truncus arteriosus Fig. 4. Heart or a human embryo at the fifth week. (From His) rv right ventricle ta truncus arteriosus Iv left ventricle laa left appendix auriculae SI sulcus mterventricularis raa right appendix auriculae In the region of the auricular canal where the auriculo-ventricular valves are subsequently fornied, the endothelial tube narrows and is markedly flattened in the sagittal direction, so that its opposite walls come nearly into contact The rudimentary ventricle (Fig. 3 v) forms a bent tube which narrows ART. 4] DEVELOPMENT OF THE HEART 21 toward the aortic bulb (to). This is soon grooved externally by a straight furrow, the sulcus interventricularis (Fig. 4 si), running from above down- wards, by which the ventricle is divided externally into a right and a left half, of which the former is continued into the truncus arteriosus. The formation of septa within the heart follows in the portion of the ventricle corresponding to the externally visible interventricular sulcus (Fig. 4 si). On the inferior and posterior wall a ridge arises (Fig. 5 vs), which is the rudiment of the septum ventriculorum, and grows from below upwards. Very soon on the posterior wall of the auricle, to the left of the venous orifice (Fig. 5 sr), a process of con- nective tissue (si) appears in the region of the auricular canal, whose walls at this stage assume the form of au annular projecting fold directed downward (the rudimentary valvular segments), and this process divides the auriculo-ventricular orifice into a right and a left half. His terms this portion of the septum the septum intermedium. Fig. 5. rv si la ra Posterior half of the heart of a human embryo at the fifth week. {_From His) left ventricle right ventricle septum intermedium left auricle right auricle ventricular septum mouth of the sinus reuniens {sinus ve- nosus of Born) auricular septum (auricular crescent of His, septum primum of Born) septum spurium * Eustachian valve In the seventh week this septum unites with the septum of the ventricles, and forms thus the middle segment of the auriculo-ventricular valves. The other segments of the mitral and tricuspid valves are formed from the wall of the ventricular cavity. The differentiation of the truncus arteriosus into an aorta and a pulmonary artery follows directly upon the formation of the ventricular septum. It begins with a flattening of the tube, and this is followed by the appearance of two longitudinal ridges on the flattened sides, which grow toward each other and then unite. Later on, the aorta and pulmonary artery become externally distinct. The process of division in the truncus arteriosus begins above, and extends downward till it reaches the ventricular cavity. The partition then unites with the ventricular septum by a secondary process of cohesion. The inferior portion of the truncus forms the membranous portion of the ventricular septum. The development of the semilunar valves begins before the division of the truncus. Four prominences of a gelatinous texture are formed ; and of these two are bisected in the process of division of the arterial channels, so that presently three prominences appear in each trunk. 22 MALFORMATIONS OP THE HBAET [CHAP. UI The auricular septum begins to develope on the superior wall of the auricle, from which point it grows (Fig. 5 as) downward, until, in the region of the auricular canal, it reaches the septum intermedium (si) and coheres with it; thus the auricle as well as the auricular canal is divided into halves. Here, however, the division again becomes incomplete, for an opening appears in the septum, the foramen ovale, which closes only after birth. The truncus arteriosus at a certain stage of embryonic development gives origin to five pairs of primitive aortic arches, from whose confluence the aorta dorsalis arises (Fig. 6). Upon the division of the heart into its several dif- ferentiated portions, transformations occur in the arterial arches, whereby the division of the circulation into the major and minor systems is effected. The plan of the embryonic vascular system, originally symmetrical, now becomes asymmetrical. The manner in which this is effected is shown in the two dia- grammatic schemes of Figs. 6 and 7. The essential points in the process of transformation are the division of the truncus into aorta and pulmonary artery, the obliteration of some of the primitive aortic arches, and the further develop- ment of the remainder. In Fig. 7 the parts which persist are black or shaded, while those ultimately obliterated are left white. The connecting link between the pulmonary artery and the aorta, the ductus arteriosus, is obliterated last, since it closes only after birth. Fig. 6. Diagrammatic scheme of the aortic akches of the embryo op an AMNIOTIC vertebrate. {From Hertwig) first to fifth aortic arches v vertebral artery aorta dorsalis s subclavian internal carotid p pulmonary artery external carotid j j 1-5 ad d ce Fig. 7. Diagrammatic scheme op the transformations of the aortic arches in a mammal. . ^ , (From Rathke) internal carotid external carotid common carotid the descending aorta fourth arch on the left side left vertebral artery k right vertebral artery h left subclavian i I right subclavian m pulmonary artery n ductus arteriosus The venous trunks, with the exception of the ascending vena cava, are origi- nally paired and symmetrical, and unite in the sinus reuniens (Fig. 5 sr) ; this later on disappears as an independent structure, and is absorbed into the auri- cles. Through the further development of some and the involution of other veins, the ultimately asymmetrical venous system is produced. A comparison of the malformations of the heart with the stages of its develop- ment shows that the malformations result essentially from defective or perverted AET. 4] REFEKENCES ON CAKDIAC ANOMALIES 23 development of the septum, the ventricle, the auricle, and the truncus arteriosus, and from failure of their normal coherences. This is true not only of defects in the septum, but also of anomalies of position and abnormal narrowness of the arteries. Union of the septum intermedium with the wall of the auricular canal leads to closure of the auriculo-ventricular orifice, or at least to an abnormal coherence of the valvular segments. Abnormal subdivision of the truncus arteriosus may also induce malformations of the valves ; and incomplete develop- ment of the rudiments of the valves may result in morbid alterations of their texture. Disorders of evolution in the aortic arches are apt to give rise to anomalies of the arterial trunks. References on the Development of the Heart. BoBN : Development of the mammalian heart A.f. mikrosk. Anat. xxxiii 1889 ; Anat. Anzeiger in (p. 606) 1888 Hertwig : Lehrb. d. Entwickelungsgeschichte Jena 1893 His : Anatomie menschl. Embryonen in Leipzig 1885 ; Beitr. z. Anal. d. menscM. Herzens Leipzig 1886 References on Malformations of the Heart. Arnold: Development of auricular septum V.A.51 1870; Congenital divertic- ulum of the heart V. A. 137 1894 Babes : Peculiar cases Jahrb. f. Kinderheilk. xiv 1879 VON Buhl : Cases Z. f. Biol, xvi 1880 Ghiari : Cor triloculare Jahrb. f. Kinderheilk. xiv, XV 1879-80 Dilg: Bare cardiac anomalies V. A. dl 1883 Dittrich: Variations in the aortic arch Prag. Z.f. Heilk. vii 1886 Eppinger : The diaphragmatico-retromediastinalis muscle and primary defects of the septum Cent. f. allg. Path, v (p. 859) Epstein : Cardiac defects Prag. Z. f. Heilk. vii 1886 FoRSTER : Die Missbildungen d. Menschen Jena 1865 GrELPKE : Selten. Fall von angeb. Herzfehler Basle 1883 Greenfield : Trans. Path. Soc. xxvii London 1876 KoLLMANN : Anomalies of vena cava inferior Anat. Anzeiger viii 1893 (with references) VON Krzywicki : The membranous interventricular septum Ziegler's Beitrage VI 1889 KussMAUL : Pulmonary stenosis Z. f. rationale Med. 1866 Leo : V. A. 103 1886 ; Pulmonary stenosis and atresia D. med. Woch. 1886 Mackenzie : Trans. Path. Soc. xxxi London 1880 Mann : Cor triloculare biatriatum Ziegler's Beitrage vi 1889 March AND : Ahlf eld's Berichte und Arbeiten 1881-82 Martinotti : Gazetta d. cliniche 1886, Anat. Anzeiger i 1886 Martinotti and Sperino : A. ital. de biol. vi 1885 Middendorp: Pulmonary atresia Internal. Monatsschr. f. Anal, in 1886 Orth: Defect in ventricular septum V. A. 82 1880 Pisenti: Rare tricuspid anomaly Lavori palol. di Perugia 1890 Pott : Foetal affections Jahrb. f. .Kinderheilk. xiii 1879 Preisz : Congenital defects of the heart Ziegler's Beitrage vii 1889 Rauchfuss : Gerhardt's Handb. d. Kinderkrankh. iv Reil : D. A.f. klin. Med. xvii RoKiTANSKY : Defecta d. Scheidewande d. Herzens Vienna 1875 RuGE : Defects of the auricular septum V. A. 126 1891 ScHMALZ : Pathogenesis of cardiac defects D. med. Woch. 1888 ToNNiES : Ueb. eine sell. Missbild. d. Herzens Gottingen 1886 Venturi : Rare cardiac lesions Eev. de med. xiii 1893 Wagner : Pulmonary atresia and tricuspid stenosis with complete ventricular septum Inaug. Diss. Giessen 1889 24 MALFOBMATIONS OF THE HEART [CHAP. HI References on Aortic Stenosis near the Ductus arteriosus. Barie : Congenital stenosis of descending aorta Rev. de med. vi 1886 Eppinger : Congenital aortic stenosis Prag. Vierleljahrsschr. 112 1871 Lebekt : Aortic stenosis near ductus arteriosus V. A. 4: 1852 LuTTiCH : Obliteration of aorta near ductus A . d. Heilk. xvii 1876 Martens : Two cases of aortic atresia V. A. 121 1890 Sommerbrodt: Obliteration of aorta near ductus V. A.91 1883 5. It is not rare for the heart to be abnormally small in pro- portion to the body-weight. This condition is described as car- diac hypoplasia. The heart is either abnormally small at birth, or fails to attain sufficient development later. Sometimes in adults the heart may be no bigger than it normally is in chil- dren of seven or eight years. Such extreme cases are rare, but minor degrees of hypoplasia are often met vi^ith. According to ViECHOW, cardiac hypoplasia is common in patients of both sexes suffering from chlorosis or haemophilia. In the majority of cases there is an accompanying hypoplasia of the arterial vascular sys- tem, the aorta and arterial trunks being narrow and thin-walled : the genital organs may also be ill-developed, and sometimes the entire body is undersized. The abnormal thinness and narrow- ness of the arteries are often associated with anomalies in their distribution ; while corrugated and lattice-lite irregularities of the surface, and fatty deposits, are observed in the inner coat of the aorta. In many cases rupture of such an aorta has been recorded. Congenital hypertrophy of the whole or a part of the heart is seen when, from alterations in the ostial orifices and vascular trunks, the forward propulsion of the blood is rendered difficult. Among the malpositions of the heart in the thorax we occasion- ally find the condition termed transpositio cordis, or deziocardia. Here the heart is situated on the right side, the malposition being part of a general situs viscerum inversus, and but rarely unac- companied by other anomalies. In cases of fissural malformation of the anterior thoracic and abdominal wall the heart is not uncom- monly displaced forwards (^ectopia cordis'). The pericardium in these cases may be present or absent. According to Thoma, the average weight of the heart in the new-born infant is 20-6 grammes; at the age of 17, 233-7 grammes; in full manhood, 303 grammes. In women this weight is about 40 grammes less. The length of the fully developed heart (Beneke) is on the average about 9-0 centimetres, the breadth 10-7 cm., the thickness 3-6 cm. The thickness of the right ventri- cular wall IS 2-0 to 3-0 millimetres ; that of the left ventricular wall, 7-0 to 8-0 mm. In cases of hypoplasia the volume of the heart may be reduced by a third or more. According to Beneke, the circumference of the ascending aorta in new- born infants, at its commencement, measures 20 mm. ; in the adult, 68 mm : the circumference of the pulmonary artery at birth and in the adult is 23 mm. and 65 mm. respectively. Above the bifurcation of the aorta into the common iliac arteries the circumference in adults is 32 mm. ART. 5] SIZE OF THE HEART 25 References on the Size of the Heart and Large Blood-vessels. Bamberger : Lehrb. d. KrankJi. d. Herzens Vienna 1857 Bbneke : Orundlagen d. Constitutionsanomalieen Marburg 1878 VON Buhl: Munch. pathol. Mittheil. Stuttgart 1878 Cammann : New York Med. Gaz. vi 1870-71 Thoma : Grosse u. Gewicht d. anat. Bestandtheile Leipzig 1882 ViERORDT : Anat. Daten u. Tabellen Jena 1893 ViRCHOW : Chlorose u. Anomal. am Gefassapparate Berlin 1872 26 MORBID ALTEKATIONS OF THE HEAET [CHAP. IV CHAPTER IV MOKBID ALTERATIONS OF THE HEART AS A WHOLE 6. Diminution in the size of the heart depends essentially upon atrophy of its muscular and adipose tissues, and occurs most frequently in persons whose general nutrition is defective, and whose blood is greatly reduced in amount. In senile marasmus and in cancerous cachexia the weight of the heart may sink below half the normal amount. The adipose layer of the atrophic heart is almost, or even entirely, absent, and is replaced by a gelatinous translucent material resembling mucous tissue. The vessels cours- ing over the surface of the heart are, as the result of the shrinking of the underlying tissue, more or less tortuous. The muscular layers, on account of the wasting of their muscle-cells, are thinned and frequently coloured brown, or yellowish-brown, by the formation of pigment and fat in their substance. The cardiac cavities are small, and the endocardium, condensed by the con- traction of the tissue that was formerly spread out over a larger surface, is less transparent than normal. Enlargement of the heart, when not due to the presence of a tumour, is caused either by dilatation of its cavities, by the hyper- plasia of its muscular structure, or by an increase of the sub- epicardial adipose tissue. Dilatation of the heart is often the result of morbid changes in its muscle, which make the walls yield more readUy to pressure (fatty degeneration). In other cases it is caused by some -resist- ance to the emptying of the heart-cavities (stenosis of the orifices, adhesions of the pericardium, diseases of the lungs, especially chronic emphysema and pleuritic adhesions), or by alterations of the valves, which, if the ventricles and auricles are relaxed, permit a regurgitation of blood from the arteries into the ven- tricles, and from the ventricles into the auricles (valvular insuf- ficiency). The dilatation, according to the cause upon which it is dependent, sometimes affects only one ventricle or auricle, some- times the entire heart, and may be so great that the circumfer- ence of the heart reaches twice the normal measurement or even more. Locally circumscribed changes in the walls (ischaemic softening of the heart-muscle, cardiac scleroses, Art. 11) cause local protrusions, which are termed aneurysms of the heart ■ (Fig. 28). ART. 6] FORMS OF HYPERTROPHY 27 Dilatation of the heart is at first accompanied by thinning of the walls of the distended portion ; but the distension may be combined with hypertrophy of the muscular structure. This occurs when the dilatation is produced by an increased resistance to the outflow of blood from the heart, or by regurgitation of blood into the heart during diastole. Hypertrophy of the cardiac muscle is the result of per- sistent increase of the work of the heart ; but this condition induces true hypertrophy only when the demands upon the heart do not exceed a certain limit and the muscle is well nourished. The causes of increased cardiac action are insufficiency and steno- FiG. 8. Hypeetrophy of the left ventbiole. (Produced btj insufficiency and stenosis of the aortic valves : transverse section : natu- ral size) a left ventricle b right Tentricle sis of the valves (Art. 9, Figs. 19 and 20), abnormal narrowness of the arterial trunks, destruction of renal tissue whereby the blood-pressure within the systemic circulation is increased, dis- eases of the lungs (emphysema, pleuritic adhesions) which in- crease the pressure in the minor circulation, adhesions of the pericardium to the heart and lungs, increase of the total amount of blood in the body, nervous excitement, and severe bodily exer- tion. Idiopathic hypertrophy of the heart, in other words, simple overgrowth of the heart-muscle from internal causes, has not been 28 MOEBIB ALTERATIONS OF THE HEABT [CHAP. IV shown to occur. The increase in size of the heart-muscle is there- fore always symptomatic ; it is dependent on increased work, from whatever cause arising. The hypertrophy accordingly appears first in that portion of the heart which is primarily exposed to the abnormal strain. In disease of the aortic valves and in cases of contracted kidney, this portion is the left ventricle (Fig. 8 a) ; in insufficiency and stenosis of the pulmonary valves, and in cases of increased resistance within the pulmonary circulation, it is the right ventricle. Hypertrophy of the heart-muscle causes in the first instance a thickening of the auricular or the ventricular wall (Fig. 8 a). The trabeculae and the papillary muscles share also in the hyper- trophy, and may undergo marked increase in their circumference. The weight of a hypertrophied heart may reach twice the normal amount, or even more ; hearts weighing 600 to 700 grammes and more are thus met with. The increase in the size of the heart-muscle is due to hyperplasia of the individual muscle-cells. It is difficult to determine whether any increase in the number of cells also occurs ; when the hyper- trophy takes place in the first years of life this is not improbable. In hypertrophied hearts the cavities are sometimes dilated, sometimes normal, and sometimes smaller than normal, present- ing the conditions known as eccentric, simple, and concentric hypertrophy, respectively. The dilatation of the heart, as a con- sequence of increased resistance to the circulation, may precede the hypertrophy, or takes place subsequently in an already hyper- trophied heart, owing to secondary degeneration of the muscles. Lipomatosis or fatty enlargement of the heart may be a local manifestation of a general deposit of fat over the entire body ; it is characterised by an increase in the yeUowish-white cardiac panniculus adiposus. More marked forms of lipomatosis or adi- posity tend to produce collections of fat in the intermuscular and sub-endocardial connective structures, so that the muscular sub- stance is as it were infiltrated with fatty tissue, and a layer of fat appears beneath the endocardium. Marked lipomatosis may im- pair the functional power of the cardiac muscle. References on Hypertrophy of the Heart. AuFRECHT : Path. Miitheil. no. 11 Magdeburg 1883 Bambekger : Volkmann's klin. Vortriige 173 Bauer and Bollinger: Idiopath. HerzvergrSsserung (from 'beer-drinking) Mu- BoLLiNGER : Idiopathic cardiac hypertrophy (from beer-drinking") Munch, path. Arbeiten 1886 &/ /' VON Buhl; Eccentric hypertrophy Munch. path. Arbeiten 1878 DU Castkl : A. gen. de me'd. 1880 Cohnhbim: AUgemeine Path, i ii Berlin 1882 Goldenberg: Atrophy and hypertrophy of cardiac muscle-fibres V. A. 103 1886 AKT. 6] EEFEEENCBS ON CAEDIAC HYPEETEOPHY 29 Grawitz and Israel : Renal disease and cardiac hypertrophy (experimental researches) V. A. 77 1879 Israel, O. : Renal disease and secondary vascular changes V. A. 86 1881 Letulle : Les hypertroph. cardiaques secondaires Paris 1879 Leyden : Cardiac disease and over-exertion Z. f. klin. Med. xi 1886 MiJLLER : Massenverhaltnisse d. menschl. Herzens Leipzig 1883 Riegel : Increased blood-pressure in nephritis Z. f. klin. Med. vii 1884 Roy and Adami : Overstrain of the heart B. M. J. 1888 Schmidt : The heart in thoracic aneurysm E. L. Wagner's Festschrift Leipzig 1887 Spatz : D. A. f. klin. Med. xxx 1882 Tangl : Hypertrophy and normal growth of the heart V. A. 116 1889 Thoma : Gevnclit d. Bestandth. d. menschl. KGrpers Leipzig 1882 Traube : Gesamm. Beitrdge m 1878 Zander : Bright's disease and cardiac hypertrophy Inaug. Diss. Konigsberg 1881 Zielonko ; Cardiac hypertrophy F. A. 62 1874. 30 MOKBID CHANGES IN THE ENDOCAEDIUM [CHAP. V CHAPTER V MORBID CHANGES IN THE ENDOCARDIUM 7. The endocardium is a delicate membrane lining the heart, composed of connective tissue, and containing few blood-vessels. The valvular segments are portions of the endocardium ; those guarding the aorta and pulmonary artery are devoid of vessels, while those at the mitral and tricuspid orifices are vascular. The chordae tendineae are provided with small vessels arising from the papillary muscles. The endocardium is frequently the seat of degenerative changes, which in most instances affect the parietal layer, and in other cases the valves. In the latter situation the degenera- tive change not rarely gives rise to disorder of the valvular functions. Fatty degeneration is the most frequent of these changes. This change is manifested by the formation of circumscribed Fig. 9. Section of fatty endocardium. {Fro7n the mitral valve of a child dead of scurvy : perosmic acid preparation, mounted ■in glycerine : X 350) Fig. 10. Mucoid degeneration op the connective tissue of the aortic valve. {Perosmic acid preparation, from a frozen section mounted in glycerine : x 350) a connective tissue 6 mucoid tissue patches of an opaque white colour, which are found most com- monly on the valves, and less frequently upon the parietal endo- cardium. The fatty changes take place first in the connective tissue, and later in the superficial endothelial cells, the protoplasm of which appears beset with oil-globules. In the graver degrees of degeneration the interstices of the connective tissue are entirely filled with od-globules of different sizes (Fig. 9). This condition usually occurs in aged persons whose vascular system elsewhere shows signs of similar change. But it may also occur in younger ART. 7] ATHEROMA AND THROMBOSIS 31 persons, and is found in association with the most varied diseases, such as chronic heart-disease, anaemia, marasmus, toxic and infec- tive conditions, and the like. Mucoid degeneration of the endocardial tissue occurs chiefly in old age, but it also accompanies morbid thickening of the valves, and is almost entirely confined to them. It generally occurs in patches, leading to the formation of circumscribed thickenings and prominences upon the free margins of the valves. These patches present a gelatinous appearance, and are composed of mucoid tissue containing cells (Fig. 10 5), or of non-cellular mucous substance. In the former case the texture of the patch resembles that of the gelatinous tissue of the valves of the foetal heart. The mucoid degeneration is often combined with fatty changes; thus one portion of the valvular tissue may appear fatty and another gelatinous, or the cells of the tissue are fatty while the ground-substance becomes mucoid. Sclerosis of the connective tissue of the endocardium is seen chiefly on the free margins of the valves, the condition being so frequently met with in old age that it may almost be regarded as a physiological change. This condition leads to the formation of flattened and diffuse thickenings of the valve, or to nodular prominences, within which the tissue is dense and either obscurely fibrillar or quite homogeneous, and contains few or no cellular elements. Sclerosis of the valvular tissue is frequently combined with fatty, mucoid, and calcareous change, and necrotic disintegration of the degenerated tissue may ultimately take place, leading to the formation of patches of softening. Ulcers arise when such softened and degenerated areas break down, and in the neighbour- hood of these ulcers reparative processes are usually set up, leading to infiltration of the tissue with leucocytes. This com- bination of morbid changes is described as atheromatous de- generation ; it is a frequent cause of valvular insufficiency in the aged. Hard calcareous masses are sometimes formed by the deposit of calcium salts in the neighbourhood of the atheromatous patches, and in many cases these masses seriously obstruct the movements of the valves. When from any cause the natural texture of the surface layer of the heart is altered, or when it becomes rough or irregular, finely-granular thrombi are apt to form on the affected spots. These take the form of circumscribed yellowish or reddish deposits, which are often (but not quite correctly) described (Art. 8) as endocarditic vegetations (Fig. 11 b). The deposits form as a rule when the circulation is irregular or weak, and appear as small yellowish or reddish-yellow nodes, or as rough warty masses. They are generally found on the valves, both about the ostial attachment and on the free surface. If these thrombi are not washed off by the blood-current, proliferation 32 MOEBID CHANGES IN THE ENDOCARDIUM [CHAP. V takes places in the underlying endocardium (Fig. 11 c) ; this penetrates the thrombus and gives rise to a more or less complete substitution of cellular connective tissue for its substance. Many gradually increasing thickenings of the valves are no doubt the result of repeated thromboses of this kind. Larger thrombi may undergo more or less complete calcareous infiltration, and cases occur in which the valvular sinuses of the aorta are beset with a number of calcified thrombi in the form of irregular serrated ex- crescences, firmly adherent to the surface of the valves. Slight amyloid degeneration of the connective tissue of the heart-wall is not infrequently observed ; it occurs under the same conditions as amyloid degenerations of other organs. Degenera- tion so marked as to be recognisable without the aid of the iodine or methyl-violet reaction is rare, though cases have been recorded (Heschl, Zibglbk, Wild) ii^i which hyaline patches and streaks, as well as circumscribed hyaline nodules, had formed in the con- nective tissue of the endocardium and in that of the myocardium and epicardium. / ^ -^ ^ /' Fig. 11. Proliferous growth of the endocardium with a thrombus. (From the slightly-thickened and vascular aortic valve of a male patient, aged 49 : prepay ration hardened in MUller's fluid, stained with alum-carmine and eosin, and mounted in Canada balsam : x 60) a hyperplastic connective tissue of 6 granular thrombi valve, wifh blood-vessels c fibro-cellular excrescences In rare cases, a combination of amyloid change with a peculiar hyaline degeneration of the connective tissue is observed. The tissue thickens and becomes completely hyaline, and then breaks up into translucent fragments, some portions yielding the characteristic iodine or methyl-violet reaction, while other portions do not. By continuous extension of the degeneration through the intermuscular connective tissue, during which the muscle-cells in the affected area disappear, a large portion of the muscular substance of the heart may be destroyed. The heart-wall is thus converted into a rigid semi-trans- lucent mass, resembling the fat or rind of boiled bacon, and the endocardium may at the same time be thickly studded with hyaline granules. References on Degeneration of the JEndocardium and on the Structure of the Valves. CoEN : Vessels of the valves A.f. mikrosk Anat. xxvn 1886 Darier : Vessels of the valves A . de physiol. ii 1888 Heschl: Amyloid heart-muscle Wien. med. TFocA. 1870 AIIT. 8] IKFECTIVE ENDOCAIMJITIS 33 HoNEGGER : Changes in the intima of the heart and arterial trunks Inauq. Diss. ^liricn 1882 Kybek: Amyloide Degeneration Dorpat 1871, and V. A.%1 1880 Soyka: Amyloid heart-musole Prag. med. Woch. 1876 ViRCHOW: Gesamm. Abhandl. Frankfort 1856 Wild: Amyloid and hyaline degeneration Ziegler's Beilrage i Jena 1885 Ziegler: Endooarditic vegetations Verh. Congr.f. inn. Med. Wiesbaden 1888 8. By endocarditis is meant an inflammatory disease of the endocardium, due to the influence of an ir-pitant which has gained access to the blood. The valves are the" structures most fre- quently affected, although the condition may be limited to other portions of the endocardium. Endocarditis is frequently a secondary affection, dependent upon inflammatory disorders in other organs, such as suppurating wounds, purulent peritonitis, and pneumonia. Not infrequently however the endocarditis forms the first local manifestation of an infection, the exciting agent of which has left no recognisable traces at the seat of its entrance into the body. Embolic occlusion of certain vessels, and metastatic inflammations in other organs, in particular the kidneys, spleen, brain, and skin, ar&^n,ot infrequently associated with endocarditis. According to tligj^searphes of Weichselbaum, Wyssoko- Vi^iTscH, Fkankbl,^anger, '*#ffe^Mk KlVes^-^irsootbeg, Stern, Netter, and others, the causatidlf : ©f endocOTdttik is not always the same. Various micro-organisms may act as the exciting cause, and among them we find certain that are known to be asso- ciated with other organic diseases, such as traumatic infections, osteomyelitis, and pneumonia, while some have not yet been correlated with any other infective disorder. Of the former the most important are the Staphylococcus pyogenes aureus, the Strep- tococcus pyogenes, and tlie Diplococcus pneumoniae ; while the Staphylococcus pyogenes albus, and the Bacillus pyogenes foetidus (Passet), seem to play only a subordinate part. Leyden and others consider that endocarditis may be caused by the Gono- coccus. The organisms found in connexion with endocarditis, but not as yet associated with other organic diseases, include both micrococci and bacilli. Thus Weichselbaum has described, as met with in some cases of endocarditis, Micrococcus endocarditidis rugatus, Micrococcus endocarditidis capsulatus, Bacillus endocar- ditidis griseus, Bacillus endocarditidis capsulatus, and a bacillus which he failed to cultivate; and Frankel and Sanger have met with a non-motile foetid bacillus. According to these authors, the experiments they have car- ried out render it very probable that all of these bacteria are pathogenic in their nature, and that the first-named organisms are certainly so. The aetiological significance of the others is not as yet established, and it may well be that their occurrence in cases of endocarditis is either a post-mortem phenomenon, or is 34 MORBID CHANGES IN THE ENDOCARDIUM [CHAP. V due to secondary settlements of the microbes in the diseased tissues during life. Thus, for example, the presence of tuber- cle-bacilli in the endocarditic deposits of tuberculous patients (CORNIL, KuNDRAT, Heller, Birch-Hirschfeld) is very proba- bly due to a secondary invasion, though it should be noted in this connexion that tubercles are occasionally found on the valves, and that these may be overlaid with thrombi. Not infrequently the areas affected with endocarditis contain at the same time two, or even three, different forms of bacteria. The action of the bacilli at their place of settlement leads in all cases to a more or less marked degeneration of the affected tissue. If the bacteria (Fig. 12 b) extend from the surface, deep zL--—- V '•'•:^X''T?>'WIm( ;i«),'^i' Ir'^oi- -i ^■;^:■■■••■.•.■.•■■'.•'^ ', ' " — r- - '' a- i * Fig. 12. Mycotic endocarditis of an aortic valve. (Staphylococcus pyogenes aureus : preparation hardened in alcohol, embedded in cel- loidln, stained with gentian-violet and vesuvin, and mounted in Canada balsam : x40) n normal valve tissue d granular lamellar thrombi 6 colonies of micrococci e fibrillar fibrin, with leucocytes c necrotic tissue containing no nuclei / red blood-corpuscles into the tissue, the result is in many cases a somewhat widely extended necrosis, so that the tissue beset with bacteria appears to have lost its nuclei (Fig. 12 c). In consequence of the changes which the chemico-physical constitution of the tissue undergoes through the growth and spread of the bacteria, thrombi very soon form on the surface of the affected areas. The thrombi mostly take the form of finely-granular flakes or films which con- tain no cellular elements. At times leucocytes and red blood- corpuscles may be found attached to the flakes (Fig. 12 f), and fibrillar fibrin is simultaneously deposited on them (e). The thrombi are thus composed of different elements, and belong to the 'mixed' variety. ART. 8] l^ORMS OF ENDOCAHDITIS 35 On the semilunar valves of the aorta and pulmonary artery, which are free from blood-vessels, inflammatory exudations appear, but only at a later stage (Fig. 12). If, however, the bacterial colonies are situated on the vascular portions of the mitral and tricuspid valves, an inflammatory exudation quickly follows, and is accompanied bj^ more or less extensive cellular infiltration of the affected valve-tissue (Fig. 13 e/). Fig. 13. Mycotic endocarditis (pustulosa) of the tricuspid valve. {Folloviing an infected wound of the left foot, accompanied by haemorrhagic septic pneumonia: preparation hardened in alcohol, and, treated with gentian-violet, iodine, and vesuvin : X 60) a tissue of the posterior segment of the valve 6 chorda tendinea c pustular elevation on the valve d Staphylococcus pyogenes aureus e pus-cells and staphylococci / pus-cells unaccompanied hy micro- cocci g small abscess The first change visible to the naked eye consists of a barely- perceptible cloudi- ness of the affected part. The course and issue of endocardi- tis is chiefly de- pendent upon the extent of the de- generation and ne- crosis to which the bacteria give rise ; but the intensity of the inflamma- tory process which has thus been started, as well as the magnitude and character of the re- sulting thrombosis, Pig. 14. Wabtt endocakditis (verrucosa) aortic valve. must also be taken into consideration. 36 MORBID CHANGES IN THE ENDOCARDIUM [CHAP. V When the extent of the degeneration and necrosis is small, and the affected area remains covered with thrombi projecting above the surface in the form of small wart-like yellowish or reddish masses, single, or in groups or rows, we have the variety known as warty endoqarditis (ver- rucosa') (Fig.>.14). When the deposits aire extensive, „ ,K ,r ^ ^„=-A 'a]i#pOlypofti'oT shaggy in Fig. 15. Villous endocarditis (polypos^. .^ ■ r j f j^i.- (Mitral valve, with recent enducardittc thrombi, appearance, the Condition seen from the auricle ; natural size) is called polypOllS Or Vil- a auricular wall joug endocarditis (Fig. posterior segment of the valve _,_ ,..,. -.rri^ -irn e thrombus 15 c and t ig. 17 6). When e auriculo-ventricular opening ^j^g nCCrOSis is mOrC CX- FiG. 16. Ulcerative endocarditis or the aorta, showing ulcers, valvulab perforations, and valvular thrombi. a aorta 6 pulmonary artery c valvular segment covered with thrombi d perforated segment covered with thrombi (Natural size) e ulcers on the ventricular septum f ulcers on the ventricular surface of the larger mitral segment ART. 8] KESULTS OF ENDOCARDITIS 37 tensive and the necrotic tissue and the thrombi formed on it have been separated, so that ulcerous excavations are visible, we have an ulcerous or diphtheritic endocarditis. Sometimes the in- fected thrombi are cast off, and passing into the circulation lodge elsewhere in the tissues as foci of suppuration -. the process may then be described as pyaemic or suppurative endocarditis (pws- tulosa) (Fig. 13). Ulceration may be combined with the formation of warty thrombi in the most various ways. On the margins of an endo- carditic ulcer (Fig. 16 c d and Fig. 17 &), new thrombi are apt to form, but they are usually larger and looser than in endocar- ditis verrucosa, and often possess rather a villous than a warty appearance. As already stated, endocarditis most frequently affects the val- vular apparatus, more rarely the parietal endocardium of the left heart, still more rarely the endocardium of the right heart ; it is most frequently observed in the latter situation when the endo- carditis is due to traumatic infection. In the course of left-sided valvular endocarditis, warty deposits may also be formed on the valves of the right side of the heart. Fig. 17. Mycotic endocarditis (villosa), with valvtilar thrombi, and acutb valvular aneurysm. a aorta (Natural size) b valvular thromljus c aneurysm Warty endocarditis affects chiefly the free margins of tlie val- vular segments ; the ulcerative forms are less frequently confaned to this situation. The ulceration attacks different portions of the valves, and very frequently spreads to the chordae tendmeae, and to the walls of the aorta and of the heart. When the tissue ot a valvular segment is gradually destroyed on one side, the diseased area sometimes yields under the pressure of the blood, and thus may 38 MORBID CHANGES IN THE ENDOCARDIUM [CHAP. V be formed an acute valvular aneurysm (Fig. 17 c). Later on the segment may be broken through (Fig. 16 c d), and valvular perforations and ruptures are then produced. Not infrequently the diseased chordae tendineae are broken. The bacterial inva- sion may penetrate deeply into the heart-muscle and into the wall of the aorta, and lead to myocarditis and arteritis, vi^ith more or less extensive ulceration. The ulceration often causes much loss of substance, leading to aneurysmal bulging of the wall, and under certain conditions to rupture. If at any time the thrombi or shreds of disintegrated tissue become detached from the aifected areas, they are carried away as emboli by the circulating blood, and are arrested in various organs, notably in the brain, spleen, and kidney. Endocarditis is often associated with myocarditis; the latter being caused by direct or indirect infection from the blood (Art. 12). The warty thombotic deposits are often referred to as endooarditio vege- tations or efflorescences, though this term, at least in so far as it is applied to the early stages of the process, is not strictly accurate ; for at first there is no true outgrowth from the endocardium (Art. 9). The term represents an opin- ion formerly held and stiU maintained by some, that the warty elevations begin as inflammatory swellings of the endocardium, that they consist chiefly of the swollen endocardial tissue, and that the thrombi which cover them are secondary deposits. As micro-organisms are found only in some of the so-called endooarditio vegetations, it is still a subject of discussion whether aU cases of endocarditis are of bacterial origin. If we regard every thrombotic deposit and the associ- ated proliferation of the underlying tissue (Arts. 7 and 9) as manifestations of endocarditis, the question must be answered in the negative, for some of the thrombi described as vegetations are not primarily due to the presence of bac- teria, but are found in association with other changes of the endocardium. In the present state of knowledge, it is better to reckon as cases of primary acute endocarditis those afEections of the endocardium only which are referable to bacterial invasion. Valvular perforations due to inflammation are not to be confounded with fenestration of the valves. This latter condition is found not infrequently as a congenital malformation, or as a consequence of loss of tissue in the neigh- bourhood of the free margins of the semilunar valves. To distinguish between the two conditions the difference in situation should be noted. Moreover signs of inflammatory infiltration, or of fibrous thickening, appear around the open- mgs m the case of valvular perforations, but are absent in cases of fenestration. 9. When the lesion caused by the presence of the bacteria has reached a certain stage, along with inflammatory infiltration certain reparative processes are set up in the adjacent tissue. These are chiefly indicated by the formation of germinal tissue (Fig. 18 d), and afterwards of connective tissue. In the rela- tively benign warty forms of endocarditis, the degenerative pro- cesses extend over a small area only, and it seems that the bacteria do not in this instance penetrate deeply. Very soon, beneath the nodular or loosely fimbriated thrombotic deposit, the infiltrated and growing endocardial connective tissue (Fig. 18 a 6) rises above the surface, and by continued proliferation extends (A) into the ART. 9] ENDOCAEDITIC VEGETATIONS 39 substance of the thrombus (e e). Cases are occasionally met with in which the fibrin of the thrombus has thus to a large extent given place to connective tissue growing from below, or is traversed from base to surface by strings of cells and fibrous strands. In this way the original thrombotic deposit is displaced by an inflammatory granulomatous growth, and this is fittingly described as an endo- carditic vegetation. In ulcerative endocarditis, in which the bacteria extend deeply into the tissue and cause necrosis, the reparative process begins only after loss of substance has taken place, and then starts in the walls and floor of the ulcer. In other respects, however, the Fig. 18. Section through an hndocaeditic vegetation. {From the auricle : preparation hardened in alcohol, stained with haematoxylin : X 150) / colourless deuucleated protoplasmic a b endocardial and subendocardial connec- tive tissue, infiltrated with leucocytes c the vegetation d inflammatory growth rising ahove the endocardial surface e granular coagula colourless masses g finely-granular masses ( ? micrococci) h zone of transition between the inflam- matory growth and the fibrinous thrombus process follows the same course as that just described, the only points of difference being that the thrombotic deposits are larger, the inflammatory infiltration more diffuse and more marked, and the proliferation more abundant, than in warty endocarditis. Small thrombotic deposits, provided they are not broken off and carried away by the blood-stream,, are as a rule entirely replaced by connective tissue. Of the larger valvular thrombi (Fig. 15 e), such as occur chiefly in ulcerative endocarditis, a con- siderable portion often remains. This becomes shrunken and cal-, cified, and the affected valve is thereafter covered with an adherent hard calcified and chalk-like deposit (Fig. 19 c, Fig. 20 6). 40 MORBID CHANGES IN THE ENDOOAEDIUM [CHAP. V These ulcerative processes, as well as the thrombotic deposits and new connective-tissue growths (provided they remain attached to the valve and attain an appreciable size), lead to deformities of the valvular segments which interfere with their function, and so give rise to the conditions known as stenosis (Fig. 21 e and Fig. 20) and insufficiency or incompetence (Fig. 19 e. Fig. 20, and Fig. 21 c e). Stenosis of a valvular orifice is due mainly to thickening and rigidity of the valves, from adherent and calcified thrombi (Fig. 19 e and Fig. 20 J), or to coherence of adjacent valvular seg- ments (Fig. 21 d). The thickened chordae tendineae (/) often become adherent to the free margins of the mitral and tricuspid Fig. 19. Postekior segment of the mitral valve, vtith thickened and calci- fied THROMBI, AND STENOSIS OF THE AURICULO-VENTRICULAR OPENING. {Seen from the auricle : natural size) a auricular wall c thrombus, partly calcified, partly organised e auriculo-ventricular opening 6 thickened posterior segment Fig. 20. Thickened and distorted aortic valves. (Seen from above, showing thickened segments, with extensive partly organised and partly calcified thrombi : aortic stenosis : natural size) a transverse section of the aorta above the valves b calcified thrombi in the sinuses of Valsalva valves, as well as to each other; so that finally the valvular apparatus is reduced to a rigid funnel, compressed from before backward, and with only a narrow slit-like opening (Fig. 21 e). From the mutual coherence of the segments guarding the aorta or pulmonary artery, and the presence thereon of calcified thrombi, the orifice of the vessel becomes a mere inextensible slit, which may be so narrow that a goose-quill can hardly be pushed through it. ABT. 9] VALVULAR ENDOCARDITIS 41 Insufficiency arises chiefly from the shortening and deformity of the valves (Fig. 21 c), and from the gradually increasing rigid- ity of their tissue, which prevents the close apposition of the segments. Ulcerative destruction and rupture of the valvular curtains and chordae tendineae may of course give rise in acute fashion to insufficiency of the valve. If the seat of the endocarditis be the parietal lining of the Fig. 21. Aortic insufficiency and mitral stenosis. {Natural size) a aorta 6 pulmonary artery c shortened and shrunken valves with thickened walls d mitral valve e stenosed opening of the mitral valve / thickened, shortened, and coherent chordae tendineae g papillary muscle heart, it leaves upon the affected area lustrous white indurated thickenings, which usually lie on the surface, but in certain c,ases radiate into the neighbouring muscular tissue. Diffuse or circum- scribed thickenings maj'^ form upon the chordae tendineae. In rare cases, the newly-formed connective tissue may undergo cicatricial contraction, which leads to stenosis of the heart, or 42 MORBID CHANGES OP THE ENDOCAEDITTM [CHAP. V rather of the conus arteriosus of a ventricle. This condition is apt to occur after foetal endocarditis, and affects most frequently the right heart ; but it may supervene during extra-uterine life, and is then found to involve the left ventricle. With the replacement of a thrombus by connective tissue, and its subsequent calcification, the progressive process in general comes to an end, though in the interior of the thickened valves changes which modify the structure of the new connective tissue may for a long time continue to take place. Usually the tissue- cells and the new blood-vessels diminish in number, the texture becomes more dense, and hyaline degeneration, fatty changes, and calcification often follow. How long the virulent bacteria retain their vitality is not known, but probably they are quickly destroyed. The appearance of new deposits upon old thickenings of the valves is not always dependent upon fresh settlements of bacteria. Very frequently these de- posits are merely thrombi due to roughnesses or other superficial alterations of the endothelium, or to some irregularity of the circu- lation. Such formations are however of considerable importance, inasmuch as they may lead to fresh proliferation, and this may still further impair the efficiency of the valves. The consequence of these affections of the valves is that the circulation of the blood is impeded (Art. 6). The difficulty of emptying the ventricles, and the regurgitation of the blood into them, causes the vessels lying behind the diseased valve to be overfilled and distended. In order to overcome the resulting hindrance to the circulation hypertrophy of the heart-muscle developes, beginning in that part of the organ which has to drive the blood through the diseased valve. References on Endocarditis. Babes : Endocarditis Ann. de I'Inst. de Path, i Bucharest 1890 BiONDi : Endocarditis in tuberculosis Cent./, path. Anat. vi (p. 105) BiRCH-HiRSCHFELD : Tuberculosis of the heart Cent.f. allg. Path, ii (p. 807) VON Buhl : Perforation of the cardiac septa Z. f. Biol, xvi Charcot and Vulpian : Ulcerative endocarditis Gaz. med. de Paris 1865 VON DusCH : Gerhardt's Handb. d. Kinderkr. iv Ebbrth: Diphtheritic endocarditis V.A.oT 1873; Mycotic endocarditis V. A. 72 1878 ; Bakteritische Mykosen Leipzig 1872 E. Frankel and Sanger : Aetiology of endocarditis V. A. 108 1887 Hanot : Tuberculous endocarditis A. gen. de med. 1893 Haushalter : Endocarditis from pneumococci Rev. de med. viii 1888 Heiberg : Ulcerat. endocard. with fungus-growth in the heart F. ^. 56 1872 ; Der puerperale pyamische Process Leipzig 1873 Heller : Bacterial (tuberculous) endocarditis V. A. 62 1874 Howard : Ulcerat. endocard. from Bacill. diphtheriae Johns Hopkins Hosp. Bullet. 1893 HucHARD : Maladies d. cceur et d. vaisseaux Paris 1893 Koster: Embolic endocarditis V. A.72 1878 Kundrat; Ulcerat. endocard. in cancer and tuberculosis Wien. med. Blatter loB5 ART. 9] EEPEKENCES ON ENDOCAEDITIS 43 KusNEZOW : Cavdiao ganglia in endocarditis V. A . 132 1893 Lancekeaux : Ulcerat. endocard. Gaz. me'd. de Paris 1862, A. gen. de me'd. 1873 VON Langek: Vessels of the valves in valvular endocarditis V. A. 109 1887 Ledoux and Lebaud : Ulcerat. endocard. A. gen. de me'd. 1886 Lbyden : Gonorrhoeal endocarditis D.med. Woch. 1893 Lion : Essai sur les endocard. infectieuses Paris 1890 Litten: Z.f. klin. Med. 1881 Mackenzie ; Ulcerat. endocard. Trans. Path. Soc. xxxiii London 1882 Maikr, 11. : Primary diphtheritic endocarditis V. A. Q2 1874 Malvoz : Parasitic tricuspid endocard. Rev. de me'd. vm 1888 Mayer : Pulmonary endocarditis D. A.f. Bin. Med. xxiv Meier, R. . Ueb. Endocarditis ulcerosa Zurich 1870 Nauwerck : Parietal endocarditis D. A.f. klin. Med. 1883 Netter and Martha : Vegetative ulcerat. endocard. in biliary affections A . de physiol. XVIII 1886 Netter : Pneumonic ulcerat. endocard. A. de physiol. xviii 1886 Osler : Malignant endocard. B.M.J. 188S PoNFiCK : Cardiac ulcers V. A. 58 1873 Ribbert : Experim. myo- and endo-carditis Fortschr. d. Med. 1886 RoLLET : Cardiac stenosis Wien. med. Jahrb. 1881 RosENBACH : Theory of endocarditis D. med. Woch. 1887 Sansom : Valvular diseases London 1886 Tapbl : Structure of endocard. vegetations Inaug. Diss. Tubingen 1888 Tripier : Tuberculous endocarditis A . de me'd. exp. ii 1890 Veraguth : Normal and inflamed cardiac valves V. A . 139 1895 ViRCHOw : Puerperal endocard. Monatsschr. f. Geburtsk. 1858 ; Ueh. die Chlorose Berlin 1871 Wbichselbaum : Pathol, anat. of endocarditis Ziegler's Beitrdge iv 1888 ; Aetiology of endocard. Cent. f. Bakteriologie ii 1887 Wilms: Gonorrhoeal endocard. Miinch. med. Woch. 1893 Wyssokowitsch : Acute endocard. Cent. f. med. Wiss. no. 33 1885 Wyssokowitsch and Orth : Theory of endocarditis V. A. 103 1886 ZiEGLER : Structure of endocarditic vegetations Verh. Congr. inn. Med. vii 1888 44 MORBID CHANGES IN THE MYOCARDIUM [CHAP. VI CHAPTER VI MORBID CHANGES IN THE MYOCARDIUM 10. Tlie myocardium is composed chiefly of cylindrical muscle-cells, whose protoplasm is to a great extent differenti- ated into transversely-striated fibrils; these fibrils are firmly united together at their ends or by lateral branches, and are surrounded by a connective tissue containing blood-vessels. Pathological changes may take place both in the muscle-cells and in the connective tissue, but they are more commonly met with in the former structures than in the latter. Atrophic and degenerative changes of the muscle-cells are those that most frequently occur, and they are often the cause of death. In such a case death takes place through paralysis of the heart. Simple atrophy of the heart-muscle is a frequent accompani- ment of senile decay, and of premature marasmus due to malig- nant disease, pulmonary tuberculosis, and other affections. It is indicated by a decrease in the size of the muscle-cells, and often also by a simultaneous increase of yellow pigment-granules within them (Fig. 22), so that the atrophied heart-muscle acquires a brownish colour, the condition being spoken of as brown atrophy. Fatty degeneration of the heart-muscle is apt to occur in the course of various forms of poisoning, of infective diseases, and of long-continued fever; also, and very frequently, as a consequence of chronic gen- eral aad local anaemia, as in steno- sis of the coronary arteries, and of general disorders of the circula- tion, as in valvular disease with imperfect compensation and in pulmonary emphysema, in which the gaseous interchanges neces- sary for the functional activity of the blood are interfered with. Histologically, fatty degeneration is characterised by the appearance of small oil-globules in the muscle-cells (Fig. 23); these are mostly arranged in rows, and Fig. 22. Brown atrophy of the cardiac muscle. (Teased preparor Hon: X 350) Fig. 23. Fatty degeneration of the cardiac mus- CLE. (X 350) AKT. 10] CARDIAC POLYPI 45 in extreme cases may pervade the entire cell. Marked fatty change is indicated to the eye by the yellowish colour imparted to the heart-muscle. In chronic fatty degeneration of the heart, the change often appears in patches, and gives rise to a yellowish mottling of the tissue, which is generally most marked on the inner surface of the heart-wall, the trabeculae, and the papillary muscles. The mottling often recalls the grain of some fine cabinet wood or the pattern of a delicately striated feather. When pigmentation accompanies the fatty change the tint becomes yellowish-brown. Granular and hyaline degeneration of the cardiac muscle, often combined with cloudy swelling or fatty degeneration of the muscular fibres, occur in the course of toxic affections and of the infective fevers (diphtheria, typhoid fever). They are also met with in connexion with traumatic injuries, inflammations, and local ischaemias (Art. 11). These forms of degeneration may, under certain conditions, reach such an intensity that the muscle presents a dull non-lustrous appearance and its section is of a grey or yellowish tint. Hyaline or waxy degeneration may be combined with segmentation or rather fragmentation of the con- tractile substance of the muscle (as in diphtheria); in such cases the lines of rupture do not always seem to correspond with the cell-bo undaries . In dilated hearts, whose substance is soft, flabby, and friable, the muscle-cells are often loosened from each other, the indi- vidual cells being then easily torn apart or actually separated by transverse clefts (Rbnaut); this change has been described as segmentary myocarditis (myoeardite segmentaire). The segmen- tation or dissociation of the fibres is not the manifestation of any definite form of heart-disease, but may occur under the most varied conditions. It is found, for example, in persons who have died from ischaemic softening or myomalacia (Art. 11), from cer- tain forms of poisoning, and from infections, such as typhoid fever, diphtheria, small-pox, pyaemia, and nephritis ; and in per- sons who have died suddenly from violence. It is therefore probable that the dissociation of the muscle-cells may take place partly by reason of morbid changes in the muscles (hyaline degeneration), partly from excessive stimulation of their fibres leading to some perverted mode of contraction (von Reck- linghausen). Thus in most cases the actual segmentation probably takes place in articulo mortis, the degenerative change not leading directly to the separation of the fibres, but only pre- disposing them to rupture. According to Dunin, when decom- position sets in soon after death (owing to the spread of the Bacillus coli within the body), the cementing substance of the muscle-cells may speedily give way. In hearts whose muscle is degenerate large thrombi are often found, particularly in the auricular appendices and in the recesses 46 MOEBID CHANGES IN THE MTOCARDrtJM [CHAP. VI between the trabeculae, whence, by continued deposition, they grow forward into the cavity of the heart, and give rise to the so-called cardiac polypi. In rare cases they form ball-like masses detached from the surface of the heart. Heschl (Oesterr. Z. f. prakt. Heilkunde I860) and Roth {Corresp. f. Schioeizer Aerzte 1884) have described cases of partial calcification of the heart- muscle, taking" the form of whitish points and streaks. Robin and Juhel- Renoy (A. gen. de me'd. 1885) have described large calcareous deposits in fibroid patches or cicatrices of the heart-wall. According to Lancereaux, Iwanowsky, Putjatin (Morbid changes in the cardiac ganglia in chronic diseases of the heart V. A.74: 1878), Ott (Nor- mal and pathological relations of the cardiac ganglia Prag. Z. f. Heitk. ix 1888), and others, in persons who have suffered from chronic heart-disease, degenerative changes and fibrous hyperplasia may be observed about the car- diac ganglia in the septum, in the wall of the auricles, and at the orifices of the aorta and pulmonary artery. , References on Atrophy and Degeneration of the Seart-muscle. Browicz : Changes in the cement-substance of the muscle-fibrils V. A. 134 1893 zuM BuscH : The composition of cardiac thrombi and their relation to the ves- sel-wall Inaug. Diss. Freiburg 1891 CoMBA : Cardiac changes in experimental diphtheria Lo Sperimentale 1894 (with references) CuRSCHMANN : Fatty degeneration from overstrain D. A. f. klin. Med. xii 1874 D0NIN : Causes of fragmentation of the cardiac muscle Ziegler's Beitrdge xvi 1894 EiCHHORST : Die tropliischen Bezieh. d. N. vagi zum Herzmuskel Berlin 1879 EiSENLOHR : Changes in cardiac nerves and ganglia Miinch.palh. Arheiten 1876 Fantino : Myocardial changes after section of the extracardiac nerves Cenl.f. med. Wiss. 1888 Friedreich : VircTiow's Handb. d. spec. Path, v 1867 GoEBEL : Fatty degeneration of the heart Cent. f. allg. Path, iv 1893 (with references) Hamilton: Waxy degeneration Journ. of Anat. xvii 1883-84 Hkssb : The heart in diphtheria Jahrb.f. Kinderheilk. xxxvi 1893 His and Romberg : Cardiac innervation Fortschr. d. Med. viii 1890 Israel : Fragmentation of the myocardium V. A. 13.3 1893 Krbhl : Idiopathic disease of cardiac muscle D. A.f. klin. Med. xlviii 1891 ; Fatty degeneration ibid, li 1893 Leyden and Munk : Die acute Phosphorvergiftung Berlin 1865 LiEBERMEiSTER : Fatty degeneration in fever D. A.f. klin. Med. 1866 Oestreich: Fragmentation of the myocardium V. A. 135 1894 Perls : Fatty degeneration in oligaemia V. A. i>Q 1873 Ponfick: Fatty degeneration in oligaemia Berl. klin. Woch. 1873 Rabot and Philippe : Acute diphtherial myocarditis A. de med. exp. iii 1891 von Recklinghausen and Zenker : Disorders of the myocardium Trans. internal, med. Congr. Ii Berlin 1891 Renaut : Chronic segmentary myocarditis Gaz. med. de Paris 1890 Romberg : The cardiac muscle in typhoid, scarlatina, and diphtheria D. A.f. klin. Med. XLviii 1891 ScHEMEN : The cardiac muscle in pharyngeal diphtheria V. A . 121 1890 Tedeschi: Fragmentation of the myocardium V. A. 128 1892 Unruh: Myocarditis in diphtheria Jahrb.f. Kinderheilk. 1883 AET. 11] SOFTENING OF THE HEART 47 11. Myomalacia cordis is the name given to softening of the cardiac muscle consequent on arterial anaemia or ischaemia, the commonest causes of the ischaemia being sclerosis, atheroma, calci- fication, and thrombosis of the coronary arteries and their branches ; more rarely it may be due to embolism of these arteries. The appearance of the areas of softening differs according to their age and the amount of blood contained in them. Shortly after the occurrence of the ischaemia the patches are still firm, and appear only as dull yellowish discolorations of the heart-muscle. After a time they become softened and friable, and assume a yel- lowish-white tint ; sometimes, if the substance has already soft- ened, the cut surface of a cross-section sinks in so as to become concave. If, in consequence of the obliteration or occlusion of the arteries, an extravasation of blood takes place from the capillaries, a haemorrhagic infarct is produced. The infarcted area is at first either uni- formly dark-red, or mottled with dark-red, brown, and yellow. It may be yellow in the middle and red at the border. After a time it may become greyish-yellow, greyish-brown, or even of a rusty tint. Later on both the anaemic and the haemor- rhagic areas take on a grey- ish translucent appearance, and the surface retracts when cut. The areas of softening are found most frequently in the left ventricle, espe- cially near the apex on the anterior or posterior wall. Occasionally they are found in other places, such as the wall of the right ventricle or of one of the auricles, though they are very seldom found in the latter situa- tion. In rare instances the papillary muscles may be the seat of softening ; under certain conditions indeed an entire papillary muscle may be con- verted into a friable yellowish mass, more or less infiltrated with extravasated blood. If the softening extends to the endocardium. ~a Fig. 24. EUPTUEE OF THE HEAKT IN ABTEBIO- SOLEKOTIC MYOMALACIA. branch of the left coronary artery, the lumen of which has been closed by sclerotic and thrombotic changes point of rupture 48 MORBID CHANGES IN THE MYOCAKDIUM [CHAP. V] > a P'^i thrombi are usually formed over the spot, in the shape of flattened superficial deposits or of polypoid coagula. If the area of softening is extensive, and involves the whole or nearly the whole thickness of the heart- wall, rupture of the heart may result (Fig. 24 6), and blood escapes into the pericar- dial sac. The rent is usually jagged and irregular. The tissue-changes underly- ^//,ii .o ing the varying appearances oi _ { * * I the softened patches . are partly retrogressive and partly con- structive in their character. The original ischaemia brings about the destruction of numbers oi muscle-cells, and consequently in the yellowish-coloured areas can be detected muscle-fibres in different stages of degeneratior and disintegration (Fig. 25 6). whose fragments ultimately break down into granular detritus (c). In the case of small lesions, aftei the disintegration of the muscle- cells the process may come to an end ; in other cases furthei changes take place in the con- nective-tissue elements. These changes are indicated by the fact that the cell-nuclei here and there no longer stain well wit! reagents (